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Circulation. 2007;116:196-206
doi: 10.1161/CIRCULATIONAHA.107.691378
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(Circulation. 2007;116:196-206.)
© 2007 American Heart Association, Inc.


Controversies in Cardiovascular Medicine

Is septal ablation preferable to surgical myomectomy for obstructive hypertrophic cardiomyopathy?

Surgical Myectomy Remains the Primary Treatment Option for Severely Symptomatic Patients With Obstructive Hypertrophic Cardiomyopathy

Barry J. Maron, MD

From the Minneapolis Heart Institute Foundation, Minneapolis, Minn.

Correspondence to Barry J. Maron, MD, Minneapolis Heart Institute Foundation, 920 E 28th St, Ste 60, Minneapolis, MN 55407. E-mail hcm.maron{at}mhif.org


*    Introduction
up arrowTop
*Introduction
down arrowSurgical Septal Myectomy
down arrowAlcohol Septal Ablation
down arrowPatient Autonomy and the...
down arrowFinal Thoughts
down arrowReferences
 
The evolving alcohol septal ablation versus surgical myectomy controversy represents a crossroad in the management of obstructive hypertrophic cardiomyopathy (HCM). Indeed, in this now polarized debate within the cardiovascular community, between the traditional and established (ie, surgery) and the new and percutaneous (ie, ablation), much is at stake for the HCM patient population. Furthermore, this issue has become increasingly important given the visibility recently afforded the pathophysiological significance and frequency of left ventricular (LV) outflow gradients in this disease.1,2

Response by Fifer p 206

In the course of this discussion, I will vigorously defend surgery as the primary treatment of choice when outflow obstruction (gradient ≥50 mm Hg at rest or with physiological exercise) produces heart failure symptoms refractory to maximal medical management (New York Heart Association functional classes III and IV).3,4 To this purpose, I will rely on the 50-year experience and substantial body of evidence available in HCM, as well as my own personal extensive association with and work in this disease spanning >30 years and several hundred publications—neither as a surgeon or interventional cardiologist nor with any particular allegiance to either discipline. The message expressed herein is prosurgery, but it is by no means antiablation, for this treatment modality has proved useful (although with a selective role) in the management of HCM.


*    Surgical Septal Myectomy
up arrowTop
up arrowIntroduction
*Surgical Septal Myectomy
down arrowAlcohol Septal Ablation
down arrowPatient Autonomy and the...
down arrowFinal Thoughts
down arrowReferences
 
Historical Context
When surgical septal myectomy (Table 1) was initially introduced in the early 1960s at several North American and European centers, it was regarded as revolutionary and has subsequently stood the test of time. The classic myectomy (Morrow operation)5 relieves obstruction by resection of a relatively small amount of muscle (2 to 5g) from the proximal ventricular septum, thereby widening the outflow tract and abolishing flow drag (or Venturi) forces that promote systolic contact between mitral valve and hypertrophied septum, resulting in immediate gradient reduction6,7 (Figure 1). More recently, some surgeons have creatively modified the myectomy resection to be wider and to extend more distally, allowing more complete reconstruction of the LV outflow tract, which may be necessary in some patients.8–12


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TABLE 1. Advantages and Disadvantages of Surgical Septal Myectomy


Figure 1184625
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Figure 1. Septal myectomy operation. Classic surgical strategy as originally depicted by Dr Andrew G. Morrow. Rectangular myectomy trough (length, {approx}3 to 4 cm) from just below aortic valve to beyond site of mitral-septal contact and intraventricular obstruction. Some myectomy surgeons now routinely extend this resection more distally. From Maron et al97 with permission from the publisher. Copyright © 1983, Oxford University Press.

Dr W.P. Cleland at Hammersmith Hospital (London) was the first surgeon to perform a myectomy,13 but the operation was soon abandoned in the United Kingdom for decades. Thereafter, Drs Andrew Morrow at the National Institutes of Health, John Kirklin at the Mayo Clinic, and Wilfred Bigelow and William Williams at Toronto General pioneered surgical intervention (first myotomy and then myectomy), permitting surgical myectomy to emerge as the primary treatment option for severely symptomatic drug-refractory patients with outflow obstruction in many centers throughout the world.3,5–12,14–32

Operative Risk
In its early years, myectomy was accompanied by ≥5% procedural mortality.17,29,31 Although such operative risk is now clearly obsolete, surgery continues to be frequently misrepresented as an outdated and risk-prone option by its opponents.33–36 Over the last 15 years, with the advantage of contemporary cardiac preservation techniques and intraoperative echocardiography, myectomy has been associated with remarkably low operative mortality approaching zero at major centers (Figure 2).9–11,14,15,22,25,28,37,38 In the combined and continuing experience of the Mayo Clinic, the Cleveland Clinic, and Toronto General Hospital over the last 10 to 12 years, >1500 consecutive isolated myectomy operations have been performed without a postoperative death. The Mayo Clinic also reports no operative deaths in young children over this period (n=56).28 It is essential that this very low operative mortality risk, rather than irrelevant data transposed from the very early surgical experience, be cited to current myectomy candidates. In contrast, the procedure-related mortality for alcohol ablation is 1.5% (up to 5%).39,40 Therefore, paradoxically, the risk of myectomy is lower than that of ablation. These contemporary data dispel the misplaced notion that myectomy is a risky undertaking because it is surgery, and that alcohol ablation is safe solely because it is percutaneous.33–36,41–45


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Figure 2. Contemporary low operative risk. Consecutive number of isolated septal myectomies (without associated cardiac operations or prior alcohol ablation) successfully performed since the last operative death at the 3 most active North American surgical centers: Mayo Clinic (Joseph Dearani, Gordon Danielson, Hartzell Schaff); Cleveland Clinic (Bruce Lytle, Nicholas Smedira); and Toronto General Hospital (William G. Williams, Anthony Ralph-Edwards). *Data to end of 2005. {dagger}Includes only adult patients. {ddagger}Includes 2 relatively new myectomy programs: Roosevelt-St Luke’s Hospital Center (Daniel Swistel) and Tufts-New England Medical Center (Hassan Rastegar), each with no operative deaths (n=51 and n=38, respectively).

Heart Failure Benefit
The vast amount of data assembled worldwide over 40 years clearly substantiates that myectomy results in immediate and permanent abolition of mechanical obstruction to LV outflow (and mitral regurgitation) with normalization of LV pressures.3–12,14–32 As a consequence, surgery achieves relief and often elimination of disabling heart failure symptoms and restores exercise capacity and quality of life. In the most recent long-term postoperative analysis, almost 85% of patients became asymptomatic or only mildly symptomatic (New York Heart Association class I or II) an average of 8 years (and up to 25 years) after myectomy.14 No evidence exists that myectomy itself increases arrhythmogenicity or predisposes to systolic dysfunction and the end stage.46 Furthermore, the preponderance of evidence from observational, comparative studies with alcohol septal ablation shows that myectomy affords more consistent and complete hemodynamic and symptomatic benefit and is associated with fewer procedural complications and reinterventions.37,47–51

Survival Benefit
In addition to heart failure reversal, myectomy also promotes long-term survival. Operated patients experience enhanced longevity indistinguishable from that expected in the general population and superior to that of nonoperated patients with obstruction15 (Figure 3). After myectomy, survival free from all-cause mortality is 98%, 96%, and 83% at 1, 5, and 10 years, and survival free from HCM-related mortality (heart failure and sudden death) is 99%, 98%, and 95%, respectively.14,15 Therefore, surgical septal myectomy favorably alters the natural course of HCM, providing a reasonable expectation for normal or nearly normal life expectancy. These data should not, however, be interpreted as a justification for intervention with either surgery or alcohol ablation at a much earlier time in the clinical course of HCM.


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Figure 3. Survival benefit from surgical myectomy. Survival from all-cause mortality after isolated myectomy at the Mayo Clinic (gold) does not differ from matched general US population (white) (P=0.2) and is superior to nonoperated HCM patients with obstruction (green) (P<0.001). From Ommen et al,15 with permission from the publisher. Copyright © 2005, the American College of Cardiology Foundation.

These substantial benefits of myectomy constitute compelling evidence supporting surgery as the gold standard treatment.3 In contrast is the unsettling and unsubstantiated claim by some in the interventional cardiology community that surgery should be marginalized or abandoned, has no significant role in the management of HCM, or in fact has already been usurped by alcohol ablation.33–35,41,42,52 Furthermore, given the available data, it seems somewhat less than responsible to arbitrarily proclaim alcohol ablation to be the "new gold standard for the 21st century"42 or, remarkably, to argue that myectomy represents an impediment to the development of alcohol ablation.41

Technical Considerations
Unlike alcohol ablation, for which precise targeting of the septum may be constrained by the size and distribution of septal perforator coronary arteries,53 the flexibility afforded the surgeon by direct visual inspection permits recognition of all morphological abnormalities that contribute to mechanical LV outflow obstruction.8,9,11,12,30,51 These include inhomogeneous thickness of the septum (Figure 4) and papillary muscle anomalies such as direct insertion into anterior mitral leaflet8,12,54 (Figure 5). In addition, recognition that greatly elongated mitral valve leaflets can produce obstruction55 (even after adequate myectomy) has led to valve repair or plication in some cases.37,56–58 Myectomy avoids mitral valve replacement3,8,11,12,30 and can be regarded as a "pure" intervention, rarely leaving behind implanted devices (pacemakers and defibrillators)3,5,11,59 and never potentially arrhythmogenic myocardial scarring.60 The complexity and heterogeneity of outflow tract morphology (and necessity for the transaortic approach) have formulated the customary recommendation that septal myectomy be performed by surgeons having specific experience with this operation and HCM.3


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Figure 4. Anatomic variant amenable to myectomy. Distribution of septal thickness that requires strategic adjustments reliable only with surgery. A, Septum is too thin at the 12 o’clock position, the standard target site for muscular resection (or ablation). B, The surgeon has been able to angulate the myectomy toward the 11 o’clock position where the septum is of sufficient thickness. The LV outflow tract is widened, and the subaortic gradient is obliterated. C, Preoperative cardiac magnetic resonance from another patient showing that the usual myectomy (or ablation) site in the anterior ventricular septum (AVS) is of normal thickness, with abrupt transitions to hypertrophied areas medially and laterally. Only the surgeon has the flexibility to compensate for such heterogeneous morphology and to provide safe (without iatrogenic septal defect) and maximally effective relief of obstruction, as in fact occurred in this patient. AFW indicates anterior free wall; PVS, posterior ventricular septum.


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Figure 5. Anatomic variant amenable only to myectomy. A, Preoperative. Anterolateral papillary muscle (APM) inserts directly in the anterior mitral leaflet (AML) and apposes the ventricular septum (VS) in systole, producing midcavity obstruction (arrowheads). This anomaly is often unrecognized with standard (transthoracic) echocardiography but is visualized by the surgeon in the operating room. B, Postoperative after standard (Morrow) myectomy (*). Muscular obstruction persists (arrowheads), underscoring the necessity for a more extended resection. C, Excised mitral valve. Massively hypertrophied papillary muscle anomalously inserts directly into the mitral valve without interposition of chordae. Ao indicates aorta; LA, left atrium. From Klues et al,54 copyright © 1991, with permission from the American Heart Association.


*    Alcohol Septal Ablation
up arrowTop
up arrowIntroduction
up arrowSurgical Septal Myectomy
*Alcohol Septal Ablation
down arrowPatient Autonomy and the...
down arrowFinal Thoughts
down arrowReferences
 
Historical Context
Despite the known benefits of myectomy, it has historically been an aspiration in HCM to develop alternative treatment strategies for operative candidates with obstacles to low-risk surgery (eg, obesity, important comorbidity, particularly advanced age, or insufficient motivation for surgery).3,4 In the early 1990s, dual-chamber pacing was promoted as an alternative (or replacement) for surgery but proved less effective than myectomy,61 and in randomized trials, perceived clinical benefit represented only a placebo effect.62

In 1995, Dr Ulrich Sigwart applied percutaneous methodology to HCM in which 2 to 4 cm3 of 96% ethanol is introduced into a septal perforator branch of the left anterior descending coronary artery (often guided by myocardial contrast echocardiography) to intentionally produce an infarction in the ventricular septum.63 After a transient drop in gradient as a result of stunning, ultimate resolution of obstruction requires several months of septal remodeling, leading to outflow tract widening and reduced mitral valve systolic anterior motion37,50,64 (ie, in effect mimicking the pathophysiology of myectomy).7

Clinical Results
Results of alcohol ablation (Table 2) have now been documented in numerous short-term observational studies (average follow-up, {approx}0.5 to 3 years).36,39,40,50,64–73 Ablation reduces LV outflow obstruction, although on average somewhat less than myectomy (residual rest gradient, 20 to 25 versus 0 to 10 mm Hg for surgery).37,47–49 Improvements in symptoms and exercise capacity may occur, according to the principle that interventions that relieve outflow gradient in HCM will likely improve heart failure symptoms. However, treatment failures have been reported in a substantial minority of patients35,39,68–71 (ie, up to 25%)69 (Figure 6), particularly in those with large outflow gradients69; induced complete heart block requiring permanent pacemaker dependency occurs in 5% to 33% of patients.35,36,39,59


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TABLE 2. Advantages and Disadvantages of Alcohol Septal Ablation


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Figure 6. Failed alcohol septal ablation. Because septal perforator distribution was inappropriate for the ventricular septal (VS) target area, thinning of the wall occurred distal to systolic anterior motion (single arrow), resulting in persistence of outflow obstruction as a result of mitral-septal contact (double arrows) and disabling heart failure symptoms. RV indicates right ventricle; LA, left atrium. From Kimmelstiel and Maron,74 copyright © 2004, with permission from the American Heart Association.

Emergence and Concerns
Over the last 7 years, enthusiasm for alcohol septal ablation has accelerated exponentially, with this technology now considered part of routine interventional practice. Interest in ablation has seemed unbridled, instinctually driven by the erroneous assumption that contemporary and percutaneous ("nonsurgical") strategies are always implicitly more benign and advantageous than traditional open heart surgery.33,41–45,74–76 Indeed, there have been more alcohol septal ablation procedures (estimated >5000) performed in the last 5 to 7 years than myectomies in >45 years51,74–76; overall, most septal reduction interventions for obstructive HCM are now probably alcohol ablations.

But do these developments in management strategy really serve the best interests of the HCM patient population? First, the disproportionate number of percutaneous versus surgical procedures is a legitimate concern, given that the professed clinical threshold (ie, magnitude of symptoms and gradient) professed for both treatments is identical.3,4,11,74–76 Consequently, it is an inescapable conclusion that less stringent patient selection criteria are used for alcohol ablation than for surgery, with many patients undergoing ablation prematurely (often with only mild symptoms after less than maximal medical management). Of note, over the past 14 years, only {approx}5% of my large HCM cohort have required referral for either surgery or ablation.

Second, we have witnessed virtual elimination of myectomy in several European countries (eg, Germany, Switzerland)17,18 and some respected centers in the United States (eg, Stanford),20 all formerly strong proponents of surgical management. In such clinical settings, myectomy has been relegated to the challenging task of relieving obstruction after a failed ablation (and in the presence of large septal scars), a circumstance that also results in pacemaker dependency and may be associated with more complicated technical considerations and hospital course.10,77,78 Certainly, the loss of myectomy expertise for a generation of cardiac surgeons cannot be viewed as advantageous for the future management of HCM. On the other hand, interventional alcohol ablation has been widely criticized for its failure to establish formal rigorous training and to define acceptable levels of expertise.11,26,35,41

Third, interest in alcohol ablation as a novel treatment strategy has created a virtual flood of observational studies (often published with priority) from a variety of clinical laboratories. This skewing of the recent literature has been so pervasive that it is likely that many newly trained cardiologists may not even be fully aware of the surgical option (Table 3). In addition, it is worth citing certain specific limitations of the available ablation literature, including incomplete patient follow-up in some reports,39,69,71 underreporting of complications and death rates in inexperienced interventional laboratories sporadically performing ablation,26 and the unfortunate forced retraction of a major ablation article from a highly respected medical journal.79


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TABLE 3. Popular Misconceptions, Myths, Rationalizations, and Excuses Used to Ignore Surgical Myectomy for Patients With Obstructive HCM*

Clinical Implications of the Scar
A major and largely unresolved issue connected to septal ablation relates to the potential long-term consequences of alcohol-induced necrosis and myocardial infarction as an arrhythmogenic substrate that predisposes susceptible patients to lethal reentrant ventricular tachyarrhythmias.60,74–76,80–88 This is not an idle consideration that can be easily dismissed, given that HCM is the most common cause of sudden death in young people.3,4

Some observers have suggested that the alcohol-induced scar does not represent a true infarction because of its chemical (rather than ischemic) origin and controlled size.41,52 However, recent morphological and magnetic resonance studies unequivocally show the alcohol ablation infarct to be both transmural and extensive, encompassing 10% of the overall LV myocardial mass (30% of the septum) (Figure 7),60,80 and with a histopathological appearance typical of necrosis and healed infarction caused by coronary occlusion.77,82 Repeated alcohol ablations (occurring in 20% to 25% of patients)41,69,74 will result in even larger areas of infarcted myocardium.35,43,60,80 Contrary to a misconception that persists for some reason,41,42,44 surgical myectomy does not produce intramyocardial scarring,60 a likely explanation for the rarity of important arrhythmias long term postoperatively.3,11,14,15,30,83 Although mild endocardial thickening may develop at the site of surgical resection, it is neither a scar nor arrhythmogenic.


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Figure 7. Consequences of ablation versus myectomy (postcontrast cardiovascular magnetic resonance delayed-enhancement images).60 Left, After alcohol ablation, large, dense transmural scar is present (arrow). Right, After surgical myectomy, intramyocardial scarring is absent.

The precise long-term risk for life-threatening arrhythmias after alcohol ablation is unresolved and requires greatly extended follow-up studies. However, the fact that such ablation-related events do frequently occur is now well established,39,42,81–87 (ie, at a rate of 8% per year,86,87 and with 13 deaths reported in 1 study81), and as evidenced by recent enthusiasm for prophylactic defibrillator implantation after ablation.83,85–87 Therefore, unlike myectomy, it is possible that alcohol-imposed infarcts could act as a new HCM risk factor, compounding the underlying myocardial electric instability already present in some patients, for whom unpredictable sudden death risk is known to extend over many decades.3,4,83,88 Consequently, for some patients, alcohol ablation could represent an unfavorable net tradeoff of gradient relief for increased arrhythmia risk.

Indeed, alcohol ablation is unique among cardiovascular treatment strategies by aspiring to hemodynamic benefit via destruction of myocardial tissue and, in the process, contradicting a major tenet of preventive cardiology, to minimize the likelihood of infarction and scarring. Recently introduced experimental septal reduction interventions, which circumvent surgery and ablation (eg, coil embolization, stenting, radiofrequency ablation), also impose sizable septal infarctions similar to those incurred with alcohol.89–92 Finally, early experience suggests that myectomy performed after failed alcohol septal ablation may be associated with more complicated technical considerations and hospital course.

Considerations for late postprocedural arrhythmias have led to the prudent recommendation that alcohol ablation should be confined largely to adults of relatively advanced age in whom the potential risk period is shortest.3,4,11,51,74–76 Although some practitioners have inadvisably lowered the age of acceptability for ablation well into childhood45,72,89,93 (remarkably, to ages as young as 3 and 5 years),89,93 it is the prevailing view of HCM experts that alcohol septal ablation should be strongly discouraged in children, adolescents, and young adults.3

Another unfortunate byproduct of this controversy and the euphoria associated with relieving obstruction with alcohol ablation is the misconception that LV outflow gradients (traditionally, a highly visible feature of HCM) are always the predominant clinical facet of this complex disease. As a consequence, other important issues such as risk stratification for sudden death, family screening, and genetic counseling may not always receive the attention they deserve.


*    Patient Autonomy and the "Gatekeeper" Effect
up arrowTop
up arrowIntroduction
up arrowSurgical Septal Myectomy
up arrowAlcohol Septal Ablation
*Patient Autonomy and the...
down arrowFinal Thoughts
down arrowReferences
 
The rapid penetration of alcohol ablation into cardiology practice has often been associated with preferential referral for this procedure without the explicit presentation of other available treatment options (ie, surgical myectomy). This strategy represents an ethical dilemma and, in effect, violates the important principle of patient autonomy (ie, that patients possess a fundamental right to full disclosure of all medical information that may potentially affect their health, safety, and risk for death or injury, as well as an opportunity to actively participate in treatment decisions that dictate their medical destiny) (Table 3). Similar considerations triggered the recent Guidant Affair, in which industry executives withheld from patients and their physicians crucial information about defective implantable defibrillators, known only by the corporation to be unreliable in preventing sudden death.94

Cardiologists in the role of gatekeeper bear a similar responsibility with respect to ablation and myectomy: to fully inform patients on the advantages and disadvantages of both septal reduction treatments (Table 3). If patients are not fully apprised of all therapeutic options, they are, in effect, deprived of the opportunity to formulate truly informed decisions. Indeed, this is a fundamental premise of those specialty centers of excellence focused on the diagnosis and management of HCM (where both expert surgery and ablation are available). Finally, recognition that the patient autonomy principle applies to decisions about ablation or surgery requires a willingness to override the inherent resistance to referring patients out of institutions and networks that lack accomplished myectomy surgeons (to those that do) when this strategy represents a clear benefit to patients. Such recommendations for HCM are not unlike those made by an American College of Cardiology/American Heart Association consensus panel regarding preferential patient referral for mitral valve repair to centers experienced with that particular operation.95


*    Final Thoughts
up arrowTop
up arrowIntroduction
up arrowSurgical Septal Myectomy
up arrowAlcohol Septal Ablation
up arrowPatient Autonomy and the...
*Final Thoughts
down arrowReferences
 
The central issue in the current myectomy versus ablation debate resides with proper patient selection. The American College of Cardiology/European Society of Cardiology expert panel recently commissioned to establish consensus guidelines for the management of HCM (including practitioners of surgery and ablation),3 and unfortunately largely ignored by the interventional community, formally advocated septal myectomy as the primary treatment option for disabling drug-refractory heart failure symptoms resulting from outflow obstruction. Alcohol septal ablation is regarded as an important but nevertheless alternative intervention for selected patients who are not optimal surgical candidates. Because a prospective randomized trial comparing alcohol ablation and myectomy is impractical and unlikely to occur to resolve this debate,96 there is little reason to look beyond the more-established surgical myectomy as the first option for most patients.

Alcohol ablation has been heavily promoted by interventional cardiology over the last several years,33,34,39,41–45,63 but now it is imperative that the pendulum swing back toward surgery.11,51 Indeed, there does not appear to be a compelling reason to aggressively advance a new invasive treatment option for obstructive HCM (ie, alcohol ablation) that may result in pacemaker and defibrillator dependency, increase the risk for late sudden death, incur potential complications from the implanted devices, and convey a not-inconsequential procedural mortality rate. This is particularly true when an established and time-honored intervention (surgical myectomy) is available that has already served this patient population exceptionally well for >45 years by virtue of extremely low operative risk, more consistent amelioration of symptoms resulting from permanent relief of mechanical impedance to LV outflow, and a documented survival benefit affording the opportunity to achieve normal life expectancy.


*    Acknowledgments
 
Disclosures

None.


*    References
up arrowTop
up arrowIntroduction
up arrowSurgical Septal Myectomy
up arrowAlcohol Septal Ablation
up arrowPatient Autonomy and the...
up arrowFinal Thoughts
*References
 
1. Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA, Cecchi F, Maron BJ. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med. 2003; 348: 295–303.[Abstract/Free Full Text]

2. Maron MS, Olivotto I, Zenovich AG, Link MS, Pandian NG, Kuvin JT, Nistri S, Cecchi F, Udelson JE, Maron BJ. Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction. Circulation. 2006; 114: 2232–2239.[Abstract/Free Full Text]

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18. Schönbeck MH, Brunner-La Rocca HP, Vogt PR, Lachat ML, Jenni R, Hess OM, Turina MI. Long-term follow-up in hypertrophic obstructive cardiomyopathy after septal myectomy. Ann Thorac Surg. 1988; 65: 1207–1214.[CrossRef]

19. Heric B, Lytle BW, Miller DP, Rosenkranz ER, Lever HM, Cosgrove DM. Surgical management of hypertrophic obstructive cardiomyopathy: early and late results. J Thorac Cardiovasc Surg. 1995; 110: 195–208.[Abstract/Free Full Text]

20. Robbins RC, Stinson EB. Long-term results of left ventricular myotomy and myectomy for obstructive hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg. 1996; 11: 586–594.

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Response to Maron

Michael A. Fifer, MD

I have the highest regard for Dr Maron’s unsurpassed experience and expertise in hypertrophic cardiomyopathy. I agree with him that the principle of patient autonomy requires that cardiologists fully inform patients about all treatment options, but I feel obliged to point out that we must compare apples to apples. It is not appropriate to compare the apples of idealized septal myectomy outcomes reported from a very few centers, beginning after the steep portions of practitioners’ learning curves and omitting patients undergoing concomitant cardiac surgery, to the oranges of actual septal ablation outcomes reported from the very early experience with the procedure. It would be misleading to equate the highly selected surgical mortality figures chosen by Dr Maron with those of patients in actual clinical practice. The mortality rate of septal myectomy is not zero! Furthermore, the need for postmyectomy permanent device therapy arises more than rarely, and we as well as others have performed septal ablation in patients who had undergone unsuccessful septal myectomy. The theoretical concern that septal ablation would increase the incidence of fatal arrhythmias has fortunately not been realized; indeed, the publication of Lawrenz et al cited by Dr Maron is actually entitled "Transcoronary Ablation of Septal Hypertrophy Does Not Alter ICD Intervention Rates in High-Risk Patients With Hypertrophic Obstructive Cardiomyopathy." I agree with Dr Maron that patients should undergo septal reduction therapy only after truly optimal medical therapy has failed, following a balanced and dispassionate presentation of the treatment options and in the context of comprehensive management of their disease.


*    Footnotes
 
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.




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