Circulation. 2007;116:196-206
doi: 10.1161/CIRCULATIONAHA.107.691378
(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
|
|---|
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
|
|---|
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 reduction
6,7 (
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

View larger version (28K):
[in this window]
[in a new window]
|
Figure 1. Septal myectomy operation. Classic surgical strategy as originally depicted by Dr Andrew G. Morrow. Rectangular myectomy trough (length, 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
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.

View larger version (11K):
[in this window]
[in a new window]
|
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

View larger version (64K):
[in this window]
[in a new window]
|
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 oclock position, the standard target site for muscular resection (or ablation). B, The surgeon has been able to angulate the myectomy toward the 11 oclock 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.
|
|

View larger version (59K):
[in this window]
[in a new window]
|
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
|
|---|
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,
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

View larger version (100K):
[in this window]
[in a new window]
|
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
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
View this table:
[in this window]
[in a new window]
|
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.

View larger version (69K):
[in this window]
[in a new window]
|
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
|
|---|
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
|
|---|
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
|
|---|
- 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]
- 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]
- Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn HJ, Seidman CE, Shah PM, Spencer WH, Spirito P, ten Cate FJ, Wigle ED. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy. J Am Coll Cardiol. 2003; 42: 1687–1713.[Free Full Text]
- Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA. 2002; 287: 1308–1320.[Abstract/Free Full Text]
- Morrow AG, Reitz BA, Epstein SE, Henry WL, Conkle DM, Itscoitz SB, Redwood DR. Operative treatment in hypertrophic subaortic stenosis: techniques, and the results of pre and postoperative assessments in 83 patients. Circulation. 1975; 52: 88–102.[Abstract/Free Full Text]
- Sherrid MV, Chaudhry FA, Swistel DG. Obstructive hypertrophic cardiomyopathy: echocardiography, pathophysiology and the continuing evolution of surgery for obstruction. Ann Thorac Surg. 2003; 75: 620–632.[Abstract/Free Full Text]
- Spirito P, Maron BJ, Rosing DR. Morphologic determinants of hemodynamic status following ventricular septal myotomy-myectomy in patients with hypertrophic cardiomyopathy. Circulation. 1984; 70: 984–995.[Abstract/Free Full Text]
- Minakata K, Dearani JA, Nishimura RA, Maron BJ, Danielson GK. Extended septal myectomy for hypertrophic obstructive cardiomyopathy with anomalous mitral papillary muscles or chordae. J Thorac Cardiovasc Surg. 2004; 127: 481–489.[Abstract/Free Full Text]
- Schoendube FA, Keith S, Flchskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. Circulation. 1995; 92 (suppl II): II-122–II-127.[Medline]
[Order article via Infotrieve]
- Dörge H, Schmitto JD, Liakopoulos OJ, Walther S, Schöndube FA. Extended myectomy for hypertrophic obstructive cardiomyopathy after failure or contraindication of septal ablation or with combined surgical procedures. Thorac Cardiovasc Surg. 2004; 52: 344–348.[CrossRef][Medline]
[Order article via Infotrieve]
- Maron BJ, Dearani JA, Ommen SR, Maron MS, Schaff HV, Gersh BJ, Nishimura RA. The case for surgery in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 2004; 44: 2044–2053.[Abstract/Free Full Text]
- Maron BJ, Nishimura RA, Danielson GK. Pitfalls in clinical recognition and a novel operative approach for hypertrophic cardiomyopathy with severe outflow obstruction due to anomalous papillary muscle. Circulation. 1998; 98: 2505–2508.[Abstract/Free Full Text]
- Cleland WP. The surgical management of obstructive cardiomyopathy. J Cardiovasc Surg. 1963; 4: 489–491.[Medline]
[Order article via Infotrieve]
- Woo A, Williams WG, Choi R, Wigle ED, Rozenblyum E, Fedwick K, Siu S, Ralph-Edwards A, Rakowski H. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy. Circulation. 2005; 111: 2033–2041.[Abstract/Free Full Text]
- Ommen SR, Maron BJ, Olivotto I, Maron MS, Cecchi F, Betocchi S, Gersh BJ, Ackerman MJ, McCully RB, Dearani JA, Schaff HV, Danielson GK, Tajik AJ, Nishimura RA. Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 2005; 46: 470–476.[Abstract/Free Full Text]
- Seiler C, Hess OM, Schoenbeck M, Turina J, Jenni R, Turina M, Krayenbuehl H-P. Long-term follow-up of medical versus surgical therapy for hypertrophic cardiomyopathy: a retrospective study. J Am Coll Cardiol. 1991; 17: 634–645.[Abstract]
- Schulte HD, Borisov K, Gams E, Gramsch-Zabel H, Losse B, Schwartzkopff B. Management of symptomatic hypertrophic obstructive cardiomyopathy: long-term results after surgical therapy. Thorac Cardiovasc Surg. 1999; 47: 213–218.[Medline]
[Order article via Infotrieve]
- 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]
- 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]
- 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.
- McCully RB, Nishimura RA, Tajik AJ, Schaff HV, Danielson GK. Extent of clinical improvement after surgical treatment of hypertrophic obstructive cardiomyopathy. Circulation. 1996; 94: 467–471.[Abstract/Free Full Text]
- Merrill WH, Friesinger GC, Graham TP Jr, Byrd BF III, Drinkwater DC Jr, Christian KG, Bender HW Jr. Long-lasting improvement after septal myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg. 2000; 69: 1732–1735.[Abstract/Free Full Text]
- Agnew TM, Barratt-Boyes BG, Brandt PW, Roche AH, Lowe JB, OBrien KP. Surgical resection in idiopathic hypertrophic cardiomyopathy subaortic stenosis with a combined approach through aorta and left ventricle. J Thorac Cardiovasc Surg. 1977; 74: 307–316.[Abstract]
- Cohn LH, Trehan H, Collins JJ Jr. Long-term follow-up of patients undergoing myotomy/myectomy for obstructive hypertrophic cardiomyopathy. Am J Cardiol. 1992; 70: 657–660.[CrossRef][Medline]
[Order article via Infotrieve]
- ten Berg JM, Suttorp MJ, Knepen PJ, Ernst SM, Vermeulen FE, Jaarsma W. Hypertrophic obstructive cardiomyopathy: initial results and long-term follow-up after Morrow septal myectomy. Circulation. 1994; 90: 1781–1785.[Abstract/Free Full Text]
- Nishimura RA, Holmes DR Jr. Hypertrophic obstructive cardiomyopathy. N Engl J Med. 2004; 350: 1320–1327.[Free Full Text]
- Diodati JG, Schenke WH, Waclawiw MA, McIntosh CL, Cannon RO. Predictors of exercise benefit after operative relief of left ventricular outflow obstruction by the myotomy-myectomy procedure in hypertrophic cardiomyopathy. Am J Cardiol. 1992; 69: 1617–1632.[CrossRef][Medline]
[Order article via Infotrieve]
- Theodoro DA, Danielson GK, Feldt RH, Anderson BJ. Hypertrophic obstructive cardiomyopathy in pediatric patients: results of surgical treatment. J Thorac Cardiovasc Surg. 1996; 112: 1589–1597.[Abstract/Free Full Text]
- Maron BJ, Merrill WH, Freier A, Kent KM, Epstein SE, Morrow AG. Long-term clinical course and symptomatic status of patients after operation for hypertrophic subaortic stenosis. Circulation. 1978; 57: 1205–1213.[Abstract/Free Full Text]
- Maron BJ. Surgery for hypertrophic obstructive cardiomyopathy: alive and quite well. Circulation. 2005; 111: 2016–2018.[Free Full Text]
- Shah PM, Adelman AG, Wigle ED, Gobel FL, Burchell HB, Hardarson T, Curiel R, De La Calzada C, Oakley CM, Goodwin JF. The natural (and unnatural) history of hypertrophic obstructive cardiomyopathy. Circ Res. 1974; 35 (suppl II): II-179–II-195.
- McIntosh CL, Maron BJ. Current operative treatment of obstructive hypertrophic cardiomyopathy. Circulation. 1988; 78: 487–495.[Free Full Text]
- Hess OM. Risk stratification in hypertrophic cardiomyopathy: fact or fiction? J Am Coll Cardiol. 2003; 42: 880–881.Editorial.[Free Full Text]
- Oakley C. Non-surgical ablation of the ventricular septum for the treatment of hypertrophic cardiomyopathy. Br Heart J. 1995; 74: 479–480.[Free Full Text]
- Seggewiss H. Percutaneous transluminal septal myocardial ablation: a new treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J. 2000; 21: 704–707.[Free Full Text]
- Lakkis NM, Nagueh SF, Kleiman NS, Killip D, He Z-X, Verani MS, Roberts R, Spencer WH. Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation. 1998; 98: 1750–1755.[Abstract/Free Full Text]
- van der Lee C, ten Cate FJ, Geleijnse ML, Kofflard MJ, Pedone C, van Herwerden LA, Biagini E, Vletter WB, Serruys PW. Percutaneous versus surgical treatment for patients with hypertrophic obstructive cardiomyopathy and enlarged anterior mitral valve leaflets. Circulation. 2005; 112: 482–488.[Abstract/Free Full Text]
- Smedira NG, Lever HM, Miluk M, Krishnaswamy G, Laing G, Thamilarasan M, Lytle BW, Blackstone EH, Topol EJ. Septal myectomy: 324 consecutive procedures without a mortality. J Am Coll Cardiol. 2006; 47 (suppl A): 275A. Abstract.
- Alam M, Dokainish H, Lakkis N. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: a systematic review of published studies. J Interv Cardiol. 2006; 19: 319–327.[CrossRef][Medline]
[Order article via Infotrieve]
- Geitzen F, Leuner CH, Raute-Kreinsen U, Dellmann A, Hegselmann J, Strunk-Mueller C, Kuhn HJ. Acute and long-term results after transcoronary ablation of septum hypertrophy (TASH): catheter interventional treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J. 1999; 20: 1342–1354.[Abstract/Free Full Text]
- Knight CJ. Alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Heart. 2006; 92: 1339–1344.[Free Full Text]
- Hess OM, Sigwart U. New treatment strategies for hypertrophic obstructive cardiomyopathy: alcohol ablation of the septum: the new gold standard. J Am Coll Cardiol. 2004; 44: 2054–2055.[Abstract/Free Full Text]
- Smith EJ, Jain AK, Knight CJ. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: how and when? Br J Cardiol. 2006; 13: 58–61.
- Roberts R, Sigwart U. Current concepts of the pathogenesis and treatment of hypertrophic cardiomyopathy. Circulation. 2005; 112: 293–296.[Free Full Text]
- Seggewiss H, Rigopoulos A. Management of hypertrophic cardiomyopathy in children. Pediatr Drugs. 2003; 5: 663–672.[CrossRef]
- Harris KM, Spirito P, Maron MS, Zenovich AG, Formisano F, Lesser JR, Mackey-Bojack S, Manning WJ, Udelson JE, Maron BJ. Prevalence, clinical profile and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy. Circulation. 2006; 114: 216–225.[Abstract/Free Full Text]
- Firoozi S, Elliott PM, Sharma S, Murday A, Brecker SJ, Hamid MS, Sachdev B, Thaman R, McKenna WJ. Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy: a comparison of clinical, haemodynamic and exercise outcomes. Eur Heart J. 2002; 23: 1617–1624.[Abstract/Free Full Text]
- Qin JX, Shiota T, Lever HM, Kapadia SR, Sitges M, Rubin DN, Bauer F, Tuzcu EM, Smedira NG, Lytle B, Thomas JD. Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery. J Am Coll Cardiol. 2001; 38: 1994–2000.[Abstract/Free Full Text]
- Ralph-Edwards A, Woo A, McCrindle BW, Shapero JL, Schwartz L, Rakowski H, Wigle ED, Williams WG. Hypertrophic obstructive cardiomyopathy: comparison of outcomes after myectomy or alcohol ablation adjusted by propensity score. J Thorac Cardiovasc Surg. 2005; 129: 351–358.[Abstract/Free Full Text]
- van Dockum WG, Beek AM, ten Cate FJ, ten Berg JM, Bondarenko O, Götte MJW, Twisk JWR, Hofman MBM, Visser CA, van Rossum AC. Early onset and progression of left ventricular remodeling after alcohol septal ablation in hypertrophic obstructive cardiomyopathy. Circulation. 2005; 111: 2503–2508.[Abstract/Free Full Text]
- Yacoub MH. Surgical versus alcohol septal ablation for hypertrophic obstructive cardiomyopathy: the pendulum swings. Circulation. 2005; 112: 450–452.Editorial.[Free Full Text]
- Batalis NI, Harley RA, Collins KA. Iatrogenic deaths following treatment for hypertrophic obstructive cardiomyopathy: case reports and an approach to the autopsy and death certification. Am J Forensic Med Pathol. 2005; 26: 343–348.[CrossRef][Medline]
[Order article via Infotrieve]
- Singh M, Edwards WD, Holmes DR, Tajik AJ, Nishimura RA. Anatomy of first septal perforating artery: a study with implications for ablation therapy for hypertrophic cardiomyopathy. Mayo Clinic Proc. 2001; 76: 799–802.[Medline]
[Order article via Infotrieve]
- Klues HG, Roberts WC, Maron BJ. Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy: significance in producing left ventricular outflow obstruction. Circulation. 1991; 84: 1188–1197.[Abstract/Free Full Text]
- Klues HG, Maron BJ, Dollar AL, Roberts WC. Diversity of structural mitral valve alterations in hypertrophic cardiomyopathy. Circulation. 1992; 85: 1651–1660.[Abstract/Free Full Text]
- McIntosh CL, Maron BJ, Cannon RO, Klues HG. Initial results of combined anterior mitral leaflet plication and ventricular septal myotomy-myectomy for relief of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. Circulation. 1992; 86 (suppl): II-60–II-67.[Medline]
[Order article via Infotrieve]
- Matsui Y, Shiiya N, Murashita T, Sasaki S, Yasuda K. Mitral valve repair and septal myectomy for hypertrophic obstructive cardiomyopathy. J Cardiovasc Surg. 2000; 41: 53–56.[Medline]
[Order article via Infotrieve]
- Kofflard MJ, van Herwerden LA, Waldstein DJ, Ruygrok P, Boersma E, Taams MA, ten Cate FJ. Initial results of combined anterior mitral leaflet extension and myectomy in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 1996; 28: 197–202.[Abstract]
- Qin JX, Shiota T, Lever HM, Asher CR, Popovi
ZB, Greenberg NL, Agler DA, Drinko JK, Smedira NG, Tuzcu EM, Lytle BW, Thomas JD. Conduction system abnormalities in patients with obstructive hypertrophic cardiomyopathy following septal reduction interventions. Am J Cardiol. 2004; 93: 171–175.[CrossRef][Medline]
[Order article via Infotrieve]
- Valeti US, Nishimura RA, Holmes DR, Araoz PA, Glockner JF, Breen JF, Ommen SR, Gersh BJ, Tajik AJ, Rihal CS, Schaff HV, Maron BJ. Comparison of surgical septal myectomy and alcohol septal ablation by cardiac magnetic resonance imaging in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 2007; 49: 350–357.[Abstract/Free Full Text]
- Ommen SR, Nishimura RA, Squires RW, Schaff HV, Danielson GK, Tajik AJ. Comparison of dual-chamber pacing versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 1999; 34: 191–196.[Abstract/Free Full Text]
- Maron BJ, Nishimura RA, McKenna WJ, Rakowski H, Josephson ME, Kieval RS. Assessment of permanent dual-chamber pacing as a treatment for drug-refractory symptomatic patients with obstructive hypertrophic cardiomyopathy: a randomized, double-blind cross-over study (M-PATHY). Circulation. 1999; 99: 2927–2933.[Abstract/Free Full Text]
- Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet. 1995; 346: 211–214.[CrossRef][Medline]
[Order article via Infotrieve]
- Henein MY, OSullivan CA, Ramzy IS, Sigwart U, Gibson DG. Electromechanical left ventricular behavior after nonsurgical septal reduction in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 1999; 34: 1117–1122.[Abstract/Free Full Text]
- Faber L, Meissner A, Ziemssen P, Seggewiss H. Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy: long-term follow-up of the first series of 25 patients. Heart. 2000; 83: 326–331.[Abstract/Free Full Text]
- Nagueh SF, Ommen SR, Lakkis NM, Killip D, Zoghbi WA, Schaff HV, Danielson CK, Quinones MA, Tajik AJ, Spencer WH. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic cardiomyopathy. J Am Coll Cardiol. 2001; 38: 1701–1706.[Abstract/Free Full Text]
- Knight C, Kurbaan AS, Seggewiss H, Henein M, Gunning M, Harrington D, Fassbender D, Gleichmann U, Sigwart U. Nonsurgical septal reduction for hypertrophic obstructive cardiomyopathy: outcome in the first series of patients. Circulation. 1997; 95: 2075–2081.[Abstract/Free Full Text]
- Yoerger DM, Picard MH, Palacios IF, Vlahakes GJ, Lowry PA, Fifer MA. Time course of pressure gradient response after first alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Am J Cardiol. 2006; 97: 1511–1514.[CrossRef][Medline]
[Order article via Infotrieve]
- Chang SM, Lakkis NM, Franklin J, Spencer WH III, Nagueh SF. Predictors of outcome after alcohol septal ablation therapy in patients with hypertrophic obstructive cardiomyopathy. Circulation. 2004; 109: 824–827.[Abstract/Free Full Text]
- Nesta F, Yoerger DM, Picard MH, Fifer MA, Palacios IF, Vlahakes GJ, Levine RA, Hung J. Mechanism of systolic anterior motion and regurgitation post septal ablation in hypertrophic cardiomyopathy. J Am Coll Cardiol. 2004; 43 (suppl A): 215A. Abstract.
- Faber L, Seggewiss H, Gietzen FH, Kuhn H, Boekstegers P, Neuhaus L, Seipel L, Horstkotte D. Catheter-based septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: follow-up results of the TASH-registry of the German Cardiac Society. Z Kardiol. 2005; 94: 516–523.[CrossRef][Medline]
[Order article via Infotrieve]
- Kuhn H, Seggewiss H, Gietzen FH, Boekstegers P, Neuhaus L, Seipel L. Catheter-based therapy for hypertrophic obstructive cardiomyopathy. Z Cardiol. 2004; 93: 23–31.
- Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H. Transcoronary ablation of septal hypertrophy for hypertrophic obstructive cardiomyopathy: feasibility, clinical benefit, and short-term results in elderly patients. Heart. 2004; 90: 638–644.[Abstract/Free Full Text]
- Kimmelstiel CD, Maron BJ. Role of percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Circulation. 2004; 109: 452–456.[Free Full Text]
- Maron BJ. Role of alcohol septal ablation in treatment of obstructive hypertrophic cardiomyopathy. Lancet. 2000; 35: 425–426.[CrossRef]
- Spirito P, Maron BJ. Perspectives on the role of new treatment strategies in hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 1999; 33: 1071–1075.[Free Full Text]
- Arrazaghi AA, Butany JW, Williams WG, Wigle DE, Rakowski H. Myectomy for hypertrophic obstructive cardiomyopathy after failed alcohol septal ablation: clinicopathological correlations. Can J Cardiol. 2001; 17: 197–202.[Medline]
[Order article via Infotrieve]
- Elbardissi AW, Stulak JM, Nishimura RA, Ommen SR, Dearani JA, Schaff HV. Septal myectomy after previous septal artery ablation. Circulation. 2006; 114: 546. Abstract.
- Coats AJ, Henein M, Flather M, Sigwart U, Seggewiss H, Wang D, Yousufuddin M, Shamim W. Nonsurgical reduction of the interventricular septum in patients with hypertrophic cardiomyopathy [retracted in: N Engl J Med. 2003;348:951]. N Engl J Med. 2002; 347: 1326–1333.[Abstract/Free Full Text]
- van Dockum WG, ten Cate FJ, ten Berg JM, Beek AM, Twisk JW, Vos J, Hofman MB, Visser CA, van Rossum AC. Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol. 2004; 43: 27–34.[Abstract/Free Full Text]
- Hori Y, Ueda M, Nakayama T, Saegusa N, Uehara M, Lee K, Sekine T, Daimon M, Kobayashi Y, Funabashi N, Komuro I. Occurrence of de novo sustained monomorphic ventricular tachycardia induced after percutaneous transluminal alcohol septal myocardial ablation for hypertrophic obstructive cardiomyopathy. Int J Cardiol. October 25, 2006[E-pub ahead of print].
- Raute-Kreinsen U. Morphology of necrosis and repair after transcoronary ethanol ablation of septal hypertrophy. Pathol Res Pract. 2003; 1999: 121–127.
- Maron BJ, Spirito P, Shen W-K, Haas TS, Formisano F, Link MS, Epstein AE, Almquist AK, Daubert JP, Lawrenz T, Boriani G, Estes NAM III, Favale S, Piccininno M, Winters SL, Santini M, Betocchi S, Arribas F, Sherrid MV, Buja G, Semsarian C, Bruzzi P. Prevention of sudden cardiac death and selection of patients for implantable cardioverter-defibrillators in hypertrophic cardiomyopathy. JAMA. In press.
- Simon RDB, Crawford FA III, Spencer WH III, Gold MR. Sustained ventricular tachycardia following alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Pacing Clin Electrophysiol. 2005; 28: 1354–1356.[CrossRef][Medline]
[Order article via Infotrieve]
- Boltwood CM Jr, Chien W, Ports T. Ventricular tachycardia complicating alcohol septal ablation. N Engl J Med. 2004; 351: 1914–1915.[Free Full Text]
- Crawford FA III, Killip D, Franklin J, Spencer WH, Gold MR, Implantable cardioverter-defibrillators for primary prevention of sudden death in patients with hypertrophic obstructive cardiomyopathy after alcohol septal ablation. Circulation. 2003; 108 (suppl): IV-386–IV-387. Abstract.
- Lawrenz T, Obergassel L, Lieder F, Leuner C, Strunk-Mueller C, Vilsendorf DMZ, Beer G, Kuhn H. Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk patients with hypertrophic obstructive cardiomyopathy. Pacing Clin Electrophysiol. 2005; 28: 295–300.[CrossRef][Medline]
[Order article via Infotrieve]
- Maron BJ, Shen W-K, Link MS, Epstein AE, Almquist AK, Daubert JP, Bardy GH, Favale S, Rea RF, Boriani G, Estes NAM III, Casey SA, Stanton MS, Betocchi S, Spirito P. Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. N Engl J Med. 2000; 342: 365–373.[Abstract/Free Full Text]
- Emmel M, Sreeram N, de Giovanni JV, Brockmeier K. Radiofrequency catheter septal ablation for hypertrophic obstructive cardiomyopathy in childhood. Z Kardiol. 2005; 94: 699–703.[CrossRef][Medline]
[Order article via Infotrieve]
- Lawrenz T, Kuhn H. Endocardial radiofrequency ablation of septal hypertrophy: a new catheter-based modality of gradient reduction in hypertrophic obstructive cardiomyopathy. Z Kardiol. 2004; 93: 493–499.[Medline]
[Order article via Infotrieve]
- Lafont A, Durand E, Brasselet C, Mousseaux E, Hagege A, Desnos M. Percutaneous transluminal septal coil embolization as an alternative to alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Heart. 2005; 91: 92.[Free Full Text]
- Anzuini A, Uretsky BF. Covered stent septal ablation for hypertrophic obstructive cardiomyopathy. Circulation. 2004; 109: e6.[Medline]
[Order article via Infotrieve]
- Subash CV, Jayranganth M, Shenoy AR. Nonsurgical septal reduction for hypertrophic cardiomyopathy in childhood. Int J Cardiol. 2006; 106: 355–359.[CrossRef][Medline]
[Order article via Infotrieve]
- Hauser RG, Maron BJ. Lessons from the failure and recall of an implantable cardioverter defibrillator. Circulation. 2005; 112: 2040–2042.[Free Full Text]
- Bonow RO, Carabello BA, Chatterjee K, de Leon AC J