Ajcc July 2013

In This Issue —

Sixty Percent of People do not Discuss their Sexual Behavior and Performance with the Doctor when they go for Consultation

—

People on Facebook are more Health Aware than Nursing Students or People not on the Net

—

Perioperative Myocardial Infarction

—

Diagnosis and Management of Diastolic Dysfunction and Heart Failure

—

An Autopsy and Echocardiographic Study of Left Ventricular Trabeculations

—

Coronary Artery Air Embolism

—

Intermittent Sudden Dyspneic Episodes

—

ACEP Policy on Evaluating Patients with Syncope in the Emergency Department

Volume 16, Number 3, July 2013 Pages 81-120

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 3, July 2013

Dr Deepak Chopra Chief Editorial Advisor

Padma Shri and Dr BC Roy National Awardee Dr KK Aggarwal Group Editor-in-Chief

from the desk of group editor-in-chief 85

Dr Veena Aggarwal MD, Group Executive Editor Dr Praveen Chandra Guest Editor, AJCC praveen.chandra@medanta.org

New Insight into COURAGE Patients (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) KK Aggarwal

Assistant Editors: Dr Nagendra Chouhan, Dr Dharmendar Jain

AJCC Speciality Panel

community health

Advisory Board 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

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

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Sixty Percent of People do not Discuss their Sexual Behavior and Performance with the Doctor when they go for Consultation KK Aggarwal

People on Facebook are more Health Aware than Nursing Students or People not on the Net KK Aggarwal

IJCP Editorial Board Obstetrics and Gynaecology Dr Alka Kriplani Dr Thankam Verma, Dr Kamala Selvaraj 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 Dentistry Dr KMK Masthan Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dermatology Dr Hasmukh J Shroff Neurology Dr V Nagarajan Orthopedics Dr J Maheshwari Journal of Applied Medicine and 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

REVIEW ARTICLE 89

93

Perioperative Myocardial Infarction Sudivya Sharma, Prashast Jain

Diagnosis and Management of Diastolic Dysfunction and Heart Failure Chhabi Satpathy, Trinath K Mishra, Ruby Satpathy, Hemant K Satpathy, Eugene Barone

CLINICAL STUDY 99

An Autopsy and Echocardiographic Study of Left Ventricular Trabeculations Deep C Pant, Hema Pant, Ajay Bahl, Uma Saikia

case report 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

106 Coronary Artery Air Embolism

Printed at New Edge Communications Pvt. Ltd, New Delhi E-mail: edgecommunication@gmail.com

Monika Maheshwari, Anand Agarwal

photo quiz

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.

108 Intermittent Sudden Dyspneic Episodes

practice guidelines

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.

111 ACEP Policy on Evaluating Patients with Syncope in the Emergency Department

lighter reading 114 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.

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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)

New Insight into COURAGE Patients (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) New insight into patients in Courage trial who crossed over their optimal medical therapy to revascularization within one year with randomization is being published in July 9 issue of Circulation.

Although crossing over from optimum medical therapy to coronary vascularization was not associated with an increased risk of death or heart attack when compared with patients who underwent upfront revascularization, angina and quality-of-life were typically worse in OMT group in that first year.

Patients who switched over were more likely to have severe angina with significantly affected quality-of-life and were dissatisfied with their current treatment.

Therefore, one can easily identify these patients in whom revascularization can be the initial process.

However, in the rest, the analysis provides the strongest to date that starting a COURAGE patient on medical therapy is reasonable and has no downside.

Though it is true that one-third of patients crossover but the critical crosover’s was only in the first year and those are the patients with severe angina who easily cannot be treated medically.

In the study, only 16% of patients crossed over in the first year; 90% underwent PCI and 10% were treated surgically. mmmmm

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community health

Sixty Percent of People do not Discuss their Sexual Behavior and Performance with the Doctor when they go for Consultation KK Aggarwal

Abstract On Doctor’s Day 2013, a survey was conducted to assess the perception of doctor-patient relationship among the people and the expectations of the patients from the doctors. Data was collected using a questionnaire and came up with some interesting changing trends among the people with regard to doctor-patient relationship.

Keywords: Family physician, specialist, sexual history, etiquette-based medicine, privacy, health insurance

A

survey of 452 people was conducted by Heart Care Foundation of India and eMedinewS on the occasion of Doctors Day 2013. The objective of the survey was to assess the perception of doctor-patient relationship among the people and the expectations of the patients from the doctors.

The survey included patients, social workers, RWAs, morning walkers, college students and government employees from NCR Delhi and consisted of middle to high socioeconomic strata. Data was collected using a questionnaire, which the survey participants were asked to answer. The data came up with some interesting changing trends among the people with regard to doctor-patient relationship.

New trend to directly go to specialists The survey revealed that only 42% had a family physician. When suffering from an illness, 52% of the people would directly opt to visit a specialist and not a family physician, which is not a good trend. The traditional concept of a ‘family physician’ that looked after all the health needs of a family regardless of his/ her specialization, is now changing.

Sexual preferences, choices and behaviors Eighty percent of the people want their doctors to ask about the sexual history in confidence. They feel Padma Shri & Dr BC Roy National Awardee President Heart Care Foundation of India E-mail: emedinews@gmail.com

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shy coming out with the history as most of the times patients are accompanied by the relations. The survey found that 60% of the patients have never opened out to their doctors and 80% of the doctors have never asked then about the sexual history. This brings them to seek help from sex quacks and advise from friends and neighborhood.

The survey found that people are sexually active even at elderly age. The proportion of man reporting no sex is 20% at age 51-60 and 87.5% at age above 75. In women, reporting no sex is 100% after the age of 70.

About 16.17% of men reported that they are facing erectile dysfunction and 17.64% are having premature ejaculation during sexual act.

The survey enlisted that the public wanted the following to be asked to them in isolation in person or through a document about the following: ÂÂ

Are you sexually active

ÂÂ

Are you satisfied with your sexual life

ÂÂ

Are you sexually attracted to men, women or both

ÂÂ

Do you have multiple partners

People want experienced doctors Sixty-five percent prefer senior doctors with white hair to treat them as they can provide better patient care than their younger fashionable counterparts with less clinical experience. Hundred percent of the people said that if their doctor cannot practice ‘compassion based medicine’ at least practice ‘etiquette-based medicine’.

community health Sixty percent of the people put their faith in the capabilities of their doctor and not on their dress code.

Fifty-seven percent however check the credentials and qualifications of a doctor before visiting them for consultation. This is a new trend in the society.

When asked about the criteria of a good doctor 90% people said that for them availability and behavior of a doctor is more important than competency. “What is the use of a competent doctor if he is not available and is arrogant”: Was the common question asked by them?

When questioned about the etiquette based medicine, 84% people said that they would like their doctor to call them with their name; would like the doctor to introduce about his credentials and competency; would like to explain and reason out the plan and duration of treatment.

Patients want privacy Forty percent of the people did not want doctors to be their friends on facebook. New International guidelines also warn doctors not to be connected with their patients on facebook. Eighty percent of the people wanted that their personal health information should not be leaked to any one without asking them including the spouse and their name should not be shouted outside the operation theatre or the intensive care unit (ICU).

Patients do not like smoking doctors Eighty-one percent people reported being disturbed when they saw their doctors smoking in public and would not like to be treated by a doctor who smoked in front of them.

Patients want doctors to spend more time with them Forty-nine percent people reported being satisfied with less 15 minutes of a doctor’s time; 26% wanted their doctor to spend more than 15 minutes with them and the rest wanted time till they were satisfied. Fifty-four percent people said that their doctors never advised them about adult vaccination. This needs immediate attention. Fifty-five percent said that their blood pressure had never been checked in both arms. Fortynine percent people said that they would prefer to take a dietary advice from their doctor and not from a dietitian.

Patient wants second opinion from the same doctor Sixty percent people wanted to get a second opinion from their regular doctor if they are not satisfied.

Seventy-two percent people do not want doctors to treat them just on clinical grounds but prefer getting investigated first. When advised investigations, 57% would ask their doctor to suggest a lab, while the rest said that they would choose their own lab.

Patient etiquette Forty-six percent people said that they preferred to call their doctor directly to fix an appointment and not the secretary. When calling for an appointment, 53% would choose to call on a mobile number and not the landline, whether the call is to the doctor or the secretary.

Ignorance is still high ÂÂ

Forty-seven percent persons did not have any health insurance.

Sixty-seven percent people felt that their doctors should have legible handwriting and favored an electronic prescription instead.

ÂÂ

Forty-nine percent did not know that when they are hiring a room in a private hospital, the insurance covers only 1% of the sum amount insured for the bed.

Patients want affordable, quality and safe medical care

ÂÂ

Fifty-two percent of the people do not know that error of judgment or difference of opinion is not an act of negligence on the part of the doctor.

ÂÂ

Forty-eight percent people were unaware of the fact that a doctor is supposed to possess only an average degree of skill and knowledge and not the maximum degree of skill and knowledge when treating a patient.

ÂÂ

Thirty percent of the people were unaware that creating violence in the hospital premises is an offence.

Patients want doctors to write legibly

Seventy-eight percent people felt that medical profession is becoming commercialized today and should be made more affordable for a common man.

Seventy-two percent people said that doctors should be transparent in their fee. Fifty-nine percent people felt that doctors’ charging less fee is not their concern. But, 41% were of the opinion that doctors should charge less as their profession is a noble one.

Asian Journal of Clinical Cardiology, Vol. 16, No. 3, July 2013

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community health

People on Facebook are more Health Aware than Nursing Students or People not on the Net KK Aggarwal

Abstract In a survey of two hundred net savvy people, 500 nursing students and 400 general public aged 14-70 years attending the Perfect Health Mela 2012, it was seen that the level of health awareness was much higher in net savvy people compared to nursing students and general public.

Keywords: Net savvy, nursing, general public, cholesterol, trans fats, garlic, turmeric

N

ew Delhi, India: Two hundred net savvy people, 500 nursing students and 400 general public aged 14-70 years attending the Perfect Health Mela 2012 were interviewed and their level of health awareness was compared. The level of awareness was highest in the net savvy people.

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Eighty percent of the net savvy people, 67% of the nursing students and 64% of general public answered correctly that foods that are of plant in origin have no cholesterol.

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Seventy-four percent of the net savvy people, 63% of nursing students and 75% of general public answered correctly that trans fats are bad for health.

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Ninety-four percent of the net savvy people, 68% of nursing students and 45% of general public answered correctly that unsaturated fat is liquid at room temperature.

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Seventy-five percent of net savvy people, 49% nursing students and 43% of the general public answered correctly that fat solid at room temperature is saturated fat.

Padma Shri & Dr BC Roy National Awardee President Heart Care Foundation of India E-mail: emedinews@gmail.com

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Asian Journal of Clinical Cardiology, Vol. 16, No. 3, July 2013

ÂÂ

All the net savvy people, 95% of nursing students and 90% of general public answered correctly that garlic is good for health.

ÂÂ

All the net savvy people, 85% of nursing students and 95% of the general public answered correctly that turmeric has anti-inflammatory properties.

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Seventy-three percent of net savvy people, 70% of the nursing students and 60% of the general public answered correctly that with advancement of age, one should eat less.

ÂÂ

Seventy-three of net savvy people, 60% of the nursing students and 65% of general public answered correctly that foods, which are bitter in taste reduce diabetes.

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All net savvy people, 80% nursing students and 90% general public answered correctly that one should include all seven colors and 6 tastes in their food.

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All net savvy people, 90% of nursing students and 90% of general public answered correctly that death is reversible in the first 10 minutes of cardiac arrest.

The level of health awareness was found to be much higher in net savvy people compared to nursing students and general public.

REVIEW ARTICLE

Perioperative Myocardial Infarction Sudivya Sharma, Prashast Jain

Abstract Myocardial infarction (MI) is defined by the World Health Organization Criteria, which includes typical ischemic chest pain, ECG criteria and raised cardiac enzymes. The perioperative period induces large, unpredictable and nonphysiological alterations in coronary plaque morphology, function and progression, and may trigger a mismatch of myocardial oxygen supply and demand. Perioperative MI (PMI) is one of the most important predictors of short- and long-term morbidity and mortality associated with noncardiac surgery. Inability to fulfil the criteria, different symptomatology and numerous differential diagnoses makes PMI our subject of detailed discussion.1

Keywords: Perioperative myocardial infarction, plaque rupture, ischemia, risk stratification

T

he incidence of perioperative cardiac injury is a cumulative result of preoperative medical condition, the specific surgical procedure, expertise of the surgeon, the diagnostic criteria used to define myocardial infarction (MI) and the overall medical care at a particular institution. Patients with or at risk of cardiac disease have a 3.9% risk of suffering a major perioperative cardiac event. A perioperative MI (PMI) has an associated in-hospital mortality of 15-25% and an increased risk of subsequent cardiovascular death or MI.2,3 Differences Most PMIs occur in the first 24-48 hours after surgery.

They are mostly of silent type, ECG changes include ST depression, tachycardia and absence of Q waves and ST elevation. There is complete reversal of ECG changes to the baseline. The pain is masked by the analgesia and residual anesthesia provided intraoperatively.

The prolonged stress-induced mismatch between oxygen supply and demand is the most likely cause of myocardial ischemia.

A study of aortic surgical patients identiďŹ ed three patterns of troponin elevation. It was proposed by the authors that coronary plaque rupture was consistent

PGIMS, Rohtak, Haryana Address for correspondence Dr Sudivya Sharma Flat No: 77, B-Wing, Mahavir krupa building TJ Road, Sewri (W), Mumbai-400 015

with early PMI due to the rapidity of troponin change, while a sustained myocardial oxygen supply-demand imbalance in the postoperative period was consistent with delayed MI.4 Pathophysiology One hypothesis supports sudden development of a thrombotic process associated with vulnerable plaque rupture. This hypothesis is based on postoperative autopsy studies and angiographic evidence of thrombus present in noncritically stenosed vessels.

Endothelial injury at the site of a plaque rupture triggers the cascade of platelet aggregation and release of mediators including thromboxane A2, serotonin, adenosine diphosphate, platelet-activating factor, thrombin and oxygen-derived free radicals. Aggregation of platelets and activation of other inflammatory and noninflammatory mediators potentiates thrombus formation and leads to dynamic vasoconstriction distal to the thrombus. The combined effects of dynamic and physical blood vessel narrowing cause ischemia and/ or infarction. In the postoperative period, changes in blood viscosity, catecholamine concentrations, cortisol levels, endogenous tissue plasminogen activator concentrations, and plasminogen activator inhibitor levels create a prothrombotic state. Changes in heart rate and blood pressure as a result of the endocrine stress response can increase the propensity for plaque fissuring and endothelial damage.

These MIs are preceded by tachycardia and ST depression, are often silent and present as non-STsegment elevation MI (NSTEMI). Patients with more severe coronary artery disease (CAD) are at greater risk.

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review article These observations support the other likely hypothesis that perioperative myocardial injury develops as a consequence of increased myocardial oxygen demand (increased blood pressure and heart rate) in the context of underlying compromised myocardial oxygen supply.

The oxygen demand is increased perioperatively due to increased heart rate, heart wall tension, preload, afterload and myocardial contractility. On the other hand, the oxygen supply is decreased due to decreased coronary blood flow, tachycardia, hypotension, hypocapnia, hypoxemia, anemia, etc.

Thus, two different pathophysiologic mechanisms can be responsible for PMI. One could be related to acute coronary thrombosis, and the other could be the consequence of increased myocardial oxygen demand in the setting of compromised myocardial oxygen supply. These processes are not mutually exclusive.

However, one process or the other can predominate in a particular patient.

In combination, these factors can precipitate thrombus formation in an atherosclerotic coronary artery and lead to the development of STEMI (Q-wave).

Tables 1-4 are guides to risk stratification for a patient, predicting likelyhood of myocardial ischemia or infarction perioperatively. The severity of surgery, the functional capacity and present cardiac clinical signs and symptoms collectively determine the prognosis and outcome of surgery. These are also a guide for further delay or optimization of the patient. Figure 1 shows a step-wise approach to patients at risk.

Table 1. Clinical Predictors of Increased Perioperative Cardiovascular Risk Major Unstable coronary syndromes

Acute or recent MI with evidence of important ischemic risk by clinical symptoms or noninvasive study

nstable or severe angina U Decompensated heart failure

Significant dysrhythmias

High-grade atrioventricular block

Symptomatic ventricular dysrhythmias in the presence of underlying heart disease

Risk Stratification

Table 2. Revised Cardiac Risk Index in Patients Undergoing Elective Major Noncardiac Surgery High-risk surgery Abdominal aortic aneurysm Peripheral vascular operation Thoracotomy

Supraventricular dysrhythmias with uncontrolled ventricular rate Severe valvular heart disease

Major abdominal operation

Intermediate

History of a positive exercise test

Mild angina pectoris

Current complaints of angina pectoris

Previous MI by history or Q waves on ECG

Use of nitrate therapy

Compensated or previous heart failure

Q waves on electrocardiogram

Diabetes mellitus (particularly insulin dependent)

Congestive heart failure

Renal insufficiency

History of congestive heart failure

Minor

History of pulmonary edema

Advanced age (older than 70 years)

History of paroxysmal nocturnal dyspnea

Abnormal ECG (left ventricular hypertrophy, left bundle branch block, ST-T abnormalities)

Physical examination showing rales or S3 gallop

Rhythm other than sinus Low functional capacity History of stroke Uncontrolled systemic hypertension (Adapted from Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA 2006 guideline update on perioperative cardiovascular evaluation for noncardiac surgery: Focused update on perioperative beta-blocker therapy: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2006;113: 2662-2674. with permission.)

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Ischemic heart disease History of myocardial infarction

Chest radiograph showing pulmonary vascular redistribution Cerebrovascular disease History of stroke History of transient ischemic attack Insulin-dependent diabetes mellitus Preoperative serum creatinine concentration > 2 mg/dl (Adapted from Lee TH, Marcantonio ER, Mangione CM, et al: Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation 1999;100:1043–1049 with permission.)

review article Table 3. Metabolic Equivalents of Functional Capacity

Table 4. Cardiac Risk Stratification for Noncardiac Surgical Procedures

MET

Functional levels of exercise

1

Eating, working at a computer, dressing

Risk stratification

2

Walking down stairs or in your house, cooking

Vascular (reported cardiac risk often > 5%)

3

Walking 1-2 blocks

4

Raking leaves, gardening

5

Climbing 1 flight of stairs, dancing, bicycling

6

Playing golf, carrying clubs

7

Playing singles tennis

8

Rapidly climbing stairs, jogging slowly

9

Jumping rope slowly, moderate cycling

10

Swimming quickly, running or jogging briskly

11

Skiing cross country, playing full-court basketball

12

Running rapidly for moderate to long distances

Step 1

Intermediate (reported cardiac risk generally 1-5%) Low (reported cardiac risk generally < 1%)

zz zz

Aortic and other major vascular surgery Peripheral vascular surgery

Intraperitoneal and intrathoracic surgery Carotid endarterectomy zz Head and neck surgery zz Orthopedic surgery zz Prostate surgery zz zz

Endoscopic procedures Superficial procedure zz Cataract surgery zz Breast surgery zz Ambulatory surgery zz zz

Operating room

Perioperative surveillance and postoperative risk stratification and risk factor management

Evaluate and treat per ACC/AHA guidelines

Consider operating room

Yes (Class I, LOE C)

Need for emergency noncardiac surgery?

Procedure examples

No Yes (Class I, LOE B)

Step 2

Active cardiac conditions

Step 3

Low risk surgery

Step 4

Functional capacity â&#x2030;Ľ4 METs without symptoms.

Step 5

Proceed with planned surgery

Yes (Class I, LOE B)

Yes (Class IIa, LOE B)

No or unknown

3 or more clinical risk factors Vascular surgery

1-2 1-2 clinical clinical risk risk factors factor

No clinical risk factor

Intermediate risk surgery Vascular surgery

Class IIa LOE B Consider testing if it will change management

Proceed with planned surgery

Intermediate risk surgery

Proceed with planned surgery with HR control (Class IIA LOE B) or consider noninvasive testing (Class IIb LOE B) if it will change management

Class IIa LOE B

Proceed with planned surgery

Figure 1. Risk stratification and management.

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review article The goal is to identify patients with heart disease who are at high-risk for perioperative cardiac morbidity or mortality or those with modifiable conditions or risk. The guidelines for cardiac evaluation before noncardiac surgery published by the ACC/AHA have become the national standard of care. These guidelines were recently revised with a marked reduction in recommendations for preoperative noninvasive stress testing and revascularization. The substantial pullback of ACC/AHA recommendations advocating noninvasive stress testing and coronary revascularization before noncardiac surgery is due to the general lack of definitive benefit and risk reduction with this approach.5 Preoperative period is an opportunity to identify patients with CAD who will benefit from long-term risk modification with statins, aspirin, exercise and diet adjustment. Patients with symptoms consistent with ischemia (but without a diagnosis of CAD) or significant risk factors without medical management such as statins and aspirin may benefit from evaluation by a cardiologist regardless of whether they are having surgery. Preoperative evaluation should not simply focus on perioperative risk.

Management The management of PMI is also different as thrombolytics cannot be given, and anticoagulant use is with caution. The risk of life-threatening bleeding cancels thrombolytics as an option, hence a more conservative approach is recommended. So, the mainstay of treatment includes good pain control, β-blockers, statins, antiplatelets, nitroglycerine and unfractionated heparin.

Conclusion Many questions relating to perioperative pharmacological therapy to prevent PMI remain unanswered.

Careful perioperative monitoring for ischemia, a low threshold for treating and preventing tachycardia while avoiding hypotension, decreased cardiac output and/or cardiac decompensation help prevent PMI. Coronary intervention is rarely indicated as the firstline of treatment, and antithrombotic therapy may exacerbate bleeding. Future studies are needed to determine, which patients with PMI require intensified postoperative surveillance, medical therapy and/or coronary intervention to improve long-term survival.

References 1. Priebe HJ. Perioperative myocardial infarctionaetiology and prevention. Br J Anaesth 2005;95(1):3-19.

2. Devereaux PJ, Goldman L, Cook DJ, Gilbert K, Leslie K, Guyatt GH. Perioperative cardiac events in patients undergoing noncardiac surgery: a review of the magnitude of the problem, the pathophysiology of the events and methods to estimate and communicate risk.

CMA J 2005;173(6):627-34.

3. Devereaux PJ. Can attenuation of the perioperative stress response prevent intermediate or long-term cardiovascular outcomes among patients undergoing noncardiac surgery? Anesthesiology 2009;111(2):223-6.

4. Le Manach Y, Perel A, Coriat P, Godet G, Bertrand M, Riou B. Early and delayed myocardial infarction after abdominal aortic surgery. Anesthesiology 2005;102(5):885-91.

5. Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery. J Am Coll Cardiol 2007; 50:159-241.

mmmmm

Risk of Stroke can be Reduced by Minor Changes in Cardiovascular Health A report, published in Stroke, showed that small improvements in cardiovascular risk factors reduce the chances a person will suffer a stroke. The report is part of an ongoing national study called Reasons for Geographic and Racial Differences in Stroke (REGARDS), which is funded by NIHâ&#x20AC;&#x2122;s National Institute of Neurological Disorders and Stroke.

Stroke is a leading cause of death and disability in the United States. Strokes are caused by abnormal changes in blood flow in the brain or the bursting of brain blood vessels.

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REVIEW article

Diagnosis and Management of Diastolic Dysfunction and Heart Failure CHHABI SATPATHY, TRINATH K MISHRA, RUBY SATPATHY, HEMANT K SATPATHY, EUGENE BARONE

Abstract Diastolic heart failure occurs when signs and symptoms of heart failure are present but left ventricular systolic function is preserved (i.e., ejection fraction greater than 45 percent). The incidence of diastolic heart failure increases with age; therefore, 50 percent of older patients with heart failure may have isolated diastolic dysfunction. With early diagnosis and proper management the prognosis of diastolic dysfunction is more favorable than that of systolic dysfunction. Distinguishing diastolic from systolic heart failure is essential because the optimal therapy for one may aggravate the other. Although diastolic heart failure is clinically and radiographically indistinguishable from systolic heart failure, normal ejection fraction and abnormal diastolic function in the presence of symptoms and signs of heart failure confirm diastolic heart failure. The pharmacologic therapies of choice for diastolic heart failure are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, and beta blockers.

Keywords: Diastolic heart failure, left ventricular systolic function, ejection fraction, diastolic dysfunction, angiotensinconverting enzyme inhibitors, angiotensin receptor blockers, diuretics, beta blockers

T

hree million Americans have congestive heart failure (CHF), and 500,000 new cases are diagnosed each year. The condition is the most common discharge diagnosis for patients older than 65 years1 and is the most expensive disease for Medicare.2 Systolic and diastolic dysfunction can cause CHF.3 All patients with systolic dysfunction have concomitant diastolic dysfunction; therefore, a patient cannot have pure systolic heart failure.4 In contrast, certain cardiovascular diseases such as hypertension may lead

CHHABI SATPATHY, M.D., is professor in the Department of Cardiology at Utkal University’s Sriram Chandra Bhanja (SCB) Medical College, Cuttack, Orissa, India.

She received her medical degree from and completed an internal medicine residency at Utkal University’s SCB Medical College.

TRINATH K. MISHRA, M.D., is professor in the Department of Cardiology at Utkal University’s SCB Medical College, where he received his medical degree and completed an internal medicine residency.

RUBY SATPATHY, M.D., is a resident in the Department of Internal Medicine at Creighton University Medical Center, Omaha, Neb. She received her medical degree from Utkal University’s SCB Medical College.

HEMANT K. SATPATHY, M.D., is professor of family medicine in the Department of Family Practice at Creighton University Medical Center. He received his medical degree from Utkal University’s SCB Medical College.

Dr. Satpathy completed a residency in obstetrics and gynecology at Vir Surendra Sai Medical College, Burla, India. He completed a family practice residency at Creighton University Medical Center, including one year as chief resident.

EUGENE BARONE, M.D., is professor and predoctoral director in the Department of Family Practice at Creighton University Medical Center where he received his medical degree and completed a family medicine residency.

Source: Adapted from Am Fam Physician. 2006;73:841-846.

to diastolic dysfunction without concomitant systolic dysfunction.5 Although diastolic heart failure accounts for approximately 40 to 60% of patients with CHF, these patients have a better prognosis than those with systolic heart failure.6 Definition and Diagnostic Criteria Diastolic heart failure is defined as a condition caused by increased resistance to the filling of one or both ventricles; this leads to symptoms of congestion from the inappropriate upward shift of the diastolic pressurevolume relation.7 Although this definition describes the principal pathophysiologic mechanism of diastolic heart failure, it is not clinically applicable. A more practical definition for use in clinical practice is: a condition that includes classic CHF findings and abnormal diastolic and normal systolic function at rest.8,9 A study group7 proposed that physicians combine clinical and echocardiographic information to categorize patients with diastolic heart failure according to the degree of diagnostic certainty (Table 110).

Prevalence and Etiology On average, 40% of patients with heart failure have preserved systolic function.11-13 The incidence of diastolic heart failure increases with age, and it is more common in older women.14,15 Hypertension and cardiac ischemia are the most common causes of

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review article Table 1 Diagnostic Criteria for Diastolic Heart Failure Definitive diastolic heart failure Definitive evidence of congestive heart

Probable diastolic heart failure* Possible diastolic heart failure Same as definitive

failure†

and

and

Objective evidence of normal left ventricular systolic function in proximity of event‡

Same as definitive

Left ventricular ejection fraction of 50 percent or more not measured within 72 hours of event

and

and

and

Objective evidence of left ventricular diastolic dysfunction§

No conclusive information on left ventricular diastolic function

Same as probable

*Patients who have definitive evidence of congestive heart failure and objective evidence of normal left ventricular systolic function in proximity of event are accepted as having probable diastolic heart failure provided that mitral valve disease, cor pulmonale, primary volume overload, and noncardiac causes are excluded. †Clinical symptoms and signs, supporting chest radiography, typical clinical response to diuretics with or without elevated left ventricular filling pressure, or low cardiac index. ‡Left ventricular ejection fraction of 50 percent or more within 72 hours of event. §Abnormal left ventricular relaxation or filling or distensibility indices on catheterization.

Table 2. Causes of Diastolic Dysfunction and Heart Failure Common causes* Cardiac ischemia Hypertension Aging Obesity Aortic stenosis

Pathophysiology Diastole is the process by which the heart returns to its relaxed state. During this period, the cardiac muscle is perfused. Conventionally, diastole can be divided into Pathophysiology of Diastolic Heart Failure Pressure overload Hypertrophy ischemia Myocardial infarction

Uncommon causes Myocardial disorders Myocardial diseases

Abnormal relaxation

Infiltrative disease (e.g., amyloidosis, sarcoidosis, fatty

Abnormal relaxation and increased stiffness

Increased stiffness

infiltration) Noninfiltrative diseases (e.g., idiopathic and hypertrophic cardiomyopathy) Endomyocardial diseases

Abnormal early filling

Hypereosinophilic syndrome

Elevated left ventricular filling pressures

Elevated pulmonary pressure during exercise

Storage diseases Glycogen storage disease

Elevated left atrial pressure and size Atrial fibrillation and decreased cardiac output

Hemochromatosis Pericardial disorders Constrictive pericarditis Effusive-constrictive pericarditis Pericardial effusion *Common causes are listed in order of prevalence.

diastolic heart failure (Table 2). Common precipitating factors include volume overload; tachycardia; exercise; hypertension; ischemia; systemic stressors (e.g., anemia, fever, infection, thyrotoxicosis); arrhythmia (e.g., atrial fibrillation, atrioventricular nodal block); increased salt intake; and use of nonsteroidal anti-inflammatory drugs.

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Normal exercise tolerance

Reduced exercise tolerance

Reduced exercise tolerance and signs of congestive heart failure

Diastolic abnormalities Diastolic dysfunction Diastolic heart failure

Figure 1. Algorithm for pathophysiology of diastolic heart failure. Abnormal relaxation and increased stiffness are associated with diastolic filling abnormalities and normal exercise tolerance in the early phase of diastolic dysfunction.

When the disease progresses, pulmonary pressures increase abnormally during exercise, producing reduced exercise tolerance. When filling pressures increase further, left atrial pressure and size increase and exercise tolerance falls as clinical signs of congestive heart failure appear.

review article four phases: isovolumetric relaxation, caused by closure of the aortic valve to the mitral valve opening; early rapid ventricular filling located after the mitral valve opening; diastasis, a period of low flow during middiastole; and late rapid filling during atrial contraction.16 Broadly defined, isolated diastolic dysfunction is the impairment of isovolumetric ventricular relaxation and decreased compliance of the left ventricle. With diastolic dysfunction, the heart is able to meet the body’s metabolic needs, whether at rest or during exercise, but at a higher filling pressure. Transmission of higher enddiastolic pressure to the pulmonary circulation may cause pulmonary congestion, which leads to dyspnea and subsequent right-sided heart failure. With mild dysfunction, late filling increases until the ventricular end-diastolic volume returns to normal. In severe cases, the ventricle becomes so stiff that the atrial muscle fails and end diastolic volume cannot be normalized with elevated filling pressure. This process reduces stroke volume and cardiac output, causing effort intolerance.

Figure 117 summarizes the pathophysiology of diastolic heart failure.

Diagnosis Heart failure can present as fatigue, dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, jugular venous distention, rales, tachycardia, third or fourth heart sounds, hepatomegaly, and edema.

Cardiomegaly and pulmonary venous congestion commonly are found on chest radiography. However, these findings are nonspecific and often occur in noncardiac conditions such as pulmonary disease, anemia, hypothyroidism, and obesity. Furthermore, it is difficult to distinguish diastolic from systolic heart failure based on physical findings alone.18 The serum brain natriuretic peptide (BNP) test can accurately differentiate heart failure from noncardiac conditions in a patient with dyspnea, but it cannot

distinguish diastolic from systolic heart failure.

Table 319 summarizes the accuracy of BNP levels for diagnosing heart failure. Physicians also should consider that patients’ New York Heart Association severity class affects BNP levels. In addition to providing fundamental information on chamber size, wall thickness and motion, systolic function, the valves, and the pericardium, two-dimensional echocardiography with Doppler is used to evaluate the characteristics of diastolic transmitral and pulmonary venous flow pattern.20 On echocardiography, the peak velocity of blood flow across the mitral valve during early diastolic filling corresponds to the E wave.

Similarly, atrial contraction corresponds to the A wave.

From these findings, the E/A ratio is calculated. Under normal conditions, E is greater than A and the E/A ratio is approximately 1.5.21 In early diastolic dysfunction, relaxation is impaired and, with vigorous atrial contraction, the E/A ratio decreases to less than 1.0. As the disease progresses, left ventricular compliance is reduced, which increases left atrial pressure and, in turn, increases early left ventricular filling despite impaired relaxation. This paradoxical normalization of the E/A ratio is called pseudonormalization. In patients with severe diastolic dysfunction, left ventricular filling occurs primarily in early diastole, creating an E/A ratio greater than 2.0.

The E- and A-wave velocities are affected by blood volume, mitral valve anatomy, mitral valve function, and atrial fibrillation, making standard echocardiography less reliable. In these cases, tissue Doppler imaging is useful for measuring mitral annular motion (a measure of transmitral flow that is independent of the aforementioned factors).

Cardiac catheterization remains the preferred method for diagnosing diastolic dysfunction. However, in day-today clinical practice, two-dimensional echocardiography with Doppler is the best noninvasive tool to confirm the diagnosis. Rarely, radionuclide angiography is used for patients in whom echocardiography is technically difficult.

Table 3. Accuracy of BNP Levels for Diagnosing Heart Failure Congestive heart failure vs. noncongestive heart failure

Systolic heart failure vs. nonsystolic heart failure

BNP level (pg per mL) Sensitivity (%) Specificity (%)

LR+

LR–

Sensitivity (%)

Specificity (%)

LR+

LR–

100

90

73

4.5

0.12

95

14

1.1

0.36

200

81

85

5.4

0.22

89

27

1.2

0.41

300

73

89

6.6

0.3

83

39

1.4

0.44

400

63

91

7

0.41

74

50

1.48

0.52

BNP = brain natriuretic peptide; LR+ = positive likelihood ratio; LR– = negative likelihood ratio.

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review article Management Primary prevention of diastolic heart failure includes smoking cessation and aggressive control of hypertension, hypercholesterolemia, and coronary artery disease. Lifestyle modifications such as weight loss, smoking cessation, dietary changes, limiting alcohol intake, and exercise are equally effective in preventing diastolic and systolic heart failure. Diastolic dysfunction may be present for several years before it is clinically evident (Figure 117). Early diagnosis and treatment is important in preventing irreversible structural alterations and systolic dysfunction.

However, no single drug has pure lusitropic properties (i.e., selective enhancement of myocardial relaxation without inhibiting left ventricular contractility or function). Therefore, medical therapies for diastolic dysfunction and diastolic heart failure often are empirical and not as well defined as therapies for systolic heart failure. On the surface, it appears that the pharmacologic treatments of diastolic and systolic heart failure do not differ dramatically; however, the treatment of diastolic heart failure is limited by the lack of large and conclusive randomized control trials.22 Furthermore, the optimal treatment for systolic heart failure may exacerbate diastolic heart failure.

Most clinical trials to date have focused exclusively on patients with systolic heart failure; only recently have trials addressed the treatment of diastolic heart failure.

Although conclusive data on specific therapies for diastolic heart failure are lacking, the American College of Cardiology and the American Heart Association joint guidelines22 recommend that physicians address blood pressure control, heart rate control, central blood volume reduction, and alleviation of myocardial ischemia when treating patients with diastolic heart failure. These guidelines target underlying causes and are likely to improve left ventricular function and optimize hemodynamics. Table 4 lists treatment goals for diastolic heart failure.

Improving Left Ventricular Function When treating a patient with diastolic dysfunction, it is important to control the heart rate and prevent tachycardia to maximize the diastolic filling period.

Beta blockers are particularly useful for this purpose; however, they do not directly affect myocardial relaxation. In addition to slowing heart rate, beta blockers have proven benefits in reducing blood pressure and myocardial ischemia, promoting regression of left ventricular hypertrophy, and antagonizing the excessive adrenergic stimulation during heart failure.

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Table 4. Goals for Treating Diastolic Heart Failure Treat precipitating factors and underlying disease.

Prevent and treat hypertension and ischemic heart disease.

Surgically remove diseased pericardium.

Improve left ventricular relaxation.

ACE inhibitors Calcium channel blockers Regress left ventricular hypertrophy (decrease wall thickness and remove excess collagen).

ACE inhibitors and ARBs Aldosterone antagonists Beta blockers Calcium channel blockers Maintain atrioventricular synchrony by managing tachycardia (tachyarrhythmia).

Beta blockers (preferred) Calcium channel blockers (second-line agents) Digoxin (controversial) Atrioventricular node ablation (rare cases) Optimize circulating volume (hemodynamics).

ACE inhibitors Aldosterone antagonists (theoretical benefit) Salt and water restriction Diuresis, dialysis, or plasmapheresis Improve survival.

Beta blockers ACE inhibitors Prevent relapse by intensifying outpatient follow-up.

Control blood pressure.

Dietary counseling (sodium) Monitoring volume status (daily weights and diuretic adjustment) Institute exercise program.

ACE = Angiotensin-converting enzyme; ARB = Angiotensin receptor blocker.

Beta blockers have been independently associated with improved survival in patients with diastolic heart failure.23 These medications should be used to treat diastolic heart failure, especially if hypertension, coronary artery disease, or arrhythmia is present.

Optimizing Hemodynamics Optimizing hemodynamics primarily is achieved by reducing cardiac preload and afterload. Angiotensinconverting enzyme (ACE) inhibitors and angiotensin

review article receptor blockers (ARBs) directly affect myocardial relaxation and compliance by inhibiting production of or blocking angiotensin II receptors, thereby reducing interstitial collagen deposition and fibrosis.24,25 The indirect benefits of optimizing hemodynamics include improving left ventricular filling and reducing blood pressure. More importantly, there is improvement in exercise capacity and quality of life.26 One retrospective study27 showed that improved survival was associated with ACE inhibitor therapy in patients with diastolic heart failure. One arm of the CHARM (Candesartan in Heart Failure Assessment of Reduction in Morbidity and Mortality) trial,28 which studied the effect of candesartan in patients with normal ejection fraction for 36.6 months, did not show a significant mortality benefit. However, it reduced the incidence of hospitalization for CHF exacerbation.

Diuretics are effective in managing optimal intravascular volume, and they minimize dyspnea and prevent acute heart failure in patients with diastolic dysfunction. Although diuretics control blood pressure, reverse left ventricular hypertrophy, and reduce left ventricular stiffness, some patients with diastolic heart failure are sensitive to the preload reduction and may develop hypotension or severe prerenal azotemia.

Intravenous diuretics should only be used to relieve acute symptoms.

The hormone aldosterone promotes fibrosis in the heart and contributes to diastolic stiffness. The aldosterone antagonist spironolactone has been studied in a large clinical trial of systolic heart failure,29 which showed a reduction in mortality related to heart failure. However, the specific effects of spironolactone on diastolic dysfunction are unclear.

Calcium channel blockers have been shown to improve diastolic function directly by decreasing cytoplasmic calcium concentration and causing myocardial relaxation or indirectly by reducing blood pressure, reducing or preventing myocardial ischemia, promoting regression of left ventricular hypertrophy, and by slowing the heart rate. However, non-dihydropyridine calcium channel blockers (e.g., diltiazem) and verapamil, should not be used in patients with bradycardia, conduction defects, or severe heart failure caused by left ventricular systolic dysfunction.30 Instead nondihydropyridines such as diltiazem and verapamil, should be used for rate control and angina when beta blockers are contraindicated or ineffective. Finally, large randomized controlled trials have not proved that calcium channel blockers reduce mortality in patients with isolated diastolic dysfunction.

Vasodilators (e.g., nitrates, hydralazine) may be useful because of their preload-reducing and anti-ischemic effects, particularly when ACE inhibitors cannot be used. The Vasodilator Heart Failure Trial,31 however, did not show significant survival benefit in patients with diastolic heart failure. Vasodilators should be used cautiously because decreasing preload may worsen cardiac output. Unlike other medications used for diastolic heart failure, vasodilators have no effect on left ventricular regression.

The exact role of digoxin for treating patients with diastolic heart failure remains unclear. Digoxin can be deleterious in older patients with left ventricular hypertrophy and hypertrophic obstructive cardiomyopathy; therefore, digoxin is only appropriate for patients with diastolic heart failure and atrial fibrillation.32 REFERENCES 1. Tecce MA, Pennington JA, Segal BL, Jessup ML. Heart failure: clinical implications of systolic and diastolic dysfunction. Geriatrics 1999;54:24-8,31-3.

2. Massie BM, Shah NB. Evolving trends in the epidemiologic factors of heart failure: rationale for preventive strategies and comprehensive disease management. Am Heart J 1997;133:703-12.

3. Litwin SE, Grossman W. Diastolic dysfunction as a cause of heart failure. J Am Coll Cardiol 1993;22(4 suppl A):49A-55A. 4. Brutsaert DL, Sys SU. Diastolic dysfunction in heart failure. J Card Fail 1997;3:225-42.

5. Vasan RS, Larson MG, Benjamin EJ, Evans JC, Reiss CK, Levy D. Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort. J Am Coll Cardiol 1999;33:1948-55.

6. Senni M, Redfield MM. Heart failure with preserved systolic function. A different natural history? J Am Coll Cardiol 2001;38:1277-82.

7. Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: pathophysiology and therapeutic implications [published correction appears in J Am Coll Cardiol 1993;22:1272]. J Am Coll Cardiol 1993;22:318-25.

8. Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation 2000;101:2118-21.

9. Grossman W. Defining diastolic dysfunction. Circulation 2000;101:2020-1.

10. van Kraaij DJ, van Pol PE, Ruiters AW, de Swart JB, Lips DJ, Lencer N, et al. Diagnosing diastolic heart failure. Eur J Heart Fail 2002;4:419-30.

11. Vasan RS, Benjamin EJ, Levy D. Prevalence, clinical features and prognosis of diastolic heart failure: an

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review article epidemiologic perspective. J Am Coll Cardiol 1995;26:1565-74.

12. Kitzman DW, Gardin JM, Arnold A, Gottdiener JS, Lyles M, Smith VE, et al., for the CHS Research Group. Heart failure with preserved systolic LV function in the elderly: clinical and echocardiographic correlates from the Cardiovascular Health Study. Circulation 1996;94(suppl 1):1-433.

13. Senni M, Tribouilloy CM, Rodeheffer RJ, Jacobsen SJ, Evans JM, Bailey KR, et al. Congestive heart failure in the community: a study of all incident cases in Olmsted County, Minnesota, in 1991. Circulation 1998;98:2282-9.

14. McCullough PA, Philbin EF, Spertus JA, Kaatz S, Sandberg KR, Weaver WD. Confirmation of a heart failure epidemic: findings from the Resource Utilization Among Congestive Heart Failure (REACH) study. J Am Coll Cardiol 2002;39:60-9.

15. Ahmed A, Nanda NC, Weaver MT, Allman RM, DeLong JF. Clinical correlates of isolated left ventricular diastolic dysfunction among hospitalized older heart failure patients. Am J Geriatr Cardiol 2003;12:82-9.

16. Kovacs SJ, Meisner JS, Yellin EL. Modeling of diastole [published correction appears in Cardiol Clin 2000;18:following table of contents]. Cardiol Clin 2000;18:459-87.

17. Mandinov L, Eberli FR, Seiler C, Hess OM. Diastolic heart failure. Cardiovasc Res 2000;45:822.

18. Philbin EF, Hunsberger S, Garg R, Lader E, Thadani U, McSherry F, et al, and the Digitalis Investigation Group.

Usefulness of clinical information to distinguish patients with normal from those with low ejection fractions in heart failure. Am J Cardiol 2002;89:1218-21.

19. Maisel AS, McCord J, Nowak RM, Hollander JE, Wu AH, Duc P, et al. Bedside B-type natriuretic peptide in the emergency diagnosis of heart failure with reduced or preserved ejection fraction. Results from the Breathing Not Properly Multinational Study. J Am Coll Cardiol 2003;41:2010-7.

the adult: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2001;38:2101-13.

23. Chen HH, Lainchbury JB, Senni M, Redfield MM. Factors influencing survival in patients with diastolic heart failure in Olmsted County, Minn. Circulation 2000;102:II412.

24. Angomachalelis N, Hourzamanis AI, Sideri S, Serasli E, Vamvalis C. Improvement of left ventricular diastolic dysfunction in hypertensive patients 1 month after ACE inhibition therapy: evaluation by ultrasonic automated boundary detection. Heart Vessels 1996;11:303-9.

25. Mitsunami K, Inoue S, Maeda K, Endoh S, Takahashi M, Okada M, et al. Three-month effects of candesartan cilexetil, an angiotensin II type 1 (AT1) receptor antagonist, on left ventricular mass and hemodynamics in patients with essential hypertension. Cardiovasc Drugs Ther 1998; 12:469-74.

26. Warner JG Jr, Metzger DC, Kitzman DW, Wesley DJ, Little WC. Losartan improves exercise tolerance in patients with diastolic dysfunction and a hypertensive response to exercise. J Am Coll Cardiol 1999;33:1567-72.

27. Philbin EF, Rocco TA Jr, Lindenmuth NW, Ulrich K, Jenkins PL. Systolic versus diastolic heart failure in community practice: clinical features, outcomes, and the use of angiotensin-converting enzyme inhibitors. Am J Med 2000;109:605-13.

28. Yusuf S, Pfeffer MA, Swedberg K, Granger CB, Held P, McMurray JJ, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial. Lancet 2003;362:777-81.

29. Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, et al., for the Randomized Aldactone Evaluation Study Investigators. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 1999;341:709-17.

20. Naqvi TZ. Diastolic function assessment incorporating new techniques in Doppler echocardiography. Rev Cardiovasc Med 2003;4:81-99.

30. Gutierrez C, Blanchard DG. Diastolic heart failure: challenges of diagnosis and treatment. Am Fam Physician 2004;69:2609-16.

21. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988;12:426-40.

31. Cohn JN, Johnson G, for the Veterans Administration Cooperative Study Group. Heart failure with normal ejection fraction. The V-HeFT Study. Circulation 1990;81(2 suppl):III48-53.

22. Hunt SA, Baker DW, Chin MH, Cinquegrani MP, Feldman AM, Francis GS, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in

32. Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med 1997;336:525-33.

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CLINICAL STUDY

An Autopsy and Echocardiographic Study of Left Ventricular Trabeculations Deep C Pant*, Hema Pant**, Ajay Bahl†, Uma Saikia‡

Abstract Background: Left ventricular (LV) trabeculations are normal anatomic variants, which can be confused with pathologic entities like mural thrombi. This was a pilot study to know the incidence and morphology of normal LV trabeculation in normal hearts both by autopsy and echocardiography. Objectives: To study the incidence of prominent LV trabeculations by autopsy and echocardiography. Material and methods: Prominent LV trabeculations, defined as trabeculations with thickness at least 50% of underlying myocardium were studied in 50 patients both by echocardiography and autopsy. Results: Prominent LV trabeculations were found in 16% of normal heart on autopsy and 14% hearts on echocardiography and incidence by two modalities was comparable. Conclusion: Prominent LV trabeculations, which are normal anatomic variants can be found in minority of hearts and can be reliably detected by echocardiography.

Keywords: Left ventricle trabeculation, incidence, autopsy, echocardiography

A

dvancement in transducers and introduction of high-resolution second harmonic technology has improved the evaluation of heart anatomy and in particular, left ventricular anatomy. Left ventricle false tendons and trabeculations are present is about half the human hearts in pathologic conditions, whereas their echocardiographic incidence in adults has been demonstrated to be very low in comparison with the prevalence on morphologic examination. Even though the echocardiographic recognition of these cavitary structures may have little clinical significance per se, these anatomic variants may be very important because of their potential to be mistaken for more important pathologic entities like mural thrombi.

AIM

This was a pilot study to see the morphology of left ventricular (LV) trabeculations by 2D echocardiography, (2D echo) and at autopsy to define the incidence and normal variations in the (LV) trabeculations.

MATERIAL AND METHODS

*Associate Professor, Dept. of Cardiology **Associate Professor, Dept. of Pathology SRMSIMS, Bareilly, Uttar Pradesh †Associate Professor, Dept. of Cardiology ‡Associate Professor, Dept. of Pathology PGIMER, Chandigarh Address for correspondence Dr Deep C Pant, Dept. of Cardiology SRMSIMS, Bareilly, Uttar Pradesh E-mail: pantpgimer@yahoo.co.in

To characterize the variations in LV trabeculations in normal heart on echocardiography and at autopsy.

OBJECTIVES ÂÂ

To study LV trabeculations in normal hearts on 2D echo.

ÂÂ

To study the variations, number and morphology of LV trabeculations at autopsy in patients without cardiac disease.

ÂÂ

To compare the echocardiographic and autopsy findings of variations in LV trabeculations in normal hearts.

2D Echocardiography Fifty consecutive individuals were included in the study with age < 50 years with no apparent cardiac sign or symptoms.

Inclusion Criterion ÂÂ

Age < 50 years.

ÂÂ

Patients attending Cardiology OPD with a negative treadmill test and no evidence of heart disease.

ÂÂ

Healthy attendants accompanying patients coming for 2D echo study of their patients who were

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Clinical Study

1 Trabeculation 11% 11%

67% 11%

Table 1. Distribution of LV Trabeculations on Gross Morphology

2 Trabeculations

No. of trabeculation

3 Trabeculations 5 Trabeculations

Figure 1. Showing percentage for the number of LV trabeculations.

No. of hearts

Percentage (%)

1

4

50

2

3

37

3

1

13

Table 2. Age and Sex Distribution of Subjects at Autopsy Sex

8 7

No. of trabeculations

6 5 No of LV trabeculations

Male

Female

18-30 yrs

24 (48%)

16

8

31-40 yrs

15 (30%)

11

6

41-50 yrs

11 (22%)

6

3

Mean age of the subjects antemortem was 32.7 ± 7.6 years.

4

Table 3. Percentage-wise Distribution of Number of Trabeculations on 2D-Echo.

3 2

Number of trabeculations

1

No. of hearts

Percentage (%)

1

4

57

2

3

43

0 Papillary muscle level

Short-axis level

Mitral value

Figure 2. Showing the number of trabeculations at different short-axis level on 2D echo.

willing to undergo screening 2D echo for LV trabeculations.

Exclusion Criterion ÂÂ

Presence of heart disease including coronary heart disease, congenital heart disease, cardiomyopathies of various types, rheumatic heart diseases.

ÂÂ

Systemic hypertension

ÂÂ

Diabetes mellitus

ÂÂ

Chronic renal failure

ÂÂ

Long-standing anemia

ÂÂ

Other medical causes, which have direct effect on cardiac functions i.e., diabetes mellitus (type 1 and type II), chronic glomerulonephritis, chronic pyleonephritis.

The above exclusion criteria were strictly followed both for echocardiography and autopsy study.

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Table 4. Percentage-wise Distribution of Site of LV Trabeculations on 2D Echo Level of short-axis

Number of heart

Percentage (%)

Mitral valve level

1

14

Papillary muscle level

3

43

Apical short-axis

3

43

2D Echo Study Left ventricle trabeculi were studied at following three levels: ÂÂ

Parasternal short-axis at mitral level

ÂÂ

Parasternal short-axis at papillary muscle level

ÂÂ

Short axis at apex

ÂÂ

Prominent LV trabeculation was defined as trabeculation with thickness at least 50% of underlying myocardium in end-systole

ÂÂ

Echocardiography of the patients was done on Acuson Sequoia C512 machine.

Clinical Study

Figure 3. Showing single prominent LV trabeculation at apex (Arrow).

Figure 4. Showing two prominent LV trabeculations at apex.

Figure 5. Showing single prominent LV trabeculations at apex.

Figure 6. Showing three prominent LV trabeculation with dilated LV cavity.

Autopsy Study

dimensions and any other abnormality. All the cases were photographed digitally, stored and the data was saved.

All the cases dying of noncardiac causes including exclusion criterion mentioned for 2D echo were included for the study. A total of 50 consecutive autopsy cases performed as standard medical autopsy with prior informed consent of the patients relatives were studied. The heart specimens were dissected along the flow of blood and fixed in 10% buffered formalin for preservation. LV and RV trabeculations were assessed for their number, coarseness, gross morphology,

Gross Features Heart weight was taken in relation to expected heart weight for body weight.

Cut section of heart in short-axis at 0.5 cm thickness from base to apex and total number of trabeculi were counted.

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Clinical Study

Figure 7. Showing two prominent LV trabeculations at apex.

Figure 8. Showing two prominent LV trabeculations at apex.

Figure 9. Showing two prominent LV trabeculations at papillary muscle level in short-axis of heart.

Figure 10. Showing single prominent LV trabeculation at apex.

ÂÂ

Ratio of thickness of trabeculi to underlying myocardium was noted.

ÂÂ

Measurement of trabeculi was done by vernier callipers.

ÂÂ

All trabeculi were photographed digitally and stored for future comparison.

ÂÂ

Prominent LV trabeculation was defined as trabeculation thickness at least 50% of underlying myocardium.

ÂÂ

102

Prominent LV trabeculations were studied and counted at short-axis at apex.

Asian Journal of Clinical Cardiology, Vol. 16, No. 3, July 2013

ÂÂ

ÂÂ

Cases were studied with routine sectioning of right and left ventricle, with massons trichrome and elastic von geisen stains performed for collagen and elastic tissue, respectively.

Any associated incidental cardiac anomaly was also noted.

OBSERVATION AND RESULTS Fifty consecutive heart specimen were studied at autopsy and the heart specimens were dissected along the flow of blood.

Clinical Study

Figure 11. Showing single prominent LV trabeculation at papillary muscle level.

Figure 12. Showing single prominent LV trabeculation at apex.

The age of the patients varied from 18 years to 50 years.

The mean age of the patients studied was 32.7 ± 7.6 years. Out of the 50 hearts selected for study, 33 hearts belonged to male subjects and 17 hearts belonged to female subjects. The weight of the heart specimens varied from 194 g to 430 g and mean weight was 274 ± 96 g.

The age of subjects ranged from 19 years to 48 years and the mean age was 32 ± 6.4 years. The mean age of the subjects examined was 32 ± 6.4 years.

Left Ventricle Trabeculations Left ventricle was studied for presence of significant trabeculations. The cases in which trabeculation thickness was least 50% of underlying myocardium in short-axis at the apex was considered as significant trabeculation.

Of the total of 50 hearts studied, eight hearts (16%) had significant LV trabeculations. Of these eight hearts with prominent trabeculations, four hearts had single trabeculation, three hearts had two trabeculations and one heart had three trabeculations. Of the eight heart with prominent trabeculations, seven heart had ratio of trabeculation to underlying myocardium between 0.5 to 1. One heart had ratio of trabeculation to underlying myocardium between 1 to 1.5. None of the heart had ratio of measured trabeculation to underlying myocardium >1.5.

ECHOCARDIOGRAPHIC STUDY

Age and Sex Distribution of Patients The number of male subjects in echocardiographic study was 29. The number of female subjects was 21.

Left Ventricle Trabeculations Fifty hearts of healthy subjects were examined for prominent LV trabeculations. Prominent trabeculation in present study was defined as trabeculations with thickness at least 50% of underlying myocardium.

Prominent LV trabeculations were detected in seven hearts out of 50 hearts of healthy subjects examined (14%). Four hearts had single LV trabeculation. Three hearts had two prominent trabeculations.

Of the hearts with prominent trabeculations the ratio of measured trabeculation to underlying myocardium thickness was between 0.5 to 1 in all the seven hearts.

In none of the hearts this observed ratio was >1.

Comparison of Echocardiographic and Autopsy Study ÂÂ

Mean age of the subjects in autopsy study was 32.7 ± 7.6 years and for echocardiographic subjects was 32 ± 6.1 years (p < 0.001) for equivalence in age two groups.

ÂÂ

At autopsy studies 34% cases were females while in echocardiographic study 42% of the subjects were female.

ÂÂ

Observations at autopsy revealed prominent LV trabeculations in eight of the total of 50 heart specimens examined (16%) while echocardiographically LV

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Clinical Study trabeculations were observed in seven hearts of the 50 hearts examined (14%). ÂÂ

The difference in incidence of LV trabeculations examined by two modalities was not statistically significant.

DISCUSSION The LV is typically less trabeculated than the right ventricle, and other than the papillary muscles it is infrequent to note coarse muscle trabeculations in the left ventricle. Occasionally trabeculated left ventricle apex is encountered, the degree of which rarely approaches that seen in right ventricle.

According to Stollberger et al, in human hearts the LV has upto three prominent trabeculations and is thus less traebeculated than the right ventricle. No study has till now simultaneously studied autopsy and echocardiography to detect the incidence of LV trabeculations in normal hearts and compared the two diagnostic modalities.

In the present study, a detailed search was made for LV trabeculations in normal human hearts.

The morphology, variations and incidence of LV trabeculations was studied both by echocardiography and at autopsy in 50 subjects and cases, respectively.

In the 2D echo study, LV trabeculations were studied in short-axis view at mitral level, papillary muscle level and at apical short-axis. All trabeculations, which had thickness ≥50% of underlying myocardium were considered prominent trabeculations and were considered for analysis for calculating the incidence and morphology of LV trabeculation.

On 2D echo study, prominent LV trabeculations were detected in seven patients (14%) of the 50 healthy hearts examined. Four (57%) of these hearts had single LV trabeculation only, while 3 (43%) hearts had two trabeculations.

In male subjects, four hearts had prominent LV trabeculation out of 29 hearts examined (28%). In female subjects, three hearts had significant LV trabeculations out of 21 hearts examined (24%). Hence, incidence of LV trabeculations was slightly more in male subjects on 2D echo.

The overall incidence of LV trabeculation was found to be 16% at autopsy and 14% on echocardiography.

The incidence of LV trabeculation in males subjects was 15% (5/33) and female subjects was 17.6% (3/17).

The mean age of the patient having LV trabeculation was 36.11 ± 8. 4 years. The mean weight of the heart specimen examined was 274 ± 96 g.

On comparison of echocardiographic incidence of LV trabeculations in our study to study done by Tamborini et al, the incidence of prominent LV trabeculation in our study is slightly lower, 14% versus 26%, respectively.

Tamborini et al, sought to review echocardiographic incidence of AI (anamolous images) such as false tendons and apical trabeculations and to define the normal echocardiographic appearance of LV endocardial surface. In 1580, patients the presence of false tendons, trabeculations or thrombi were evaluated with transthoracic echocardiography and correlated to clinical characteristics and echocardiographic parameters. The incidence of AI was 46.2 (75% false tendons, 23% trabeculations, 2% thrombi) slightly higher in pathologic (48.9%) then in normal hearts (40.8%). In AI was more frequent in male patient (52%) then female patients (39.7%) and associated with LV dilatation, hypertrophy and systolic dysfunction. False tendons and LV trabeculations were not related to age. Male sex was the most significant independent predictor of anamolous image.

There is need of correct technical approach for a complete examination of the LV apex for detection of LV trabeculations. All studies included not only the standard views from all the echocardiographic windows, but also off axis views obtained by angulating the probe to better visualize the apex and insertion points and orientation of the suggested trabeculation.

In the present study, we also used one additional echocardiographic view of apical short-axis to visualize the LV trabeculations.

At autopsy, LV trabeculations were seen in eight hearts (16%) out of total 50 hearts examined. All trabeculations were studied at apical short-axis in heart specimen and measured with a scale.

Trabeculations also were observed between two points on the ventricular septum in 37 (6%) of the hearts and between two points along the free wall in 36 (6%). Less common patterns included trabeculations between the ventricular septum and the posteromedial papillary muscle in 10 hearts (2%), the ventricular septum and the anterolateral papillary muscles in two, the two papillary muscles in one and the apex and the ventricular septum in one heart.

Of all hearts having LV trabeculation, four heart had single LV trabeculations, while two trabeculations were seen in two hearts. One heart had three LV trabeculation.

In our study, solated right ventricular hypertrabeculation was found in one heart at autopsy. In this heart, non-compacted portion of right ventricular myocardium

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Clinical Study was more than three times the underlying compacted right ventricular myocardium at apex with dilated RV cavity. In the above heart left ventricular apex was relatively spared but however both the papillary muscles of left ventricle were poorly developed. Poorly developed papillary muscle on left side of heart is one of the criteria at autopsy for diagnosis of left ventricular noncompaction. However, the significance of isolated noncompaction of right ventricle with poorly formed papillary muscle on left side is not known.

Study Limitations The sample size was small in our study both in echocardiography and at autopsy, which could have resulted in lower incidence of LV trabeculations in our study when compared to other similar large studies.

Another limitation of our study was that success of patients for echocardiography and autopsy study were different, so a comparison cannot be made between the diagnostic accuracy of echocardiography against the bench mark of autopsy study for detection of LV trabeculations.

Summary And Conclusions ÂÂ

ÂÂ

Incidence and morphologic variations in prominent LV trabeculations in 50 normal hearts on 2D echo and at autopsy were studied.

Prominent LV trabeculations were seen in eight hearts (16%) out of the 50 normal hearts examined at autopsy.

ÂÂ

On 2D echo, prominent LV trabeculation were found in seven hearts (14%) of 50 heart examined.

ÂÂ

The echoc and autopsy incidence of prominent LV trabeculations is comparable i.e. 14% versus 16% (p = 0.16).

ÂÂ

No of prominent trabeculations detected by autopsy varied between one to three (mean 1 ± 0.56).

ÂÂ

No of prominent trabeculations detected by echocardiography varied between one and two (mean 1 ± 0.49)

ÂÂ

In the autopsy study, the ratio of prominent LV trabeculations to underlying myocardium thickness was between 0.5 to 1 in seven hearts ,while in one

heart this ratio was between 1 to 1.5. None of the examined hearts had this ratio >1.5. ÂÂ

In the echocardiography study, all prominent LV trabeculations had ratio of trabeculation to underlying myocardium thickness between 0.5 to 1. None of the measured trabeculation had this ratio >1.

Conclusion ÂÂ

Prominent LV trabeculations are seen in 14-16% of normal hearts.

ÂÂ

Only 1-3 prominent LV trabeculation were seen in studied normal hearts.

ÂÂ

None of the hearts had ratio of trabeculation to underlying myocardium thickness >1.5 by autopsy and 1 by echocardiography study.

SUGGESTED READING 1. Tamborini G, Pepi M, Celeste F, Muratori M, Susini F, Maltagliati A, et al. Incidence and characteristics of left ventricular false tendons and trabeculations in the normal and pathologic heart by second harmonic echocardiography.

J Am Soc Echocardiogr 2004;17(4):367-74.

2. Stöllberger C, Finsterer J, Valentin A, Blazek G, Tscholakoff D. Isolated left ventricular abnormal trabeculation in adults is associated with neuromuscular disorders. Clin Cardiol 1999;22(2):119-23.

3. Burke A, Mont E, Kutys R, Virmani R. Left ventricular noncompaction: a pathological study of 14 cases. Hum Pathol 2005;36(4):403-11.

4. Ritter M, Oechslin E, Sütsch G, Attenhofer C, Schneider J, Jenni R. Isolated noncompaction of the myocardium in adults. Mayo Clin Proc 1997;72(1):26-31.

5. Pignatelli RH, McMahon CJ, Dreyer WJ, Denfield SW, Price J, Belmont JW, et al. Clinical characterization of left ventricular noncompaction in children: a relatively common form of cardiomyopathy. Circulation 2003;108(21):2672-8.

6. Ichida F, Hamamichi Y, Miyawaki T, Ono Y, Kamiya T, Akagi T, et al. Clinical features of isolated noncompaction of the ventricular myocardium: long-term clinical course, hemodynamic properties, and genetic background. J Am Coll Cardiol 1999;34(1):233-40.

7. Agmon Y, Connolly HM, Olson LJ, Khandheria BK, Seward JB. Noncompaction of the ventricular myocardium. J Am Soc Echocardiogr 1999;12(10):859-63.

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case report

Coronary Artery Air Embolism MONIKA MAHESHWARI*, ANAND AGARWAL**

Abstract Coronary artery air embolization is a rare event leading to catastrophic hemodynamic compromise within seconds after introduction of air emboli within the coronary arteries. The management of massive air embolism should be extremely quick so as to save life of the patient. We present a case of a 35-year-old, diabetic and hypothyroid female who had massive air embolism in both LAD and LCX arteries during coronary angiography, which resolved within a few minutes with prompt treatment.

Keywords: Coronary artery air embolism, angiography, percutaneous interventions, hemodynamic compromise

C

oronary artery air embolization is a rare event, with overall incidence ranging from 0.2% to 0.8% during percutaneous interventions.1 Catastrophic hemodynamic compromise can occur within seconds after introduction of air emboli within the coronary arteries and may resolve within a few minutes if prompt treatment is undertaken, as we did in our case.

CASE REPORT A 35-year-old, diabetic and hypothyroid female with treadmill test (TMT) positive for inducible ischemia, was planned for coronary angiography. The right radial artery was cannulated with 5F tiger catheter.

Engagement and initial injections of left coronary angiogram was uneventful showing a smooth, normal left anterior descending (LAD) and left circumflex arteries (LCX). However, while shooting subsequently RAO cranial view suddenly patient on table began to experience severe chest pain and ST segments in leads V1-V6 began to rise upto 3 mm in amplitude.

Angiography demonstrated massive air embolism in both LAD and LCX arteries with no contrast flow

*DM (Cardio) 3rd Year Resident **DM (Cardio) Assistant Professor Dept. of Cardiology Jawaharlal Nehru Medical College Address for correspondence Navin Niwas, 434/10, Bapu Nagar, Ajmer - 305 001, Rajasthan E-mail: opm11@rediffmail.com

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Figure 1. Massive with no contrast flow beyond the midsegments of both arteries.

Figure 2. Showing TIMI-3 flow and no residual air embolism.

case report beyond the mid-segments of both arteries (Fig. 1).

The patient was soon hemodynamically unstable with hypotension and bradycardia. Immediately an attempt was made to suck out the air from the left coronary arteries via the guiding catheter. Cardiopulmonary resuscitation (CPR) was initiated with vigorous external cardiac massage. The patient was given 100% oxygen, intravenous (IV) atropine injections and was also put on IV dopamine. External cardiac massage and prompt aspiration was maintained for almost four minutes by which time the patient recovered both his heart rate and blood pressure with settled ST-segment on ECG monitor. After ascertaining that the patient was hemodynamically stable and had fully recovered her consciousness, left coronary angiogram was retaken, which showed TIMI-3 flow and no residual air emboli (Fig. 2).

Discussion Air can be introduced in coronary vessels inadvertently by inadequate aspiration of the guiding catheters, rupture of balloon and leakage of air via a defective manifold system.2 The management of massive air embolism should be extremely quick so as to save life of the patient. Case reports have described mechanical methods in the treatment of an air embolus including disruption or dislodgement by the guidewire,3 forceful injection of saline1 to fragment the air embolus and allow dispersal distally. Such interventions may result in main vessel patency but have a potential to damage the distal microvasculature due to widespread, smaller embolizations. In contrast, aspiration aims at resolving the blockage by removing the air. Aspiration has been attempted with nondedicated devices such as over the wire (OTW) balloons4 or the angiography catheter itself.1 The lumen of such an OTW balloon system is just large enough to allow 0.014 inch wire passage and

this may limit rapid aspiration. Use of the angiography catheter is limited by the ability to manipulate it deeply enough to affect the distal embolus and the risk of damage while attempting this. In contrast, the export aspiration catheter is a dedicated system for coronary artery aspiration.5 As such, it has the favorable qualities of being a monorail system that has the flexibility and slenderness to reach distal lesions down tortuous vessels Dudar et al6 reported a case of massive air embolism in which AngioJet catheter was utilized to aspirate coronary air embolus with successful restoration of coronary blood flow. Along with these mechanical efforts, supportive measures with 100% oxygen, opoid analgesia, external cardiac massage (CPR), DC cardioversion and if needed intraaortic balloon support are warranted for life saving.

Treatment has to be rapid and prompt as we did in our case.

REFERENCES 1. Khan M, Schmidt DH, Bajwa T, Shalev Y. Coronary air embolism: incidence, severity, and suggested approaches to treatment. Cathet Cardiovasc Diagn 1995;36(4):313-8.

2. Dib J, Boyle AJ, Chan M, Resar JR. Coronary air embolism: a case report and review of the literature. Catheter Cardiovasc Interv 2006;68(6):897-900.

3. Inoue T, Yaguchi I, Mizoguchi K, Hoshi K, Takayanagi K, Morooka S, et al. Air embolism in the right coronary artery occurring during the left coronary angioplasty using the guiding catheter with a side hole. Catheter Cardiovasc Interv 2000;49(3):331-4.

4. Solodky A, Birnbaum Y, Assali A, Ben Gal T, Strasberg B, Herz I. Coronary air embolism treated by bubble aspiration.

Catheter Cardiovasc Interv 2000;49(4):452-4.

5. Patterson MS, Kiemeneij F. Coronary air embolism treated with aspiration catheter. Heart 2005;91(5):e36.

6. Dudar BM, Kim HE. Massive air embolus treated with rheolytic thrombectomy. J Invasive Cardiol 2007;19(7):E182-4.

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New Way to Block Inflammation in Alzheimer’s, Atherosclerosis and Type 2 Diabetes Researchers at NYU Langone Medical Center have discovered a mechanism that triggers chronic inflammation in Alzheimer’s, atherosclerosis and type 2 diabetes. The results, published in Nature Immunology, suggest a common biochemical thread to multiple diseases and point the way to a new class of therapies that could treat chronic inflammation in these noninfectious diseases without crippling the immune system. Alzheimer’s, atherosclerosis and type 2 diabetes – diseases associated with aging and inflammation – affect more than 100 million Americans.

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photo quiz

Intermittent Sudden Dyspneic Episodes

A

62-year-old nursing home patient presented with dyspnea. He had recently been discharged from the intensive care unit after treatment for urosepsis with multiple organ failure. While in the hospital, he required vasopressors and mechanical ventilation for more than three weeks.

After discharge to a skilled nursing facility, the patient had several episodes of acute respiratory failure. The episodes were sudden and self-limited, resolving rapidly with minimal intervention, such as nebulizers, supplemental oxygen, or head repositioning, and were associated with clear lungs on auscultation. The episodes occurred when the patient was recumbent with his head slightly elevated, or when he was sitting and reached forward. Imaging was performed (Figures 1 and 2).

Figure 1.

Question Based on the patientâ&#x20AC;&#x2122;s history, physical examination, and imaging findings, which one of the following is the most likely diagnosis?

A. Flash pulmonary edema.

B. Gastroesophageal reflux with sudden aspiration

and pneumonitis.

C. Tracheomalacia.

D. Ventilator-induced lung damage.

E. Ventilator-related persistent pneumonia and atelectasis.

Figure 2.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2013;87(3):217-219.

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photo quiz Summary Table Condition

Characteristics

Flash pulmonary edema

Decreased breath sounds, rales, rhonchi, or wheezing, and jugular venous distention

Gastroesophageal reflux with sudden aspiration and pneumonitis

Bronchospasm symptoms after aspiration, such as wheezing, rales, and fine expiratory rhonchi

Tracheomalacia

Diffuse or segmental tracheal cartilage weakness related to recent intubation; symptoms occur suddenly and resolve spontaneously

Ventilator-induced lung damage

Findings during or immediately after mechanical ventilation, no breath sounds in the affected hemithorax, signs of intrathoracic hypertension

Ventilator-related persistent pneumonia and atelectasis

Findings arising after mechanical ventilation; respiratory symptoms, such as rales and rhonchi; systemic symptoms, such as fever and cough; not relieved with changes in position; insidious onset

Discussion The answer is C: tracheomalacia.

Tracheomalacia refers to diffuse or segmental tracheal cartilage weakness. It can be classified by appearance (anteroposterior tracheal narrowing or lateral), distribution (diffuse or segmental), or timing of appearance (congenital or acquired).1 The acquired form is most common in adults, particularly in those who were intubated or had a tracheostomy. Tracheostomy or endotracheal intubation can destroy tracheal cartilage at the stoma or inflatable cuff site, respectively, which weakens the tracheal wall.2 This type of tracheomalacia is usually segmental, with a length of 3 cm or less.

Possible risk factors for tracheomalacia include recurrent or prolonged intubation, and concurrent high-dose steroid therapy. The mechanism is uncertain but may be related to pressure necrosis, impaired blood flow, recurrent infections, mucosal friction, or mucosal inflammation.2 Other causes include recurrent infections, severe emphysema with chronic inflammation due to the inhalation of irritants (e.g., cigarette smoke), history of trauma from high-impact sports, and chronic external compression of the trachea (e.g., goiter, extrinsic vascular congestion).3

Figure 3. Computed tomography scan showing anteroposterior, segmental narrowing of the trachea (arrow) in a patient with tracheomalacia.

This patientâ&#x20AC;&#x2122;s symptoms are explained by an anteroposterior, segmental narrowing of the trachea a few centimeters below the vocal cords (Figure 3).

Air entry and movement were compromised when he moved his head forward or flexed at the neck while in a seated position. Figure 4 shows a three-dimensional reconstruction of the lungs and trachea, where the tracheomalacia lesion is evident.

Sudden shortness of breath in a frail patient with recent intubation and multiple organ failure raises the possibility of flash pulmonary edema. This patientâ&#x20AC;&#x2122;s shortness of breath was related to positional changes

Figure 4. Three-dimensional image of the lungs and trachea showing a tracheomalacia lesion (arrow).

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photo quiz of his head or neck and was not associated with signs of volume overload. Flash pulmonary edema leads to decreased breath sounds, rales, rhonchi, or wheezing, and jugular venous distention.

cells. The presentation is slower than tracheomalacia, and it does not resolve spontaneously. There are no breath sounds in the affected hemithorax, but there are signs of intrathoracic hypertension.

Gastroesophageal reflux causing a chronic aspiration syndrome with bronchospasm is associated with signs of bronchospasm, such as wheezing, rales, and fine expiratory rhonchi. A history of gastroesophageal reflux disease would make this diagnosis more likely.

Persistent pneumonia and atelectasis arising after mechanical ventilation has a slower presentation. It causes systemic symptoms, such as fever and cough, accompanied by respiratory signs (e.g., rales, rhonchi) on physical examination.

Lung damage, such as barotrauma, that causes gross air leaks or volutrauma is a more subtle type of lung injury that can occur secondary to pulmonary overdistention.

This type of damage can be induced by mechanical ventilation. Cyclical atelectasis, also called atelectrauma, refers to the damage that can occur when lungs become atelectatic and then are reexpanded. Biotrauma is the inflammatory response to increased cytokine recruitment in the alveoli after overstretching lung

REFERENCES 1. Nuutinen J. Acquired tracheobronchomalacia. Eur J Respir Dis. 1982;63(5):380-387.

2. Ferguson GT, Benoist J. Nasal continuous positive airway pressure in the treatment of tracheobronchomalacia. Am Rev Respir Dis. 1993;147(2):457-461.

3. Collard P, Freitag L, Reynaert MS, Rodenstein DO, Francis C. Respiratory failure due to tracheobronchomalacia.

Thorax. 1996;51(2):224-226.

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Me Lord I Am Not Guilty

plaint cannot Me Lord, this email com tion 27 of sec er und ed be entertain act Delhi Medical Council

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Note: Delhi Medical Council Act mandates that â&#x20AC;&#x201C; â&#x20AC;&#x153;No complaint shall be entertained unless it is in writing and signed by the person making it. Therefore, email complaints cannot be entertained.(Reference: DMC/DC/F14/496/2008).

[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

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practice guidelines

ACEP Policy on Evaluating Patients with Syncope in the Emergency Department

S

yncope, which involves a brief loss of consciousness followed by spontaneous recovery, accounts for 1 to 1.5 percent of emergency department visits and 6 percent of hospital admissions each year. It is estimated that more than $2 billion is spent annually in the United States on hospitalizing patients with syncope. In 2007, the American College of Emergency Physicians (ACEP) updated its 2001 clinical policy on assessing patients with syncope in the emergency department.

Level C recommendations indicate a strategy based on preliminary, inconclusive, or conflicting evidence, or panel consensus if published literature is unavailable.

Patients with syncope are often asymptomatic when they arrive at the hospital, making it difficult to evaluate them and obtain an accurate history. Patients may appear well, but be at risk of sudden death, which often prompts extensive evaluations or hospital admission. It is unknown whether admitting asymptomatic patients for observation and evaluation affects patient outcomes.

Older age, structural heart disease, or a history of coronary artery disease should be considered risk factors for adverse outcomes. Younger patients with syncope that is non-exertional, or without a history or signs of cardiovascular disease, a family history of sudden death, or comorbidities, are at low risk of adverse events (Level B recommendations).

Physicians must identify patients with life-threatening conditions who require hospital admission. However, the initial evaluation may not indicate a clear etiology.

Rather than determining a specific diagnosis, the physician should implement risk stratification similar to that of chest pain evaluation. All symptoms and complaints should be considered, and a complete history should be obtained. Associated symptoms may reveal an underlying medical condition that must be addressed. Life-threatening conditions in patients with syncope are uncommon, but they must be identified. These include dysrhythmias, pulmonary embolism, aortic dissection, subarachnoid hemorrhage, and acute coronary symptoms. Patients with bradycardia and medication-induced orthostatic hypotension are among those who may benefit from intervention.

The history and physical examination will assist with syncope risk stratification. Because the patient may not recall the event, the physician should ask eyewitnesses to estimate the duration of the loss of consciousness and evidence of seizure activity. If the patient cannot remember the experience, witnesses should also be asked to describe falls or trauma that accompanied the syncope, as well as any confusion or focal neurologic deficits exhibited by the patient. A prodrome of less than five seconds may be present with dysrhythmias. Longer prodromes, nausea, or vomiting may indicate neurally mediated syncope, also known as vasovagal syncope, which is associated with a good prognosis. If the syncope occurs while the patient is seated or reclining, it is more likely to have a cardiac etiology. Syncope that occurs after two minutes of standing may indicate orthostatic hypotension (i.e., a decrease in systolic blood pressure of at least 20 mmHg after standing).

This policy focuses on three critical questions when evaluating patients with syncope. Evidence-based recommendations were made following a careful review and analysis of the medical literature. Level A recommendations indicate generally accepted principles for patient management that reflect a high degree of clinical certainty. Level B recommendations indicate a strategy or range of strategies that reflect moderate clinical certainty.

What history and physical examination data help to risk-stratify patients with syncope?

History or physical examination findings consistent with heart failure may be used to identify patients at higher risk of adverse outcomes (Level A recommendation).

Syncope may also be caused by medications or drug interactions. Some drugs prolong the QT interval and are linked to life-threatening dysrhythmias.

Syncope may be caused by vasoactive drugs, such as antihypertensive agents, vasodilators for angina, and

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practice guidelines those used for erectile dysfunction. Older patients taking multiple medications may be more likely to experience drug-related syncope.

A family history of premature sudden cardiac death is a possible indication of serious congenital conduction abnormalities, such as pre-excitation syndromes, long QT syndromes, or brugada syndrome. The patient's sex, race, and age may also be risk factors for cardiovascular disease, which increases the risk of sudden death in patients with syncope. Two studies found that cardiovascular risk, not syncope, was the best predictor of cardiovascular events and mortality. Patients younger than 45 years tend to have a lower risk of adverse outcomes, although there is no definitive age cutoff for assessing this risk or making a firm age-based recommendation about risk stratification.

Patients with diagnosed heart failure, which predicts poor left ventricular function, are consistently at higher risk of sudden death. Patients with heart failure and syncope have a poor prognosis, even if the syncope is not of cardiac etiology.

Vital Signs Loss of consciousness, as well as hypoperfusion or hypotension, is transient in syncope. Persistent hypotension may suggest the presence of another disease. Orthostatic hypotension may identify syncope caused by volume depletion, autonomic insufficiency, or medications. Light-headedness or syncope after standing is more significant than a change in blood pressure. The diagnosis of orthostatic hypotension as a cause of syncope should be symptom-related and is a diagnosis of exclusion in otherwise low-risk patients with syncope.

Cardiopulmonary Findings Congestive heart failure found during the physical examination indicates a high risk of sudden death or early mortality after syncope. Murmurs that indicate valvular heart disease should prompt an evaluation for structural heart disease.

Head and Face Injuries Lateral tongue biting has a high specificity for convulsive seizures, although the absence of tongue biting is not significant to a diagnosis. Head trauma caused by syncope is not linked to a particular type of syncope or short-term outcome.

Abdominal Pain Pain or tenderness in the abdomen associated with syncope could point to significant pathology

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or hemorrhage. If gastrointestinal hemorrhage is suspected, a rectal examination should be performed to check for bleeding.

What diagnostic testing data help to riskstratify patients with syncope?

Obtain a standard 12-lead electrocardiography (ECG) in patients with syncope (Level A recommendation).

Laboratory testing and advanced investigative testing, such as echocardiography or cranial computed tomography (CT), are unnecessary unless indicated by specific findings in the patient history or physical examination (Level C recommendation).

When a diagnosis of syncope is made, the history and physical examination will identify the cause in most patients. An ECG will identify the cause in less than 5% of patients; however, the test is not invasive or expensive, and it can identify life-threatening conditions such as pre-excitation syndromes, prolonged QT syndromes, or brugada syndrome in young adults who appear to be in good health. When the ECG result is normal, dysrhythmias are unlikely to be the cause of syncope.

Cardiac Monitoring Continuous cardiac monitoring may detect arrhythmia that is not detected on a single 12-lead tracing. If arrhythmias are suspected, inpatient or ambulatory monitoring may be advised, although monitoring for more than 24 hours is not likely to increase detection.

One study found that four factors identified patients likely to have an abnormality after monitoring of up to 72 hours: age older than 65 years, male sex, history of heart disease, and nonsinus rhythm on ECG.

Laboratory Testing Routine laboratory testing for patients with syncope is not recommended because useful information is rarely found. One study found that hematocrit levels of less than 30% is a useful predictor of adverse events among patients with syncope of any cause.

Advanced Tests and Imaging Advanced imaging, such as CT, and advanced testing, such as functional cardiac echocardiography or electrophysiologic testing, are not recommended for routine screening of patients with syncope. Advanced testing should be guided by the patient's history and

practice guidelines physical examination results that may suggest the presence of a life-threatening condition.

Who should be admitted after an episode of syncope of unclear cause?

Patients with syncope and evidence of heart failure or structural heart disease should be admitted. Patients with syncope and other factors determined to be highrisk for adverse outcomes should be admitted (Level B recommendations).

Patients with syncope who are determined to be at risk for significant dysrhythmia or sudden death should be admitted to an inpatient unit, observation unit, or other

monitored area. The literature does not adequately describe which patients will benefit from hospital admission or observation. The literature also has not demonstrated the value of admission in preventing future adverse outcomes. Typical end points for patient follow-up are six months to one year or longer.

Admission should be based on patients' specific risks, with high-risk patients requiring admission. However, other symptoms, medical problems, and social factors should also be considered when deciding whether hospital admission is appropriate. Additional testing, consultation, or anticipated therapy may also warrant admission.

Source: Adapted from Am Fam Physician. 2008;78(4):516-518.

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Me Lord I Am Not Guilty ct CI A er M en p s d. A be giv isse to dism need ours e s Ca ecords n 72 h i r with

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Note: As per Medical Council of India 1.3.1: Every physician shall maintain the medical records pertaining to his / her indoor patients for a period of 3 years from the date of commencement of the treatment in a standard proforma laid down by the Medical Council of India and attached as Appendix 3. Nowhere it is written that a person shall maintain medical records pertaining to outpatients.

1.3.2. If any request is made for medical records either by the patients / authorized attendant or legal authorities involved, the same may be duly acknowledged and documents shall be issued within the period of 72 hours.

[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

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113

lighter reading

An American businessman was at a pier in a small coastal Mexican village when a small boat with just one fisherman docked. Inside the small boat were several large yellow–fin tuna.

The American complimented the Mexican on the quality of his fish and asked how long it took to catch them.

The Mexican replied, "only a little while". The American then asked why didn’t he stay out longer and catch more fish. The Mexican said he had enough to support his family’s immediate needs. The American then asked the Mexican how he spent the rest of his time.

The Mexican fisherman said, "I sleep late, fish a little, play with my children, take siesta with my wife, Maria, stroll into the village each evening where I sip wine and play guitar with my amigos. I have a full and busy life, senor."

The American scoffed, "I am a Harvard MBA and could help you. You should spend more time fishing and with the proceeds, buy a bigger boat. With the proceeds from the bigger boat, you could buy several boats; eventually you would have a fleet of fishing boats. Instead of selling your catch to a middleman you would sell directly to the processor, eventually opening your own cannery. You would control the product, processing and distribution. "You would need to leave this small coastal fishing village and move to Mexico City, then LA and eventually NYC where you will run your expanding enterprise."

The Mexican fisherman asked, "But senor, how long will this all take?" To which the American replied, "15–20 years.""But what then, senor?" asked the Mexican.

laugh a while

MBA and the fisherman

Never ask a woman her age Nurse to Patient: How old are you, Mrs. Smith?

Patient: None of your business.

Nurse: But the doctor must know your age for his records.

Patient: Well, first, multiply twenty by two, then add ten. Got that?

Nurse: Yes. Fifty.

Patient: All Right, now subtract fifty, and tell me, what do you get?

Nurse: Zero.

Patient: And that's exactly the chance of me telling you my age.

QUOTE

An Inspirational Story

Lighter Side of Medicine

“Success is not measured by what you accomplish but by the opposition you have encountered, and the courage with which you have maintained the struggle against overwhelming odds”.

—H. Jackson Brown, Jr.

Dr. Good and Dr. Bad Situation: A type 1 diabetic wanted to observe

Ramadan fast

Go ahead

Avoid it

©IJCP Academy

The American laughed, and said, "That’s the best part! When the time is right, you would announce an IPO and sell your company stock to the public.

You’ll become very rich, you would make millions!"

"Millions, senor?" replied the Mexican. "Then what?"

The American said, "Then you would retire. Move to a small coastal fishing village where you would sleep late, fish a little, play with your kids, take siesta with your wife, stroll to the village in the evenings where you could sip wine and play your guitar with your amigos."

Then the Mexican Fisherman says: THEN WHAT AM I DOING NOW?

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Asian Journal of Clinical Cardiology, Vol. 16, No. 3, July 2013

Lesson: Fasting is especially risky for those with

type 1 diabetes [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 -

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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).

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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.

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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.

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Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the

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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. 3, July 2013

117

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 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.

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.

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Do not use clips/staples on photographs and artwork.

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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.)_______________________________ 2. Total number of pages ________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________ 5. Special requests _____________________________

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.

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The legend must include enough information to permit interpretation of the figure without reference to the text.

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Asian Journal of Clinical Cardiology, Vol. 16, No. 3, July 2013

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