TREATMENT OF HYPERTROPHIC CARDIOMYOPATHY: POINT-COUNTERPOINT
The case for surgery in obstructive hypertrophic cardiomyopathy
Barry J. Maron, MD, FACC*,*,
Joseph A. Dearani, MD ,
Steve R. Ommen, MD, FACC,
Martin S. Maron, MD ,
Hartzell V. Schaff, MD, FACC,
Bernard J. Gersh, MB, MBChB, DPhil, FACC and
Rick A. Nishimura, MD, FACC
* Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota
Departments of Cardiovascular Surgery and Cardiology, Mayo Clinic, Rochester, Minnesota
Hypertrophic Cardiomyopathy Center, Tufts-New England Medical Center, Boston, Massachusetts
Manuscript received December 18, 2003;
accepted April 27, 2004.
* Reprint requests and correspondence: Dr. Barry J. Maron, The Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, 920 E. 28th Street, Suite 60, Minneapolis, Minnesota 55407 (Email: hcm.maron{at}mhif.org).
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Abstract
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Relief of left ventricular (LV) outflow obstruction in patients with hypertrophic cardiomyopathy (HCM) and disabling symptoms refractory to maximum medical management has historically been a surgical problem. Surgical septal myectomy permanently abolishes systolic anterior motion of the mitral valve and mitral regurgitation, while normalizing LV pressures and wall stress. Also, these salutary goals are achieved without encumbering patients with post-procedural devices (e.g., pacemakers or defibrillators) or creating potentially arrhythmogenic substrates, as may occur with alcohol septal ablation. Procedural morbidity and mortality risk with myectomy is similar to, and in some institutions less than those for alcohol septal ablation. Over four decades, reports from numerous centers worldwide have consistently and unequivocably documented the benefits of surgery on hemodynamic and functional state, restoring normal and acceptable quality of life to patients of all ages by largely reversing the complications of heart failure. Long-term survival after myectomy is similar to that of the general population and superior to non-operated patients with obstruction. The LV outflow tract morphology in HCM is heterogeneous and not uncommonly includes congenital anomalies of the mitral valve apparatus for which the surgeon has the flexibility to adapt the repair, often employing an extended myectomy. In the current atmosphere of increasing and perhaps excessive enthusiasm for newer catheter-based interventions, it is a critical time to promote and re-emphasize that surgery is the time-honored (and presently the most effective) treatment strategy for relieving heart failure-related disability resulting from dynamic LV outflow obstruction in HCM, and is the primary treatment option for this subgroup of severely symptomatic drug-refractory patients.
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Abbreviations and Acronyms
| | HCM = hypertrophic cardiomyopathy | | LV = left ventricular |
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Historical context
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Historically, surgery has been the primary strategy for relieving left ventricular (LV) outflow obstruction in patients with hypertrophic cardiomyopathy (HCM) and severe limiting symptoms unresponsive to maximum medical management (1,2). A recently introduced catheter-based intervention (alcohol septal ablation) has experienced a surge in popularity among interventional cardiologists (1). In the present discussion, we wish to re-emphasize the appropriate role and visibility of surgical septal myectomy in the treatment of obstructive HCM, and in the process prudently balance the presently skewed ongoing debate between percutaneous techniques and cardiac surgery.
Since the first modern reports in the late 1950s (3,4), HCM has been regarded as a genetic heart disease characterized by asymmetric LV hypertrophy and dynamic outflow obstruction (1,2,5–18). Indeed, the common nonobstructive form of HCM was not fully appreciated until the advent of echocardiography in the early 1970s (1). Despite periodic controversy (19–21), substantial clinical importance has been attributed to LV outflow obstruction through the years, with patient management often predicated on the presence (or absence) of a subaortic gradient (1,2,7–11).
However, only recently was the long-term pathophysiologic significance of obstruction leading to progressive heart failure and cardiovascular death substantiated in a large and prospectively enrolled HCM population (22). It is now generally accepted that outflow tract gradients (and associated mitral regurgitation) represent adverse consequences of HCM, cause mechanical impedance to LV ejection, and are a major cause of disabling symptoms at any age.
Surgical intervention for obstructive HCM was first performed by Cleland (23) in the United Kingdom, but the procedure was abandoned owing to high operative mortality. Subsequently, surgical techniques were pioneered in North America by Morrow (24) at the National Institutes of Health, Kirklin (25) at Mayo Clinic, and Bigelow et al. (26) at Toronto General Hospital, and then quickly adopted by other U.S. and Western European centers. Paradoxically, early surgical efforts in the 1960s went forward even though the mechanism by which obstruction occurs, that is, systolic anterior motion of the mitral valve with prolonged mid-systolic septal apposition, had not yet been recognized, and subaortic gradients were regarded as the consequence of a sphincter-like, muscular outflow tract contraction ring (5,6,24).
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The surgical approach
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Surgery for obstructive HCM, traditionally performed in specialized tertiary centers, has evolved over the past four decades, from ventricular septal myotomy (i.e., without muscular resection) (26), to the classic Morrow myectomy (24). More recently, an extended and more extensive myectomy (up to about 7 cm long compared with 3 cm for the standard Morrow resection), combined with repair of mitral valve and submitral abnormalities, is practiced by some surgeons (27–30).
Septal myectomy is performed through an aortotomy. A rectangular trough is created by first making two parallel longitudinal incisions in the basal septum. Incisions are extended distally and then transversely connected proximally below the aortic valve and distally just beyond the level of mitral-septal contact and subaortic obstruction (with standard Morrow myectomy) or to mid-ventricular level at the base of papillary muscles (with extended myectomy), yielding 3 to 12 grams of septal muscle. It has been prudent practice to perform myectomy under intraoperative transesophageal echocardiographic guidance to directly monitor the efficacy of the resection (to identify the level of obstruction and distribution of septal hypertrophy) and allow for possible surgical revision.
Mitral valve repair, in addition to myectomy, may be most appropriate for selected patients with severe mitral regurgitation caused by primary valvular disease (e.g., myxomatous or rheumatic or ruptured chordae) (31–34). Occasionally, if intrinsic mitral valve disease is of sufficient severity to preclude repair, or the proximal septum is only mildly thickened and the risks for either septal perforation (by excessive muscular resection) or residual post-operative obstruction (by inadequate resection) are increased, then replacement with a low-profile mitral prosthesis without myectomy may be prudent (31,35,36). Mitral valve replacement is, however, not routinely recommended as a primary treatment for obstruction, because of the potential post-operative complications related to durability, thromboembolism, and anticoagulation (1,2,37).
Occasionally, greatly elongated and flexible mitral leaflets will contribute substantially to the generation of mitral-septal contact (38,39). In such selected cases, mitral valve plication combined with myectomy has been performed to restrict mitral valve motion and allow for more complete relief of subaortic obstruction and mitral regurgitation (32,33,39–42). Septal myectomy also offers an opportunity to repair associated major cardiac lesions such as atherosclerotic obstructive coronary artery disease or forms of fixed aortic stenosis, or surgically treat atrial fibrillation with the MAZEprocedure (43,44).
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Traditional role for septal myectomy
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Limiting exertional dyspnea (often with anginal or atypical chest pain), fatigue, and occasionally orthopnea, paroxysmal nocturnal dyspnea, or syncope can frequently be controlled largely by conventional drug treatment with negative inotropic agents such as beta-blockers, verapamil, and disopyramide (1,2,7,9–11) (Fig. 1). However, septal myectomy is the preferred treatment intervention should such heart failure symptoms become refractory to maximal medical management with substantial lifestyle limitation equivalent to New York Heart Association functional classes III or IV, in the presence of LV outflow tract obstruction (gradient  50 mm Hg under resting [basal] conditions or when physiologically provoked with exercise) (1,2) (Fig. 1). Children with obstruction may be regarded as surgical candidates when experiencing somewhat lesser degrees of limitation.
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Figure 1 Presentation and treatment strategies for patient subgroups within the broad clinical spectrum of hypertrophic cardiomyopathy (HCM). AF = atrial fibrillation; DDD = dual-chamber; ICD = implantable cardioverter-defibrillator; MAZE = surgical procedure to abolish atrial fibrillation;PV = pulmonary vein; SD = sudden death; w/o = without. *No specific treatment or intervention indicated, except under exceptional circumstances. Adapted from Maron et al. (1) and reproduced with permission of the American College of Cardiology.
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Intervention with septal myectomy (or alcohol ablation) based primarily on other disease features such as atrial fibrillation or unexplained syncope, in patients with the nonobstructive form of HCM, or in asymptomatic (or mildly symptomatic) patients with outflow obstruction, is not recommended. Of particular note, these guidelines governing the selection of HCM patients for myectomy represent the contemporary recommendations of the 2003 American College of Cardiology-European Society of Cardiology Expert Consensus Panel on the Management of HCM (1). Furthermore, it should be emphasized that the stated guidelines governing selection of patients for surgical septal myectomy are identical to those for alcohol septal ablation (1).
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Surgical risks
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The evolution of septal myectomy, aided by improved myocardial preservation techniques and post-operative care, as well as intraoperative echocardiography, has produced substantial reduction in operative mortality. In the 1980s, reasonably high operative mortality rates of 5% were reported from some centers, disproportionately reflecting the initial surgical experience of up to 40 years ago (23,24,45–49). However, over the last 10 to 15 years, myectomy has been performed with low mortality rates of 1% to 2% or even less (although somewhat higher with associated coronary artery bypass grafting or valve replacement) (46,49–52). Of particular note, the major centers performing septal myectomy report virtually no operative deaths in the most recent consecutive cases (including children) spanning the last decade (e.g., involving up to >250 cases per institution) (1,52–57). It is most appropriate to cite these very low contemporary mortality rates to current candidates for myectomy, rather than to characterize the risks of surgery with older and obsolete data. Such surgical considerations are predicated on the strong preference that septal myectomy be performed at centers (and by surgeons) having considerable experience with obstructive HCM, and in which patient outcomes have been analyzed.
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Post-surgical results
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Heart failure symptoms.
Based on the experience and data assembled from more than 25 centers worldwide over almost 45 years (1,2,9,10,27–33,35,39–42,45–73), septal myectomy is established as a proven approach for reversing the consequences of heart failure by providing permanent amelioration of obstruction (and relief of mitral regurgitation) at rest, and restoring functional capacity and an acceptable quality of life at any age, exceeding that achievable with chronic administration of cardioactive drugs (1). These salutary benefits are demonstrable subjectively by patient history and objectively by increased treadmill time, maximum workload, peak oxygen consumption, and improved myocardial oxygen demand, metabolism, and coronary flow (66–69).
Gradient reduction results from basal septal thinning with resultant widening of the LV outflow tract area (and re-direction of forward flow with loss of the drag and Venturi effects on mitral valve) (15–17), and consequently abolition of systolic anterior motion of the mitral valve and mitral-septal contact (16,18,65,70,71,73). Mitral regurgitation is usually virtually eliminated without the need for additional mitral valve surgery (72), left atrial size (and possibly the long-term risk for atrial fibrillation) are reduced (7,11,28,74), and LV systolic and end-diastolic pressures as well as wall stress are normalized (1,2,7,11,15,72,73,75).
Long-term survival.
Whether relief of outflow obstruction by septal myectomy also extends the longevity of patients with HCM has been an important but largely unresolved issue, owing to the impracticality and ethical considerations involved in designing a controlled trial comparing patients randomized to surgery and other treatments. Nevertheless, previous reports (46,49,52–55,59–61,64) and a recently available retrospective and controlled analysis of the Mayo Clinic surgical series (75) provide evidence that myectomy results in excellent long-term survival, may alter the natural history of the disease, and consequently obstructive HCM could be regarded as a surgically correctable form of heart failure in many severely symptomatic patients. After septal myectomy, long-term actuarial survival was 99%, 98%, and 95%, at 1, 5, and 10 years, respectively (when considering HCM-related mortality). Survival of myectomy patients did not differ from that expected in a matched general U.S. population and, in fact, was superior to that achieved by non-operated obstructed patients (75). Myectomy was also associated with reduced long-term risk for sudden cardiac death (75), suggesting that the long-term consequences of surgical myectomy and ablation may well be paradoxical in this regard—that is, myectomy can decrease sudden death risk, whereas ablation may increase that risk (at least in some patients) (1). However, relevant long-term data for alcohol septal ablation will not be available for decades.
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Alternatives to surgery
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The impetus to developing alternative strategies for relieving LV outflow obstruction in severely symptomatic HCM patients is based on the awareness that not all patients deserving of surgery can be regarded as satisfactory candidates (1,2) (Fig. 1). For example, there may be important geographic issues (and resistance to travel) for some patients without ready access to a specialized center within the U.S. and particularly in countries without an experienced surgical option, as well as medical conditions constituting obstacles to low-risk surgery—for instance, co-morbidity or particularly advanced age, or insufficient patient motivation (1).
Pacing.
In the early 1990s, dual-chamber pacing was offered as an alternative to surgery to reduce outflow obstruction and heart failure symptoms (76–79). Observational studies attributed considerable benefit to pacing, but subsequent data from randomized trials demonstrated gradient reduction to be modest and inconsistent, and the perceived functional improvement largely explained as a placebo effect (69,77–79). Although a small subset of mostly older patients may benefit from implantation of a dual-chamber pacemaker, this treatment has fallen from favor as a primary alternative to myectomy in obstructive HCM and has evolved to only a limited role (1).
Alcohol septal ablation.
A nonsurgical, catheter-based technique (known by a number of acronyms) has recently emerged as an additional interventional therapy for obstructive HCM—in the process generating considerable visibility at the expense of the older surgical option (80–90). Alcohol septal ablation is a percutaneous approach in which 1 to 3 mlof 96% to 98% alcohol is introduced into a major septal perforator artery to create necrosis and permanent myocardial infarction in the proximal septum (80–90). Subsequent intramyocardial septal scarring (91) leads to progressive LV thinning, restricted septal excursion, outflow tract enlargement, and consequent reduction in obstruction and mitral regurgitation, thereby mimicking the remodeling that results from myectomy. Therefore, alcohol ablation is a unique therapeutic strategy, in which hemodynamic and clinical benefit is promoted by virtue of intentionally creating myocardial damage.
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The challenge of alcohol septal ablation to surgery
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We are concerned that the unbridled enthusiasm in interventional practice for alcohol septal ablation (88,90–94) has become excessive without proper technical regulation and training requirements. This circumstance has also apparently obscured the appropriate selection of patients for major intervention, and has far too often made this new percutaneous strategy the initial treatment for symptomatic patients with obstructive HCM, and in the process distorted the management strategies for patients within this heterogeneous disease spectrum. Unfortunately, in increasing numbers, the surgical option is being relegated to those patients referred directly to surgeons or with failed ablations (a clinical scenario in which surgical myectomy is more difficult) (95), or portrayed in a negative light with the potential risks exaggerated while those attributable to ablation are minimized (96). Remarkably, a recent editorial (96) misrepresented management strategies in HCM by completely excluding surgery from the overall HCM treatment algorithm, thereby arbitrarily declaring myectomy to be outdated and obsolete. These developments could unnecessarily undermine future patient access to what should be considered the preferred treatment for symptomatic obstructive HCM (i.e., septal myectomy).
Of note, even though the acknowledged hemodynamic and symptomatic criteria for the selection of patients undergoing either myectomy or ablation are the same (1), the vast number of alcohol ablations performed over the last four to six years (estimated >3,500 worldwide) has reached epidemic proportions, far exceeding—by 10- to 35-fold—the number of surgical myectomies during the same time period and also the total number of operations performed worldwide over 45 years (88). Paradoxically, HCM surgery in Germany is now in danger of extinction because of the euphoria for alcohol ablation, despite the fact that myectomy was pioneered in Europe 40 years ago by German surgeons (45); however, this is not the case in many other European countries (such as France and Sweden) where alcohol ablations have been performed in only limited numbers.
To account for the excess number of alcohol septal ablations performed over a short period of time, it is undeniable that the threshold for limiting symptoms and outflow gradient has been lowered well below that generally recommended for myectomy (1,92–94). Furthermore, it has been the practice at some centers to target patients for alcohol septal ablation by provoking outflow obstruction with non-physiologic methods, for example, administration of dobutamine, a powerful inotropic drug known to induce subaortic gradients even in normal hearts (84,87,88,97–99), and the use of which has been strongly discouraged (1). These less strict patient selection criteria for alcohol ablation contrast sharply with the contemporary international guidelines of the 2003 American College of Cardiology-European Society of Cardiology consensus panel (1).
Obstacles to surgical myectomy derive from certain emerging patterns, such as the difficulties perceived by many cardiologists acting as "gate-keepers" for referring patients with obstructive HCM to surgery (particularly if alternative centers are required) (73). Certainly, economic pressures in the cardiology marketplace may understandably skew treatment choices toward catheter-based interventions, which can be performed promptly in the laboratory. Surgical septal myectomy has been traditionally performed in tertiary referral centers with subspecialists who are knowledgeable about the HCM disease process. Similarly, it is preferred that alcohol ablation be undertaken in centers having a comprehensive understanding of HCM and surgical myectomy, rather than preferentially in interventional practices focused solely on ablation, to allow for prudent management decisions in an environment not unduly biased toward either therapeutic option. Certainly, the perceived relative simplicity of alcohol ablation has resulted in less experienced practices performing this technique without the advantage of formal training, or an expansive cardiac assessment which is necessary for a heterogeneous and complex disease such as HCM.
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The case for surgery: the "gold standard"
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Although surgery and alcohol septal ablation both reduce LV outflow obstruction and symptoms, these two interventional options cannot be regarded as entirely equivalent procedures. For example, two single-institution comparison studies report certain end points (gradient reduction and peak oxygen consumption with exercise) to be superior with myectomy (66,85). Indeed, with a well-performed myectomy, patients can expect a preoperative gradient of any magnitude at rest to be invariably reduced to 0 to 10 mm Hg and not recur over time (1), and to be much less variable than reported short-term after alcohol ablation. Because available follow-up information is considerable for surgery over an eight-fold greater period of time (i.e., 45 years) than for ablation (about 5 years with average cohort follow-up <2 years) (88), it remains unresolved as to whether ablation-related benefits will prove to be sustainable and truly long-lasting as with surgery. Also, immediate relief of marked outflow obstruction, which may be necessary in some particularly symptomatic patients, can only be achieved with surgical intervention, because alcohol ablation requires gradual and unpredictable remodeling with progressive scarring for up to one year in order to effect consistent gradient reduction (1,81).
Finally, rates of permanent pacemaker implantation for procedure-related complete heart block are 10-fold higher in patients undergoing ablation (5% to 25% of patients, many who are young) (1,87,88,100,101), and some patients are now receiving implantable defibrillators for high-risk status created by the ablation itself (102). Therefore, based on current practice and results, the most complete, permanent, and pure repair for severely symptomatic patients with obstructive HCM and heart failure can be expected with surgical myectomy.
It should be emphasized that intramyocardial scarring of the septum is not a consequence of septal myectomy (although localized endocardial thickening can occur) (103), nor is there evidence that surgery increases the risk for ventricular fibrillation and sudden death (1,2,73,75) or predisposes to LV systolic dysfunction (104). However, there are important unresolved issues surrounding the long-term clinical significance of the potentially arrhythmogenic substrate created by alcohol-induced myocardial infarcts (either transmural or multi-focal) (91,102). Given that many patients with HCM already harbor a pre-existing and unpredictable predisposition to ventricular tachyarrhythmias (1,2,105–109), it is likely that this additional necrosis and scarring could only enhance the level of electrical instability and thereby constitute a risk factor for life-threatening arrhythmias and sudden death in susceptible patients (9,107). This circumstance was documented by the recent report of potentially lethal arrhythmic events frequently occurring shortly after ablation (102). These considerations apply, in particular, to youthful patients with long and unpredictable periods of future risk (1,2,105–109) in whom the "trade-off" with reduced obstruction derived from alcohol ablation may not convey a net benefit. However, to date, there has been little apparent reluctance to performing ablations in young patients. Certainly, although longer follow-up is needed, there is sufficient reason to presume (based on experience with atherosclerotic coronary artery disease) that even the relatively small infarcts produced in HCM patients by alcohol ablation could well increase subsequent risk for an arrhythmic event or death (110).
Because sudden death due to ventricular arrhythmia may occur unexpectedly decades after diagnosis (1,2,105–109), the relatively short follow-up available after septal ablation at this time precludes knowledge regarding the magnitude of that risk. Therefore, these remaining uncertainties can only be resolved by comprehensive post-ablation follow-up studies over many years. Unfortunately, however, there are as yet virtually no systematic reports characterizing arrhythmias or assessing risk stratification after ablation. Surgical myectomy and alcohol ablation have not been subjected to a randomized trial, but such a study design seems unlikely given the numerous ethical and practical obstacles, including the substantial and largely consistent observational data already available for each technique, and the anticipated obstacles to organizing such an investigation of sufficient duration to assess late occurring cardiac events.
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Selection of patients for intervention
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Given the aforementioned considerations, specialized HCM centers which offer both septal myectomy and ablation consistently express a strong preference for surgery, especially in younger patients (<55 years), but always in the presence of severe drug-refractory heart failure symptoms (New York Heart Association functional classes III/IV) (Fig. 2). Although there are few absolute exclusions for myectomy, alcohol ablation would be most appropriately reserved largely for specific patient subgroups including those of advanced age, with significant co-mortality and relative contraindications to surgery, or with a strong personal preference for avoiding an operative procedure—in whom proximal ventricular septal anatomy and septal perforator distribution and size are also judged appropriate (1,88,111) (Fig. 2). Alcohol ablation should be, however, strongly discouraged in children or young adults, because of the potential long-term consequences of the septal scar. Otherwise, the basic hemodynamic criteria for intervention with surgery or alcohol ablation do not differ—that is, LV outflow tract obstruction caused by systolic anterior motion of the mitral valve with septal contact, producing a subaortic gradient 50 mm Hg either under resting conditions or by physiologically based provocation with exercise (1). The LV outflow gradients induced by the administration of dobutamine or other catecholamine-stimulating pharmacologic agents are generally regarded to be of questionable physiologic and clinical significance (1).
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Figure 2 Each of the individual factors which favor management decisions for respective therapeutic options in patients with obstructive hypertrophic cardiomyopathy and drug-refractory severe symptoms (New York Heart Association functional classes III/IV). LVH = left ventricular hypertrophy; MAZE = surgical procedure to abolish atrial fibrillation.
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The diverse LV outflow tract morphology characteristic of HCM may impact on proper selection of patients for myectomy (vs. ablation) and the likelihood of a favorable hemodynamic result (1,2,29,30,38,111,112) (Fig. 2). For example, in a large consecutive surgical myectomy series, almost 20% of patients had complex and important congenital, structural LV outflow tract anomalies involving the mitral apparatus, which produced or contributed to obstruction (30). These include, most prominently, the direct insertion of papillary muscle into the anterior mitral leaflet (associated with exaggerated anterior displacement of the papillary muscles), producing mid-cavitary muscular obstruction (29,30,112). Importantly, failure to identify this particular outflow tract anomaly will assuredly result in persistence of obstruction with potentially adverse procedural outcome (112). Other important abnormalities include extensive fusion of hypertrophied papillary muscles to either ventricular septum or LV free wall, as well as fibrous attachments between septum and papillary muscle, LV free wall, or mitral valve which restrict mitral valve mobility and tether the mitral apparatus toward the septum. Such morphologic abnormalities are challenging to identify with standard echocardiographic examination (even by expert observers) (29,112), but are evident with intraoperative echocardiographic imaging (31,113,114) and to the operating surgeon by direct visualization, aided by fiber-optic headlight and magnification with optical loupes.
In this regard, an extended septal myectomy (27–30) (although not required in many patients) allows the surgeon to relieve muscular obstruction in the mid-cavity as well as reconstruct and widen the LV outflow tract by excising all anomalous and accessory submitral fibrous attachments to the septum and selectively reduce the size of hypertrophied papillary muscles and their attachment to LVfree wall. This affords greater flexibility and mobility to the mitral apparatus, ensuring the most complete and sustained relief of outflow obstruction and mitral regurgitation without prosthetic valve replacement. The surgeon may also tailor the precise length and location of the myectomy trough to account for mitral leaflet elongation and the potentially variable level of subaortic obstruction.
In contrast, creation of a myocardial infarct by alcohol is restricted by dependency on the variable anatomic size and the unpredictable course and perfusion distribution of the septal perforator arteries (86,88,111). Also, it is possible that some failed alcohol septal ablations (95,115,116) are attributable to unrecognized anomalies of the mitral valve and submitral structures. Indeed, a major distinction between the methodology of myectomy and ablation is the greater awareness of overall outflow tract morphology by the operating surgeon.
Part of the considerable interest in alcohol septal ablation resides in the apparent ease with which this procedure is performed, in comparison to surgery, involving far less discomfort, shorter hospital stay, less expense, and avoidance of cardiopulmonary bypass (6,80–90). Nevertheless, the risk of procedure-related mortality due to alcohol ablation is in fact similar to (or even higher than) that achieved in recent years at certain major centers with septal myectomy (1,2,49,52–57,60). Furthermore, therapeutic ablation failures requiring multiple procedures are common (115,116); in one recent report, almost 25% of patients experienced unsatisfactory clinical outcome, including those with the highest pre-procedural gradients (115). The need for repeat alcohol-based interventions would not seem desirable, particularly from the standpoint of the myocardial scar produced, and unavoidably complicates any subsequent surgical myectomy. The true rate of nonfatal complications and mortality associated with alcohol ablation is, however, unknown because such events may occur not uncommonly in lower volume practices and be under-reported in the literature.
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Future directions
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The future management of obstructive HCM will require expanded patient access to surgery, to be promoted in selected regional centers for which at least 10 myectomy operations would be performed annually. This would, in a proactive fashion, counteract the possible contraction of surgical services available to patients in the future. At present, with the permanent closure of both the medical and surgical HCM programs at the National Institutes of Health (Bethesda, Maryland), a limited number of North American centers remain most dedicated to the HCM surgical option: Mayo Clinic, Cleveland Clinic, and Toronto General Hospital, and emerging programs at St. Luke's-Roosevelt Hospital Center (New York) and Tufts-New England Medical Center (Boston).
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Conclusions
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At this crossroads in the management of obstructive HCM, it would seem prudent to adopt a measure of restraint before allowing an intoxication with novel interventional technology—relatively untested over time (alcohol ablation)—to impair the availability of the established treatment (septal myectomy) which has served patients with HCM exceedingly well over decades and continues to merit the confidence of the cardiovascular community. However, our arguments for surgery are not intended to represent an indictment or rejection of the alcohol septal ablation procedure. To the contrary, alcohol ablation is a promising alternative therapy for selected patients and an important addition to the therapeutic armamentarium of obstructive HCM. However, its ultimate role in management is not yet fully defined or resolved, and requires further long-term evaluation. Indeed, there is presently no justification for promoting alcohol ablation as the standard primary therapeutic strategy for all severely symptomatic patients refractory to maximal medical management and with marked obstruction to LV outflow. Septal myectomy remains the gold standard treatment option for this HCM patient subset.
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References
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1. Maron BJ, McKenna WJ, Danielson GK, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic CardiomyopathyA report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines Committee to Develop an Expert Consensus Document on Hypertrophic Cardiomyopathy. J Am Coll Cardiol 2003;42:1687-1713.[Free Full Text]
2. Maron BJ. Hypertrophic cardiomyopathy: a systematic review JAMA 2002;287:1308-1320.[Abstract/Free Full Text]
3. Teare D. Asymmetrical hypertrophy of the heart in young adults Br Heart J 1958;20:1-18.[Free Full Text]
4. Brock R. Functional obstruction of the left ventricle (acquired aortic subvalvular stenosis) Guy's Hospital Report 1957;106:221-238.
5. Wigle ED, Heinbecker RO, Gunton RW. Idiopathic ventricular septal hypertrophy causing muscular subaortic stenosis Circulation 1962;26:325-340.[Abstract/Free Full Text]
6. Braunwald E, Lambrew C, Rockoff D, et al. Idiopathic hypertrophic subaortic stenosis: IA description of the disease based upon an analysis of 64 patients. Circulation 1964;30(Suppl IV):1-217.[Free Full Text]
7. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy: clinical spectrum and treatment Circulation 1995;92:1680-1692.[Free Full Text]
8. Maron BJ, Epstein SE. Clinical significance and therapeutic implications of the left ventricular outflow tract pressure gradient in hypertrophic cardiomyopathy Am J Cardiol 1986;58:1093-1096.[CrossRef][Medline]
9. Maron BJ. Hypertrophic cardiomyopathy Lancet 1997;350:127-133.[CrossRef][Medline]
10. Spirito P, Seidman CE, McKenna WJ, Maron BJ. The management of hypertrophic cardiomyopathy N Engl J Med 1997;336:775-785.[Free Full Text]
11. Wigle ED, Sasson Z, Henderson MA, et al. Hypertrophic cardiomyopathy: the importance of the site and the extent of hypertrophy: a review Prog Cardiovasc Dis 1985;28:1-83.[CrossRef][Medline]
12. Klues HG, Schiffers A, Maron BJ. Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in 600 patients J Am Coll Cardiol 1995;26:1699-1708.[Abstract]
13. Shah PM, Gramiak R, Kramer DH. Ultrasound localization of left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy Circulation 1969;40:3-11.[Abstract/Free Full Text]
14. Spirito P, Maron BJ. Patterns of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography Am J Cardiol 1984;54:1039-1046.[CrossRef][Medline]
15. 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]
16. Shah PM, Gramiak R, Adelman AG, Wigle ED. Echocardiographic assessment of the effects of surgery and propranolol on the dynamics of outflow obstruction in hypertrophic subaortic stenosis Circulation 1972;45:516-521.[Abstract/Free Full Text]
17. Sherrid MV, Chu K, DeLia E, Mogtader A, Dwyer Jr EM. An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy J Am Coll Cardiol 1993;22:816-824.[Abstract]
18. Maron BJ, Harding AM, Spirito P, Roberts WC, Waller BF. Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy Circulation 1983;68:282-293.[Abstract/Free Full Text]
19. Murgo JP, Alter BR, Dorethy JF, Altobelli SA, McGranahan Jr GM. Dynamics of left ventricular ejection in obstructive and nonobstructive hypertrophic cardiomyopathy J Clin Invest 1980;66:1369-1382.[Medline]
20. Criley JM. Unobstructed thinking (and terminology) is called for in the understanding and management of hypertrophic cardiomyopathy J Am Coll Cardiol 1997;29:741-743.[CrossRef][Medline]
21. Ross Jr. J, Braunwald E, Gault JH, Mason DT, Morrow AG. The mechanisms of the intraventricular pressure gradient in idiopathic hypertrophic subaortic stenosis Circulation 1966;34:558-578.[Free Full Text]
22. Maron MS, Olivotto I, Betocchi S, et al. 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]
23. Cleland WP. The surgical management of obstructive cardiomyopathy J Cardiovasc Surg 1963;4:489-491.[Medline]
24. Morrow AG. Hypertrophic subaortic stenosis: operative methods utilized to relieve left ventricular outflow obstruction J Thorac Cardiovasc Surg 1978;76:423-430.[Abstract]
25. Kirklin JW, Ellis Jr FH. Surgical relief of diffuse subvalvular aortic stenosis Circulation 1961;24:739-742.[Abstract/Free Full Text]
26. Bigelow WG, Trimble AS, Auger P, Marquis, Wigle ED. The ventriculomyotomy operation for muscular subaortic stenosis J Thorac Cardiovasc Surg 1966;52:514-524.[Medline]
27. Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus Circulation 1995;92(Suppl II):122-127.[Abstract/Free Full Text]
28. Woo A, Williams WG, Choi R, et al. Clinical and echocardiographic determinants of long-term survival following surgical myectomy in obstructive hypertrophic cardiomyopathy. Circulation 2005. In Press..
29. 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]
30. Minakata K, Dearani JA, Nishimura RA, et al. 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]
31. McIntosh CL, Maron BJ. Current operative treatment of obstructive hypertrophic cardiomyopathy Circulation 1988;78:487-495.[Free Full Text]
32. 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]
33. Joyce F, Lever H, Cosgrove D. Treatment of hypertrophic cardiomyopathy by mitral valve repair and septal myectomy Ann Thorac Surg 1994;54:1025-1027.
34. Petrone RK, Klues HG, Panza JA, Peterson E, Maron BJ. Coexistence of mitral valve prolapse in a consecutive group of 528 patients with hypertrophic cardiomyopathy assessed with echocardiography J Am Coll Cardiol 1992;20:55-61.[Abstract]
35. Krajcer Z, Leachman RD, Cooley DA, Ostojie M, Coronado R. Mitral valve replacement and septal myectomy in hypertrophic cardiomyopathy: ten-year following in 80 patients Circulation 1988;78:I-35-43.[Medline]
36. McIntosh CL, Greenberg CJ, Maron BJ, Leon MB, Cannon III RO, Clark RE. Clinical and hemodynamic results after mitral valve replacement in patients with obstructive hypertrophic cardiomyopathy Ann Thorac Surg 1989;47:236-246.[Abstract]
37. Roberts WC. Operative treatment of hypertrophic obstructive cardiomyopathy: the case against mitral valve replacement Am J Cardiol 1973;32:377-381.[CrossRef][Medline]
38. 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]
39. McIntosh CL, Maron BJ, Cannon RO, et al. 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:II60-7.[Medline]
40. van der Lee C, Kofflard MJM, van Herwerden LA, et al. Sustained improvement after combined anterior mitral leaflet extension and myectomy in hypertrophic obstructive cardiomyopathy Circulation 2003;108:2088-2092.[Abstract/Free Full Text]
41. Cooley DA. Surgical technique for hypertrophic left ventricular obstructive myopathy including mitral valve plication J Cardiac Surg 1991;6:29-33.[Medline]
42. Matsuda H, Nomura F, Kadoba K, et al. Transatrial and transmitral approach for left ventricular myectomy and mitral valve plication for diffuse-type hypertrophic obstructive cardiomyopathy: a novel approach J Thorac Cardiovasc Surg 1996;112:195-196.[Free Full Text]
43. Siegman I, Maron BJ, Permut L, McIntosh C, Clark R. Results of operation for coexistent obstructive hypertrophic cardiomyopathy and coronary artery disease J Am Coll Cardiol 1989;13:1527-1533.[Abstract]
44. Sorajja P, Ommen SR, Nishimura RA, Gersh BJ, Berger PB, Tajik AJ. Adverse prognosis of patients with hypertrophic cardiomyopathy who have epicardial coronary artery disease Circulation 2003;108:2342-2348.[Abstract/Free Full Text]
45. Schulte HD, Bircks WH, Losse B, Godehardt EA, Schwartzkopff B. Prognosis of patients with hypertrophic obstructive cardiomyopathy after transaortic myectomy: late results up to twenty-five years J Thorac Cardiovasc Surg 1993;106:709-717.[Abstract]
46. 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]
47. Maron BJ, Merrill WH, Freier PA, et al. Long-term clinical course and symptomatic status of patients after operation for hypertrophic subaortic stenosis Circulation 1978;57:1205-1213.[Abstract/Free Full Text]
48. Maron BJ, Epstein SE, Morrow AG. Symptomatic status and prognosis of patients after operation for hypertrophic obstructive cardiomyopathy: efficacy of ventricular septal myotomy and myectomy Eur Heart J 1983;4:175-185.
49. Schulte HD, Borisov K, Gams E, et al. Management of symptomatic hypertrophic obstructive cardiomyopathy—long-term results after surgical therapy Thorac Cardiovasc Surg 1999;47:213-218.[Medline]
50. Cooper MM, McIntosh CL, Tucker E, Clark RE. Operation for hypertrophic subaortic stenosis in the aged Ann Thorac Surg 1987;44:370-378.[Abstract]
51. Mohr R, Schaff HV, Danielson GK, Puga FJ, Pluth JR, Tajik AJ. The outcome of surgical treatment of hypertrophic obstructive cardiomyopathy: experience over 15 years J Thorac Cardiovasc Surg 1989;97:666-674.[Abstract]
52. Mohr R, Schaff HV, Puga FJ, Danielson GK. Results of operation for hypertrophic obstructive cardiomyopathy in children and adults less than 40 years of age Circulation 1989;80:I191-6.[Medline]
53. ten Berg JM, Suttorp MJ, Knaepen 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]
54. Robbins RC, Stinson EB. Long-term results of left ventricular myotomy and myectomy for obstructive hypertrophic cardiomyopathy J Thorac Cardiovasc Surg 1996;111:586-594.[Abstract/Free Full Text]
55. Cohn LH, Trehan H, Collins Jr JJ. Long-term follow-up of patients undergoing myotomy/myectomy for obstructive hypertrophic cardiomyopathy Am J Cardiol 1992;70:657-660.[CrossRef][Medline]
56. Theodoro DA, Danielson GK, Feldt RH, Anderson BJ. Hypertrophic obstructive cardiomyopathy in pediatric patients: results of surgical treatment J Thorac Cardiovasc Surg 1966;112:1589-1599.
57. Merrill WH, Friesinger GC, Graham Jr. T, et al. Long-lasting improvement after septal myectomy for hypertrophic obstructive cardiomyopathy Ann Thorac Surg 2000;69:1732-1735.[Abstract/Free Full Text]
58. Morrow AG, Reitz BA, Epstein SE, et al. Operative treatment in hypertrophic subaortic stenosis: techniques, and the results of pre and postoperative assessments in 83 patients Circulation 1975;52:88-8102.[Abstract/Free Full Text]
59. Williams WG, Wigle ED, Rakowski H, Smallhorn J, LeBlanc J, Trusler GA. Results of surgery for hypertrophic obstructive cardiomyopathy Circulation 1987;76(Suppl V):104-108.
60. 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]
61. Schönbeck MH, Brunner-LaRocca PH, Vogt PR, et al. Long-term follow-up in hypertrophic cardiomyopathy after septal myectomy Ann Thorac Surg 1998;65;:1207-1214.
62. Agnew TM, Barratt-Boyes BG, Brandt PW, et al. 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]
63. Reis R, Bolton MR, King JF, Pugh DM, Dunn MI, Mason DT. Anterior-superior displacement of papillary muscles producing obstruction and mitral regurgitation in idiopathic hypertrophic subaortic stenosis Circulation 1974;50:II181-8.[Medline]
64. Seiler C, Hess OM, Schoenbeck M, et al. Long-term follow-up of medical versus surgical therapy for hypertrophic cardiomyopathy: a retrospective study J Am Coll Cardiol 1991;17:634-645.[Abstract]
65. Schapira JN, Stemple DR, Martin RP, Rakowski H, Stinson EB, Popp RL. Single and two-dimensional echocardiographic visualization of the effects of septal myectomy in idiopathic hypertrophic subaortic stenosis Circulation 1978;58:850-860.[Abstract/Free Full Text]
66. Firoozi S, Elliott PM, Sharma S, et al. Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy: a comparison of clinical, hemodynamic and exercise outcomes Eur Heart J 2002;20:1617-1624.
67. Cannon RO, McIntosh CL, Schenke WH, et al. Effect of surgical reduction of left ventricular outflow obstruction on hemodynamics, coronary flow, and myocardial metabolism in hypertrophic cardiomyopathy Circulation 1989;79:766-775.[Abstract/Free Full Text]
68. Diodati JG, Schenke WH, Waclawiw MA, et al. Predictors of exercise benefit after operative relief of left ventricular outflow obstruction by the myotomy-myectomy procedure in hypertrophic cardiomyopathy Am J Cardiol 1992;69:1617-1622.[CrossRef][Medline]
69. 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: a comparison of objective hemodynamic and exercise end points J Am Coll Cardiol 1999;34:191-196.[Abstract/Free Full Text]
70. Spirito P, Maron BJ, Rosing DR. Morphologic determinants of hemodynamic state after ventricular septal myectomy-myectomy in patients with obstructive hypertrophic cardiomyopathy: M-mode and two-dimensional echocardiographic assessment Circulation 1984;70:984-995.[Abstract/Free Full Text]
71. Franke A, Schöendube FA, Kühl HP, et al. Quantitative assessment of the operative results after extended myectomy and surgical reconstruction of the subvalvular mitral apparatus in hypertrophic obstructive cardiomyopathy using dynamic three-dimensional transesophageal echocardiography J Am Coll Cardiol 1998;31:1641-1649.[Abstract/Free Full Text]
72. Yu EH, Omran AS, Wigle ED, Williams WG, Siu SC, Rakowski H. Mitral regurgitation in hypertrophic obstructive cardiomyopathy: relationship to obstruction and relief with myectomy J Am Coll Cardiol 2000;36:2219-2225.[Abstract/Free Full Text]
73. Nishimura RA, Holmes DR. Hypertrophic obstructive cardiomyopathy N Engl J Med 2004;350:1320-1327.[Free Full Text]
74. Watson DC, Henry WL, Epstein SE, et al. Effects of operation on left atrial size and the occurrence of atrial fibrillation in patients with hypertrophic subaortic stenosis Circulation 1977;55:178-181.[Abstract/Free Full Text]
75. Ommen SR, Olivotto I, Betocchi S, et al. The effect of surgical myectomy on survival of patients with hypertrophic cardiomyopathy(abstr) J Am Coll Cardiol 2004;43(Suppl A):215A.
76. Fananapazir L, Epstein ND, Curiel RV, Panza JA, Tripodi D, McAreavey D. Long-term results of dual-chamber (DDD) pacing in obstructive hypertrophic cardiomyopathy: evidence for progressive symptomatic and hemodynamic improvement and reduction of left ventricular hypertrophy Circulation 1994;90:2731-2742.[Abstract/Free Full Text]
77. Maron BJ, Nishimura RA, McKenna WJ, et al. 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]
78. Nishimura RA, Trusty JM, Hayes DL, et al. Dual-chamber pacing for hypertrophic cardiomyopathy: a randomized, double-blind, cross-over trial J Am Coll Cardiol 1997;29:435-441.[Abstract]
79. Linde C, Gadler F, Kappenberger L, Ryden L. Placebo effect of pacemaker implantation in obstructive hypertrophic cardiomyopathyPIC Study Group. Pacing in Cardiomyopathy. Am J Cardiol 1999;83:903-907.[CrossRef][Medline]
80. Faber L, Meissner A, Ziemssen P. 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]
81. Boekstegers P, Steinbigler P, Molnar A, et al. Pressure-guided nonsurgical myocardial reduction induced by small septal infarctions in hypertrophic obstructive cardiomyopathy J Am Coll Cardiol 2001;38:846-853.[Abstract/Free Full Text]
82. Gietzen FH, Leuner CJ, Raute-Kreinsen U, et al. Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH): catheter interventional treatment for hypertrophic obstructive cardiomyopathy Eur Heart J 1999;20:1342-1354.[Abstract/Free Full Text]
83. Gietzen FH, Leuner CJ, Obergassel L, Strunk-Muller C, Kuhn H. Role of transcoronary ablation of septal hypertrophy in patients with hypertrophic cardiomyopathy: NYHA functional class III or IV and outflow obstruction only under provocable conditions Circulation 2002;106:454-459.[Abstract/Free Full Text]
84. Nagueh SF, Ommen SR, Lakkis NM, et al. 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]
85. Qin JX, Shiota T, Lever HM, et al. 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]
86. Knight C, Kurbaan AS, Seggewiss H, et al. Nonsurgical septal reduction for hypertrophic obstructive cardiomyopathy: outcome in the first series of patients Circulation 1997;95:275-281.[Medline]
87. Lakkis NM, Nagueh SF, Dunn JK, et al. Nonsurgical septal reduction therapy for hypertrophic cardiomyopathy J Am Coll Cardiol 2000;36:852-855.[Abstract/Free Full Text]
88. Kimmelstiel CD, Maron BJ. Percutaneous septal ablation in hypertrophic obstructive cardiomyopathy: role within the treatment armamentarium and other considerations Circulation 2004;109:1180-1185.[Abstract/Free Full Text]
89. Seggewiss H, Gleichmann U, Faber L, Fassbender D, Schmidt HK, Strick S. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: acute results and 3-month follow-up in 25 patients J Am Coll Cardiol 1998;31:252-258.[Abstract/Free Full Text]
90. Wigle ED, Schwartz L, Woo A, Rakowski H. To ablate or operate? That is the question! J Am Coll Cardiol 2001;38:1708-1710.
91. Raute-Kreinsen U. Morphology of necrosis and repair after transcoronary ethanol ablation of septal hypertrophy Pathol Res Pract 2003;199:121-127.[CrossRef][Medline]
92. Maron BJ. Role of alcohol septal ablation in treatment of obstruction hypertrophic cardiomyopathy(editorial) Lancet 2000;355:425-426.[Medline]
93. Maron BJ. New interventions for obstructive hypertrophic cardiomyopathy: promise and prudence Eur Heart J 1999;20:1292-1294.[Free Full Text]
94. Spirito P, Maron BJ. Perspectives on the role of new treatment strategies in hypertrophic cardiomyopathy J Am Coll Cardiol 1999;33:1071-1075.[Free Full Text]
95. 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]
96. Hess OM. Risk stratification in hypertrophic cardiomyopathy: fact or fiction? J Am Coll Cardiol 2003;42:880-881.[Free Full Text]
97. Luria D, Klutstein MW, Rosenmann D, Shaheen J, Sergey S, Tzivoni D. Prevalence and significance of left ventricular outflow gradient during dobutamine echocardiography Eur Heart J 1999;20:386-392.[Abstract/Free Full Text]
98. Okeie K, Shimizu M, Yoshio H, et al. Left ventricular systolic dysfunction during exercise and dobutamine stress in patients with hypertrophic cardiomyopathy J Am Coll Cardiol 2000;36:856-863.[Abstract/Free Full Text]
99. Luria D, Klutstein MV, Rosenmann D, Shaheen J, Sergey S, Tzivoni D. Prevalence and significance of left ventricular outflow gradient during dobutamine echocardiography Eur Heart J 1999;20:386-392.[Abstract/Free Full Text]
100. Qin JX, Shiota T, Lever HM, et al. Conduction system abnormalities in patients with obstructive hypertrophic cardiomyopathy following septal reduction intervention Am J Cardiol 2004;93:171-175.[CrossRef][Medline]
101. Runquist LH, Nielsen CD, Killip D, Gazes P, Spencer III WH. Electrocardiographic findings after alcohol septal ablation therapy for obstructive hypertrophic cardiomyopathy Am J Cardiol 2002;90:1020-1021.[CrossRef][Medline]
102. Crawford FA, Killip D, Franklin J, et al. Implantable cardioverter-defibrillator for primary prevention of sudden cardiac death in patients with hypertrophic obstructive cardiomyopathy after alcohol septal ablation(abstr) Circulation 2003;108:IV-386-7.
103. Roberts CS, Roberts WC. Morphologic featuresIn: Zipes DP, Rowlands DJ, editors. Progress in Cardiology, Vol. 2-2. Philadelphia, PA: Lea & Febiger; 1989. pp. 3-22.
104. Harris KM, Zenovich AG, Casey SA, Wilson J, Maron BJ. Significance and clinical profile of the end-stage phase in a large hypertrophic cardiomyopathy cohort(abstr) Circulation 2003;108:IV626.
105. Maron BJ, Shen W-K, Link MS, et al. Efficacy of implantable cardioverter-defibrillators for prevention of sudden death in patients with hypertrophic cardiomyopathy N Engl J Med 2000;342:365-373.[Abstract/Free Full Text]
106. Maron BJ, Olivotto I, Spirito P, et al. Epidemiology of hypertrophic cardiomyopathy-related deathRevisited in a large non-referral-based patient population. Circulation 2000;102:858-864.[Abstract/Free Full Text]
107. Maron BJ, Estes III NAM, Maron MS, Almquist AK, Link MS, Udelson J. Primary prevention of sudden death as a novel treatment strategy in hypertrophic cardiomyopathy Circulation 2003;107:2872-2875.[Free Full Text]
108. Elliott PM, Poloniecki J, Dickie S, et al. Sudden death in hypertrophic cardiomyopathy: identification of high risk patients J Am Coll Cardiol 2000;36:2212-2218.[Abstract/Free Full Text]
109. Spirito P, Bellone P, Harris KM, Bernabo P, Bruzzi P, Maron BJ. Magnitude of left ventricular hypertrophy predicts the risk of sudden death in hypertrophic cardiomyopathy N Engl J Med 2000;342:1778-1785.[Abstract/Free Full Text]
110. Burns RJ, Gibbons RJ, Yi Q, et al. The relationships of left ventricular ejection fraction, end-systolic volume index and infarct size to six-month mortality after hospital discharge following myocardial infarction treated by thrombolysis J Am Coll Cardiol 2002;39:30-36.[Abstract/Free Full Text]
111. Mandeep S, Edwards WD, Holmes DR. Anatomy of first septal perforating artery: a study with implications for ablation therapy for hypertrophic cardiomyopathy Mayo Clinic Proc 2001;76:799-802.[Abstract]
112. 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]
113. Ommen SR, Park SH, Click RL, et al. Impact of intraoperative transesophageal echocardiography in the surgical management of hypertrophic cardiomyopathy Am J Cardiol 2002;90:1022-1024.[CrossRef][Medline]
114. Grigg LE, Wigle ED, Williams WG. Transesophageal echocardiography in obstructive hypertrophic cardiomyopathy: clarification of pathophysiology and importance of intraoperative decision making J Am Coll Cardiol 1992;20:42-52.[Abstract]
115. Chang SM, Lakkis NM, Franklin J, Spencer WH, 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]
116. Nesta F, Yoerger DM, Picard MH, et al. Mechanism of systolic anterior motion and regurgitation post septal ablation in hypertrophic cardiomyopathy(abstr) J Am Coll Cardiol 2004;43(Suppl A):215A.
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Abstract
Historical context