European Heart Journal Advance Access originally published online on May 4, 2007
European Heart Journal 2007 28(21):2583-2588; doi:10.1093/eurheartj/ehm117
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Surgical septal myectomy decreases the risk for appropriate implantable cardioverter defibrillator discharge in obstructive hypertrophic cardiomyopathy
1 Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
2 Division of Pediatric Cardiology, Department of Pediatrics, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
3 Division of Thoracic and Cardiovascular Surgery, Department of Surgery, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
Received 15 December 2006; revised 16 March 2007; accepted 22 March 2007; online publish-ahead-of-print 4 May 2007.
* Corresponding author. Tel: +1 507 284 2511; fax: +1 507 266 0103. E-mail address: ommen.steve{at}mayo.edu
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Abstract |
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Aims: To determine the impact of surgical myectomy on ventricular arrhythmias in obstructive hypertrophic cardiomyopathy (HCM). Left ventricular outflow tract obstruction (LVOTO) correlates with adverse outcomes, including sudden cardiac death (SCD) in patients with HCM. Surgical myectomy is the primary treatment strategy for relief of symptoms owing to LVOTO and has been hypothesized to decrease the potential for ventricular tachyarrhythmias.
Methods and results: We reviewed the Mayo Clinic HCM database for those patients with HCM who had received implantable cardioverter defibrillator (ICD) and grouped the patients into myectomy and non-myectomy groups. Retrospective analysis of the incidence of SCD and appropriate ICD discharge was performed in addition to the analysis of ICD interrogation records. A total of 125 patients defined by these parameters were followed at the Mayo Clinic between 1992 and 2005. New York Heart Association functional class, anti-arrhythmic drug usage, wall thickness, and reasons for ICD implantation were similar between the groups; 118 patients underwent ICD implantation for primary prevention and seven for secondary prevention after sustained ventricular arrhythmias. There were no SCDs during this follow-up period in either group, whereas 12 (17%) patients in the non-myectomy group and only one (2%) patient in the myectomy group sustained appropriate ICD discharges. The average annualized event rate was 4.3% per year in the non-myectomy group, compared with 0.24% per year following myectomy (P = 0.004).
Conclusion: These data suggest that surgical myectomy, primarily performed to relieve outflow tract obstruction and severe symptoms in HCM, is associated with a marked reduction in the incidence of appropriate ICD discharge and risk for SCD.
Key Words: Hypertrophic cardiomyopathy • Implantable defibrillator • Surgical myectomy
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Introduction |
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Since its initial description in the literature, sudden cardiac death (SCD) has been recognized as one of the most devastating outcomes of hypertrophic cardiomyopathy (HCM).1 Early reports, predominantly from referral centres, suggested that the annual frequency of SCD ranged 4–6% and was even higher in younger asymptomatic patients,2–4 thus identifying prevention as an integral and challenging component of management strategies. Subsequent population-based studies have shown that the SCD rate is much lower overall, on the order of
1% per year.5 The principal mechanism of SCD in patients with HCM appears to be ventricular tachycardia or fibrillation, and the implantable cardioverter defibrillator (ICD) has been demonstrated to be highly effective in terminating these lethal arrhythmias in high-risk groups.6 Importantly, the presence of left ventricular outflow tract obstruction (LVOTO) has been demonstrated to increase the rate of SCD.7 Among drug-refractory, symptomatic patients with HCM and significant haemodynamic outflow tract obstruction, surgical myectomy has been recognized as the therapeutic ‘gold standard’ resulting in substantial long-term improvements in haemodynamics, symptoms, morbidity, and mortality.8–10
To what extent surgical myectomy could have a beneficial impact upon SCD has not been established but the concept is intuitively attractive given the association between obstruction and SCD in prior studies. Moreover, observational data from a large multi-centre cohort of patients with HCM recently alluded to a significantly lower risk for SCD in myectomy patients compared with non-operated obstructive HCM patients.8 This retrospective study evaluates the impact of septal myectomy on the incidence of lethal arrhythmias on the basis of the analysis of ICD histories.
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Methods |
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Patient selection
Patients were eligible for inclusion in this retrospective analysis if they underwent ICD implantation at Mayo Clinic, Rochester between 1992 and 2005. The overall study population of 125 ICD recipients with HCM is composed of two subgroups: group 1 consisted of 56 patients who had undergone surgical ventricular septal myectomy (myectomy group) and were compared with group 2, 69 non-operated HCM patients (non-myectomy group). The latter group of patients who were managed medically did not meet criteria for surgery because there was insignificant outflow obstruction or minimal symptoms (see Surgery). The follow-up of patients who underwent septal ablation as a management option (n = 3 patients in the non-myectomy group) was censored at the time of the procedure. This study was approved by the Mayo Institutional Review Board.
Echocardiography
The diagnosis of HCM was based on the presence of a hypertrophied non-dilated LV in the absence of other conditions that could be responsible for the magnitude of LV hypertrophy (LVH).11 Echocardiographic parameters were measured as described previously.7,11 The LV outflow tract gradient was assessed under resting (basal) conditions, using continuous wave Doppler echocardiography at initial presentation or prior to myectomy.
Surgery
The cohort of patients who underwent septal myectomy with placement of an ICD consisted of 56 patients. Surgery was performed to relieve LVOTO, with the criteria for surgical intervention at the Mayo Clinic being as follows: LVOTO 
50 mmHg at rest or with provocative manoeuvres attributable to systolic anterior motion of the mitral valve, associated with New York Heart Association functional classes III–IV limitation (or repetitive effort-related syncope) despite maximum medical management.12–14 The septal myectomy operation in this cohort was extended to include a larger resection than that originally described by Morrow et al.15,16 Our surgical modifications have been described in detail elsewhere.17,18 In this cohort, the average maximal outflow tract gradient at rest decreased from 59 ± 35 mmHg pre-operatively to 1 ± 3 mmHg post-operatively (P < 0.0001).
Implantable cardioverter defibrillator implants
The ICD devices were implanted between 1992 and 2005, with implantation performed via the transvenous route (70% were placed after 1998). Most of the devices were able to provide defibrillation and anti-tachycardia pacing (ATP) therapies, together with diagnostic memory capacity. There were no significant differences between the two groups of patients with respect to device type or capabilities. The indication for ICD placement was determined to be either primary or secondary. Primary prevention was defined as device placement for perceived increased risk of SCD on the basis of the presence of one or more SCD risk factors and no history of prior SCD, ventricular fibrillation, or sustained ventricular tachycardia. Secondary prevention was defined as occurring after either resuscitation from cardiac arrest (with documented ventricular fibrillation) or sustained, spontaneous ventricular tachycardia.6 The defibrillation thresholds were routinely tested to ensure efficient functionality in terminating ventricular tachyarrhythmias. Programmed ATP was activated at the discretion of the clinical cardiologist,19 and stored intracardiac electrogram data, when available, were reviewed after all discharges and at routine visits.20
Implantable cardioverter defibrillator event interpretation
Defibrillator discharges or ATP was analysed in conjunction with intracardiac electrogram recordings prior to these events. Stringent definitions were applied to event and electrogram interpretation and were in keeping with previous standards.6 Briefly, ventricular fibrillation was defined as irregular tachycardia with regard to QRS or electrographic polarity, amplitude, morphology, and sequence, with a mean cycle length 
240 ms. Ventricular tachycardia was defined as regular (monomorphic) or irregular (polymorphic) tachycardia with regard to QRS or electrographic polarity, amplitude, and morphology, with a mean cycle length >240 ms. Sinus tachycardia was defined as regular tachycardia with a gradual acceleration identical to that recorded during sinus rhythm and a mean rate exceeding the programmed cutoff rate. AF was defined as irregular tachycardia with RR interval variation >60 ms and similar ventricular electrogram morphology compared with sinus rhythm with ventricular rate <180 b.p.m. and/or cycle lengths ranging 220–120 ms with variable amplitude and morphology. If the ventricular rate exceeded tachycardia detection, beat-to-beat RR interval variation would be >60 ms, whereas ventricular electrogram morphology would be similar to sinus rhythm. The nominal VT detection was set at 150–200 b.p.m. and the VF detection rate was >200 b.p.m. Although some individual variations in device programming can occur because of electrophysiological characteristics of ventricular arrhythmias on average, the detection rates were not different between the two groups of patients.
Classification of discharges as appropriate or inappropriate
Defibrillator discharges or anti-tachycardia overdrive pacing was considered appropriate if the device was triggered by ventricular tachycardia or fibrillation, and which was documented by stored intracardiac electrogram or cycle-length data in conjunction with patient's symptoms immediately before and after device discharge. Inappropriate discharges were defined as those triggered by a rapid ventricular rate exceeding the programmed threshold rate as a consequence of supraventricular tachycardia, exercise-related sinus tachycardia, or a malfunction of the device. Each discharge and ATP therapy for ventricular arrhythmias were classified as either appropriate or inappropriate by experienced electrophysiologists. Only one patient did not have EGMs reviewed at our institution. All patients had adjudication as per the previously described and accepted methods.6 There were six (11%) patients in the myectomy group with inappropriate ICD discharge and 11 (16%) in the non-myectomy group (P = 0.5).
Follow-up
The median and (interquartile range) follow-up period from the time of ICD implantation was 4.4 ± 4.1 years. Those patients who underwent myectomy were followed for 4.6 ± 5 years, compared with 4.4 ± 4 years (P = 0.02), in the non-myectomy group. Seven patients underwent implantation of ICDs prior to myectomy, with a median insertion period of 2.5 ± 3 years prior to surgery (range 2 weeks to 7.6 years). There were no ICD therapies prior to myectomy in these seven patients. The other 49 patients received ICDs, following the myectomy as part of a primary prevention strategy, i.e. no patient had suffered SCD, sustained VT, or VF as the indication for ICD placement after myectomy. Follow-up was obtained at the time of clinical visit or by contact with the patient and their primary physician utilizing telephone and written medical records. One patient from the non-myectomy group was lost to follow-up, whereas no patients from the myectomy group were lost.
Statistical analysis
The survival analysis model utilized proportional hazards regression methodology and Kaplan–Meier survival curves using log-rank statistics to assess time to first appropriate ICD discharge. To determine whether differences in the risk for sudden death between the myectomy and the non-myectomy population could be explained by disease-related variables other than the operation, univariate and multivariable Cox proportional hazard regression analyses were performed. The endpoint was the first occurrence of appropriate ICD discharge or ATP.
Two multivariable models were utilized. The first entered only those variables that demonstrated significant univariate association with time to first appropriate ICD discharge (specifically, group and non-sustained ventricular tachycardia as outlined Results). Because of the dramatic differences observed between the two groups, a second model was constructed that entered all variables that were significantly different between the two groups. The two-sided t-tests and contingency table analyses were used to compare baseline characteristics between the two groups. The significance level used was set at P < 0.05.
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Results |
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Characteristics at the time of implantable cardioverter defibrillator implantation
Table 1 summarizes the baseline data at the time of ICD implantation. Patients who underwent myectomy were younger than those included in the non-myectomy group (38 ± 15 vs. 44 ± 13 years, P = 0.03). LV ejection fraction and maximal wall thickness did not differ significantly between the groups (70 ± 9 vs. 68 ± 10%, P = 0.4; 22 ± 9 vs. 21 ± 5 mm, P = 0.4, respectively).
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Evaluation of cardiac medication usage reflected more intensive drug therapy in the non-myectomy group at the time of ICD implantation as outlined in Table 1. All patients in the myectomy group had been treated with one or more negative inotropic agents prior to the surgical myectomy procedure. The prevalence of atrial fibrillation (either paroxysmal or chronic) was similar between both groups (11 vs. 16%; P = 0.5).
Indications for implantable cardioverter defibrillator implantation
Among the myectomy patients, ICDs were implanted for primary prevention in 52 patients (90.9%) and secondary prevention in five patients (9.0%). Among the non-myectomy group, 97.1% (67 patients) were implanted for primary prevention and only 2.9% (two patients) were implanted for secondary prevention of SCD (P = 0.2 for comparison of distributions, Table 2). The principal reasons for primary prevention ICD placement included a family history of one or more sudden deaths (49%); syncope or near-syncope (40% of patients); non-sustained ventricular tachycardia (defined as three or more consecutive ventricular beats at a rate >120 b.p.m. with a duration <30 s) on Holter electrocardiographic monitoring or telemetry (38%); abnormal (hypotensive) blood pressure response to exercise (26%), an LV wall thickness of at least 30 mm (6%); and inducible ventricular tachycardia or fibrillation with programmed ventricular stimulation (14%).
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Other than a higher proportion of maximal wall thickness >30 mm in the myectomy group and a greater frequency of non-sustained ventricular tachycardia in the non-myectomy group, there was no significant difference in the distribution of SCD risk factors. Patients in the myectomy group presented an average of 1.54 + 1.1 risk factors (48% with two or more), whereas patients in the non-myectomy group had an average of 1.77 + 0.8 risk factors (63% with two or more) for SCD (P = 0.2 for the comparison of mean number of risk factors, and P = 0.1 for the proportion of patients with two or more risk factors between the two groups).
Appropriate discharges
The rate of first appropriate discharge for the overall study group was 1.8% per year, with an average follow-up of 4.1 ± 3 years after implantation. In the non-myectomy group, 12 (16%) patients sustained 122 appropriate discharges from their ICD during the follow-up period for 78 episodes of ventricular tachycardia and 44 episodes of ventricular fibrillation. Of these, the initial appropriate ICD therapy was defibrillation in 11 patients and ATP in the other. Their average annualized first event rate was 4.3% per year, and their events occurred on average 1.8 years (±1.8) after implanting the device. One of these patients received the ICD as a secondary prevention strategy, whereas the remainder were primary prevention recipients.
Only one patient in the myectomy group received three appropriate ICD discharges, all occurring on 1 day, for ventricular tachycardia and fibrillation, yielding an average annualized ICD discharge rate of 0.24% (P = 0.004 in comparison with the non-myectomy group, Figure 1). These defibrillation events occurred 14 years after myectomy and 1.5 years following ICD implantation. There were no episodes of ATP therapy observed in the myectomy group.
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Among the patients in the non-myectomy group, 14 out of 69 (20%) had resting LV outflow tract gradients >30 mmHg at rest. Notably, two of these 14 patients (14%) received at least one appropriate ICD discharge.
Significant univariate association with time to first ICD discharge included surgical group (myectomy vs. non-myectomy, P = 0.0009) and non-sustained ventricular tachycardia (P = 0.02). Multivariable analysis including both of these variables demonstrated that myectomy (hazard ratio 0.33, confidence limits 0.08–0.8, P = 0.007) retained the most significant independent association with time to appropriate ICD discharge (Table 3). Because the observed event rates were markedly different between the myectomy and non-myectomy groups, an additional multivariable model was constructed that incorporated all variables that were significantly different between the two groups (age, sex, medication use, non-sustained ventricular tachycardia, and maximal wall thickness >30 mm) and again identified myectomy (hazard ratio 0.16, confidence limits 0.02–0.5, P = 0.0008) as the most significant variable (Table 3).
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Discussion |
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For several decades, it has been an accepted practice to proceed to surgical myectomy for those patients with HCM who have outflow tract obstruction and limiting symptoms, and among whom there has been an inadequate response to medications.13 Subsequent to surgery, this group of patients has an overall postoperative survival free from all-cause mortality at 10 years, which in fact did not differ from that of the general population.8 Moreover, the same analysis suggests that those patients with LVOTO who did not undergo myectomy experienced greater than twice the overall mortality risk observed in myectomy patients.
This current analysis identifies that ventricular arrhythmias, as defined by appropriate ICD discharge, in those patients who underwent myectomy were far less common than that observed in the non-myectomy group: 0.24 vs. 4.3% per year. It is notable that the observed rates of ICD discharge in the non-myectomy group are identical to that observed in the original report of the HCM ICD registry when implanted for primary prevention,6 whereas the myectomy patients, despite similar risk profile, experienced over 10-fold fewer events. The results from this study complement those observations that the presence of outflow tract obstruction is associated with higher rates of overall and sudden death mortality and that relief of obstruction is associated with near-normalization of overall mortality.7,8,21 The mechanisms whereby surgical septal myectomy may reduce the frequency of ventricular arrhythmias remain speculative, yet reduction in the amount of arrhythmogenic substrate and normalization of LV pressures are integral to the putative pathophysiology.
In a previous retrospective analysis,22 the risk of sudden death has been shown to increase progressively and in direct relation to the LV wall thickness. Moreover, other studies have also highlighted the vulnerability to SCD in patients with severe LVH, particularly in younger individuals.23 In addition, the degree of ventricular hypertrophy in genetically confirmed patients with HCM has also been found to parallel the inducibility of ventricular arrhythmias in electrophysiology studies,24 whereas arrhythmias in HCM patients were less frequently inducible after myectomy than prior to their surgery.25 This substrate of hypertrophy coupled with myocyte disarray, and interstitial fibrosis have also been suggested as potential sources of interference to conduction and refractoriness—features that reductive surgery may inherently address.26–28 Consistent with these clinical findings, animal models of HCM have also verified that the magnitude of ventricular hypertrophy is significantly associated with an increase in arrhythmia susceptibility.29
It is also relevant that severe microvascular dysfunction is a potent long-term predictor of adverse LV remodelling and systolic dysfunction in HCM,30 and one could postulate that with normalization in LV pressures and associated improvements in regional myocardial blood flow, one can halt the progression towards LV dysfunction and associated dysrhythmias.
A limitation of this retrospective analysis and the assimilation of basic science data originates in the vast genetic heterogeneity that underlies the HCM phenotype. Although there is a significant reduction in ICD discharges potentially across a diverse array of gene defects in the myectomy group, the question remains whether highly symptomatic patients represent a genotypically distinct subset apart from those whose symptoms have not been severe enough to warrant surgery. To this effect, genetic testing in HCM has shown that there was no correlation between myectomy status and genotype-positive status.31
Another limitation includes those patients who underwent ICD implantation and/or follow-up elsewhere. Although every attempt was made to obtain details of device interrogations at both Mayo Clinic and outside institutions, there may be some missing data. We do not, however, expect this contribution to significantly impact the results of this analysis, as the rate of SCD after myectomy, as reported in previous studies,8,32 has been characterized as being extremely low and in the same range as the observed rate of appropriate ICD discharge in the current analysis. The relatively long enrollment period necessarily encompassed a period of considerable expansion in the knowledge regarding SCD risk assessment in HCM patients such that there was not a uniform risk strategy applied to all patients. Specifically, the use of electrophysiology study was only utilized early in this study period, whereas the use of massive hypertrophy in clinical decision-making was utilized only in the latter part. There was some discrepancy in the distribution of risk factors among the patients, notably the prevalence of and proportion of patients with massive hypertrophy and non-sustained ventricular tachycardia. Although these differences may be important, massive hypertrophy did not show independent association with appropriate ICD discharge on multivariable analysis. Although non-sustained ventricular tachycardia did show independent association, it was a weaker association than that observed with respect to operative status. Finally, the overall number of patients with events (n = 12) is relatively low and does raise the possibility of findings reflecting chance. However, we feel that the robust differences and consistency across models as well as the clinical plausibility all support these data.
Although the findings in this study are quite striking and intriguing, it is clear that SCD can occur late after surgical myectomy and thus the need for continued SCD risk assessment remains necessary even after operation. Moreover this study from a single institution cannot be used to change current guidelines for ICD implantation. Likewise, these data cannot be construed to suggest reduction of SCD risk as the sole indication for referral for septal myectomy. The myectomy patients in this study all demonstrated advanced symptoms despite pharmacotherapy prior to the myectomy procedure, and the results should not be extrapolated to less symptomatic patients, nor to other procedures designed to reduce LVOTO. These current data do provide further insight into the natural history of arrhythmias, following myectomy for obstructive HCM. This procedure has long been established as providing substantive and durable relief from previously refractory symptoms, is accomplished with very low procedural morbidity and mortality, and is associated with normalization of long-term survival. The current data confirm that the rate of appropriate ICD discharge and potentially fatal arrhythmia following surgical myectomy is impressively small.
Conflict of interest: none declared.
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