Effect of Left Ventricular Outflow Tract Obstruction on Clinical Outcome in Hypertrophic Cardiomyopathy

doi:10.1056/NEJMoa021332

Volume 348:295-303		January 23, 2003		Number 4

Effect of Left Ventricular Outflow Tract Obstruction on Clinical Outcome in Hypertrophic Cardiomyopathy

Martin S. Maron, M.D., Iacopo Olivotto, M.D., Sandro Betocchi, M.D., Susan A. Casey, R.N., John R. Lesser, M.D., Maria A. Losi, M.D., Franco Cecchi, M.D., and Barry J. Maron, M.D.

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ABSTRACT

Background The influence of left ventricular outflow tract obstructionon the clinical outcome of hypertrophic cardiomyopathy remainsunresolved.

Methods We assessed the effect of outflow tract obstructionon morbidity and mortality in a large cohort of patients withhypertrophic cardiomyopathy who were followed for a mean (±SD)of 6.3±6.2 years.

Results Of the 1101 consecutive patients, 273 (25 percent) hadobstruction of left ventricular outflow under basal (resting)conditions with a peak instantaneous gradient of at least 30mm Hg. A total of 127 patients (12 percent) died of hypertrophiccardiomyopathy, and 216 surviving patients (20 percent) hadsevere, disabling symptoms of progressive heart failure (NewYork Heart Association [NYHA] functional class III or IV). Theoverall probability of death related to hypertrophic cardiomyopathywas significantly greater among patients with outflow tractobstruction than among those without obstruction (relative risk,2.0; P=0.001). The risk of progression to NYHA class III orIV or death specifically from heart failure or stroke was alsogreater among patients with obstruction (relative risk, 4.4;P<0.001), particularly among patients 40 years of age orolder (P<0.001). Age-adjusted multivariate analysis confirmedthat outflow tract obstruction was independently associatedwith an increased risk of both death related to hypertrophiccardiomyopathy (relative risk, 1.6; P=0.02) and progressionto NYHA class III or IV or death from heart failure or stroke(relative risk, 2.7; P<0.001). The likelihood of severe symptomsand death related to outflow tract obstruction did not increaseas the gradient increased above the threshold of 30 mm Hg.

Conclusions In patients with hypertrophic cardiomyopathy, leftventricular outflow tract obstruction at rest is a strong, independentpredictor of progression to severe symptoms of heart failureand of death.

Hypertrophic cardiomyopathy is a genetic cardiac disease withheterogeneous phenotypic expression and a diverse clinical coursecharacterized by both sudden death and disabling symptoms relatedto heart failure.¹^,²^,³^,⁴^,⁵^,⁶^,⁷^,⁸^,⁹^,¹⁰^,¹¹^,¹² Historically, evenfrom the first clinical descriptions, the left ventricular outflowtract gradient has been a prominent and quantifiable featureof hypertrophic cardiomyopathy.¹^,²^,³^,⁴^,⁵^,¹³^,¹⁴^,¹⁵^,¹⁶^,¹⁷^,¹⁸^,¹⁹^,²⁰^,²¹^,²²Major therapeutic interventions (such as ventricular septalmyectomy, percutaneous alcohol septal ablation, and dual-chamberpacing) have been introduced to relieve disabling symptoms associatedwith outflow tract obstruction.⁵^,⁶^,²³^,²⁴^,²⁵^,²⁶ However, thelong-term effect of the subaortic gradient on clinical outcomecontinues to be a source of uncertainty. Therefore, we analyzeda large cohort of patients with hypertrophic cardiomyopathyin order to define the relation between the outflow tract gradientand the clinical course.

Methods

Study Population

A total of 1101 consecutive patients with hypertrophic cardiomyopathywere enrolled: 364 at Azienda Ospedaliera Careggi in Florence,Italy; 200 at Federico II University of Naples in Naples, Italy;and 537 at the Minneapolis Heart Institute in Minneapolis. Theinitial clinical evaluation was defined as the time at whichthe left ventricular outflow tract gradient was first assessedby continuous-wave Doppler echocardiography at each institutionfrom July 1983 to December 2001. The mean (±SD) durationof follow-up, from the initial measurement of the gradient tothe most recent evaluation or death, was 6.3±6.2 years.All patients enrolled in the study signed a statement, previouslyapproved by Allina Health System in Minneapolis or conformingto the Authority for Privacy Act in Italy, agreeing to the useof their medical information for research purposes.

Echocardiography

Echocardiographic studies were performed with the use of commerciallyavailable instruments. Obstruction of the left ventricular outflowtract, which was due to the anterior motion of the mitral valveduring systole and septal contact,²²^,²⁷ was considered to bepresent when the peak instantaneous outflow gradient was estimatedto be at least 30 mm Hg with the use of continuous-wave Dopplerechocardiography under basal (resting) conditions.²² Care wastaken to avoid contamination of the left ventricular outflowwaveform by the mitral regurgitation jet.²²

Definitions

The diagnosis of hypertrophic cardiomyopathy was based on thedemonstration by two-dimensional echocardiography of a hypertrophied,nondilated left ventricle (wall thickness of at least 15 mmin adults or the equivalent relative to body-surface area inchildren)²⁸ in the absence of another cardiac or systemic diseasecapable of producing a similar degree of hypertrophy.²⁹ Suddendeath was defined as a sudden and unexpected collapse in patientswho had previously had a relatively uneventful clinical course.³⁰Death related to heart failure was regarded as that occurringin the context of cardiac decompensation and a progressive coursewith limiting symptoms, particularly when it was complicatedby pulmonary edema or required hospitalization for treatment,or both.³⁰ In addition, potentially lethal events in which patientswere successfully resuscitated from cardiac arrest or receivedappropriate shocks from an implanted defibrillator were regardedas equivalent to sudden death. Heart transplantation in patientswith advanced, end-stage disease and systolic dysfunction⁵^,⁶was considered to be a surrogate for death related to heartfailure.³⁰ Stroke-related deaths were judged to be a consequenceof embolic events related to hypertrophic cardiomyopathy, usuallyin the setting of atrial fibrillation.³¹

Statistical Analysis

Data are expressed as means ±SD. The unpaired Student'st-test or one-way analysis of variance was used to compare normallydistributed data. Fisher's exact test was used to compare noncontinuousvariables expressed as proportions. Relative risks and 95 percentconfidence intervals were calculated with univariate and multivariateCox proportional-hazards regression models. Multivariate analyseswere performed with a stepwise forward regression model, inwhich each variable with a P value of 0.05 or less (based onthe univariate analysis) was entered into the model. Survivalcurves were constructed according to the Kaplan–Meiermethod. P values are two-sided, and a P value of less than 0.05was considered to indicate statistical significance. Calculationswere performed with use of SPSS software (version 8.0).

The primary clinical end points used in this study were deathfrom any cause, death related to hypertrophic cardiomyopathy(i.e., sudden death or death as a consequence of heart failureor stroke), a combined end point of death from heart failureor stroke or progression to New York Heart Association (NYHA)functional class III or IV (i.e., severe symptoms), and sudden,unexpected death alone. Analyses of deaths from all causes anddeaths related to hypertrophic cardiomyopathy included the totalstudy group of 1101 patients. Evaluations of progression toNYHA class III or IV and death from heart failure or strokeor of sudden death alone were confined to the 994 patients whowere in NYHA class I or II at entry into the study and thusexcluded the 107 patients who were already in NYHA class IIIor IV. For the 66 severely symptomatic patients who underwentmajor therapeutic interventions known to relieve outflow tractgradient most effectively (septal myectomy, mitral-valve replacement,or alcohol septal ablation),¹^,³^,⁵^,⁶^,⁷^,²³^,²⁴^,²⁵^,²⁶ follow-upwas terminated at the time of the procedure.

Results

Base-Line Characteristics

The clinical and demographic characteristics of the overallstudy population of 1101 patients are shown in Table 1. Themean age at initial evaluation was 45±20 years. A totalof 273 patients (25 percent) had peak instantaneous left ventricularoutflow tract gradients of at least 30 mm Hg under basal conditions(range, 30 to 176 mm Hg); the other 828 patients (75 percent)had a gradient of less than 30 mm Hg or no gradient and wereconsidered to be without obstruction. As compared with patientswithout obstruction, those with left ventricular outflow tractobstruction were older (and less commonly male), more oftenhad severe limiting symptoms (NYHA class III or IV), and hadthicker left ventricular walls and larger left atrial dimensions(Table 1).

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Table 1. Characteristics of 1101 Patients with Hypertrophic Cardiomyopathy According to the Presence or Absence of Left Ventricular Outflow Tract Obstruction at Base Line.

At the time of the last follow-up visit, 914 patients (83 percent)were still alive, 60 patients (5 percent) had died of causesunrelated to hypertrophic cardiomyopathy, and 127 patients (12percent) had died of hypertrophic cardiomyopathy, either suddenlyor as a consequence of heart failure or stroke. Among the 914surviving patients, 216 had severe, disabling symptoms of exertionaldyspnea (with or without chest pain) and were in NYHA classIII or IV (Table 1).

Mortality and Heart Failure–Related Morbidity

During the follow-up period, patients with obstruction had asignificantly greater likelihood of death related to hypertrophiccardiomyopathy than patients without obstruction (relative risk,2.0; 95 percent confidence interval, 1.3 to 3.0; P=0.001) (Figure 1).Similarly, the probability of reaching the end point ofprogression to NYHA class III or IV or death from heart failureor stroke was significantly greater in patients with obstruction(relative risk, 4.4; 95 percent confidence interval, 3.3 to5.9; P<0.001) (Figure 2).

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Figure 1. Probability of Hypertrophic Cardiomyopathy (HCM)–Related Death among 273 Patients with a Left Ventricular Outflow Gradient of at Least 30 mm Hg under Basal Conditions and 828 Patients without Obstruction at Entry.

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Figure 2. Probability of Progression to Severe Heart Failure (NYHA Class III or IV) or Death from Heart Failure or Stroke among 224 Patients with Left Ventricular Outflow Tract Obstruction and 770 Patients without Obstruction.
Patients who were already in NYHA class III or IV at entry were excluded from the analysis.

Among patients with obstruction, those with mild symptoms (NYHAclass II) at entry were more likely to have progression to moresevere symptoms or to die from heart failure or stroke thanwere asymptomatic patients (P<0.001) (Figure 2). When theeffect of age at the time of measurement of the gradient wasanalyzed, patients with obstruction who were at least 40 yearsold were more likely to die of causes related to hypertrophiccardiomyopathy or to have complications of this condition thanwere younger patients with obstruction (P<0.001) (Figure 3).In addition, patients with obstruction had a significantlyincreased risk of death from any cause, as compared with patientswithout obstruction (relative risk, 2.0; 95 percent confidenceinterval, 1.4 to 2.7; P<0.001).

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Figure 3. Effect of Age and the Presence or Absence of Left Ventricular Outflow Tract Obstruction of at Least 30 mm Hg on the Probability of Progression to Severe Heart Failure (NYHA Class III or IV) or Death from Heart Failure or Stroke.
Patients who were already in NYHA class III or IV at entry were excluded from the analysis.

Sudden Death from Hypertrophic Cardiomyopathy

The probability of sudden death among patients with obstructionwas significantly higher than that among patients without obstruction(relative risk, 2.1; 95 percent confidence interval, 1.1 to3.7; P=0.02) (Figure 4). However, the difference in the annualrate of sudden death between patients with obstruction and patientswithout obstruction was small (1.5 percent vs. 0.9 percent,or 0.6 percent per year). Outflow tract obstruction was alsoassociated with a particularly low positive predictive valuefor sudden death (7 percent), although the negative predictivevalue was high (95 percent).

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Figure 4. Probability of Sudden Death among 224 Patients with a Left Ventricular Ouflow Tract Gradient of at Least 30 mm Hg and 770 Patients without Obstruction.
Patients who were already in NYHA class III or IV at entry were excluded from the analysis.

Magnitude of the Outflow Gradient

When clinical outcome was assessed with respect to the magnitudeof the outflow gradient among the 994 patients in NYHA classI or II at study entry — 30 to 49 mm Hg (in 62 patients),50 to 69 mm Hg (in 73), or 70 mm Hg or greater (in 89) —there were no significant differences in the overall risk ofdeath related to hypertrophic cardiomyopathy, progression toNYHA class III or IV (Figure 5), or sudden death. Furthermore,there was no significant difference in the average outflow tractgradient among patients with obstruction who died from variouscauses related to hypertrophic cardiomyopathy (sudden death,71±18 mm Hg; heart failure, 52±20 mm Hg; and stroke,82±48 mm Hg) or among survivors, as compared with patientswho died of causes unrelated to hypertrophic cardiomyopathy(69±29 mm Hg vs. 71±32 mm Hg). Also, among patientswith obstruction, the absolute gradient measured as a continuousvariable was not associated with a significant increase in therisk of any of the study end points in the age-adjusted multivariateanalysis.

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Figure 5. Relation of the Magnitude of Left Ventricular Outflow Tract Gradient or the Absence of a Gradient to the Probability of Progression to Severe Heart Failure (NYHA Class III or IV) or Death from Heart Failure or Stroke.
P<0.001 for the comparison of the group without obstruction with each subgroup with obstruction; P>0.30 for each comparison among the subgroups with obstruction. Patients who were already in NYHA class III or IV at entry were excluded from the analysis.

Predictors of Outcome

Age-adjusted multivariate analysis showed that left ventricularoutflow tract obstruction was a strong, independent determinantof outcome, including the overall risk of death related to hypertrophiccardiomyopathy (relative risk, 1.6; P=0.02), progression tosevere heart failure or death from heart failure or stroke (relativerisk, 2.7; P<0.001), and death from any cause (relative risk,1.6; P=0.02) (Table 2). Other disease variables that were independentlyassociated with an increased risk of death related to hypertrophiccardiomyopathy were atrial fibrillation, limiting symptoms (NYHAclass II, III, or IV) at study entry, and maximal left ventricularwall thickness of at least 30 mm (Table 2). Only a minorityof patients with obstruction had associated severe mitral regurgitationidentified by color-flow imaging³² (27 of 273, or 10 percent),and this finding itself was not consistently associated withdeath related to hypertrophic cardiomyopathy or to progressionto NYHA class III or IV (P=0.50 for both comparisons).

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Table 2. Results of Age-Adjusted Multivariate Cox Proportional-Hazards Analysis of the Relation between Base-Line Clinical Variables and Outcome.

With regard to sudden death, left ventricular outflow tractobstruction was the only clinical variable independently associatedwith this outcome (relative risk, 1.9; P=0.01). None of thepharmacologic agents commonly used to control symptoms of hypertrophiccardiomyopathy (i.e., beta-blockers, calcium-channel blockers,and disopyramide) or amiodarone significantly affected any ofthe study end points when taken for more than 50 percent ofthe follow-up period.

Analyses among Centers

The patients enrolled at the three participating centers didnot differ significantly with regard to several demographicand disease-related variables, including age, sex, and the prevalenceof outflow tract obstruction. The annual rates of death relatedto hypertrophic cardiomyopathy were also similar: 2.1 percentin Florence, 1.8 percent in Naples, and 1.7 percent in Minneapolis.Also, all three centers had higher annual rates of death amongpatients with obstruction than among those without obstruction:1.8 percent vs. 1.4 percent in Florence, 3.3 percent vs. 1.3percent in Naples, and 2.6 percent vs. 1.7 percent in Minneapolis.

Discussion

The left ventricular outflow tract gradient has been the mostrecognizable feature of hypertrophic cardiomyopathy from itsinitial clinical descriptions.¹^,²^,³^,⁴^,⁵^,⁶^,⁷^,⁸^,⁹^,¹⁰^,¹¹^,¹²^,¹³^,¹⁴^,¹⁵^,¹⁶^,¹⁷^,¹⁸^,¹⁹^,²⁰^,²¹^,²²^,²³^,²⁴^,²⁵^,²⁶^,²⁷^,³³^,³⁴^,³⁵^,³⁶A gradient of at least 50 mm Hg has historically been the thresholdfor performing major invasive interventions, such as septalmyectomy, alcohol septal ablation, and dual-chamber pacing,in patients with severe symptoms refractory to maximal medicalmanagement.³^,⁵^,⁶^,²³^,²⁴^,²⁵^,²⁶ Most previous studies addressingthe clinical significance of obstruction have involved relativelysmall or highly selected populations, and reports have oftenbeen conflicting.⁴^,⁸^,⁹^,¹³^,¹⁴^,¹⁵^,¹⁶^,¹⁷^,¹⁸^,¹⁹^,³³^,³⁴ Indeed, theissue of obstruction in patients with hypertrophic cardiomyopathyhas periodically been the subject of intense controversy,¹^,²^,³^,⁴^,¹³^,¹⁸^,¹⁹and the long-term effect of the outflow gradient on outcomeremains largely unresolved. Consequently, we took this opportunityto investigate the clinical significance of subaortic obstructionin a large cohort of patients with hypertrophic cardiomyopathy.

Our data show that obstruction of left ventricular outflow isof prognostic importance in patients with hypertrophic cardiomyopathy.Patients with outflow tract obstruction (defined here as a basalgradient of at least 30 mm Hg) had an increased risk of deathfrom hypertrophic cardiomyopathy or progression to severe congestivesymptoms, which was more than four times that among patientswithout obstruction. Outflow tract obstruction also proved tobe a strong independent determinant of limiting symptoms anddeath after adjustment for other relevant disease-related anddemographic variables. Patients with obstruction and mild symptoms(NYHA class II) were more likely than asymptomatic patientsto have progression to severe symptoms or to die from heartfailure. Furthermore, we have previously shown that the combinationof outflow tract obstruction with atrial fibrillation is particularlydeleterious in patients with hypertrophic cardiomyopathy.³¹

Our data have certain potentially important therapeutic implicationsfor patients with the obstructive form of hypertrophic cardiomyopathy.Currently accepted clinical practice¹^,²^,³^,⁴^,⁵^,⁶ encourages theuse of aggressive medical therapy for patients with symptomswho have obstruction, including the use of drugs capable ofreducing the outflow gradient under basal conditions or duringexercise (predominantly beta-blockers and disopyramide)⁴^,⁵^,⁶^,³⁵;our data support this strategy. However, when symptoms and thelimitation in exercise capacity become refractory to maximalmedical management, major interventions to reduce obstructionbecome necessary.¹^,²^,³^,⁴^,⁵^,⁶^,⁷^,²³^,²⁴^,²⁵^,²⁶^,³⁶

In this regard, our findings indicate that nonpharmacologicinterventions (i.e., surgery or alcohol septal ablation) maybe a reasonable treatment option earlier and at somewhat lowergradient thresholds than current clinical practice dictates.¹^,³^,⁵^,³⁶Such a strategy may be beneficial for some patients who haveclear progression of symptoms despite medical treatment butwho have not yet become substantially disabled, particularlythose judged to have long-standing gradients.¹^,³^,⁵^,⁶^,³⁶

We could not directly assess the effects of treatment interventionson mortality. Furthermore, we do not believe that our data canbe used to infer that a basic and sweeping alteration in thestandard management of symptomatic obstructive hypertrophiccardiomyopathy is required. Indeed, the interventions that relieveobstruction most reliably (i.e., septal myectomy and alcoholseptal ablation)⁵^,⁶^,²³^,²⁴^,²⁵^,²⁶ should not be performed in patientswithout symptoms or with only mild symptoms, since such proceduresare associated with some risk of complications and death.¹^,³^,⁴^,⁵^,⁶^,⁷^,²³^,²⁴^,²⁵^,²⁶^,³⁶Therefore, our observations emphasize the importance of clinicaljudgment in planning a strategy to reduce left ventricular outflowtract obstruction in patients with hypertrophic cardiomyopathy.

We found that the likelihood of sudden death was also greateramong patients with obstruction than among those without obstruction.However, because of the low annual rate of sudden death andthe particularly low positive predictive value of obstruction,we believe that the contribution of obstruction to risk stratificationremains limited. Indeed, although obstruction can probably beregarded as another potential risk factor for sudden death onthe basis of present and prior analyses,⁸^,⁹ the relation betweenthe gradient and sudden death is not sufficiently strong forobstruction to be considered the sole or a substantial determinantof decisions to implant cardioverter–defibrillators prophylactically.³⁷

The threshold value for the outflow tract gradient that provedto be clinically relevant was relatively low — 30 mm Hg.Furthermore, values above this threshold did not add to thelikelihood of complications and death related to hypertrophiccardiomyopathy. This inability to stratify outcome with respectto the magnitude of the gradient probably reflects the dynamicnature of outflow tract obstruction in hypertrophic cardiomyopathy.¹⁵^,²⁰^,²¹Consequently, we cannot exclude the possibility that particularlymarked degrees of obstruction may adversely affect prognosisin certain patients.

We assessed the clinical significance of the subaortic gradientunder basal conditions, the variable traditionally used to formulateclinical decisions in patients with symptomatic hypertrophiccardiomyopathy.¹^,²^,³^,⁴^,⁵^,⁶^,⁷^,⁸^,⁹^,²³^,²⁴^,²⁵^,²⁶^,³⁶ The participatinginstitutions did not routinely provoke outflow tract gradientsunder physiologic conditions in ambulatory patients with hypertrophiccardiomyopathy. Nevertheless, in symptomatic patients with relativelylow gradients at rest (e.g., 30 to 50 mm Hg), much more substantialgradients are likely to develop with exertion under conditionsin which symptoms of hypertrophic cardiomyopathy usually occur.It is therefore reasonable to assume that the relatively lowbasal gradient threshold of 30 mm Hg probably increases greatlywith physical exertion and thus probably leads to disablingsymptoms.

Because our study was designed to assess longitudinally therelation of the basal left ventricular outflow tract gradientto outcomes, we used the value obtained during the initial continuous-waveDoppler assessment to evaluate in a standardized fashion theclinical effect of obstruction over the longest possible follow-upperiod. Although we are aware of the potential limitations ofthe use of single measurements in individual patients, we believethis consideration is largely compensated for by the substantialsize of our cohort.

The mechanisms by which chronic subaortic obstruction causessymptoms of or death from heart failure in patients with hypertrophiccardiomyopathy are largely unknown. It is likely, however, thatthe greatly elevated left ventricular pressures created by obstructionlead to increased wall stress, myocardial ischemia, and eventually,cell death and replacement scarring.³⁸^,³⁹^,⁴⁰ This cellular remodeling,in turn, probably increases the likelihood that the left ventriclewill become stiff and noncompliant, leading to diastolic dysfunction,¹^,³^,³⁶and may also increase susceptibility to electrical instabilityand sudden death.³⁷ Consistent with this hypothesis is our findingthat older patients (those at least 40 years of age) with obstructivehypertrophic cardiomyopathy were more likely to have diseaseprogression than younger patients. This observation suggests(if chronologic age is assumed to approximate the duration ofobstruction) that longer periods of exposure to left ventricularoutflow tract obstruction and systolic pressure overload aredeleterious. In addition, most patients who undergo interventionsto relieve outflow tract obstruction (i.e., septal myectomyor alcohol septal ablation) have substantial relief of disablingsymptoms¹^,²^,³^,⁴^,⁵^,⁶^,⁷^,³⁶; this finding also supports the principlethat the outflow gradient in patients with hypertrophic cardiomyopathyhas important pathophysiological implications.

Supported in part by grants from the Minneapolis Heart InstituteFoundation and the Italian Ministry for Scientific and TechnologicResearch (COFIN, 2002).

Source Information

From the Division of Cardiology, Tufts–New England Medical Center, Boston (M.S.M.); the Regional Referral Center for Myocardial Diseases, Azienda Ospedaliera Careggi, Florence, Italy (I.O., F.C.); the Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University of Naples, Naples, Italy (S.B., M.A.L.); and the Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis (S.A.C., J.R.L., B.J.M.).

Address reprint requests to Dr. Barry Maron at the Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, 920 E. 28th St., Suite 60, Minneapolis, MN 55407, or at hcm.maron{at}mhif.org.

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Hypertrophic Cardiomyopathy and Outflow Tract Obstruction
Monserrat L., Penas-Lado M., Castro-Beiras A., Iqbal K., Tramboo N. A., Mohi-Ud-Din K., Spevack D. M., Maron M. S., Olivotto I., Maron B. J.
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N Engl J Med 2003; 348:1815-1816, May 1, 2003. Correspondence

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Writing Committee Members, , Maron, B. J., McKenna, W. J., Danielson, G. K., Kappenberger, L. J., Kuhn, H. J., Seidman, C. E., Shah, P. M., Spencer, W. H. III, Spirito, P., Ten Cate, F. J., Wigle, E. D., ACCF Task Force on Clinical Expert Consensus Docum, , Vogel, R. A., Abrams, J., Bates, E. R., Brodie, B. R., Danias, P. G., Gregoratos, G., Hlatky, M. A., Hochman, J. S., Kaul, S., Lichtenberg, R. C., Lindner, J. R., O'Rourke, R. A., Pohost, G. M., Schofield, R. S., Tracy, C. M., Winters, W. L. Jr, ESC Committee for Practice Guidelines Members, , Klein, W. W., Priori, S. G., Alonso-Garcia, A., Blomstrom-Lundqvist, C., De Backer, G., Deckers, J., Flather, M., Hradec, J., Oto, A., Parkhomenko, A., Silber, S., Torbicki, A. (2003). American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. Eur Heart J 24: 1965-1991 [Full Text]
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