In This Issue —
Outpatient Diagnosis of Acute Chest Pain in Adults
—
Echocardiographic Evaluation of Left Ventricle Functions in Left Ventricle Anterior Infarction
—
Superficial Brachial Artery: Its Embryological and Clinical Significance
—
Left Atrial Myxoma Presenting as Severe Pulmonary Hypertension
—
AHA Releases Statement on Sexual Activity and Cardiovascular Disease
—
Acute Chest Pain in an Adolescent
—
What is the Importance of Aldosterone and Resistin in Resistant Hypertension?
Volume 16, Number 5, September 2013 Pages 161-200
Asian
Journal of
IJCP Group of Publications
CLINICAL CARDIOLOGY
Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor
Volume 16, Number 5, September 2013
Dr Deepak Chopra Chief Editorial Advisor
Padma Shri and Dr BC Roy National Awardee Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor
from the desk of group editor-in-chief 165 Five Foods That Fight High Cholesterol
Dr Praveen Chandra Guest Editor, AJCC praveen.chandra@medanta.org Assistant Editors: Dr Nagendra Chouhan, Dr Dharmendar Jain
AJCC Speciality Panel International Dr Fayoz Shanl Dr Alain Cribier Dr Kohtian Hai Dr Tanhuay Cheem Dr Ayman Megde Dr Alan Young Dr Gaddy Grimes Dr Jung bo Geg Dr Rosli Mohd. Ali Dr S Saito National Dr Mansoor Hassan Dr RK Saran Dr SS Singhal Dr Mohd. Ahmed
Advisory Board Dr PK Jain Dr PK Gupta Dr Naresh Trehan Dr Sameer Shrivastava Dr Deepak Khurana Dr Ganesh K Mani Dr K S Rathor Dr Rajesh Kaushish Dr Sandeep Singh Dr Yugal Mishra Faculty Dr GK Aneja Dr Ramesh Thakur Dr Balram Bhargava Dr HK Bali Dr HM Mardikar
Dr Sanjay Mehrotra Dr Vivek Menon Dr Keyur Parikh Dr Ajit Mullasari Dr Kirti Punamiya Dr MS Hiramath Dr VS Narain Dr SK Dwivedi Dr Raja Baru Panwar Dr Vijay Trehan Dr Rakesh Verma Dr Suman Bhandari Dr Ravi Kasliwal Dr Atul Abhyankar Dr Tejas Patel Dr Samir Dani
REVIEW ARTICLE 166 Outpatient Diagnosis of Acute Chest Pain in Adults
Cardiology: Dr Praveen Chandra, Dr SK Parashar Paediatrics: Dr Swati Y Bhave Diabetology: Dr CR Anand Moses, Dr Sidhartha Das, Dr A Ramachandran, Dr Samith A Shetty ENT: Dr Jasveer Singh, Dr Chanchal Pal Dentistry: Dr KMK Masthan, Dr Rajesh Chandna Gastroenterology: Dr Ajay Kumar, Dr Rajiv Khosla Dermatology: Dr Hasmukh J Shroff, Dr Pasricha, Dr Kaushik Lahiri Nephrology: Dr Georgi Abraham Neurology: Dr V Nagarajan, Dr Vineet Suri Orthopedics: Dr J Maheshwari Journal of Applied Medicine & Surgery: Dr SM Rajendran, Dr Jayakar Thomas Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions
John R. McConaghy, Rupal S. Oza
CLINICAL STUDY 172 Echocardiographic Evaluation of Left Ventricle Functions in Left Ventricle Anterior Infarction
IJCP Editorial Board Obstetrics and Gynaecology: Dr Alka Kriplani, Dr Thankam Verma, Dr Kamala Selvaraj
KK Aggarwal
Monika Maheshwari, SR Mittal
CASE REPORT 178 Superficial Brachial Artery: Its Embryological and Clinical Significance
M Khullar, Meenakshi Khullar
182 Left Atrial Myxoma Presenting as Severe Pulmonary Hypertension
Deep Chandra Pant, Hema Pant
practice guidelineS 184 AHA Releases Statement on Sexual Activity and Cardiovascular Disease
photo quiz 186 Acute Chest Pain in an Adolescent
EXPERT'S OPINION Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com
188 What is the Importance of Aldosterone and Resistin in Resistant Hypertension?
Printed at New Edge Communications Pvt. Ltd, New Delhi E-mail: edgecommunication@gmail.com
SC Tiwari, KK Aggarwal
MEDILAW
Š Copyright 2013 IJCP Publications Ltd. All rights reserved. The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.
190 Can Docs be Booked in 304-A When DMC Says no Negligence?
KK Aggarwal
ALGORITHM
Editorial Policies The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article.
191 Algorithm for the Evaluation of Suspected Orthostatic Hypotension in the Outpatient Setting
Around the Globe 192 News and Views
lighter reading 194 Lighter Side of Medicine
Note: Asian Journal of Clinical Cardiology does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.
IJCP’s Editorial & Business Offices Delhi
Mumbai
Kolkata
Bangalore
Chennai
Hyderabad
Dr Veena Aggarwal 9811036687 E - 219, Greater Kailash, Part - I, New Delhi - 110 048 Cont.: 011-40587513 editorial@ijcp.com drveenaijcp@gmail.com Subscription Dinesh: 9891272006 subscribe@ijcp.com Ritu: 09831363901 ritu@ijcp.com
Mr. Nilesh Aggarwal 9818421222
Ritu Saigal Sr. BM 9831363901
H Chandrashekar GM Sales & Marketing 9845232974
Chitra Mohan Sr. BM 9841213823 40A, Ganapathypuram Main Road Radhanagar Chromepet Chennai - 600 044 Cont.: 22650144 chitra@ijcp.com
Venugopal GM Sales & Marketing 9849083558
Pravin Dhakne 8655611025, 24452066 Unit No. 210 2nd Floor Shreepal Complex, Suren Road, Near Cine Magic Cinema Andheri (E) Mumbai - 400 093 nilesh.ijcp@gmail.com
Flat 7E Merlin Jabakusum 28A, SN Roy Road Kolkata - 700 038 Cont.: 24452066 ritu@ijcp.com
Sr.: Senior; BM: Business Manager; GM: General Manager
Arora Business Centre, 111/1 and 111/2, Dickenson Road (Near Manipal Centre) Bangalore - 560 042 Cont.: 25586337 chandra@ijcp.com
H. No.16-2-751/A/70 First Floor Karan Bagh Gaddiannaram Dil Sukh Nagar Hyderabad 500 059 Cont.: 65454254 venu@ijcp.com
from the desk of group editor-in-chief Dr KK Aggarwal
Padma Shri and Dr BC Roy National Awardee Sr. Physician and Cardiologist, Moolchand Medcity, New Delhi President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Vice President, Elect, IMA Chairman, Ethical Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)
Five Foods That Fight High Cholesterol ÂÂ
Oats give you soluble fiber. Add a banana or some strawberries for more soluble fibers.
ÂÂ
Beans are especially rich in soluble fiber. They also take a while for the body to digest, meaning you feel full for longer after a meal.
ÂÂ
Nuts: Eating almonds, walnuts, peanuts and other nuts is good for the heart. Eating 2 ounces of nuts a day can slightly lower low-density lipoprotein (LDL) by about 5%. Nuts have additional nutrients that protect the heart in other ways.
ÂÂ
Foods fortified with sterols and stanols: Companies are adding them to foods ranging from margarine and granola bars to orange juice and chocolate. They’re also available as supplements. Getting 2 g of plant sterols or stanols a day can lower LDL cholesterol by about 10%.
ÂÂ
Fatty fish: Eating fish 2-3 times a week can lower LDL in two ways: By replacing meat, which has LDL-boosting saturated fats and by delivering LDL-lowering omega-3 fats.
Stay away from saturated and trans fats Saturated fats are found in red meat, milk and other dairy foods and coconut and palm oils. Trans fats are a byproduct of the chemical reaction that turns liquid vegetable oil into solid margarine or shortening and that prevents liquid vegetable oils from turning rancid. Trans fats boost LDL as much as saturated fats do. They also lower protective HDL, rev up inflammation and increase the tendency for blood clots to form inside blood vessels. ■■■■
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
165
REVIEW ARTICLE
Outpatient Diagnosis of Acute Chest Pain in Adults JOHN R. MccONAGHY, RUPAL S. OZA
Abstract Approximately 1 percent of primary care office visits are for chest pain, and 1.5 percent of these patients will have unstable angina or acute myocardial infarction. The initial goal in patients presenting with chest pain is to determine if the patient needs to be referred for further testing to rule in or out acute coronary syndrome and myocardial infarction. The physician should consider patient characteristics and risk factors to help determine initial risk. Twelve-lead electrocardiography is typically the test of choice when looking for ST segment changes, new-onset left bundle branch block, presence of Q waves, and new-onset T wave inversions. For persons in whom the suspicion for ischemia is lower, other diagnoses to consider include chest wall pain/costochondritis (localized pain reproducible by palpation), gastroesophageal reflux disease (burning retrosternal pain, acid regurgitation, and a sour or bitter taste in the mouth), and panic disorder/anxiety state. Other less common but important diagnostic considerations include pneumonia (fever, egophony, and dullness to percussion), heart failure, pulmonary embolism (consider using the Wells criteria), acute pericarditis, and acute thoracic aortic dissection (acute chest or back pain with a pulse differential in the upper extremities). Persons with a higher likelihood of acute coronary syndrome should be referred to the emergency department or hospital.
Keywords: Chest pain, unstable angina acute, myocardial infarction, twelve-lead electrocardiography, acute coronary syndrome
A
pproximately 1 percent of all ambulatory visits in the primary care setting are for chest pain.1 Cardiac disease is the leading cause of death in the United States, yet only 1.5 percent of patients presenting to a primary care office with chest pain will have unstable angina or an acute myocardial infarction (MI).2 The most common causes of chest pain in the primary care population include chest wall pain (20 percent); reflux esophagitis (13 percent); and costochondritis (13 percent),2 although in practice, costochondritis is often included in the chest wall pain category. Other considerations include pulmonary (e.g., pneumonia, pulmonary embolism), gastrointestinal (e.g., gastroesophageal reflux disease [GERD]), and psychological (e.g., anxiety, panic disorder) etiologies, and cardiovascular disorders (e.g., acute congestive heart failure, acute thoracic aortic dissection). Table 1 lists the differential diagnosis of chest pain.3-15 Initial Evaluation Algorithmic approaches to the diagnosis and workup of the patient presenting with chest pain in the
JOHN R. McCONAGHY, MD, CPE, FAAFP, is a professor, the associate residency director, and the practice medical director in the Department of Family Medicine at The Ohio State University, Columbus. RUPAL S. OZA, MD, MPH, is a clinical assistant professor in and the director of the Urban Family Medicine Residency Program at The Ohio State University. Source: Adapted from Am Fam Physician. 2013;87(3):177-182.
166
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
office setting have not been specifically studied. Differentiating ischemic from nonischemic causes often is difficult, and patients with chest pain with an ischemic etiology often appear well. As such, the initial diagnostic approach should always consider a cardiac etiology for the chest pain, unless other causes are apparent.16 The first decision point for most physicians is whether or not the chest pain is caused by coronary ischemia.16 Acute coronary syndrome (ACS) is a constellation of clinical findings that suggests acute myocardial ischemia encompassing unstable angina and acute MI. Angina has been described as deep, poorly localized chest or arm discomfort (pain or pressure) that is reproducibly associated with physical exertion or emotional stress and is relieved promptly with rest or sublingual nitroglycerin.17 Unstable angina is defined as angina at rest, new-onset angina, or angina that has become more severe or longer in duration.18 Acute MI is defined as ST segment changes (elevation or depression) on electrocardiography (ECG) and positive laboratory markers of myocardial necrosis (e.g., troponin I).17 In office and ambulatory settings, the clinical impression is, in most cases, shaped by the presenting symptoms, physical examination, and initial ECG, combined with the patient’s risk of ACS.16,19 The initial goal is to determine if the patient needs to be referred for further testing (e.g., troponin I or
review article Table 1. Differential Diagnosis of Chest Pain Diagnosis
Clinical findings
LR+
LR–
Acute myocardial infarction3
Chest pain radiates to both arms
7.1
0.67
Third heart sound on auscultation
3.2
0.88
Hypotension
3.1
0.96
At least two of the following findings: localized muscle tension; stinging pain; pain reproducible by palpation; absence of cough
3.0
0.47
Gastroesophageal reflux disease5,6
Burning retrosternal pain, acid regurgitation, sour or bitter taste in the mouth; one-week trial of high-dose proton pump inhibitor relieves symptoms
3.1
0.30
Panic disorder/anxiety state7
Single question: In the past four weeks, have you had an anxiety attack (suddenly feeling fear or panic)?
4.2
0.09
Pericarditis8,9
Clinical triad of pleuritic chest pain (increases with inspiration or when reclining, and is lessened by leaning forward), pericardial friction rub, and electrocardiographic changes (diffuse ST segment elevation and PR interval depression without T wave inversion)
NA
NA
Pneumonia10,11
Egophony
8.6
0.96
Chest wall
Heart
pain4
failure12
Pulmonary embolism13,14
Acute thoracic aortic dissection15
Dullness to percussion
4.3
0.79
Fever
2.1
0.71
Clinical impression
2.0
0.24
Pulmonary edema on chest radiography
11.0
0.48
Clinical impression/judgment
9.9
0.65
History of heart failure
5.8
0.45
History of acute myocardial infarction
3.1
0.69
High pretest probability based on Wells criteria
6.8
1.8
Moderate pretest probability based on Wells criteria
1.3*
0.7
Low pretest probability based on Wells criteria
0.1
7.6
Acute chest or back pain and a pulse differential in the upper extremities
5.3
NA
Note: The higher the LR is above 1, the better it rules in disease (greater than 10 is considered good). Conversely, the lower the LR is below 1, the better it rules out disease (less than 0.1 is considered good). LR+ = Positive likelihood ratio; LR– = Negative likelihood ratio; NA = Not available. *Does not change posttest probability. Information from references 3 through 15.
stress testing, coronary angiography) to rule in or out a potentially catastrophic ACS and acute MI. One recent meta-analysis concluded that the history and physical examination were mostly not helpful in diagnosing ACS or acute MI in patients presenting with chest pain, especially in a low prevalence setting.20 Although individual characteristics may not rule in or out a diagnosis, a combination of signs and symptoms may increase diagnostic accuracy.21 Characteristics traditionally associated with increased likelihood of acute MI include male sex plus age older than 60 years; diaphoresis; pain that radiates to the shoulder, neck, arm, or jaw; and a history of angina or acute MI.22 Predictability may be influenced by patient description
of their symptoms. Patients often do not use the term pain to describe their symptoms, but frequently use other terms like discomfort, tightness, squeezing, or indigestion.16 Other clinical features that increase the likelihood of MI in patients with acute chest pain include pain that radiates to both arms (positive likelihood ratio [LR+] = 7.1), a third heart sound on auscultation (LR+ = 3.2), and hypotension (LR+ = 3.1). Clinical features that decrease the likelihood of acute MI include pleuritic chest pain (negative likelihood ratio [LR–] = 0.2), sharp or stabbing chest pain (LR– = 0.3), and chest pain reproduced by palpation (LR– = 0.2 to 0.4).3
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
167
review article The presence or absence of comorbidities, such as diabetes mellitus, tobacco use, hyperlipidemia, or hypertension, as cardiac risk factors weakly predict ACS in patients older than 40 years (LR+ = 2.1 in persons 40 to 65 years of age; LR+ = 1.1 in patients older than 65 years)23; however, evaluating for presence or absence of comorbidities is still an important component of the initial assessment. One recently developed and validated clinical decision rule (Table 2) outlines five items that best predict coronary artery disease as the cause of chest pain: age/sex (55 years or older in men or 65 years or older in women); known coronary artery disease, occlusive vascular disease, or cerebrovascular disease; pain that is worse during exercise; pain not reproducible by palpation; and patient assumption that the pain is of cardiac origin.24 Among those with none or one of these clinical factors, only 1 percent had coronary artery disease, whereas 63 percent of the patients with four or five of the factors had coronary artery disease. The study results suggest that patients with chest pain and four or five of these factors require urgent workup. Physicians should consider applying a validated clinical decision rule to predict heart disease as a cause of chest pain.24 Twelve-lead ECG is typically the test of choice in the initial evaluation of patients with chest pain.19 ST segment changes (elevation or depression), newonset left bundle branch block, presence of Q waves, and new-onset T wave inversion increase the likelihood Table 2. Validated Clinical Decision Rule to Predict CAD as a Cause of Chest Pain Component
Points
Age/sex: men 55 years or older, women 65 years or older
1
Known vascular disease (CAD, occlusive vascular disease, cerebrovascular disease)
1
Pain worse with exercise
1
Pain not elicited with palpation
1
Patient assumes pain is of cardiac origin
1
Likelihood of CAD as Cause of Chest Pain Score
of ACS or acute MI.3,25 Concern based on the clinical impression (history, physical examination, risk factors, and 12-lead ECG) often will influence the physician’s decision regarding whether to refer the patient to a higher level of care (emergency department or hospital) for further workup and treatment, or to look for other possible diagnoses for the chest pain.16,19 Other Diagnostic Considerations If the initial evaluation indicates that a cardiac cause of ACS is less likely, other noncardiac causes of chest pain should be considered. Understanding that there are common conditions that often occur, with the clinical impression, will help lead to a correct diagnosis.
Chest Wall Pain One prospective cohort study identified four clinical factors that predict a final diagnosis of chest wall pain in patients presenting to the primary care office with chest pain: localized muscle tension, stinging pain, pain reproducible by palpation, and the absence of a cough. Having at least two of these findings had a 77 percent positive predictive value for chest wall pain, and having none or one had an 82 percent negative predictive value.4
Costochondritis Often considered a subset of chest wall pain, costochondritis is a self-limited condition characterized by pain reproducible by palpation in the parasternal/ costochondral joints. It is sometimes called Tietze syndrome, which is distinguished from costochondritis by the presence of swelling over the affected joints.26 Costochondritis is a clinical diagnosis and does not require specific diagnostic testing in the absence of concomitant cardiopulmonary symptoms or risk factors.27
GERD Classic symptoms of GERD include a burning retrosternal pain, acid regurgitation, and a sour or bitter taste in the mouth.5 No useful physical examination maneuvers exist to assist in establishing the diagnosis, and there is no standard test to rule it in or out. However, a one-week trial of a high-dose proton pump inhibitor is modestly sensitive and specific for GERD, with modest LRs (LR+ = 3.1; LR– = 0.3).6
Positive likelihood ratio
Negative likelihood ratio
0 to 1 point
1.09
0.00
2 to 3 points
1.83
0.03
Panic Disorder and Anxiety State
4 to 5 points
4.52
0.16
Panic disorder and anxiety state are common. One in four persons with a panic attack will have chest pain
CAD = Coronary artery disease.
168
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
review article and shortness of breath.28 Yet, concomitant panic disorder and chest pain are often not recognized, leading to more testing, follow-up, and higher costs of care.28,29 Panic may cause chest pain and vice versa.28 Several validated brief questionnaires are used to diagnose panic disorder and anxiety state. One question (In the past four weeks, have you had an anxiety attack [suddenly feeling fear or panic]?) is sensitive (93 percent) and modestly specific (78 percent) in detecting panic disorder (LR+ = 4.2; LR– = 0.09).7 Less Common, but Important, Diagnostic Considerations
Pericarditis Pericarditis is the clinical triad of pleuritic chest pain, pericardial friction rub, and diffuse electrocardiographic ST-T wave changes.8 ECG usually demonstrates diffuse ST segment elevation and PR interval depression without T wave inversion. Acute pericarditis should be considered in patients presenting with new-onset chest pain that increases with inspiration or when reclining, and is lessened by leaning forward.9
Pneumonia Community-acquired pneumonia is a cause of chest pain and respiratory symptoms in the outpatient setting. Common symptoms include fever, chills, productive cough, and pleuritic chest pain.30 Fever, egophony heard during auscultation of the lungs, and dullness to percussion of the posterior thorax are suggestive of pneumonia.10 Clinical impression is modestly useful for ruling in or out pneumonia (LR+ = 2.0; LR– = 0.24).10 The test of choice for diagnosing pneumonia is chest radiography,11 although it has been more recently recommended that it be performed only if other diagnoses are being considered in the uncomplicated outpatient setting.31
Heart Failure Most patients with heart failure present with dyspnea on exertion, although some will have chest pain.12 A history of heart failure or acute MI best predicts the presence of heart failure (LR+ = 5.8 and 3.1, respectively).12 Clinical impression/judgment is predictive of heart failure (LR+ = 9.9; LR– = 0.65), as is pulmonary edema on chest radiography (LR+ = 11.0).12
Pulmonary Embolism Diagnosing pulmonary embolism in the office based on signs and symptoms is difficult because of its highly
Table 3. Wells Clinical Prediction Rule for PE Component
Points
Clinical signs of DVT (asymmetric leg swelling, palpable calf pain)
3
Diagnosis of PE is more likely than an alternative diagnosis
3
Heart rate greater than 100 beats per minute
1.5
Previous diagnosis of DVT or PE
1.5
Bed rest immobilization or surgery within the past four weeks
1.5
Hemoptysis
1
Malignancy within the past six months
1
Probability of PE Points
Risk of PE
Probability of PE (%)
0 to 1 point
Low
1.3
2 to 6 points
Moderate
16
Greater than 6 points
High
41
DVT = Deep venous thrombosis; PE = Pulmonary embolism.
variable presentation. Although dyspnea, tachycardia, and/or chest pain are present in 97 percent of those diagnosed with pulmonary embolism,32 there is no single clinical feature that effectively rules it in or out.33 The physician can estimate the patient’s likelihood of pulmonary embolism by using a validated clinical decision rule, such as the Wells criteria (Table 313,34), to determine if further testing should be performed (e.g., d-dimer assay, ventilation-perfusion scan, helical computed tomography of the pulmonary arteries).13,14,35
Acute Thoracic Aortic Dissection Patients with acute thoracic aortic dissection may present with chest or back pain.36 History and physical examination are only modestly useful for ruling in or out the condition; acute chest or back pain and a pulse differential in the upper extremities modestly increase the likelihood of an acute thoracic aortic dissection (LR+ = 5.3).15 REFERENCES 1. Hsiao CJ, Cherry DK, Beatty PC, Rechtsteiner EA. National ambulatory medical care survey: 2007 summary. Natl Health Stat Report. 2010;(27):1-32. 2. Klinkman MS, Stevens D, Gorenflo DW; Michigan Research Network. Episodes of care for chest pain: a preliminary report from MIRNET. J Fam Pract. 1994;38(4):345-352.
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
169
review article 3. Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256-1263.
16. Kontos MC, Diercks DB, Kirk JD. Emergency department and office-based evaluation of patients with chest pain. Mayo Clin Proc. 2010;85(3):284-299.
4. Bösner S, Becker A, Hani MA, et al. Chest wall syndrome in primary care patients with chest pain: presentation, associated features and diagnosis. Fam Pract. 2010;27(4):363-369.
17. Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA focused update of the guidelines for the management of patients with unstable angina/nonST-elevation myocardial infarction (updating the 2007 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [published corrections appear in Circulation. 2011;124(12):e337-e340, and Circulation. 2011;123(22):e625-e626]. Circulation. 2011;123(18): 2022-2060.
5. Zimmerman J. Validation of a brief inventory for diagnosis and monitoring of symptomatic gastro-oesophageal reflux. Scand J Gastroenterol. 2004;39(3):212-216. 6. Wang WH, Huang JQ, Zheng GF, et al. Is proton pump inhibitor testing an effective approach to diagnose gastroesophageal reflux disease in patients with noncardiac chest pain?: a meta-analysis. Arch Intern Med. 2005;165(11):1222-1228. 7. Löwe B, Gräfe K, Zipfel S, et al. Detecting panic disorder in medical and psychosomatic outpatients: comparative validation of the Hospital Anxiety and Depression Scale, the Patient Health Questionnaire, a screening question, and physicians’ diagnosis. J Psychosom Res. 2003;55(6):515-519. 8. Imazio M, Brucato A, Cemin R, et al.; CORP (COlchicine for Recurrent Pericarditis) Investigators. Colchicine for recurrent pericarditis (CORP): a randomized trial. Ann Intern Med. 2011;155(7):409-414. 9. Maisch B, Seferovic’ PM, Ristic’ AD, et al.; Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology. Guidelines on the diagnosis and management of pericardial diseases executive summary. Eur Heart J. 2004;25(7):587-610. 10. Diehr P, Wood RW, Bushyhead J, Krueger L, Wolcott B, Tompkins RK. Prediction of pneumonia in outpatients with acute cough–a statistical approach. J Chronic Dis. 1984;37(3):215-225. 11. Metlay JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA. 1997;278(17):1440-1445. 12. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA. 2005;294(15):1944-1956. 13. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001;135(2):98-107.
18. Braunwald E. Unstable angina. Circulation. 1989;80(2):410-414.
A
classification.
19. Cooper A, Timmis A, Skinner J; Guideline Development Group. Assessment of recent onset chest pain or discomfort of suspected cardiac origin: summary of NICE guidance. BMJ. 2010;340:c1118. 20. Bruyninckx R, Aertgeerts B, Bruyninckx P, Buntinx F. Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis. Br J Gen Pract. 2008;58(547):105-111. 21. Bösner S, Becker A, Abu Hani M, et al. Accuracy of symptoms and signs for coronary heart disease assessed in primary care. Br J Gen Pract. 2010;60(575):e246-e257. 22. Rouan GW, Lee TH, Cook EF, Brand DA, Weisberg MC, Goldman L. Clinical characteristics and outcome of acute myocardial infarction in patients with initially normal or nonspecific electrocardiograms (a report from the Multicenter Chest Pain Study). Am J Cardiol. 1989;64(18):1087-1092. 23. Han JH, Lindsell CJ, Storrow AB, et al. The role of cardiac risk factor burden in diagnosing acute coronary syndromes in the emergency department setting. Ann Emerg Med. 2007;49(2):145-152, 152.e1. 24. Bösner S, Haasenritter J, Becker A, et al. Ruling out coronary artery disease in primary care: development and validation of a simple prediction rule. CMAJ. 2010;182(12):1295-1300. 25. Rude RE, Poole WK, Muller JE, et al. Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients. Am J Cardiol. 1983;52(8):936-942. 26. Proulx AM, Zryd TW. Costochondritis: diagnosis and treatment. Am Fam Physician. 2009;80(6):617-620.
14. Tamariz LJ, Eng J, Segal JB, et al. Usefulness of clinical prediction rules for the diagnosis of venous thromboembolism: a systematic review. Am J Med. 2004;117(9):676-684.
27. Disla E, Rhim HR, Reddy A, Karten I, Taranta A. Costochondritis. A prospective analysis in an emergency department setting. Arch Intern Med. 1994;154(21): 2466-2469.
15. von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection. Arch Intern Med. 2000;160(19):2977-2982.
28. Huffman JC, Pollack MH, Stern TA. Panic disorder and chest pain: mechanisms, morbidity, and management. Prim Care Companion J Clin Psychiatry. 2002;4(2):54-62.
170
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
review article 29. Katerndahl DA, Trammell C. Prevalence and recognition of panic states in STARNET patients presenting with chest pain. J Fam Pract. 1997;45(1):54-63. 30. Watkins RR, Lemonovich TL. Diagnosis and management of community-acquired pneumonia in adults. Am Fam Physician. 2011;83(11):1299-1306. 31. Lim WS, Baudouin SV, Georbe RC, et al.; Pneumonia Guidelines Committee of the BTS Standards of Care Committee. BTS guidelines for the management for community acquired pneumonia in adults: update 2009. Thorax. 2009;64(suppl 3):iii1-iii55.
deep venous thrombosis. Ann Intern Med. 2005;143(2): 129-139. 34. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: Increasing the models utility with the SimpliRED d-dimer. Thromb Haemost. 2000;83(3): 416-420.
32. Perrier A, Desmarais S, Miron MJ, et al. Non-invasive diagnosis of venous thromboembolism in outpatients. Lancet. 1999;353(9148):190-195.
35. Qaseem A, Snow V, Barry P, et al.; Joint American Academy of Family Physicians/American College of Physicians Panel on Deep Venous Thrombosis/ Pulmonary Embolism. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Fam Med. 2007;5(1):57-62.
33. Goodacre S, Sutton AJ, Sampson FC. Meta-analysis: The value of clinical assessment in the diagnosis of
36. Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA. 2002;287(17):2262-2272.
■■■■
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
171
CLINICAL STUDY
Echocardiographic Evaluation of Left Ventricle Functions in Left Ventricle Anterior Infarction Monika Maheshwari*, SR Mittal**
Abstract Assessment of global left ventricle (LV) functions has important diagnostic, prognostic and therapeutic implications in patients with coronary artery disease. 2D-echocardiography with it’s new parameters such as MPI and LAVI is currently the most useful and reproducible noninvasive, investigative modality of choice to assess LV functions in such patients.
Keywords: Global left ventricle functions, 2D-echocardiography
A
ssessment of global left ventricle (LV) functions has important diagnostic, prognostic and therapeutic implications in patients with coronary artery disease.1 Hence, earliest recognition of LV dysfunction is warranted. 2D-echocardiography has gained widespread use in the clinical evaluation of global LV functions because it allows comprehensive evaluation of anatomy and functions in a short period of time and is noninvasive, mobile and relatively inexpensive compared with radionuclide angiography2 and other emerging imaging techniques such as magnetic resonance imaging.3 No risk of ionizing radiation exposure, no need for contrast material and easy and immediate availability makes 2D-echocardiography currently the investigative modality of choice to assess LV functions.4 Aims and Objective ÂÂ
To study LV functions in various subgroups of patients with LV anterior myocardial infarction classified angiographically.
ÂÂ
To correlate LV myocardial performance index (LV-MPI) and left atrial volume index (LAVI) with LV ejection fraction (LVEF).
*Assistant Professor Dept. of Medicine **Ex-Senior Professor and Head Dept. of Cardiology JLN Medical College, Ajmer, Rajasthan Address for correspondence Dr Monika Maheshwari Navin Niwas, 434/10 Bapu Nagar, Ajmer - 305 001, Rajasthan E-mail: Opm11@rediffmail.com
172
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
Material and Methods The present study was conducted at Dept. of Cardiology of Jawaharlal Nehru Medical College and Associate Group of Hospitals, Ajmer, Rajasthan.
Grouping of Subjects Control Group (n = 25): This group consisted of 25 age, sex, body mass index (BMI), pulse and blood pressure matched healthy subjects without history of heart disease, systemic hypertension, diabetes, any other systemic illness and with normal findings in resting and exercise ECG, echocardiography and coronary angiography. Study Group (n = 50): This group consisted of 50 patients with LV anterior myocardial infarction, which were further subdivided into two subgroups according to the infarct related artery. Group 1 (n = 25): Hemodynamically significant stenosis of proximal left anterior descending (LAD) artery. Group 2 (n = 25): Hemodynamically significant stenosis of both LAD and left circumflex (LCx) artery. Inclusion Criteria Patients with ST-segment elevated LV anterior wall myocardial infarction having. ÂÂ History of characteristic ischemic chest pain (>30 minutes) ÂÂ >1 mm ST segment elevation with sequential changes in anterior leads I, aVL, V1-V6. Exclusion Criteria ÂÂ
Inferior/Posterior/Right infarction.
ventricle
myocardial
Clinical Study ÂÂ
Significant valve disease (stenosis/regurgitation).
ÂÂ
Atrial fibrillation, atrial flutter, supraventricular or ventricular ectopics.
frequent
Lead
Criteria
V5
Q ≥3 0ms
1
R/Q ≤ 1
2
Bundle branch block/Advanced atrioventricular block.
R/S ≤ 1
ÂÂ
Significant pericardial effusion.
R/S ≤ 2
ÂÂ
Poor acoustic window.
R ≤ 0.7 mV
ÂÂ
Point each criteria
R/Q ≤ 2 1
Notched R
Design of Study
V6
Q ≥ 30 ms
1
In all patients with isolated LV anterior myocardial infarcts following detailed analysis was done.
R/Q ≤ 1
2
ECG
R/S ≤ 3
A complete and through analysis of various leads was done as described below.5
R < 0.6 mV
Lead
Criteria
Point each criteria
I
Q ≥ 30 ms
1
R/Q ≤ 1
1
R ≤ 0.3 mV II aVF
aVL V1 V2
Q ≥ 40 ms
2
Q ≥ 30 ms
1
Q ≥ 50 ms
3
Q ≥ 40 ms
2
Q ≥ 30 ms
1
R/Q ≤ 1
2
R/Q ≤ 2
1
Q ≥ 30 ms
1
R/Q ≤ 1
1
Any Q
1
S ≥ 1.8 mV
1
R/S ≤ 1 R/Q ≤ 3
1
Notched R Infarct size: Total ECG points X 3 = % LV infarcted. Estimated ejection fraction: 65 - % LV infarcted.
Right and Left Coronary Angiography This was performed through a percutaneus femoral/ radial artery approach under local anesthesia using LAD
Any Q R ≤ 10 ms
1
R ≤ 0.1 mV
Figure 1. Stenosis of isolated proximal LAD artery.
R ≤ 0.1 mV V3
Any Q
LAD
R ≤ 20 ms R < 0.2 mV
1
RV3 ≤ RV1 V4
Q ≥ 20 ms
1
R/Q ≤ 0.5
2
R/S ≤ 0.5 R/Q ≤ 1
LCx
1
R/S ≤ 1 R < 0.7 mV Notched R
Figure 2. Showing stenosis of both LAD and LCx arteries.
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
173
Clinical Study
ECG c d
a Mitral fow ICT ICT=(a-b)-IRT
b ET
IRT IRT=c-d
well-validated and recommended by the American Society of Echocardiography Guidelines.7 Values of left atrial volume were indexed to body surface area (LVAI). The time interval (a) from the cessation to onset of mitral inflow was equal to the sum of isovolumetric contraction time (ICT), ejection time (ET) and isovolumetric relaxation time (IRT). LVET (b) was the duration of LV outflow velocity profile. The sum of ICT and IRT was thus obtained by subtracting b from a. The MPI of combined LV systolic and diastolic function (the sum of ICT and IRT divided by ET) was calculated as ‘a-b’ (Fig. 3). Discussion
LV outfow
Figure 3. Myocardial performance index of combined LV systolic and diastolic function.
Judkin’s left and right-6/Tiger-5 French catheter. Left coronary artery (LCA) was visualized with nonionic dye in RAO caudal 40/40°, RAO cranial 40/30°, LAO cranial 60/35°, LAO caudal 60/40°, AP caudal 0/35° and AP cranial 0/30° views. Right coronary artery (RCA) was visualized in LAO cranial 40° and left lateral views. Views were changed when required for optimal visualization of the coronary arteries. Patients of anterior myocardial infarction showing stenosis of isolated proximal LAD artery (Fig. 1) or stenosis of both LAD and LCx arteries (Fig. 2) with fully patent RCA from proximal to it’s distal end along with it’s branches were included in study. Transthoracic 2D-echocardiography In all patients transthoracic 2D, M-mode, pulsed Doppler echocardiographic examination was performed in left lateral decubitus and supine position using Siemen echocardiographic machine G-50 and CV-70 with 3.5 MHz transducer. LV volumes and ejection fraction were obtained with Simpson’s Biplane method.6 M-mode echocardiograms were recorded from the parasternal window at rest to determine left atrial and LV dimensions. Pulsed Doppler recordings of the mitral flow velocities were obtained from the apical 4-chamber view by placing the sample volume between the tips of the mitral leaflets and LV outflow velocities were obtained by placing the sample volume in the outflow tract below the aortic valve. Estimation of left atrial volume was done by Simpson’s method of disc,
174
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
LV Systolic Functions Mitral valve EPSS and LV end-diastolic and endsystolic dimensions and volumes were increased in both subgroups of anterior myocardial infarction (Table 1), suggestive of LV systolic dysfunction in patients of anterior myocardial infarction compared to control group. However, LV systolic functions were deranged more in subgroup 2 compared to subgroup 1. Percentage of systolic thickening was also significantly lower in group 2 than in the control group and group 1. LVEF measured by M-mode and Simpson’s method and LV fractional shortening were also decreased more in subgroup 2 patients having stenosis of both LAD and LCx arteries compared to subgroup 1 patients having isolated stenosis of LAD artery (Table 2).
LV Diastolic Functions On pulse Doppler of mitral valve, ‘E’ wave peak velocity, velocity time integral and pressure half-time were reduced in both subgroups of anterior myocardial infarction, while ‘A’ wave peak velocity and velocity time integral were increased in both subgroups of anterior myocardial infarction (Table 3), suggestive of impaired relaxation of LV in both subgroups of anterior myocardial infarction compared to control group. However, LV diastolic dysfunction was greater in subgroup 2 compared to subgroup 1.
LV Myocardial Performance Index LV-MPI was significantly increased in both study subgroups as compared to control group (Table 4). We found that LV-MPI is a simpler and reproducible marker of LV functions. It integrates isovolumic and ejection phase indices and therefore becomes abnormal before an ejection phase measure such as Simpson’s
Clinical Study Table 1. LV Systolic Functions Parameters
M-mode echocardiographic parameters Control (n = 25)
Group 1 (LAD) (n = 25)
Group 2 (LAD + LCx) (n = 25)
P value
5.44 ± 2.22
9.20 ± 4.6
11.39 ± 7.02
C vs 1 → *** C vs 2 → ***
44.9 ± 6.38
48.50 ± 92.03
54.2 ± 8.4
C vs 2→ ***
151 ± 52
197.70 ± 92.03
269 ± 105.5
C vs 1 → * C vs 2 → ***
ESD (mm)
27.4 ± 6.36
33.50 ± 10.50
38.6 ± 09.8
C vs 1 → * C vs 2 → ***
ESV (ml/m2)
36.9 ± 20.3
74.90 ± 68.60
107 ± 78.5
C vs 1→ ** C vs 2 → ***
LVEF (%)
77.22 ± 9.92
65.26 ± 18.1
62.27 ± 14.7
C vs 1 → *** C vs 2 → ***
Interventricular septum
45 ± 45
42 ± 43
33 ± 60
NS
Posterior wall
70 ± 53
69 ± 58
48 ± 67
C vs 2 → ***
Mitral valve-EPSS (mm) LV cavity EDD (mm) EDV
(ml/m2)
Percentage of systolic thickening
P value: ***<0.005; **< 0.01; *< 0.025 C = Control group: 1 = Group 1; 2 = Group 2
Table 2. LV Systolic Functions Parameters
2D-echocardiographic parameters Control (n = 25)
Group 1 (LAD) (n = 25)
Group 2 (LAD + LCx) (n = 25)
P value
73.5 ± 9.6
50.9 ± 14.6
46.81 ± 11.8
C vs 1 → *** C vs 2 → ***
39.5 ± 10.1
32 ± 13.10
29.3 ± 9.89
C vs 1 → * C vs 2 → *
Ejection fraction Simpson’s (%) Fractional shortening (%)
P value: ***<0.005; *<0.025 C = Control group: 1 = Group 1; 2 = Group 2
LVEF indicates abnormality.8 Further, it needs no geometric assumptions and provides global assessment of systolic and diastolic functions of LV independent of heart rate and loading conditions.9
Left Atrial Volume Index Though LAD was not significantly larger in patients of anterior myocardial infarction as compared to healthy subjects, LAVI was markedly raised in subgroup 2 patients (Table 4), suggestive of increased LV filling pressure and more advanced LV dysfunction in them.10 Accuracy of measuring anteroposterior dimension of left atrium by M-mode is limited by anatomic confinement afforded by spine and sternum and asymmetrical (pillow-shaped) enlargement of left atrium.11 Hence, we recommend estimating LAVI is superior and more accurate than LAD alone for reflecting LV functions.
Correlation of LV-MPI and LAVI with LVEF On regression analysis, both LV-MPI and LAVI correlated well with LVEF. Patients of subgroup 2 with maximally reduced LVEF (46.8 ± 11%) had largest LAVI (38.76 ± 2.14 ml/m2) and LV-MPI (0.75 ± 0.12). Hence, we interpret that these new markers are valuable tools for clinical and prognostic implications, and should be routinely incorporated in clinical practice. Conclusion LV functions are relatively more deranged in patients of anterior myocardial infarction having stenosis of both LAD and LCx arteries. 2D-echocardiography with it’s new parameters such as MPI and LAVI is currently the most useful and reproducible noninvasive, investigative modality of choice to assess LV functions in such patients.
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
175
Clinical Study Table 3. LV Diastolic Functions Parameters
Pulse Doppler echocardiographic parameters of mitral valve flow Control (n = 25)
Group 1 (LAD) (n = 25)
Group 2 (LAD + LCx) (n = 25)
P value
Velocity (m/s)
0.67 ± 0.15
0.57 ± 0.17
0.54 ± 0.17
C vs 1 → * C vs 2 → **
VTI (cm)
10.50 ± 3.09
8.18 ± 02.29
7.24 ± 1.83
C vs 1 → ** C vs 2 → ***
0.59 ± 0.16
0.56 ± 0.14
0.78 ± 0.64
C vs 1 → *
5.7 ± 1.7
6.16 ± 0.12
7.12 ± 0.81
C vs 2 → ** C vs 1 → * C vs 2 → **
1.21 ± 0.49
1.12 ± 0.67
1.03 ± 0.51
NS
58 ± 16.0
54 ± 17.4
45 ± 11.3
NS
E wave
A wave Velocity (m/s) VTI (cm)
E/A velocity Pressure half-time (ms) LV-IVRT (ms)
110 ± 36.20
118 ± 26.90
121 ± 22.5
C vs 1 → *
LV-IVCT (ms)
38.4 ± 13.70
52.4 ± 16.90
62 ± 13.6
C vs 2 → ** C vs 1 → * C vs 2 → ***
P value: ***<0.005; **<0.01; *<0.025; NS > 0.05 C = Control group: 1 = Group 1; 2 = Group 2
Table 4. Overall Left Ventricle Functions Parameters
Common echocardiographic parameters Control (n = 25)
Group 1 (LAD) (n = 25)
Group 2 (LAD + LCx) (n = 25)
P value
Left atrium (mm)
34.51 ± 6.27
34.8 ± 5.33
36.87 ± 4.43
NS
Left atrium volume index (LAVI) (ml/m2)
24.00 ± 6.20
32.81 ± 8.21
38.76 ± 2.14
C vs 1 → ** C vs 2 → ***
LV-MPI
0.55 ± 0.18
0.62 ± 0.17
0.75 ± 0.12
C vs 1 → ** C vs 2 → ***
P value: ***<0.005; **<0.01; *<0.025; NS > 0.05 C = Control Group: 1 = Group 1; 2 = Group 2
References 1. The Multicentre Post Infarction Research Group. Risk Stratification and survival after myocardial infarction. N Engl J Med 1983;309(6):331-6. 2. Lee D, Fuisz AR, Fan PH, Hsu TL, Liu CP, Chiang HT. Realtime 3-dimensional echocardiographic evaluation of left ventricular volume: correlation with magnetic resonance imaging - validation study. J Am Soc Echocardiogr 2001;14(10):1001-9. 3. Nosir YF, Fioretli PM, Vietter WB, Boersma E, Salustri A, Postma JT, et al. Accurate measurement of left ventricular ejection fraction by three-dimensional echocardiography. A comparison with radionuclide angiograph. Circulation 1996;94(3):460-6. 4. Krenning BJ, Voormolen MM, Roelandt JR. Assessment of left ventricular function by three-dimensional echocardiography. Cardiovasc Ultrasound 2003;1: 12-15. 5. Startt RH, Wagner GS, Idekar RE. Myocardial infarction. In: Comprehensive Electrocardiology. Theory and Practice
176
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
in Health and Disease. Vol. 1 Macfarlane PW, (Ed.), TD Veitch Lawrie, New York 1989:565-629. 6. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2(5):358-67. 7. Lang RM, Bierig M, Devereux RB, Flachskampt FA, Foster E, Pellika PA, et al; Chamber Quantification Writing Group; American Society of Echocardiography’s Guidelines and Standards Committee; European Association of Echocardiography. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European
Clinical Study Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18(12):1440-63. 8. Miller D, Farah MG, Liner A, Fox K, Schluchter M, Hoti BD. The relation between quantitative right ventricular ejection fraction and indices of tricuspid annular motion and myocardial performance. J Am Soc Echocardiogr 2001;17(5):443-7. 9. Krikpatrick JN, Vannuan MA, Narula J, Lang RM. Echocardiography in heart failure: applications, utility,
and new horizons. J Am Coll Cardiol 2007;50(5): 381-96. 10. Kedia G, Habibzadeh MR, Kudilhipudi V, Molls F, Sorrell VL. Using traditional measurements of the left atrial diameter to predict the left atrial volume index. Echocardiography 2008;25(1):36-9. 11. Lester SJ, Ryan EW, Schiller NB, Faster E. Best method in clinical practice and in research studies to determine left atrial size. Am J Cardiol 1999;84(7):829-32.
■■■■
Intense lifestyle changes and metformin both helped modify lipid particles in patients with type 2 diabetes, presumably improving their cardiovascular risk profile, according to a new study reported online in the Journal of Clinical Endocrinology & Metabolism. In a subgroup analysis of the Diabetes Prevention Program, patients who were randomized to either metformin or to an intense lifestyle intervention had lower levels of various particles of low-density lipoprotein (LDL) cholesterol, and increases in high-density lipoprotein (HDL) particles. According to Ronald Goldberg, MD, principal investigator of the Diabetes Research Program at the University of Miami, these findings demonstrate that the same therapies used to slow the onset of diabetes also may help allay the risk of heart disease.
A remote preconditioning procedure used prior to coronary artery bypass graft (CABG) surgery significantly improved perioperative myocardial protection among surgical patients treated at a single center in Germany. More important, long-term follow-up suggested that patients who underwent ischemic preconditioning had a lower risk of mortality compared with patients who underwent conventional CABG surgery. The primary endpoint of the study was cardiac damage reflected by the release of the biomarker troponin I, which was significantly reduced in patients undergoing remote preconditioning, indicating that in fact that there was cardiac protection.
Among patients with non-ST-segment elevation acute coronary syndrome (ACS), pre-treatment with prasugrel (Effient) before angiography did not improve outcomes and worsened bleeding, a randomized trial showed. The rate of cardiovascular death, myocardial infraction, stroke, urgent revascularization or glycoprotein IIb/IIIa inhibitor rescue therapy through Day 7 was 10% with pre-treatment of all patients and 9.8% when prasugrel was given only after angiography resulted in planned use of percutaneous coronary intervention (hazard ratio [HR] 1.02, 95% confidence interval [CI] 0.84-1.25). That lack of efficacy was accompanied by a significant increase in all TIMI major bleeding - regardless of whether it was related to CABG - through Day 7 (2.6% vs 1.4%; HR 1.90, 95% CI 1.19-3.02). These findings were reported by Gilles Montalescot, MD, PhD, of Pitié-Salpêtrière University Hospital in Paris at the European Society of Cardiology meeting and were published simultaneously online in the New England Journal of Medicine. (Source: Medpage Today)
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
177
CASE REPORT
Superficial Brachial Artery: Its Embryological and Clinical Significance M Khullar*, Meenakshi Khullar**
Abstract The principal arteries of the upper limb show a wide range of variations that are of considerable interest to orthopedic surgeons, plastic surgeons, radiologists and anatomists. We present here a case of bilateral superficial brachial artery found during the routine dissection of the upper limbs of a 50-year-old female cadaver. In both the limbs, the third part of the axillary artery divided into superficial brachial and deep brachial arteries; denominated according to their relation to the median nerve. The superficial brachial artery continued in the arm without giving any branches and ended in the cubital fossa dividing into radial and ulnar arteries. The deep brachial artery gave rise to anterior circumflex humeral, posterior circumflex humeral and profunda brachii arteries. Earlier superficial brachial artery has been reported with a prevalence rate varying from 0.2 to 25% but bilateral variation is extremely rare. The great variability of this arterial pattern may be attributed to the failure of regression of some paths of the embryonic arterial trunks.1 The embryological and clinical significance of this variant are also discussed in detail.
Keywords: Axillary artery, superficial brachial artery, deep brachial artery
A
xillary artery (AA) is a continuation of the subclavian artery from the outer border of the first rib. It ends at the inferior border of the teres major and continues in the arm as brachial artery. According to textbooks, an AA penetrates the dorsoventral divisions of the brachial plexus by passing between the lateral and medial roots of the median nerve. Rarely, an aberrant AA is unable to penetrate the brachial plexus. In this case, the AA is positioned superficial to the brachial plexus and then, this is known the superficial brachial artery (SBA).
The SBA has been reported by many authors because of its relatively high frequency in comparison with other vascular variations.2,3 It is necessary, however, to pay attention to the branches originating from the aberrant AAs, in addition to the various courses of the AA, in order to understand their morphogenesis. Case report During the routine undergraduate dissections on the upper limbs of a 50-year-old female cadaver, it was *Assistant Professor Dept. of Anatomy Guru Gobind Singh Medical College Faridkot, Punjab Address for correspondence Dr Meenakshi Khullar 43, Vikas Vihar (Phase-1), Ferozepur City - Punjab E-mail: meenakshikhullar8@gmail.com
178
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
observed that on both the sides, the third part of the AA after giving the subscapular artery bifurcated into a SBA and a deep brachial artery. The SBA descended superficial to the lateral root of the median nerve; did not give any branch in the arm and continued as the brachial artery proper. Finally, on reaching the cubital fossa it terminated by dividing into radial and ulnar arteries. The deep brachial artery passed deep to the medial root of the median nerve and gave anterior and posterior circumflex humeral branches of AA and profunda brachii branch of brachial artery. Then it terminated by giving twigs to the muscles of arm (Fig. 1). Discussion Variations in the arterial pattern of the upper limb are common and have been reported by several investigators.1 The presence of a SBA and the usual pattern of its branching in the upper arm or forearm have also been reported.4-6 The definition of the SBA was set for the first time by Adachi in 1928 and runs as follows: â&#x20AC;&#x153;The SBA is the one that runs superficial to the median nerve.â&#x20AC;?7 It may replace the main trunk or may be accompanied by an equally important, less important or more important trunk running deep to median nerve. Table 1 shows the prevalence of SBA as observed by different authors from time-to-time.
case report
SBA
SBA
(I)
(II)
UA
SPA (III)
AIA MA
MA MA
AIA
AIA
SC
SPA (IV)
RA
AIA MA
UA UA
SPA (V)
Figure 2. Stages of development of arteries of upper arm. Figure 1. Photograph showing the third part of the axillary artery (AA) dividing into the superficial brachial artery (SBA) and the deep brachial artery [BA(p)]; MN(lr) - (lateral root of median nerve) , MN(mr) - (medial root of the median nerve), MN (median nerve).
SC = Subclavian artery; MA = Median artery; AIA = Anterior interosseous artery; SBA = Superficial brachial artery; UA = Ulnar artery; SPA = Superficial palmar arch; RA = Radial artery.
artery fuses with the lower portion of interosseous artery and ultimately forms the main channel for the digital branches becoming the principle artery of the forearm.
Ontogeny The embryological background of these variations in the vasculature of the upper limb may be explained as abnormal deviations in the normal vascular patterns. Arey and Jurjus mentioned six explanations for the variations observed:8,9 ÂÂ
The choice of unusual paths in the primitive vascular plexus
ÂÂ
The persistence of vessels which are normally obliterated
ÂÂ
The disappearance of vessels which are normally retained
ÂÂ
An incomplete development
ÂÂ
The fusion and absorption of parts which are normally distinct
ÂÂ
A combination of factors leading to an atypical pattern normally encountered.
Ontogenic basis of the present case can be easily made out if we look at Singer’s five stages of development of the brachial artery (Fig. 2):10 ÂÂ
ÂÂ
Stage I: Originally the subclavian artery extends to the wrist, where it terminates by dividing into terminal branches for the fingers. The distal portion of the artery becomes the interosseous artery of the adult. Stage II: The median artery arises from the interosseous artery and becomes larger while interosseous artery subsequently undergoes retrogression. During this process, the median
ÂÂ
Stage III: In embryos of 18 mm, the ulnar artery arises from brachial artery and unites distally with the median artery to form superficial palmar arch. Digital branches arise from this arch.
ÂÂ
Stage IV: In embryo of 21 mm length, the SBA develops in the axillary region and traverses the medial surface of the arm and runs diagonally from the ulnar to the radial side of the forearm to the posterior surface of the wrist. There it divides over the carpus into branches for the dorsum of the thumb and index finger.
ÂÂ
Stage V: Finally three changes occur. When the embryo reaches the length of 23 mm the median artery undergoes retrogression becoming a small slender structure, now known as 'arteria nervi mediani'. The SBA gives off a distal branch, which anastomoses with the superficial palmar arch already present. At the elbow an anastomotic branch between brachial artery and SBA becomes enlarged sufficiently to form with the distal portion of the latter, the radial artery, as a major artery of the forearm; the proximal portion of the SBA atrophies correspondingly.10
In the present case, it seems that in Stage III of Singer, ulnar artery came from brachial artery as usual.10 SBA continued as radial artery and anastomosis between SBA and brachial artery developed normally (See Fig. 3). However, brachial artery between origin of SBA and ulnar artery (‘A' in Fig. 3) retrogressed and lost its communication with common interosseous
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
179
case report Clinical Significance
B
A
SBA
C
B
A
C RA
UA
MA
MA
UA AIA
RA
AIA
SBA
SPA "A"
SPA "B"
Figure 3. Showing the normal development of the brachial artery in “A” and that in the present case in “B”. SBA = Superficial brachial artery; RA = Radial artery; UA = Ulnar artery; MA = Median artery; AIA = Anterior interosseous artery; SPA = Superficial palmar arch.
Table 1. Showing the Incidence of the SBA in Various Studies Name of Author
Year
% of cases with SBA
Quain12
1844
0.2
Gruber13
1848
0.4
Muller14
1903
1
Adachi7
1928
3.1
Miller15
1939
3
McCormack et al6
1953
0.12
Skopakoff4
1959
19.7
Fuss et al5
1985
17
Rao and Chaudhary16
2001
4.2
Rodriguez-Niedenführ et al17
2001
4.9
al18
2002
6
Kachlik et al19
2010
5
Patnaik et
artery. The SBA failed to retrogress and continued to supply radial artery. The anastomosis between SBA and brachial artery (‘B’ in Fig. 3), which usually forms proximal part of radial artery now formed proximal part of ulnar artery, thus giving appearance that ulnar artery and radial artery are terminal branches of SBA and common interosseous artery (‘C’ in Fig. 3) came as a branch of ulnar artery.
180
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
Gonzalez-Compta highlighted the diagnostic, interventional and surgical significance of such a vascular variation.11 Diagnostically, it may disturb the evaluation of angiographic images. Interventionally, accidental puncture of superficially placed arteries may occur while attempting venipuncture. Surgically, it is vulnerable in both orthopedic and plastic surgery operations. Hence, the anatomic knowledge of the vascular patterns of upper limb is of crucial importance not only for neurosurgeons, but for all those involved in radiodiagnostics, particularly in cases involving traumatic injuries, as improved knowledge would allow more accurate diagnostic interpretation and surgical treatment. References 1. Rodríguez-Baeza A, Nebot J, Ferreira B, Reina F, Pérez J, Sañudo JR, et al. An anatomical study and ontogenetic explanation of 23 cases with variations in the main pattern of the human brachio-antebrachial arteries. J Anat 1995;187(Pt 2):473-9. 2. Aharinejad S, Nourani F, Hollensteiner H. Rare case of high origin of the ulnar artery from the brachial artery. Clin Anat 1997;10(4):253-8. 3. Jurjus A, Sfeir R, Bezirdjian R. Unusual variation of the arterial pattern of the human upper limb. Anat Rec 1986;215(1):82-3. 4. Skopakoff C. Variability of branches and distribution of the superficial brachial artery. Anat Anz 1959;106 (17-20):356-68. 5. Fuss FK, Matula CW, Tschabitscher M. The superficial brachial artery. Anat Anz 1985;160(4):285-94. 6. McCormack LJ, Cauldwell EW, Anson BJ. Brachial and antebrachial arterial patterns; a study of 750 extremities. Surg Gynecol Obstet 1953;96(1):43-54. 7. Adachi B. Arterensystem des japaner. Kyoto 1928; 1:205-10. 8. Arey LB. Development anatomy. In: Development of Arteries. 6th edition, WB Sounders Copmany: Philadelphia 1957:p.375-7. 9. Jurjus AR, Correa-De-Aruaujo R, Bohn RC. Bilateral double axillary artery: embryological basis and clinical implications. Clin Anat 1999;12(2):135-40. 10. Singer E. Embryological pattern persisting in the arteries of the arm. Anat Rec 1933;55(4):403-9. 11. Gonzalez-Compta X. Origin of the radial artery from the axillary artery and associated hand vascular anomalies. J Hand Surg Am 1991;16(2):293-6.
case report 12. Quain R. Anatomy of the arteries of the human body. Taylor & Wolton: London 1844:p.326-37.
17. Rodríguez-Niedenführ
M,
Vázquez
T,
Nearn
L,
Ferreira B, Parkin I, Sañudo JR. Variations of the arterial
13. Gruber W. Zur Anatomie der Arteria radialis. Arch Anat Physiol Wissen Med 1864:p.434-55.
pattern in the upper limb revisited: a morphological and
14. Muller E. Beitrage zur Morphologie des Gefässytstems. I. Die Armarterien des Menschen. Anat Hefte 1903;22:377-575.
2001;199(Pt 5):547-66.
15. Miller RA. Observations upon the arrangement of the axillary artery and brachial plexus. Am J Anat 1939;64(1):143-63. 16. Rao PV, Chaudhary SC. Superficial brachial artery terminating as radial and superficial ulnar arteries: a case report. Centr Afr J Med 2001; 47(3):78-80
statistical study, with a review of the literature. J Anat 18. Patnaik VVG, Kalsey G, Singla RK. Branching pattern of brachial artery: a morphological study. J Anat Soc Ind 2002;51(2):176-86. 19. Kachlik D, Konarik M, Baca V. Vascular patterns of upper limb: an anatomical study with accent on superficial brachial artery. Bosn J Basic Med Sci 2011;11(1):4-10.
■■■■
Vitamin D No Help for High BP in Older Adults Supplementation with high doses of oral cholecalciferol (or vitamin D3) every three months did not have a significant effect on blood pressure (BP) in older patients with isolated systolic hypertension, a small randomized trial showed. At both three months and one year, there were no differences in office BP between the supplementation and placebo groups, according to Miles Witham, PhD, of the University of Dundee in Scotland and colleagues.
Preterm Birth Tied to Smaller Right Ventricle Preterm babies were more likely than term babies to have a smaller right ventricle and enlarged right ventricular mass, researchers found. Compared with babies who were born at term, preterm birth was associated with small right ventricle (end diastolic volume 79.8 ml/m2 vs 88.5 ml/m2, p < 0.001) and large right ventricular mass (24.5 g/m2 vs 20.3 g/m2, P <0.001), according to Paul Lesson, PhD, of the John Radcliffe Hospital in Oxford, and colleagues.
High Normal PTH Still Poses Heart Risk Even when they’re within the normal range, higher levels of parathyroid hormone (PTH) are associated with heart disease in older patients, researchers found. In a cross-sectional population study, older patients in the highest quintile of normal serum PTH levels had a significantly higher risk of cardiovascular disease compared with those in the lowest quintile (OR 2.22, 95% CI 1.39-3.56), Elisabeth Eekhoff, PhD, of VU University Medical Center in Amsterdam and colleagues reported online in the Journal of Clinical Endocrinology and Metabolism. (Source: Medpage Today)
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
181
CASE REPORT
Left Atrial Myxoma Presenting as Severe Pulmonary Hypertension Deep Chandra Pant,* Hema Pant**
Abstract Myxomas are usually benign tumors of the heart and their most common site of presentation is left atrial septal region. 2-D transthoracic or transesophageal echocardiography is useful in the diagnosis of cardiac myxoma and allows determination of site of tumor attachment and tumor size, which are important considerations in planning of surgical excision.
Keywords: Atrial myxoma, embolic infarcts, tumor plop
M
yxomas are usually benign tumors of the heart and their most common site of presentation is left atrial septal region. These can be solitary or multiple (usually familial) and present more commonly in females. Patients can present with episodes of embolic infarcts, Raynaudâ&#x20AC;&#x2122;s phenomenon and symptomatology can mimic those of severe mitral stenosis. These tumors respond very well to curative excision and do not usually recur unless they are part of familial syndromes.
Case Report A 48-year-nondiabetic, nonhypertensive, nonsmoker gentleman presented with 2-year history of shortness of breath, exertional chest pain and exertional dizziness. Breathlessness had increased to New York Heart Association (NYHA) Class III/IV at the time of presentation with history of pedal edema, congested neck veins and history of paroxsysmal nocturnal dyspnea since one month. There was no history of postural aggravation of his symptoms or of syncope. On examination, patient was of normal built, afebrile, pulse rate was 100/min (normal volume, regular), blood pressure was 110/76 mmHg, jugular venous pressure
*Associate Professor Dept. of Cardiology **Assistant Professor Dept. of Pathology UFHT Medical College, Haldwani, Uttarakhand Address for correspondence Dr Deep Chandra Pant Associate Professor Dept. of Cardiology UFHT Medical College, Haldwani, Uttarakhand E-mail: pantpgimer@yahoo.co.in
182
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
(JVP) was not raised, 6 cm congestive hepatomegaly was seen with pitting pedal edema. On examination of cardiovascular system, S1 was normal, P2 component of S2 was loud, S3, S4 was not heard and there was a short mid-diastolic murmur, which did not radiate and there was no positional variation of the murmur. No additional sounds were heard. Examination of chest revealed fine basilar crepitations. On investigation, his hemogram showed normochromic, normocytic anemia, normal erythrocyte sedimentation rate (ESR) with normal reticulocyte count and hemoglobin of 9 g/dl. Blood biochemistry was within normal limits. Electrocardiogram (ECG) revealed a normal sinus rhythm with evidence of left atrial enlargement. Chest X-ray PA view revealed normal cardiac silhouette with mild pulmonary plethora. Two-dimensional (2D) echocardiography revealed 55 Ă&#x2014; 26 mm mass attached to left atrial septum and protruding into mitral valve orifice resulting in severe left inflow obstruction with mean diastolic gradient across the valve of 20 mmHg. Mild tricuspid regurgitation (TR) was seen with TR gradient of 76 mmHg. There was no mitral regurgitation or evidence of rheumatic activity on any of the valves. His left ventricle systolic function was within normal limits. Rest of the echocardiographic findings were within normal limits. A diagnosis of left atrial myxoma with severe pulmonary venous hypertension with severe pulmonary arterial hypertension with congestive heart failure was made. Patient was referred to Dept. of Cardiothoracic Surgery for evaluation for excision of the tumor.
case report
Discussion Atrial myxomas are the most common primary heart tumors. Myxomas account for 40-50% of the primary cardiac tumors. Most cases are sporadic and 10% tumors can be familial. Most common site of attachment is at the border of the fossa ovalis in the left atrium, although myxomas can originate from the posterior atrial wall, the anterior atrial wall or the atrial left atrial appendage. Early diagnosis is a challenge because of nonspecific symptoms. 2D echocardiography is the diagnostic procedure of choice. Left atrial myxoma may present with general malaise, fever, embolic phenomenon like embolic cerebral infarcts or symptoms mimicking mitral stenosis.1,2 The common clinical presentation mimics that of mitral valve disease either stenosis due to tumor prolapse into mitral orifice, or regurgitation due to tumorinduced valvular trauma.4 Ventricular myxomas may cause outflow obstruction similar to that caused by subaortic or subpulmonic stenosis. The symptoms and signs of myxomas may be of sudden onset or positional in nature, reflecting changes in tumor position due to gravity and auscultatory findings, termed as ‘tumor plop’, is a characteristic low-pitched sound that may be audible during early or mid diastole and is thought to result from the tumor abruptly stopping as it strikes the ventricular wall. Presentation of cardiac myxoma with severe pulmonary hypertension as a result of left inflow obstruction is theoretically possible but has not been reported in medical literature till now. This is the first case report of left atrial myxoma presenting with secondary severe pulmonary hypertension.
2D transthoracic or transesophageal echocardiography is useful in the diagnosis of cardiac myxoma and allows determination of site of tumor attachment and tumor size, which are important considerations in planning of surgical excision. Computed tomography (CT) and particularly magnetic resonance imaging (MRI) may provide important information regarding size, shape, composition and surface characteristics of the tumor.3 Although cardiac catheterization and angiography have previously been performed routinely before surgery, catheterization of the chamber from which the tumor arises carries the risk of tumor emboli. Catheterization is no longer considered mandatory when adequate noninvasive information is available and other cardiac diseases (e.g. coronary artery disease) are not considered likely. Suggested reading 1. Pinede L, Duhaut P, Loire R. Clinical presentation of left atrial cardiac myxoma. A series of 112 consecutive cases. Medicine 2001;80(3):159-72. 2. Aggarwal SK, Barik R, Sarma TC, Iyer VR, Sai V, Mishra J, et al. Clinical presentation and investigation findings in cardiac myxoma, new insights from the developing world. Am Heart J 2007;154(6):1102-7. 3. Sharpiro LM. Cardiac tumors: diagnosis and management Heart 2001;85(2):218-22. 4. Whitlock R, Evans R, Lonn E, Teoh K. Giant left atrial myxoma and associated mitral valve pathology. J Cardiothoracic Vasc Anesth 2007;21(1):103-5. 5. Reynen K. Cardiac myxomas. N Engl J Med 1995;333 (24):1610-7.
■■■■
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
183
practice guidelineS
AHA Releases Statement on Sexual Activity and Cardiovascular Disease
D
ecreased sexual activity and sexual dysfunction are common in patients with cardiovascular disease (CVD), and can lead to anxiety and depression. The American Heart Association (AHA) has published a scientific statement synthesizing data relevant to sexual activity and heart disease to provide recommendations and to foster communication between physicians and patients about sexual activity.
General Recommendations Patients with stable CVD who have no or minimal symptoms during routine activities, and who are found on clinical examination to be at low risk of cardiovascular complications, can safely engage in sexual activity. In patients who are at greater risk or in whom risk is unknown, exercise stress testing should be performed. If these patients can exercise at 3 to 5 metabolic equivalents or more without angina, excessive dyspnea, ischemic ST-segment changes, cyanosis, hypotension, or arrhythmia, they can be advised that sexual activity is reasonable. Cardiac rehabilitation and regular exercise can be useful to reduce the risk of cardiovascular complications. Patients with unstable, decompensated, or severe symptomatic CVD, and those who experience cardiovascular symptoms precipitated by sex, should defer sexual activity until their condition is stabilized and optimally managed. Women with CVD should be counseled about the safety and advisability of contraceptive methods and pregnancy, when appropriate.
symptoms during mild to moderate physical activity at least one week after uncomplicated myocardial infarction; uncomplicated vascular access site several days after percutaneous coronary intervention for complete coronary revascularization; or a well-healed sternotomy six to eight weeks after standard coronary artery bypass graft surgery or noncoronary open heart surgery. Exercise stress testing can be considered to assess the extent and severity of residual ischemia in patients with incomplete coronary revascularization. Sexual activity should be deferred in patients with unstable or refractory angina until their condition is stabilized and optimally managed.
Heart Failure Sexual activity is reasonable in patients with compensated or mild heart failure. It is not advised for patients with decompensated or advanced heart failure until the condition is stabilized and optimally managed.
Valvular Heart Disease Sexual activity is reasonable in patients with mild or moderate valvular heart disease and no or mild symptoms, and in those with normally functioning prosthetic valves, successfully repaired valves, and successful transcatheter valve interventions. Sexual activity is not advised for patients with severe or significantly symptomatic valvular disease until the condition is stabilized and optimally managed.
Disease-Specific Recommendations
Arrhythmias
Coronary Artery Disease
Sexual activity is reasonable in patients with arrhythmias if they meet one or more of the following criteria: a well-controlled ventricular rate in patients with atrial fibrillation or atrial flutter; a history of atrioventricular nodal reentry tachycardia, atrioventricular reentry tachycardia, or atrial tachycardia with controlled arrhythmias; implantation of a pacemaker or an internal cardioverter-defibrillator (ICD) for primary prevention; or use of an ICD for secondary prevention in a patient who can tolerate moderate exercise without
Sexual activity is reasonable in patients with coronary artery disease if they meet one or more of the following criteria: no or mild angina; no cardiac
Source: Adapted from Am Fam Physician. 2012;86(11):1074-1076.
184
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
practice guidelineS experiencing ventricular tachycardia or fibrillation, and who does not receive frequent multiple appropriate shocks. Sexual activity should be deferred in patients with atrial fibrillation and a poorly controlled ventricular rate, uncontrolled or symptomatic supraventricular arrhythmias, and spontaneous or exercise-induced ventricular tachycardia until the condition is optimally managed. Patients with an ICD who have received multiple shocks also should defer sexual activity until the arrhythmia is stabilized and optimally managed.
Congenital Heart Disease Sexual activity is reasonable in most patients with congenital heart disease who do not have decompensated or advanced heart failure, severe or significantly symptomatic valvular disease, or uncontrolled arrhythmias.
Hypertrophic Cardiomyopathy Sexual activity is reasonable in most patients with hypertrophic cardiomyopathy. It should be deferred in patients with severe symptoms until the condition is stabilized. Cardiovascular Drugs and Sexual Function Several classes of cardiovascular drugs, including beta blockers and diuretics, are thought to cause erectile dysfunction. However, recent studies have not shown a clear relationship between this condition and many contemporary cardiovascular drugs. Cardiovascular drugs that can improve symptoms and survival should not be withheld because of concerns about their potential effect on sexual function. If a patient who is being treated with a cardiovascular drug reports sexual dysfunction, efforts should be made to assess whether the dysfunction is more likely related to underlying vascular or cardiac disease or psychological factors. Pharmacotherapy for Sexual Dysfunction
Phosphodiesterase-5 Inhibitors Phosphodiesterase-5 inhibitors are useful in the treatment of erectile dysfunction in patients with stable CVD. However, they should not be used in patients receiving nitrate therapy, and nitrates should
not be administered within 24 hours of sildenafil or vardenafil, or within 48 hours of tadalafil. The safety of these drugs in patients with acute aortic stenosis or hypertrophic cardiomyopathy is not known.
Estrogen Vaginal dryness and pain with sexual intercourse are common in postmenopausal women. Vaginal administration of estrogen can relieve symptoms of vaginal atrophy, and topical estrogen preparations can also be used on the vulva to treat insertional pain. Concerns have been raised that combined estrogen and progesterone therapy may increase cardiovascular risk in women, but trials of estrogen therapy alone did not show any increased risk. Furthermore, systemic absorption of estrogen with vaginal administration is minimal, so topical estrogen therapy is unlikely to pose any cardiac risk in women with CVD.
Herbal Medications Numerous herbal medications are advertised for the treatment of sexual dysfunction. Some of these may contain drugs such as phosphodiesterase-5 inhibitors (or chemically similar substances), yohimbine, or l-arginine. These substances can interact with cardiovascular medications, have vasoactive or sympathomimetic properties, can elevate or reduce blood pressure or have been associated with adverse outcomes in patients with coronary artery disease. It may be reasonable to caution patients with CVD about the potential for adverse effects with the use of herbal medications with unknown ingredients that are taken for the treatment of sexual dysfunction. Psychological Issues and Patient Counseling Changes in sexual activity after a cardiac event may impair a patient’s quality of life, negatively affect psychological health, and strain marital or other intimate relationships. The resulting anxiety and depression may be an important contributing cause of sexual dysfunction, including decreased libido, difficulty with arousal and orgasm, and dyspareunia. Physicians should assess patients with CVD for anxiety and depression, and refer patients and their partners for sexual counseling, if necessary.
■■■■
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
185
photo quiz
Acute Chest Pain in an Adolescent
A
16-year-old patient presented to the emergency department with sudden onset of chest pain and shortness of breath while playing basketball. There was no history of trauma. Physical examination revealed an otherwise healthy male in no acute distress with a blood pressure of 129/66 mm Hg, heart rate of 71 beats per minute, respiratory rate of 20 breaths per minute, and a pulse oximetry reading of 97 percent. Swelling and crepitus were noted in the neck. On auscultation, a crunching sound was noted over the precordium with each heartbeat. Pulmonary examination was unremarkable, and results of electrocardiography were normal. Chest radiography was performed (see accompanying figure).
Question Based on the patient's history and physical examination, which one of the following is the most likely diagnosis? A. Aortic dissection. B. Pneumomediastinum. C. Atypical chest pain. D. Reactive airways disease. E. Esophageal rupture.
Source: Adapted from Am Fam Physician. 2006;74(3):473-474.
186
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
SEE THE FOLLOWING PAGE FOR DISCUSSION.
photo quiz Discussion The answer is B: pneumomediastinum. Physical examination demonstrated subcutaneous emphysema and Hamman's sign, the audible crunching accompanying each heartbeat. These findings are characteristic of pneumomediastinum. Chest pain and dyspnea are the most common symptoms. The chest radiograph shows a radiolucent outline of the mediastinum as well as the continuous diaphragm sign.1 Pneumomediastinum is extra-alveolar air within the mediastinum. Numerous etiologies have been identified, including penetrating or crushing chest trauma, rapid shearing of the fixed carina, and increased intrabronchial pressure.2 Other causes include esophageal rupture in Boerhaave's syndrome, repeated Valsalva maneuver during inhalation drug use, or colonic perforation during colonoscopy.3-5 Spontaneous pneumomediastinum is rare, especially episodes not related to chest trauma, tracheobronchial or esophageal procedures, mechanical ventilation, cardiac catheterization, or chest surgery. Pneumomediastinum mainly affects previously healthy young men.6 Pulmonary alveolar rupture is the most common etiology. Potential precipitating conditions include asthma, vomiting, Valsalva maneuver, esophageal rupture, and intense exercise or sports participation.7 Rapid recovery is common, and interventions such as needle decompression and ventilatory assistance rarely are needed. An important associated or causative condition to rule out is spontaneous pneumothorax. In this patient, a small left pneumothorax was visible on computed tomography. Etiologies include alveolar rupture secondary to straining against a closed glottis or rupture of subpleural blebs.8 Aortic dissection is a rare but potentially fatal occurrence. Prevalence increases with age and is higher in men. Risk factors include hypertension, trauma, and collagen-vascular disorders (e.g., Marfan syndrome). Patients may present with sudden, severe, tearing abdominal or back pain. Radiographic findings may include mediastinal widening. Atypical chest pain is a diagnosis of exclusion. In this case, there is a clear diagnosis based on chest radiography. Reactive airways disease, in particular exercise-induced asthma, could present with chest pain and shortness of breath after exercise. Wheezing does not have to be present. This patient had no history of reactive airways disease, and chest radiography provided the diagnosis. However, some cases of spontaneous pneumomediastinum are associated with
Selected Differential Diagnosis of Acute Chest Pain in an Adolescent Condition
Characteristics
Aortic dissection
Sudden tearing pain with widened mediastinum; possible history of collagen-vascular disorders or trauma
Pneumomediastinum
Air within the mediastinum; subcutaneous emphysema, Hamman's sign, chest pain, dyspnea
Atypical chest pain
Exclusionary diagnosis once cardiopulmonary etiologies have been ruled out; may be musculoskeletal, gastrointestinal, or psychological
Reactive airways disease
Inflammatory response to allergens, infection, climate, exercise; dyspnea with or without wheezing
Esophageal rupture
Often seen as air within the mediastinum; usually history of trauma or forceful vomiting; chest pain, especially worsened by swallowing
asthma or other pulmonary disease, leading some experts to recommend pulmonary function testing after recovery.7 The presentation of esophageal rupture is similar to that of pneumomediastinum. Subcutaneous emphysema and chest pain, especially worsened by swallowing, are common. However, the patient's history usually includes trauma or forceful vomiting. REFERENCES 1. Murray JF, Nadel JA, eds. Textbook of Respiratory Medicine. 3rd ed. Philadelphia, Pa.: Saunders, 2000. 2. Ullman EA, Donley LP, Brady WJ. Pulmonary trauma emergency department evaluation and management. Emerg Med Clin North Am. 2003;21:291-313. 3. Howton JC. Boerhaave's syndrome in a healthy adolescent male presenting with pneumomediastinum. Ann Emerg Med. 2004;43:785. 4. Hazouard E, Koninck JC, Attucci S, FauchierRolland F, Brunereau L, Diot P. Pneumorachis and pneumomediastinum caused by repeated Muller's maneuvers: complications of marijuana smoking. Ann Emerg Med. 2001;38:694-7. 5. Chao D. Air, air everywhere. Am Fam Physician. 2003;68:1381-3. 6. Mihos P, Potaris K, Gakidis I, Mazaris E, Sarras E, Kontos Z. Sports-related spontaneous pneumomediastinum. Ann Thorac Surg. 2004;78:983-6. 7. Chalumeau M, Le Clainche L, Sayeg N, Sannier N, Michel JL, Marianowski R, et al. Spontaneous pneumomediastinum in children. Pediatr Pulmonol. 2001;31:67-75. 8. Kirchner JT. Diagnosis and management of spontaneous pneumothorax. Am Fam Physician. 2000;62:1398-400.
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
187
EXPERT'S OPINION
What is the Importance of Aldosterone and Resistin in Resistant Hypertension? SC Tiwari,* KK Aggarwal**
T
he proportion of obese hypertensive patients with higher plasma aldosterone concentrations (PAC) is significantly higher than those in the nonobese hypertensive patients. Ehrhart-Bornstein et al reported that there are some substances extracted from the supernatant of fat cell culture stimulating aldosterone production of cultured human adrenal cortical cells. But these aldosterone-stimulating substance(s) have not been well-identified.1
Increased levels of plasma angiotensinogen (AGT), renin and aldosterone, and angiotensin-converting enzyme (ACE) activity have been found in obese patients.2-4 High PAC has been associated with increased fat mass in several studies in recent years,5-8 and the association was more significant in women than in men. Reduction of weight has shown to lead to a fall in PAC.9-11 Adipose tissue is now recognized as a highly active endocrine organ rather than a simple depot for fuel storage that can produce and secrete many hormones and proteins, the so-called adipokines, which exert a wide range of biological actions.12,13 A link between adipose tissue and the production of glucocorticoid in adrenal gland has been demonstrated. The adiposetissue related adipokine, resistin plays a role in the regulation of aldosterone secretion of human adrenal cortical cells. Resistin up regulates both CYP11B2 mRNA expression and the aldosterone secretion by way of activating the intracellular signaling molecules including protein-kinase C (PKC) and cyclic adenosine monophosphate (cAMP). There is growing evidence showing that circulating resistin level and resistin gene single nucleotide polymorphisms are associated with the development
*Professor and Chairman Dept. of Nephrology Fortis Group of Hospitals, New Delhi **Senior Physician and Cardiologist Moolchand Medcity, New Delhi
188
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
of diabetes, hypertension and atherosclerosis.14-18 A cross-sectional study demonstrated that patients in prehypertension had higher plasma resistin levels than those with normotension. In the Nursesâ&#x20AC;&#x2122; Health Study, the association between plasma resistin levels and the risk for incident hypertension among 872 women without a history of hypertension or diabetes was evaluated. The investigators identified 361 incident cases of hypertension during 14 years of follow-up. After adjustment for potential confounders, resistin levels in the highest tertile conferred a 75% higher risk for hypertension than the lowest tertile (relative risk [RR] 1.75; 95% confidence interval [CI] 1.19-2.56). Further adjustment for other adipokines did not change the RR substantially. In stratified analysis, resistin levels in the highest tertile significantly increased the risk for hypertension among women aged â&#x2030;Ľ55 years (adjusted RR 2.40; 95% CI 1.55-3.73) but not among women aged <55 years (adjusted RR 0.64; 95% CI 0.25-1.62). In a subset analysis of 362 women who also had measurements of inflammatory and endothelial biomarkers, plasma resistin levels significantly correlated with interleukin-6 (IL-6), soluble tumor necrosis factor (TNF) receptor 2, intercellular adhesion molecule 1, vascular adhesion molecule 1 and E-selectin after controlling for age and body mass index. After further adjustment for these biomarkers and C-reactive protein, resistin levels remained significantly associated with incident hypertension. It was concluded that higher plasma resistin levels independently associated with an increased risk for incident hypertension among women without diabetes.16 Increased systolic blood pressure (BP), diastolic BP and resting heart rate as well as increased insulin and resistin plasma levels and decreased adiponectin plasma levels have been shown to pre-exist in young healthy offspring with positive family history for essential hypertension.19
EXPERT'S OPINION References 1. Ehrhart-Bornstein M, Lamounier-Zepter V, Schraven A, et al. Human adipocytes secrete mineralocorticoid-releasing factors. Proc Natl Acad Sci USA 2003;100(24):14211-6. 2. Bloem LJ, Guo C, Pratt JH. Identification of a splice variant of the rat and human mineralocorticoid receptor genes. J Steroid Biochem Mol Biol 1995;55(2):159-62. 3. Cooper R, McFarlane-Anderson N, Bennett FI, et al. ACE, angiotensinogen and obesity: a potential pathway leading to hypertension. J Hum Hypertens 1997;11(2):107-11. 4. Messerli FH, Christie B, DeCarvalho JG, et al. Obesity and essential hypertension. Hemodynamics, intravascular volume, sodium excretion, and plasma renin activity. Arch Intern Med 1981;141(1):81-5. 5. Licata G, Scaglione R, Ganguzza A, et al. Central obesity and hypertension. Relationship between fasting serum insulin, plasma renin activity, and diastolic blood pressure in young obese subjects. Am J Hypertens 1994;7(4 Pt1): 314-20. 6. Egan BM, Stepniakowski K, Goodfriend TL. Renin and aldosterone are higher and the hyperinsulinemic effect of salt restriction greater in subjects with risk factors clustering. Am J Hypertens 1994;7(10 Pt 1): 886-93. 7. El-Gharbawy AH, Nadig VS, Kotchen JM, et al. Arterial pressure, left ventricular mass, and aldosterone in essential hypertension. Hypertension 2001;37(3):845-50. 8. Goodfriend TL, Kelley DE, Goodpaster BH, et al. Visceral obesity and insulin resistance are associated with plasma aldosterone levels in women. Obes Res 1999;7(4):355-62. 9. Engeli S, Böhnke J, Gorzelniak K, et al. Weight loss and the renin-angiotensin-aldosterone system. Hypertension 2005;45(3):356-62.
10. Harp JB, Henry SA, DiGirolamo M. Dietary weight loss decreases serum angiotensin-converting enzyme activity in obese adults. Obes Res 2002;10(10):985-90. 11. Tuck ML, Sowers J, Dornfeld L, et al. The effect of weight reduction on blood pressure, plasma renin activity, and plasma aldosterone levels in obese patients. N Engl J Med 1981;304(16):930-3. 12. Arner P. The adipocyte in insulin resistance: key molecules and the impact of the thiazolidinediones. Trends Endocrinol Metab 2003;14(3):137-45. 13. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004;89(6): 2548-56. 14. Takata Y, Osawa H, Kurata M, et al. Hyperresistinemia is associated with coexistence of hypertension and type 2 diabetes. Hypertension 2008;51(2):534-9. 15. Anderson DE, McNeely JD, Windham BG. Regular slowbreathing exercise effects on blood pressure and breathing patterns at rest. J Hum Hypertens 2010;24(12):807-13. 16. Zhang L, Curhan GC, Forman JP. Plasma resistin levels associate with risk for hypertension among nondiabetic women. J Am Soc Nephrol 2010;21(7):1185-91. 17. Loscertales MP, Brabin BJ. ABO phenotypes and malaria related outcomes in mothers and babies in The Gambia: a role for histo-blood groups in placental malaria? Malar J 2006;5:72. 18. Iacobellis G, Petramala L, Cotesta D, et al. Adipokines and cardiometabolic profile in primary hyperaldosteronism. J Clin Endocrinol Metab 2010;95(5):2391-8. 19. Papadopoulos DP, Makris TK, Perrea D, et al. Adiponectin - insulin and resistin plasma levels in young healthy offspring of patients with essential hypertension. Blood Press 2008;17(1):50-4.
■■■■
Remnant cholesterol and not low-density lipoprotein (LDL) may be the cause of inflammation in atherosclerosis. A new study has found that the cholesterol transported by remnant lipoproteins is associated with ischemic heart disease (IHD) and low-grade inflammation, whereas LDL cholesterol is associated with IHD without any signs of inflammation. Using data from the Copenhagen General Population Study, the Copenhagen City Heart Study and the Copenhagen Ischemic Heart Disease Study, the study included 10 668 individuals diagnosed with IHD between 1977 and 2011. Dr Anette Varbo from Herlev Hospital, Copenhagen, Denmark and colleagues in their report, published online August 7, 2013 in Circulation said that while the statins might have pleiotropic effects that reduce inflammation, these results might also be explained by statins lowering not only LDL cholesterol but also remnant cholesterol levels and consequently also reducing atherosclerosis and inflammation. (Source: Medscape)
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
189
MEDILAW
Can Docs be Booked in 304-A When DMC Says no Negligence? KK Aggarwal
S
ix doctors of Apollo Hospital have been booked for causing death by negligence of a 70-year-old man in 2009 as per police.
As per the hospital, there is no medical negligence. The patient had multiple pre-existing comorbid conditions including uncontrolled diabetes, heart and kidney disease. Appropriate care and treatment was provided by a competent multidisciplinary team but the patient, sadly, succumbed to his illness. The Delhi Medical Council (DMC) also ordered that the patient was duly treated as per established norms. A case has been filed with police station on May 31 over an order of district court. The patient, complainant’s father was admitted to the hospital on March 6, 2009 with perianal abscess with diabetes and coronary artery disease on blood thinners.
Charges The hospital and the doctors now face charges under Sections 304-A (causing death by negligence), 465 (forgery) and 471 (using forged document as genuine). Defense ÂÂ
The patient was in sepsis at the time of admission.
ÂÂ
He had other comorbidities which needed to be stabilized.
ÂÂ
The patient was evaluated by the cardiologist, nephrologist and anesthetist.
ÂÂ
After the patient had been preoperatively evaluated, stabilized, he was taken up for surgery under highrisk consent.
ÂÂ
Debridement was done every-day till as hence the blood thinners were not given till debridement was necessary.
Allegations ÂÂ
After remaining in the hospital for 27 days, the patient died on April 1, 2009 due to gross, grave, reckless and culpable criminal negligence of the accused, who had vision, reasonable foresight and complete knowledge and awareness of the consequences of their acts, but showed thorough disregard and indifference.
ÂÂ
There was unreasonable delay in conducting surgery for drainage of perianal abscess.
ÂÂ
The surgery was performed after an unjustified delay of 20 hours from the time of admission.
ÂÂ
Blood thinners were discontinued prior to surgery and were not restarted again. This contributed to a heart attack on March 27, 2009 as per the allegation.
eMedinews Comments ÂÂ
Once the State Medical Council has cleared the complainant should appeal the order in Medical Council of India. Till that the police should not take any cognizance.
ÂÂ
Difference of opinion and error of judgment are not negligence.
ÂÂ
For it to be a criminal negligence it has to be willful, grossly negligent and reckless, which would have been observed by the State Medical Council if it was there.
ÂÂ
Stopping blood thinner is a normal practice for 5-7 days before any surgery.
ÂÂ
Anemia was not corrected on time.
ÂÂ
ÂÂ
Hyponatremia, very low albumin and plasma proteins and blood gases were not managed at all.
Being on blood thinners does not guarantee that a person will not get a heart attack.
ÂÂ
Had proper diagnosis been made in time the heart attack could have been prevented.
Death does not mean negligence or a criminal negligence.
ÂÂ
If two experts differ the benefit of doubt should go to the doctor.
ÂÂ
These types of case hurt doctors and makes them practice defensive practice which in long run is not in the interest of the patients.
ÂÂ
Senior Physician and Cardiologist Moolchand Medcity, New Delhi
190
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
ALGORITHM
Algorithm for the Evaluation of Suspected Orthostatic Hypotension in the Outpatient Setting Patient with signs and symptoms of orthostatic hypotension Loss of consciousness? Yes High-risk cardiac or neurologic patient?
No
Yes
No
Evaluate for cardiac or neurologic disorders Cause identified? Yes
No Orthostatic hypotension likely
Obtain orthostatic vital signs
Positive
Negative No
Suspicion for orthostatic hypotension?
Orthostatic hypotension unlikely
Yes Evaluate and treat non-orthostatic cause of symptoms
Assess for volume depletion
Go to A Volume depleted
Not dehydrated
Treat for volume depletion Symptoms resolve?
No
Yes
Evaluate for non-neurologic cause
Cause not identified A
Stable for discharge?
No Admit for further evaluation and treatment
Cause identified Treat likely cause
Yes Discharge with outpatient follow-up
Source: Adapted from Am Fam Physician. 2011;84(5):527-536.
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
191
Around the Globe
News and Views Thrombolytic Therapy for Acute Stroke Women are less likely than men to receive intravenous (IV) thrombolytic therapy for acute stroke, researchers reported online in Stroke: Journal of the American Heart Association. This could be due to the delayed arrival at the hospital. In a group of patients presenting within 24 hours of stroke onset, IV tissue plasminogen activator (tPA) was used in 11% of women and 14% of men. But this gender difference was not found in the subgroup of patients who presented with an acute ischemic stroke within four hours of symptom. (Source: Medpage Today) Patients with pulmonary arterial hypertension Two Phase III trials reported in the July 25 issue of the New England Journal of Medicine state that riociguat (proposed trade name Adempas), an investigational agent improved exercise capacity and other outcomes in patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Compared with placebo, riociguat provided net gains in the 6-minute walk distance of 36 and 46 meters in patients with PAH and CTEPH, respectively (p < 0.001 for both). (Source: Medpage Today) Common Blood Pressure Drugs May Slow Dementia Decline A class of drug used to lower blood pressure could potentially slow the rate of cognitive decline in dementia and even boost brain power, according to a study published by BMJ Open. Researchers from Ireland analyzed the cognitive decline and brain power of 361 patients with an average age of 77. All had been diagnosed with either Alzheimer's disease, vascular dementia or a mixture of both. A new study appears to confirm that when you eat is just as important for health as what and how much you eat? US researchers asked men to complete questionnaires about what they ate and when they ate it, then tracked their health for 16 years. Those who said they skipped
192
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
breakfast were found to have a higher risk of heart attack or fatal coronary heart disease. Blood Pressure Measurement May Detect Proneness To Heart Attack The ankle brachial index (ABI), a simple, noninvasive 10-minute test should be incorporated into a routine physical exam for diagnosing peripheral arterial disease in the middle aged and the elderly, especially those with heart attack risk factors like smokers, diabetics and the ones with high blood pressure (BP) or cholesterol levels. With the patient in a supine position, the doctor takes BP readings from both arms; he then takes BP readings from both ankles with a sphygmomanometer and Doppler device. ABI value is calculated by dividing the higher systolic pressure in each leg by the higher systolic brachial pressure. ABI scores should be interpreted as follows: ÂÂ
Greater than 0.90: Normal
ÂÂ
0.71-0.90: Mild obstruction
ÂÂ
0.41-0.70: Moderate obstruction
ÂÂ
Less than 0.40: Severe obstruction
ÂÂ
More than 1.30: Calcification of the vessels
Presence of peripheral arterial disease may indicate associated blockages in the heart and proneness to heart attack or paralysis. Kidney Patients More at Risk For Future Heart Attacks Chronic kidney disease (CKD) patients with kidney function less than 60% have now been added in the list of criteria for defining people at highest risk for future heart attacks. In a large cohort Canadian study published in The Lancet led by Dr Marcello Tonelli at University of Alberta, patients with only CKD had a significantly higher rate of heart attacks than those who only had diabetes. Those who had already had a heart attack had the highest overall rate of heart attacks.
Around the Globe CKD should be regarded as a coronary heart disease risk equivalent, similar to diabetes, as patients with the condition have high rates of cardiovascular events, particularly when they also have proteinuria.
and may be harmful, writes Amir Qaseem, MD, PhD, MHA, from the ACP, Philadelphia, Pennsylvania, and colleagues in the January 17, 2012 issue of the Annals of Internal Medicine.
When CKD was defined more stringently with kidney function less than 45% and increased proteinuria, the rate of first heart attack was higher in those with both CKD and diabetes than in those with either disorder alone.
ACP Committee has identified 37 clinical scenarios in which screening does not promote patient health, and might even have adverse consequences. Those related to cardiac scenarios: ÂÂ
Performing coronary angiography in patients with chronic stable angina who have well-controlled symptoms on medical therapy, or who lack specific high-risk criteria on exercise testing.
ÂÂ
Routinely repeating echocardiography in asymptomatic patients with mild mitral regurgitation and normal left ventricular size and function.
ÂÂ
Obtaining ECG to screen for cardiac disease in patients at low to average risk for coronary artery disease.
ÂÂ
Obtaining exercise electrocardiogram for screening low-risk, asymptomatic adults.
Donating Blood Reduces Chances of Heart Attack One should donate blood at least once in a year. Donating blood regularly has been shown in many reports to reduce chances of future heart attacks. Blood donation is also one of the best charities that one can do as it can save multiple lives through various components taken out of a single blood transfusion. All those who are going for elective surgery should donate their blood well in advance and the same should be used at the time of surgery. In the current medical tourism scenario, many Christian patients from Jehovah’s Witnesses refuse blood transfusion on religious grounds. They do not accept transfusion of whole blood or any of the four major components (blood cells, platelets, plasma and white cells). They are prepared to die rather than receive the blood. They also do not accept transfusion of stored blood including their own due to the belief that blood should not be taken out of the body and stored for any length of time. In such cases, every effort should be made to reduce blood loss, conserve blood and give drugs that can enhance hemoglobin formation. A new concept called 'Bloodless Medicine' has now become a reality where treatment, surgery and even emergency surgery can be done without using any blood. Judicious Use of Cardiac Screening Unnecessary screening can have a considerable cost beyond that of the test itself, warn members of an ad hoc committee convened by the American College of Physicians. Screening tests should be performed judiciously, and the committee has assembled a list of common clinical situations in which more testing is unlikely to be helpful
Does Good Cholesterol Still Predict Heart Risk After Bad Cholesterol Is Controlled By Statin Therapy? Yes, according to a post-hoc analysis of data from the controversial courage trial, appearing in the Journal of the American College of Cardiology. No, according to Dutch researchers whose report on the secondary manifestations of arterial disease (SMART) study also appears in the journal. Optimal medical therapy after acute myocardial infarction Although nearly all heart attack patients leave the hospital on secondary prevention medications, only about a third get appropriate doses, registry data showed. Initial dose was key, because about threequarters of those who didn’t go home on a dose within 75% of the dose proven effective in landmark trials didn’t get an increase during follow-up care, Suzanne V. Arnold, MD, MHA, of St. Luke’s Mid America Heart Institute in Kansas City, Mo., and colleagues found. "Integration of dose intensity into performance measures may help improve the use of optimal medical therapy after acute myocardial infarction," the group suggested online in the Journal of the American College of Cardiology.
■■■■
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
193
lighter reading
The yogi Raman was a true master of the art of archery. One morning, he invited his favorite disciple to watch a display of his skill. The disciple had seen this more than a hundred times before, but he nevertheless obeyed his teacher. They went into the wood beside the monastery and when they reached a magnificent oak tree, Raman took a flower which he had tucked in his collar and placed it on one of the branches. He then opened his bag and took out three objects: His splendid bow made of precious wood, an arrow and a white handkerchief embroidered with lilacs. The yogi positioned himself one hundred paces from the spot where he had placed the flower. Facing his target, he asked his disciple to blindfold him with the embroidered handkerchief. The disciple did as his teacher requested. ‘How often have you seen me practice the noble and ancient sport of archery?’ Raman asked him. ‘Every day,’ replied his disciple. ‘And you have always managed to hit the rose from three hundred paces away.’ With his eyes covered by the handkerchief, the yogi Raman placed his feet firmly on the ground, drew back the bowstring with all his might-aiming at the rose placed on one of the branches of the oak treeand then released the arrow.
A family is driving in their car on holidays. A frog crosses the road and the husband, who is driving, is able to stop the car. He gets out and takes the frog and carries him to the side of the road. The frog is grateful, thanks the man and tells him that he will grant him a wish. The man says, "Please make my dog win the next dog race."
laugh a while
Power of thought: Hitting unseen target
The frog asks to look at the dog, which limps out of the car. The frog notices that the dog only has three legs, it very fat, and can barely move at all so he tells the man that he thinks it is almost impossible to fulfill his wish and asks that the man will tell him another wish. The man says, "Well, then please make my wife win the next beauty contest in the area. The frog asks him to tell his wife to get out of the car. Wife comes out of the car and approaches the frog. The frog turns to the man and says, "Could I please have another look at the dog?"
QUOTE
An Inspirational Story
Lighter Side of Medicine
"Problems are only opportunities in work clothes." — Henry John Kaiser
Dr. Good and Dr. Bad Situation: A patient with CAD developed diabetes.
We can start with any antidiabetic drug
We will start treatment with metformin
‘No, you missed completely,’ replied the disciple. ‘I thought you were going to demonstrate to me the power of thought and your ability to perform magic.’ ‘I have just taught you the most important lesson about the power of thought,’ replied Raman. ‘When you want something, concentrate only on that: no one will ever hit a target they cannot see.
194
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
©IJCP Academy
The arrow whistled through the air, but it did not even hit the tree, missing the target by an embarrassingly wide margin. ‘Did I hit it?’ said Raman, removing the handkerchief from his eyes. Lesson: In patients with no contraindication, metformin is the drug of choice for oral treatment of diabetes with different suggestive of reduced risk for macrovascular and microvascular complications. Diabetes care 2013;36:1304. [Dr. K K Aggarwal, Padma Shri and Dr. B C Roy National Awardee; Chairman Legal Cell Indian Academy of Echocardiography; Chairman, Ethical Committee Delhi Medical Council; Editor, eMedinewS and President, Heart Care Foundation of India]
KK Aggarwal
Asian
Journal of
CLINICAL CARDIOLOGY
Information for Authors
Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767). Asian Journal of Clinical Cardiology strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so. The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript. Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper. Covering letter -
- -
The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper. Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors. Articles must be accompanied by a declaration by all authors stating that the article has not been published in any other Journal/Book. Authors should mentioned complete designation and departments, etc. on the manuscript.
Manuscript - Three complete sets of the manuscript should be submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures). -
The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), Introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures.
-
All pages should be numbered consecutively beginning with the title page.
departments and institutions where the work was performed, name of the corresponding authors, acknowledgment of financial support and abbreviations used. - The title should be of no more than 80 characters and should represent the major theme of the manuscript. A subtitle can be added if necessary. - A short title of not more than 50 characters (including inter-word spaces) for use as a running head should be included. - The name, telephone and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page. - A list of abbreviations used in the paper should be included. In general, the use of abbreviations is discouraged unless they are essential for improving the readability of the text. Summary - The summary of not more than 200 words. It must convey the essential features of the paper. - It should not contain abbreviations, footnotes or references. Introduction - The introduction should state why the study was carried out and what were its specific aims/objectives. Methods - These should be described in sufficient detail to permit evaluation and duplication of the work by others. - Ethical guidelines followed by the investigations should be described. Statistics The following information should be given: - The statistical universe i.e., the population from which the sample for the study is selected. - Method of selecting the sample (cases, subjects, etc. from the statistical universe). - Method of allocating the subjects into different groups. - Statistical methods used for presentation and analysis of data i.e., in terms of mean and standard deviation values or percentages and statistical tests such as Student’s ‘t’ test, Chi-square test and analysis of variance or non-parametric tests and multivariate techniques.
Note: Please keep a copy of your manuscript as we are not responsible for its loss in the mail. Manuscripts will not be returned to authors.
-
Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the
-
Confidence intervals for the measurements should be provided wherever appropriate.
Results These should be concise and include only the tables and figures necessary to enhance the understanding of the text.
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
197
Discussion -
This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g. practicality and cost.
References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses). At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution. Examples of common forms of references are: Articles
Figures - Two complete sets of glossy prints of high quality should be submitted. The labelling must be clear and neat. - All photomicrographs should indicate the magnification of the print. - Special features should be indicated by arrows or letters which contrast with the background. - The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen. - Color illustrations will be accepted if they make a contribution to the understanding of the article. -
Do not use clips/staples on photographs and artwork.
-
Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as ‘Fig.’. Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected summary, etc.)_______________________________
Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes. Q. J. Expt. Physiol. 1955;40:89-111.
2. Total number of pages ________________________
Books
6. Suggestions for reviewers (name and postal address)
Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.
Indian 1.____________Foreign 1.________________
2.____________ 2.________________
Articles in Books
3.____________ 3.________________
Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470.
4.____________ 4.________________
Tables -
These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.
Legends - These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text. -
The legend must include enough information to permit interpretation of the figure without reference to the text.
198
Asian Journal of Clinical Cardiology, Vol. 16, No. 5, September 2013
3. Number of tables ____________________________ 4. Number of figures ___________________________ 5. Special requests _____________________________
7. All authors’ signatures________________________ 8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers __________________________________________
Online Submission Also e-issue @ www.ijcpgroup.com For Editorial Correspondence
Dr KK Aggarwal
Group Editor-in-Chief Asian Journal of Clinical Cardiology E - 219, Greater Kailash, Part - 1, New Delhi - 110 048. Phone: 011-40587513 E-mail: editorial@ijcp.com, emedinews@gmail.com Website: www.ijcpgroup.com
Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD and Group Executive Editor Dr Alka Kriplani Dr Praveen Chandra Dr Swati Y Bhave Dr CR Anand Moses Dr Sidhartha Das Dr Wiqar Sheikh Dr Ajay Kumar Dr A Ramachandran Dr Samith A Shetty Dr SK Parashar Dr Kamala Selvaraj Dr Georgi Abraham Dr V Nagarajan Dr Thankam Verma Dr KMK Masthan Dr Hasmukh J Shroff Dr Rajesh Chandna Dr SM Rajendran
Volume 22, Number 11 Peer Reviewed Journal
Drug Review
Review Article
Original Article
Case Report
Photo Quiz
Lighter Reading
April 2012, Pages 545-596
R.N.I. No. 71217/98 Date of Publishing 25 of Same Month Date of Posting 25-26 Same Month
REGISTRATION NO. DL (S)-01/3288/2013-2015 POSTED IN NDPSO NEW DELHI