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Acute effects of alcohol septal ablation on systolic and diastolic left ventricular function in patients with hypertrophic obstructive cardiomyopathy P Steendijk, E Meliga, M Valgimigli, F J Ten Cate and P W Serruys Heart 2008;94;1318-1322; originally published online 1 May 2008; doi:10.1136/hrt.2007.139535
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Original article
Acute effects of alcohol septal ablation on systolic and diastolic left ventricular function in patients with hypertrophic obstructive cardiomyopathy P Steendijk,1 E Meliga,2,3 M Valgimigli,2 F J Ten Cate,2 P W Serruys2 1
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands; 2 Department of Interventional Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands; 3 Department of Interventional Cardiology, S Giovanni Battista Hospital, University of Turin, Turin, Italy Correspondence to: Dr Paul Steendijk, Leiden University Medical Center, Department of Cardiology, PO Box 9600, 2300 RC Leiden, The Netherlands; p.steendijk@lumc. nl Accepted 11 March 2008 Published Online First 1 May 2008
ABSTRACT Objective: Hypertrophic obstructive cardiomyopathy (HOCM) often leads to heart failure, severe symptoms and death. Percutaneous transluminal septal myocardial ablation (PTSMA) by alcohol injection efficiently reduces left ventricular (LV) outflow tract pressure gradient and improves symptoms. We determined acute changes in haemodynamics and systolic and diastolic LV function after PTSMA. Methods: In 17 consecutive patients with symptomatic HOCM referred for PTSMA, the target vessel was determined by myocardial contrast transthoracic echocardiography. An over-the-wire balloon was inflated in the target vessel and multiple 0.5-ml alcohol injections were performed. LV systolic and diastolic function was assessed by online pressure-volume loops obtained by conductance catheter at baseline and acutely after the procedure. Results: In all patients except two, a single septal branch was treated using a total of 2.0 (0.5) ml ethanol per patient. The rest and post-extrasystolic gradient were significantly decreased after PTSMA (79 (38) to 14 (16) mm Hg and 130 (50) to 34 (33) mm Hg, respectively, both p,0.001). Ejection fraction decreased (78% (9%) to 67% (13%), p,0.001). Cardiac output, heart rate and stroke work were unchanged, but systolic and diastolic volume increased. End-systolic and end-diastolic pressure significantly decreased (166 (27) to 129 (26) mm Hg, p,0.001 and 25 (6) to 21 (7) mm Hg, p = 0.049, respectively). Significant rightward shift (p,0.001) and decreased slope (p = 0.041) of the end-systolic pressurevolume relation indicated reduced contractility, whereas diastolic stiffness, 2dP/dtMIN, and tau were significantly improved after the procedure. Conclusions: PTSMA acutely reduced systolic function but promptly improved diastolic function with maintained cardiac output and stroke work. Improved diastolic function and increased end-diastolic volume compensated for the systolic loss and resulted in maintained haemodynamics.
Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic cardiac disease which is characterised by interventricular septum hypertrophy, a narrowed left ventricular outflow tract (LVOT), mitral regurgitation and mitral valve systolic anterior motion (SAM) resulting in LVOT obstruction.1 Patients with HOCM are at high risk of dying or developing severe symptoms, and LVOT obstruction has been shown to be an independent predictor of development of heart failure symptoms and death.2 3 In patients who remain symptomatic despite optimal medical 1318
therapy, surgical removal of a small amount of muscle from the basal interventricular septum has been shown to be an effective therapy.4 Recently, percutaneous transluminal septal myocardial ablation (PTSMA) was introduced as an attractive alternative procedure.5–10 PTSMA induces myocardial infarction by selective injection of alcohol into one or more septal branches of the left anterior descending coronary artery aiming at contractile dysfunction and thinning of the septum to reduce the LVOT pressure gradient.11 Significant and sustained decreases in LV outflow tract pressure gradients have been reported in several studies after PTSMA at long-term follow-up,6 7 12 although a recent study indicated less favourable effects in young patients with high baseline resting gradients.13 The role of PTSMA in reducing mitral regurgitation and SAM is still uncertain.5 The aim of this study was to establish the acute changes in systolic and diastolic left ventricular function after PTSMA in order to better understand the complex series of events that follow the procedure and that result in a new haemodynamic status.
METHODS Patient population The study population consisted of 17 consecutive patients with symptomatic HOCM despite optimal medical treatment who were referred for PTSMA at the Thoraxcenter. The HOCM diagnosis was based on typical clinical, echocardiographic and angiocardiographic findings. The inclusion criteria were New York Heart Association (NYHA) classification class II–IV, associated with any sign of obstructive LVOT: resting systolic gradient greater than 50 mm Hg or septal thickness greater than 15 mm, or a less than 7-mm LVOT diameter or SAM of anterior mitral leaflet. The study group included two patients with confirmed familial HOCM and four patients in whom HOCM was presumably related to previous hypertension. In the remaining patients the origin was unknown. The study was approved by the internal review board of the Erasmus Medical Centre and all patients provided informed consent before participation.
PTSMA procedure A 6F transfemoral temporary pacemaker was positioned in the right ventricle. Baseline haemodynamic data, including LVOT gradient at rest and at provocation with the Valsalva manoeuvre, were measured via two retrograde 6F catheters introduced percutaneously via the femoral artery and Heart 2008;94:1318–1322. doi:10.1136/hrt.2007.139535
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Original article placed one in the left ventricle and one in the ascending aorta. Intraprocedural myocardial contrast transthoracic echocardiography (TTE) was performed to determine the target vessel. The vessel was then selectively probed with a 0.014-inch guide wire through a 6F percutaneous coronary angioplasty guiding catheter. A 9-mm long, oversized over-the-wire balloon (1.5– 2.5 mm) was introduced and inflated and the distal vessel bed was contrasted. After verification of the correct balloon position and inflation, 1–2 ml of the echo contrast agent (Levovist, concentration 350 mg/ml, Schering or Sonovue, Bracco) were injected through the balloon catheter lumen under continuous TTE imaging. Once dye reflux into the left anterior descending (LAD) coronary artery was excluded and if probatory vessel closure by the inflated balloon had resulted in significant LVOT gradient reduction, multiple 0.5-ml alcohol injections were performed. Each injection was performed slowly, over a period of 30 seconds. Special care was taken to avoid leakage of alcohol into the LAD and its major branches. The balloon remained inflated for 10 minutes after the alcohol administration to enhance tissue contact and to exclude alcohol reflux into the LAD. Finally, all the haemodynamic measurements (see below) were repeated. The pacemaker lead was left in situ for at least 48 hours and the patient had a telemetric recording during the whole hospitalisation period.
catheter (CD Leycom, Zoetermeer, The Netherlands) introduced retrogradely into the LV and placed along the LV long axis. The catheter was connected to a Cardiac Function Lab (CFL-512, CD Leycom) for display and acquisition of pressurevolume loops. The conductance catheter was calibrated by matching the baseline conductance-derived volume signals with end-diastolic and end-systolic volumes obtained by echocardiography before the procedure. Data analysis was performed offline by custom-made software. Haemodynamics and LV function were quantified by cardiac output and stroke volume, end-diastolic and end-systolic volume, LV ejection fraction, endsystolic and end-diastolic pressure, maximal and minimal rate of LV pressure change (dP/dtMAX, 2dP/dtMIN). The time constant of relaxation (tau) was determined using phase-plot analysis. Stroke work was calculated as the area of the pressure-volume loop. The end-systolic pressure-volume relation (ESPVR) was estimated using a single-beat method adopted from Takeuchi et al14 as illustrated in figure 1. The ESPVR was characterised by its slope EES (end-systolic elastance) and its position as defined by the volume intercept at 150 mm Hg (ESV150, see fig 1). The enddiastolic stiffness constant KED was determined by fitting an exponential curve, P = A.exp(KED.V), to the diastolic trajectory of the pressure-volume loop, and we also determined enddiastolic stiffness, EED, as the linear slope of the diastolic trajectory (P = B+ EED.V).
Haemodynamics and LV function Left ventricular (LV) function before, during and after the PTSMA procedure was assessed by online LV pressure-volume signals obtained by a 7F combined pressure-conductance
Statistical analysis Continuous variables are shown as mean (SD) and were compared using Student t tests. Categorical variables are presented as counts and percentage and compared with the Fisher’s exact test. Differences were considered significant if the p value was ,0.05. All statistical tests were two tailed. Statistical analyses were performed by SPSS (version 12.0.1).
RESULTS Baseline patient characteristics Baseline clinical and haemodynamic characteristics are presented in tables 1 and 2. Mean age at the time of the procedure was 62 (13) years. Angina occurred in six patients (35%), syncope in three (18%) and dyspnoea was present in eight (47%). All patients were symptomatic despite optimal medical treatment with b-blockers (53%), calcium channel antagonists (59%) and diuretics (35%): eight patients (47%) were in NYHA class III and nine (53%) were in NYHA class II. In this series, no patients were in NYHA class IV. The mean gradient at rest was Table 1 Baseline patient (n = 17) characteristics
Figure 1 Single-beat estimation of the end-systolic pressure-volume relation (ESPVR) and end-diastolic pressure-volume relation (EDPVR). dP/dtMAX, maximal rate of LV pressure increase; ESV, end-systolic volume; LV, left ventricular; PMAX, isovolumic peak pressure. Heart 2008;94:1318–1322. doi:10.1136/hrt.2007.139535
Age, years (mean (SD)) Male Female Symptoms Angina Syncope Dyspnoea Medications b-blockers Calcium channel antagonists Diuretics NYHA functional class II III IV
62 (13) 11 (64%) 6 (36%) 6 (35%) 3 (18%) 8 (47%) 9 (53%) 10 (59%) 6 (35%) 9 (53%) 8 (47%) 0 (0%)
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Original article Table 2 Baseline (Pre) and post-procedural (Post) haemodynamic measurements (n = 17) Gradient (mm Hg) Post-extrasystolic gradient (mm Hg) HR (beats/min) SV (ml) CO (l/min) SW (l.mm Hg) ESV (ml) EDV (ml) EF (%) ESP (mm Hg) EDP (mm Hg) LVPPEAK (mm Hg) LVPMIN (mm Hg) dP/dtMAX (mm Hg/s) 2dP/dtMIN (mm Hg/s) Tau (ms) PMAX (mm Hg) EES (mm Hg/ml) ESV150 (ml) EED (mm Hg/ml) KED (1/ml)
Pre
Post
79 (38) 130 (50) 69 (12) 86 (28) 6 (2.3) 10.7 (3.7) 33 (14) 110 (30) 78 (9) 166 (27) 25 (6) 187 (32) 8.1 (3.3) 1549 (289) 1611 (248) 111 (61) 268 (40) 1.93 (1.16) 36 (15) 0.32 (0.24) 0.025 (0.021)
14 (16) 34 (33) 67 (11) 81 (38) 5.3 (2.5 9.2 (4.4) 44 (19) 119 (36) 67 (13) 129 (26) 21 (7) 147 (24) 7.2 (3.7) 1438 (244) 1310 (333) 67 (15) 230 (36) 1.38 (0.62) 58 (22) 0.19 (0.09) 0.021 (0.019)
p Value ,0.001 ,0.001 0.326 0.794 0.409 0.135 0.004 0.073 ,0.001 ,0.001 0.049 ,0.001 0.322 0.069 0.001 0.011 0.011 0.041 ,0.001 0.014 0.275
CO, cardiac output; dP/dtMAX, maximal rate of LV pressure increase; 2dP/dtMIN, maximal rate of LV pressure decline; EED, diastolic stiffness; EES, end-systolic elastance (slope of ESPVR); EDP, end-diastolic pressure; EDV, end-diastolic volume; EF, ejection fraction; ESP, end-systolic pressure; ESV, end-systolic volume; ESV150, intercept of ESPVR; HR, heart rate; KED, diastolic stiffness constant; LVPMIN, minimal LV pressure; LVPPEAK, peak left ventricular (LV) systolic pressure; PMAX, isovolumic peak pressure; SV, stroke volume; SW, stroke work; tau, relaxation time constant.
79 (38) mm Hg, the mean post-extrasystolic gradient was 130 (50) mm Hg and the mean septal thickness was 21.7 (0.5) mm.
Procedural results An average of 2.0 (0.5) ml of ethanol was injected per patient. In all patients except two, only one septal branch was treated. In eight patients the first septal branch was treated, in six patients the second, in one the third. In two patients both the first and the second septal branches were treated because of incomplete gradient relief after the treatment of the first one. No death or sustained ventricular arrhythmias occurred. Eight patients developed right bundle branch block, which was persistent in four. No patient required permanent pacemaker implantation after the procedure. Acute haemodynamic findings are
summarised in figure 2 and table 2. The mean rest and postextrasystolic gradient were both significantly decreased after the procedure (79 (38) to 14 (16) mm Hg and 130 (50) to 34 (33) mm Hg, respectively, both with p value ,0.001). The CO, HR, SV and SW were unchanged. The ESV increased from 33 (14) to 44 (19) ml (p = 0.004); the EDV tended to increase from 110 (30) to 119 (36) ml (p = 0.07) and the ejection fraction significantly decreased from 78% (9%) to 67% (13%) (p,0.001). Both ESP and EDP significantly decreased from 166 (27) to 129 (26) mm Hg (p,0.001) and from 25 (6) to 21 (7) mm Hg, respectively. LVPPEAK decreased from 187 (32) to 147 (24) (p,0.001). LV dP/dtMAX tended to decrease from 1549 (289) to 1438 (244) mm Hg/s (p = 0.069) and 2dP/dtMIN significantly decreased from 1611 (248) to 1310 (333) mmHg/s (p = 0.001). Both tau and EED were reduced from 111 (61) to 67 (15) ms (p = 0.011) and from 0.32 (0.24) to 0.19 (0.09) mm Hg/ml (p = 0.014), respectively. The ESPVR showed a decreased slope (EES from 1.93 (1.16) to 1.38 (0.62) mm Hg/ml, p = 0.041) and a shift to the right (ESV150 from 36 (15) to 58 (22) ml, p,0.001). Figure 3 shows a typical example of pressure-volume loops before and after PTSMA.
DISCUSSION
Figure 2 Acute effect of percutaneous transluminal septal myocardial ablation: left ventricular (LV) outflow tract gradient before (Pre) and after (Post) procedure. 1320
HOCM was first described in the late 1950s.15 16 A morphological difference is made between subaortic obstruction and the more rare mid-ventricular obstruction. Symptoms and disease manifestations in patients with HOCM include dyspnoea, angina, palpitations, syncope, heart failure and sudden cardiac death. Obstruction of LVOT, diastolic dysfunction, cardiac ischaemia and rhythm disturbances are the main problems and underlying mechanisms in patients with HOCM.1 10 Symptomatic patients not only have impaired quality of life but also seem to have an adverse prognosis; the occurrence of atrial fibrillation, ventricular tachycardia17 and myocardial ischaemia18 are all prognostically unfavourable factors. Heart 2008;94:1318–1322. doi:10.1136/hrt.2007.139535
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Original article
Figure 3 Typical example of pressure-volume loops before (Pre) and after (Post) percutaneous transluminal septal myocardial ablation. LV, left ventricular. Symptomatic HOCM patients are usually treated first with negatively inotropic substances, especially b-blockers, calcium antagonists like verapamil, or disopyramide.19 These drugs may favourably modify LV diastolic function through their antiischaemic actions although the effect on symptoms and LVOT obstruction is often limited and present only in a select group of patients. Moreover, verapamil may prolong tau and increase filling pressures in some patients. A recent study indicated that disopyramide combined with b-blockers may provide amelioration of symptoms without proarrhythmic effects.19 Atrioventricular sequential pacing has been applied20 and was reported to reduce the outflow tract gradient up to 30%, to limit cavity obliteration and reduce systolic pressures probably by inducing dyssynchronous apical contraction,21 which was leading to a decrease in symptoms in patients without affecting septal thickness.22 Surgical myectomy has been the therapeutic option of choice for decades since the late 1950s,4 23 and patients tend to have improved markers of diastolic LV function and a favourable prognosis. Recently, PTSMA has been shown to be an attractive alternative to surgical myectomy. The induction of a limited ‘‘therapeutic’’ infarction as a result of ethanol injection24 within the hypertrophied septal myocardium leads to localised thinning and regional contractile dysfunction, which expands the left ventricular outflow tract, eliminates or reduces the mitral valve SAM and thus reduces LVOT gradient and the resulting symptoms.25–28 Previous echocardiographic and magnetic resonance imaging studies have shown that LVOT gradient reduction is associated with a decreased afterload and an increased cardiac output,29–31 resulting in a higher diastolic pressure in the aorta along with a lower diastolic pressure in the LV. These changes enhance coronary flow and myocardial perfusion by increasing coronary filling pressure, leading to reduced subendocardial ischaemia and improved LV relaxation.32 33 Moreover, the gradual regression of hypertrophy and the changes in LV geometry may explain the further long-term improvement in diastolic function.32–34 Most of these changes are assumed to achieve their maximum effect generally weeks or months after the procedure, but what happens immediately after the procedure is still poorly understood. In the present study we used invasive conductance catheter-derived pressure-volume loops to assess the acute effects of PTSMA on general haemodynamics, and systolic and diastolic LV function. This methodology has been validated extensively35 and has the unique advantage of providing Heart 2008;94:1318–1322. doi:10.1136/hrt.2007.139535
continuous, online haemodynamics and relatively loadindependent indexes of systolic and diastolic LV function. The results indicate that, despite the acute gradient reduction, general haemodynamics reflected by CO and SW were not greatly affected. However, systolic function was acutely reduced: this was evidenced by a reduced ejection fraction resulting from increased EDV with maintained SV. Consistently, dP/dtMAX decreased, although this effect just failed to reach statistical significance (p = 0.069). Since these traditional indexes may be affected by the greatly altered loading conditions we also assessed systolic LV function by the ESPVR, a relatively load-independent relation: the significant reduction in slope and the rightward shift of the ESPVR both clearly indicated a reduction in intrinsic systolic function. Conversely, diastolic LV function showed an acute improvement: EDP decreased significantly despite the increase in EDV, and tau also improved significantly. In line with these finding, the EDPVR showed a decreased slope indicating improved diastolic compliance. The improved diastolic function and increased EDV (Frank-Starling effect) presumably compensated for the systolic loss and resulted in maintained stroke volume. The reduced systolic function most likely reflects the iatrogenic loss of functional cardiac muscle induced by the alcohol injection. The amount of the loss is related both to the site and the size of the infarct area, which in turn depends on the quantity of ethanol delivered and on the number of septal branches treated. In our series all patients, except two, had a single septal branch treated and the infarct area was similar in all patients (22.4 (6.9) mm2, evaluated by echocardiography). The acute improvement in diastolic function is in line with previously reported long-term effects. However, whereas longterm improvements may be mainly due to regression of myocardial hypertrophy, the current findings suggest an improvement in intrinsic myocardial function: we speculate that relief of subendocardial ischaemia may partly explain this acute effect. In addition, relaxation is known to be affected by systolic load via changes in intracellular calcium transients.36 Potentially, acute systolic load reduction may also have improved relaxation via this pathway. Interestingly, 2dP/dtMIN was reduced, suggesting a worsening of the isovolumic relaxation. This, however, can be explained because 2dP/dtMIN reflects the very early part of diastole, this ‘‘active’’ relaxation phase is largely dependent on systolic properties that, in this acute setting, are iatrogenically depressed.37 38
Limitations Ideally, ESPVR and EDPVR are derived from multiple beats at altered loading conditions. In most pressure-volume loop studies a gradual reduction in preload is induced by balloon occlusion of the inferior vena cava. In the present study group we were hesitant to apply this intervention because these patients with diastolic dysfunction and near cavity obliteration at end-systole have very little reserve capacity and preload reduction was anticipated to result in large pressure drops and unstable haemodynamics. Therefore we applied single-beat methodologies to derive ESPVR and EDPVR. These approaches were previously used and generally found to be reasonable estimates of multi-beat pressure-volume relations.14 39 40 In conclusion, our mechanistic findings describe the complex haemodynamic effects acutely induced by PTSMA and help to explain how treatment may result in immediate symptom relief well before remodelling of the LV cavity takes place. PTSMA acutely reduced systolic function but promptly improved diastolic function with maintained general haemodynamics. 1321
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Original article Most previous studies indicated that 3–6 months after the procedure, both systolic and diastolic performance indexes are improved; this difference is probably the result of the influence the tissue loss has on the systolic function in the acute phase while the compensatory and remodelling processes have not yet started. More generally, the present data could be relevant for operative risk assessment, post-procedural patient management and future optimisation of the procedure in high-risk heart failure patients. Our findings suggest that PTSMA can be safely applied in patients with severe heart failure symptoms.
18.
Competing interests: None.
23.
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Heart 2008;94:1318–1322. doi:10.1136/hrt.2007.139535