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(Circulation. 2000;102:858.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Epidemiology of Hypertrophic Cardiomyopathy–Related Death
Revisited in a Large Non–Referral-Based Patient Population
From Minneapolis Heart Institute Foundation, Minneapolis, Minn (B.J.M., S.A.C., T.E.G., K.J.G.); Ente Ospedaliero Ospedali Galliera, Genoa, Italy (P.S.); Ospedale Santa Corona, Pietra Ligure (P.B.); Children’s Heart Clinic, Minneapolis, Minn (D.A.B.); and Ospedale di Careggi, Florence, Italy (I.O., F.C.). Correspondence to Barry J. Maron, MD, Minneapolis Heart Institute Foundation, 920 E 28th St, Suite 40, Minneapolis, MN 55407.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—Death resulting from hypertrophic cardiomyopathy (HCM), particularly when sudden, has been reported to be largely confined to young persons. These data emanated from tertiary HCM centers with highly selected referral patterns skewed toward high-risk patients.
Methods and Results—The present analysis was undertaken in an international population of 744 consecutively enrolled and largely unselected patients more representative of the overall HCM spectrum. HCM-related death occurred in 86 patients (12%) over 8±7 years (mean±SD). Three distinctive modes of death were as follows: (1) sudden and unexpected (51%; age, 45±20 years); (2) progressive heart failure (36%; age, 56±19 years); and (3) HCM-related stroke associated with atrial fibrillation (13%; age, 73±14 years). Sudden death was most common in young patients, whereas heart failure– and stroke-related deaths occurred more frequently in midlife and beyond. However, neither sudden nor heart failure–related death showed a statistically significant, disproportionate age distribution (P=0.06 and 0.5, respectively). Stroke-related deaths did occur disproportionately in older patients (P=0.002). Of the 45 patients who died suddenly, most (71%) had no or mild symptoms, and 7 (16%) participated in moderate to severe physical activities at the time of death.
Conclusions—HCM-related cardiovascular death occurred suddenly, or as a result of heart failure or stroke, largely during different phases of life in a prospectively assembled, regionally based, and predominantly unselected patient cohort. Although most sudden deaths occurred in adolescents and young adults, such catastrophes were not confined to patients of these ages and extended to later phases of life. This revised clinical profile suggests that generally held epidemiological tenants for HCM have been influenced considerably by skewed reporting from highly selected populations. These data are likely to importantly affect risk stratification and treatment strategies importantly for the prevention of sudden death in HCM.
Key Words: cardiomyopathy • death, sudden • heart failure
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Hypertrophic cardiomyopathy (HCM) is a complex primary and genetically transmitted cardiac disease with a diverse clinical course that includes a benign or stable clinical course over many years, progressive congestive symptoms requiring therapeutic intervention, and the possibility of sudden and unexpected death.1 2 3 4 5 6 7 8 9 Since the initial description of HCM in 1958,10 sudden death occurring in young and usually asymptomatic patients has received substantial exposure in the literature as the most devastating consequence of the disease.11 12 13 14 15 16 17 18 19 20 21 However, until recently, natural history data for HCM were predominantly assembled at a few large, tertiary centers with patient referral patterns preferentially comprised of high-risk patients.1 2 3 6 7 21 22 In the present study, we have reassessed the epidemiology and clinical profile of HCM-related death in a largely unselected cohort of 744 patients that more closely reflects the overall clinical spectrum of the disease.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Selection
Patient populations from 3 regional centers were combined to assemble a consecutive cohort of 744 patients evaluated between 1975 and 1998: (1) the Minnesota cohort: 297 patients from the Minneapolis Heart Institute and Children’s Heart Clinic, consisting primarily of Minnesota residents but also those from the adjacent states of Wisconsin, Iowa, and North and South Dakota7 ; (2) the Tuscany cohort: 237 patients, predominantly from the region of Tuscany in central Italy and the Careggi Hospital in Florence23 ; and (3) the Genoa cohort: 210 patients from metropolitan Genoa and adjacent regions of northwestern Italy and the Galliera Hospital.24 The period of follow-up from first hospital evaluation for the overall study group was 8.0±7 years. Portions of these databases have been used in other clinical studies.7 23 24
Echocardiography
Echocardiographic studies were performed with
commercially available Hewlett-Packard and Toshiba instruments. Left
ventricular hypertrophy was assessed with
2-dimensional echocardiography, and the site of
maximum wall thickness was identified.25 26 Peak
instantaneous left ventricular outflow gradient was
estimated with continuous-wave Doppler under basal
conditions.27
Statistical Analysis
Data are expressed as mean±SD. Differences between means were
analyzed with 1-way ANOVA with the Bonferroni test for post hoc
group comparisons or unpaired Student’s t test, as
appropriate. The uniformity of age distributions at death was assessed
statistically by use of the nonparametric Kruskal-Wallis
test. Comparison of nominal variables expressed as proportions were
performed by use of the Pearson 
2 test.
Definitions
HCM
The diagnosis of HCM was based on the 2-dimensional
echocardiographic identification of a hypertrophied,
nondilated left ventricle (wall thickness 
15 mm in adults and
the equivalent relative to body surface area in
children)28 in the absence of another cardiac or systemic
disease capable of producing the magnitude of wall thickening
evident.29
Sudden cardiac death was defined as unexpected sudden collapse occurring <1 hour from the onset of symptoms in patients who had previously experienced a relatively stable or uneventful clinical course. In addition, potentially lethal cardiovascular events in which 14 patients either were successfully resuscitated from cardiac arrest (with documented ventricular fibrillation; n=11) or received appropriate defibrillation shocks from an implanted cardioverter-defibrillator (ICD; n=3) were regarded as equivalents of sudden cardiac death in the present data analysis. Two patients who survived their first cardiac arrest ultimately died in refractory heart failure 34 months and 17 years later but are tabulated as sudden deaths for the purposes of this study.30
Congestive heart failure–related death was defined as occurring in the
context of cardiac decompensation and progressive disease course 1
year before death, particularly if complicated by pulmonary
edema or evolution to the end-stage phase31 and/or
requiring hospitalization for heart failure. Seven patients with
advanced refractory heart failure who received heart
transplants32 were considered equivalent to HCM-related
heart failure deaths in this analysis.
Stroke-related deaths were judged to be a direct consequence of embolic or other events related to HCM, usually in the setting of paroxysmal or chronic atrial fibrillation.33
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Demographics
Clinical and demographic variables are tabulated for the overall patient population and individually for each of the 4 patient cohorts in Table 1
. The vast
majority of these parameters were similar among the 4
populations. However, patients from Minnesota and Genoa had been
treated with amiodarone less frequently than were the patients
from Tuscany (Table 1).
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Mode of Death
Of the 744 study patients, 125 (17%) died during the follow-up
period. These included 36 from causes unrelated to HCM (such as cancer,
suicide, accident, or acute myocardial infarction resulting from
advanced coronary artery disease); 3 others occurred
perioperatively as a result of complications of
ventricular septal myotomy-myectomy. In the remaining 86
patients, death was judged to be probably or definitely a result of
HCM, although 3 of these patients also had atherosclerotic
coronary artery disease documented during life or at autopsy.
Three modes of death were defined (Figure 1 and Table 1
): (1) sudden and
unexpected (44 patients, including 11 with aborted cardiac arrest and 3
with appropriate ICD interventions for ventricular
tachycardia or fibrillation); (2) resulting from
progressive, refractory heart failure (31 patients, including 8 with
heart transplantation)32 ; and (3) as a consequence of
HCM-related ischemic stroke, largely compatible with a
cardioembolic origin (11 patients; Figure 1 and Table 2). Three other patients died
postoperatively after ventricular septal myotomy-myectomy
operation.1 2 3 4 5
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Relation of Mode of Death to Clinical Parameters
Age
The distribution of age at death was dissimilar for the 3 modes
(P<0.001). In the group analysis for the study
population, sudden deaths occurred in the younger patients (mean age,
45±20 years; Figure 1 and Table 1). Nevertheless, with
individual patient analysis, the 44 sudden deaths were
distributed throughout a wide range of ages (7 to 78 years); 14 (32%)
occurred in patients 35 years of age, but 15 patients (34%) were
55 years of age (Figure 2).
Consequently, the risk of sudden death was not confined to young
patients but extended into later phases of life (Figure 2) and
without a statistically significant predilection for any age group
(P=0.06). The distribution of sudden deaths was not
substantially altered with or without inclusion of the 13 patients with
either aborted cardiac arrest or appropriate ICD intervention.
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In contrast, the 31 congestive heart failure–related deaths occurred
frequently in midlife and beyond (mean age, 56±19 years), with 26 of
31 or 84% in patients >35 years of age. There was no significant
difference in the distribution of these deaths among age groups
(P=0.5; Figure 2). Of these 31 patients, 13 were
judged to be in the end-stage phase31 (Figure 1 and Table 1).
The 11 deaths related to stroke occurred in patients of the most
advanced ages (mean age, 73±14 years; Figures 1 and 2
and Table 1), with 10 of the 11 (91%) >65 years of age at the
time of their event (Figure 2 and Table 1). Consequently,
the age distribution of stroke-related deaths was skewed significantly
to older patients (P=0.0001; Figure 2). Ten of the 11
strokes (91%) were also associated with a history of chronic or
paroxysmal atrial fibrillation, suggesting cardioembolic origin (Table 2).
Overall, 30 of the 86 HCM-related deaths (35%) occurred after 65 years of age, including 12 deaths in patients >75 years of age (2 of whom died suddenly).
Sex and Family History
No significant differences in sex were evident between patients
who died suddenly or of heart failure (Table 2). However, a
striking predominance of women (9 of 11 patients; 82%) experienced
stroke-related death. Of the 86 patients who died, only 15 (17%) had a
family history of 1 relative with HCM-related death.
Left Ventricular Wall Thickness
Maximum wall thicknesses did not differ significantly among the 3
patient subgroups according to mode of death (Table 2). However,
particularly marked hypertrophy (30 mm) was
present in 18 patients, including 9 (20%) of the 44 who died
suddenly.
Outflow Gradient
No significant differences in magnitude of the outflow gradient
were evident between patients who died suddenly or of heart failure
(27±40 versus 22±34 mm Hg, P=NS); however, patients
with stroke-related death showed substantially higher outflow gradients
(60±53 mm Hg, P=0.02; Table 2).
Antiarrhythmic Drug Treatment
Of the 744 study patients, 106 (14%) received amiodarone
(usually 200 mg/d) for 6 months, including 20 (23%) of the 86
patients who died of HCM, either for nonsustained
ventricular tachycardia on Holter ECG or
prevention of atrial fibrillation recurrence. Seven of the 44
patients who died suddenly (16%) had been taking amiodarone at
the time of death; of the 106 patients taking amiodarone, 10
(9%) experienced heart failure–related death.
Annual Mortality Analysis
Clinical outcome was also prospectively analyzed with
respect to annual HCM mortality from the time of study entry (ie, at
initial evaluation; Figure 3). Annual
mortality for deaths occurring either suddenly and unexpectedly, as a
result of heart failure, and as a consequence of stroke or for all
HCM-related deaths combined were 0.7%, 0.5%, 0.2%, and 1.4%,
respectively. Furthermore, for sudden or heart failure–related deaths,
no statistically significant differences in annual mortality were
evident with respect to the age groups (P=0.10 and 0.09,
respectively). In contrast, annual mortality resulting from stroke was
highest in the oldest patients (P<0.001).
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Circumstances of Sudden Deaths
Prior Symptoms
Sudden cardiac death occurred predominantly in those patients with
no or mild symptoms (NYHA functional class I and II; 31 of 44 patients,
71%), and 17 of these patients had been asymptomatic
before death. The remaining 13 patients (29%) who died suddenly had
experienced substantial limiting symptoms (functional class III);
however, each was clinically stable and had not experienced progressive
deterioration before death (Figure 4).
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Prior Activity
Most patients (37, 84%) died suddenly during or immediately after
a variety of sedentary or mild physical activities such as watching
television, walking, or driving a car (including 7 who
died while sleeping in bed); 37 deaths occurred outside the hospital,
and 2 inpatients died. The remaining 7 patients (16%) died during
moderate to severe physical exertion, including only 1 who had been
engaged in competitive athletics (a 33-year-old man in master’s level
sports who survived a cardiac arrest incurred during burst exertion;
Figure 4).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study revisits the epidemiology and profile of death in HCM by using a largely unselected and longitudinally assessed, consecutive population of patients who were previously diagnosed with the disease. This large HCM cohort of
750
patients differs importantly from tertiary center cohorts in which
referral patterns are skewed toward those patients perceived to be at
high risk.1 3 6 7 21 22 In contrast, our study population
was assembled by combining all HCM patients from 3 regional centers
virtually free of tertiary center referral bias and therefore was more
closely representative of the overall disease spectrum.
The relatively low mortality rates reported here for sudden and other
HCM-related modes of death (<1%/y) are consistent with the
relatively unselected nature of the study
group.6 7 8 22 23 In the present profile, we defined 3 distinctive modes of HCM-related death occurring largely during different periods of life. For example, sudden and unexpected death often occurred in younger patients, although without a clear predilection for any particular age group. Most heart failure–related deaths were in midlife and beyond. Death as a consequence of stroke (usually embolic and associated with atrial fibrillation) was virtually confined to much older patients, many of whom had already achieved normal longevity in statistical terms.
Numerous prior reports from HCM referral centers emphasized that sudden
cardiac death (or resuscitated cardiac arrest) preferentially occurred
during a particular period of life—ie, in asymptomatic (or
mildly symptomatic) children and adults younger than 35
years of age.4 5 11 12 13 14 15 16 17 18 19 20 21 34 Therefore, we have reported a
profile of sudden death that modifies in certain important respects the
profile previously described for HCM.4 5 11 12 13 14 15 16 17 18 19 20 21 In our
regional and largely unselected population, we could not replicate
prior descriptions of a sharp peak in sudden death during adolescence
and young adulthood21 and little risk for sudden death
after 35 years of age. In contrast, although the present
analysis demonstrates a trend toward greater frequency of
sudden death among younger patients (adolescents and young adults),
these events were neither confined to young patients nor
disproportionately distributed across a broad expanse of ages from 7 to
78 years and continued to occur in midlife and beyond (including 20%
after 65 years of age). Similarly, heart failure–related deaths did
not show statistically significant differences among the age groups
with respect to occurrence and annual mortality. Only with stroke were
differences according to age identified, with significantly increased
occurrence of death and annual mortality in the elderly.
We believe that the important differences cited between HCM data sets regarding clinical course are explained largely by patient selection, usually younger and higher-risk patients preferentially referred to tertiary centers.21 22 When such selection bias is removed (as in the present study cohort), the clinical profile of sudden death is considerably altered, emphasizing that patient referral patterns are probably the strongest determinants of our prevailing perceptions regarding the clinical expression and impact of HCM.1 6 7 22
Our observations that sudden death in HCM is not limited to young patients and that the risk period in this disease extends virtually throughout life have important clinical implications. Such revised perceptions are relevant to risk stratification and treatment for the prevention of sudden cardiac death, particularly with respect to the potential role of the ICD in this disease.35 Indeed, in contrast to coronary artery disease,36 patients with HCM are often much younger (average, 40 years of age) and have long periods of potential risk when regarded as candidates for the primary prevention of sudden death.35
We are uncertain about the potential impact that the administration of
amiodarone to a segment of the patient population had on our
findings. It has been suggested that amiodarone may be
protective against sudden cardiac death in HCM,37 38 and
15% of the patients in this study population received this drug
prophylactically. However, an important observation of this
study is that 15% of our patients who died suddenly were treated
with amiodarone (usually 200 mg/d), clearly demonstrating that
the administration of this drug is not absolutely protective against
the risk for arrhythmic death.37 Furthermore, the finding
that only 10% of those patients treated with amiodarone
developed progressive heart failure–related death confirms our
suspicion that administration of this drug probably does not predispose
to cardiac death in HCM.38
We identified a relatively low frequency of sudden deaths (or
cardiac arrest) occurring during or just after moderate to severe
physical exertion (15%). These observations contrast somewhat with
the data assembled in highly selected HCM tertiary referral
institutions that included patients without prior clinical evaluation
initially identified at autopsy.21 First, it should be
emphasized that none of the patients in the present consecutive
population were known to be trained competitive athletes (although 1
patient died while engaged in sports). Second, our reduced frequency of
exertion-related sudden death probably reflects the current widespread
awareness of risks for young HCM patients engaged in intense
sports,39 40 41 42 43 as well as the changing attitudes and
recommendations against competitive athletics for such
individuals.39 40 41 42 44 Third, the vast majority of athletes
with HCM who die suddenly are not aware of their underlying disease and
therefore would not be likely to appear in a consecutively diagnosed
and enrolled cohort such as the present one. Indeed, we cannot be
certain how many additional patients in this generally low-risk cohort
would have died had they been systematically exposed to an athletic
lifestyle. Consequently, the present data should not undermine the
well-established link between intense competitive sports and the risk
for sudden death with HCM.39 40 44
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Acknowledgments |
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Supported in part by grants from the Consiglio Nazionale delle Ricerche and Telethon-Italy (to Dr Spirito) and the Minneapolis Heart Institute Foundation and Paul G. Allen Foundation (to Dr Maron).
Received February 11, 2000; revision received March 22, 2000; accepted March 27, 2000.
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A Esposito, F De Cobelli, G Perseghin, M Pieroni, E Belloni, R Mellone, T Canu, F Gentinetta, P Scifo, C Chimenti, et al. Impaired left ventricular energy metabolism in patients with hypertrophic cardiomyopathy is related to the extension of fibrosis at delayed gadolinium-enhanced magnetic resonance imaging Heart, February 1, 2009; 95(3): 228 - 233. [Abstract] [Full Text] [PDF]
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I. Olivotto, M. S. Maron, F. Cecchi, and B. J. Maron Reply. J. Am. Coll. Cardiol., January 27, 2009; 53(4): 399 - 399. [Full Text] [PDF]
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F. A. Cuoco, W. H. Spencer III, V. L. Fernandes, C. D. Nielsen, S. Nagueh, J. L. Sturdivant, R. B. Leman, J. M. Wharton, and M. R. Gold Implantable Cardioverter-Defibrillator Therapy for Primary Prevention of Sudden Death After Alcohol Septal Ablation of Hypertrophic Cardiomyopathy J. Am. Coll. Cardiol., November 18, 2008; 52(21): 1718 - 1723. [Abstract] [Full Text] [PDF]
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K Sakata, H Ino, N Fujino, M Nagata, K Uchiyama, K Hayashi, T Konno, M Inoue, H Kato, Y Sakamoto, et al. Exercise-induced systolic dysfunction in patients with non-obstructive hypertrophic cardiomyopathy and mutations in the cardiac troponin genes Heart, October 1, 2008; 94(10): 1282 - 1287. [Abstract] [Full Text] [PDF]
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P Elliott and P Spirito Prevention of hypertrophic cardiomyopathy-related deaths: theory and practice Heart, October 1, 2008; 94(10): 1269 - 1275. [Abstract] [Full Text] [PDF]
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U. Sigwart Catheter Treatment for Hypertrophic Obstructive Cardiomyopathy: For Seniors Only? Circulation, July 8, 2008; 118(2): 107 - 108. [Full Text] [PDF]
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P P Dimitrow, A Undas, M Bober, W Tracz, and J S Dubiel Obstructive hypertrophic cardiomyopathy is associated with enhanced thrombin generation and platelet activation Heart, June 1, 2008; 94(6): e21 - e21. [Abstract] [Full Text] [PDF]
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 A. J. Mittnacht, M. Fanshawe, and S. Konstadt Anesthetic Considerations in the Patient With Valvular Heart Disease Undergoing Noncardiac Surgery Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2008; 12(1): 33 - 59. [Abstract] [PDF]
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H. Rakowski and S. Carasso Quantifying Diastolic Function in Hypertrophic Cardiomyopathy: The Ongoing Search for the Holy Grail Circulation, December 4, 2007; 116(23): 2662 - 2665. [Full Text] [PDF]
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D. Szczesna-Cordary, M. Jones, J. R. Moore, J. Watt, W. G. L. Kerrick, Y. Xu, Y. Wang, C. Wagg, and G. D. Lopaschuk Myosin regulatory light chain E22K mutation results in decreased cardiac intracellular calcium and force transients FASEB J, December 1, 2007; 21(14): 3974 - 3985. [Abstract] [Full Text] [PDF]
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T. Kubo, J. R. Gimeno, A. Bahl, U. Steffensen, M. Steffensen, E. Osman, R. Thaman, J. Mogensen, P. M. Elliott, Y. Doi, et al. Prevalence, Clinical Significance, and Genetic Basis of Hypertrophic Cardiomyopathy With Restrictive Phenotype J. Am. Coll. Cardiol., June 26, 2007; 49(25): 2419 - 2426. [Abstract] [Full Text] [PDF]
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P Melacini, B J Maron, F Bobbo, C Basso, B Tokajuk, M Zucchetto, G Thiene, and S Iliceto Evidence that pharmacological strategies lack efficacy for the prevention of sudden death in hypertrophic cardiomyopathy Heart, June 1, 2007; 93(6): 708 - 710. [Abstract] [Full Text] [PDF]
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P M Elliott, J R Gimeno, R Thaman, J Shah, D Ward, S Dickie, M T Tome Esteban, and W J McKenna Historical trends in reported survival rates in patients with hypertrophic cardiomyopathy Heart, June 1, 2006; 92(6): 785 - 791. [Abstract] [Full Text] [PDF]
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T. Kubo, H. Kitaoka, M. Okawa, Y. Matsumura, N. Hitomi, N. Yamasaki, T. Furuno, J. Takata, M. Nishinaga, A. Kimura, et al. Lifelong Left Ventricular Remodeling of Hypertrophic Cardiomyopathy Caused by a Founder Frameshift Deletion Mutation in the Cardiac Myosin-Binding Protein C Gene Among Japanese J. Am. Coll. Cardiol., November 1, 2005; 46(9): 1737 - 1743. [Abstract] [Full Text] [PDF]
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B. Schumacher, F. H. Gietzen, H. Neuser, J. Schummelfeder, M. Schneider, S. Kerber, R. Schimpf, C. Wolpert, and M. Borggrefe Electrophysiological Characteristics of Septal Hypertrophy in Patients With Hypertrophic Obstructive Cardiomyopathy and Moderate to Severe Symptoms Circulation, October 4, 2005; 112(14): 2096 - 2101. [Abstract] [Full Text] [PDF]
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S. R. Ommen, B. J. Maron, I. Olivotto, M. S. Maron, F. Cecchi, S. Betocchi, B. J. Gersh, M. J. Ackerman, R. B. McCully, J. A. Dearani, et al. Long-Term Effects of Surgical Septal Myectomy on Survival in Patients With Obstructive Hypertrophic Cardiomyopathy J. Am. Coll. Cardiol., August 2, 2005; 46(3): 470 - 476. [Abstract] [Full Text] [PDF]
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I. Olivotto, M. S. Maron, A. S. Adabag, S. A. Casey, D. Vargiu, M. S. Link, J. E. Udelson, F. Cecchi, and B. J. Maron Gender-Related Differences in the Clinical Presentation and Outcome of Hypertrophic Cardiomyopathy J. Am. Coll. Cardiol., August 2, 2005; 46(3): 480 - 487. [Abstract] [Full Text] [PDF]
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P. A. Kaufmann and P. G. Camici Myocardial Blood Flow Measurement by PET: Technical Aspects and Clinical Applications J. Nucl. Med., January 1, 2005; 46(1): 75 - 88. [Full Text] [PDF]
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B. J. Maron, J.G. Seidman, and C. E. Seidman Proposal for contemporary screening strategies in families with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., December 7, 2004; 44(11): 2125 - 2132. [Abstract] [Full Text] [PDF]
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B. J. Maron, J. A. Dearani, S. R. Ommen, M. S. Maron, H. V. Schaff, B. J. Gersh, and R. A. Nishimura The case for surgery in obstructive hypertrophic cardiomyopathy J. Am. Coll. Cardiol., November 16, 2004; 44(10): 2044 - 2053. [Abstract] [Full Text] [PDF]
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S. L. Van Driest, V. C. Vasile, S. R. Ommen, M. L. Will, A. J. Tajik, B. J. Gersh, and M. J. Ackerman Myosin binding protein C mutations and compound heterozygosity in hypertrophic cardiomyopathy J. Am. Coll. Cardiol., November 2, 2004; 44(9): 1903 - 1910. [Abstract] [Full Text] [PDF]
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F H Gietzen, C J Leuner, L Obergassel, C Strunk-Mueller, and H Kuhn Transcoronary ablation of septal hypertrophy for hypertrophic obstructive cardiomyopathy: feasibility, clinical benefit, and short term results in elderly patients Heart, June 1, 2004; 90(6): 638 - 644. [Abstract] [Full Text] [PDF]
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M. P Frenneaux Assessing the risk of sudden cardiac death in a patient with hypertrophic cardiomyopathy Heart, May 1, 2004; 90(5): 570 - 575. [Full Text] [PDF]
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T. Konno, M. Shimizu, H. Ino, M. Yamaguchi, H. Terai, K. Uchiyama, K. Oe, T. Mabuchi, T. Kaneda, and H. Mabuchi Diagnostic value of abnormal Q waves for identification of preclinical carriers of hypertrophic cardiomyopathy based on a molecular genetic diagnosis Eur. Heart J., February 1, 2004; 25(3): 246 - 251. [Abstract] [Full Text] [PDF]
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P. Sorajja, S. R. Ommen, R. A. Nishimura, B. J. Gersh, P. B. Berger, and A. J. Tajik Adverse Prognosis of Patients With Hypertrophic Cardiomyopathy Who Have Epicardial Coronary Artery Disease Circulation, November 11, 2003; 108(19): 2342 - 2348. [Abstract] [Full Text] [PDF]
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B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, F. J. Ten Cate, et al. 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 J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1687 - 1713. [Full Text] [PDF]
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Writing Committee Members, B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, et al. 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., November 1, 2003; 24(21): 1965 - 1991. [Full Text] [PDF]
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H. Terai, M. Shimizu, H. Ino, M. Yamaguchi, K. Uchiyama, K. Oe, K. Nakajima, J. Taki, M. Kawano, and H. Mabuchi Changes in Cardiac Sympathetic Nerve Innervation and Activity in Pathophysiologic Transition from Typical to End-Stage Hypertrophic Cardiomyopathy J. Nucl. Med., October 1, 2003; 44(10): 1612 - 1617. [Abstract] [Full Text] [PDF]
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F. Cecchi, I. Olivotto, R. Gistri, R. Lorenzoni, G. Chiriatti, and P. G. Camici Coronary Microvascular Dysfunction and Prognosis in Hypertrophic Cardiomyopathy N. Engl. J. Med., September 11, 2003; 349(11): 1027 - 1035. [Abstract] [Full Text] [PDF]
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B J Maron Contemporary considerations for risk stratification, sudden death and prevention in hypertrophic cardiomyopathy Heart, September 1, 2003; 89(9): 977 - 978. [Full Text] [PDF]
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S. L. Van Driest, E. G. Ellsworth, S. R. Ommen, A. J. Tajik, B. J. Gersh, and M. J. Ackerman Prevalence and Spectrum of Thin Filament Mutations in an Outpatient Referral Population With Hypertrophic Cardiomyopathy * Note Added in Proof Circulation, July 29, 2003; 108(4): 445 - 451. [Abstract] [Full Text] [PDF]
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B. J. Maron, N. A. M. Estes III, M. S. Maron, A. K. Almquist, M. S. Link, and J. E. Udelson Primary Prevention of Sudden Death as a Novel Treatment Strategy in Hypertrophic Cardiomyopathy Circulation, June 17, 2003; 107(23): 2872 - 2875. [Full Text] [PDF]
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M. J. M. Kofflard, F. J. Ten Cate, C. van der Lee, and R. T. van Domburg Hypertrophic cardiomyopathy in a large community-based population: clinical outcome and identification of risk factors for sudden cardiac death and clinical deterioration J. Am. Coll. Cardiol., March 19, 2003; 41(6): 987 - 993. [Abstract] [Full Text] [PDF]
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A. J. Marian On predictors of sudden cardiac death in hypertrophic cardiomyopathy J. Am. Coll. Cardiol., March 19, 2003; 41(6): 994 - 996. [Full Text] [PDF]
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M. S. Maron, I. Olivotto, S. Betocchi, S. A. Casey, J. R. Lesser, M. A. Losi, F. Cecchi, and B. J. Maron Effect of Left Ventricular Outflow Tract Obstruction on Clinical Outcome in Hypertrophic Cardiomyopathy N. Engl. J. Med., January 23, 2003; 348(4): 295 - 303. [Abstract] [Full Text] [PDF]
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I. Olivotto, R. Gistri, P. Petrone, E. Pedemonte, D. Vargiu, and F. Cecchi Maximum left ventricular thickness and risk of sudden death in patients with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., January 15, 2003; 41(2): 315 - 321. [Abstract] [Full Text] [PDF]
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L. Choudhury, H. Mahrholdt, A. Wagner, K. M. Choi, M. D. Elliott, F. J. Klocke, R. O. Bonow, R. M. Judd, and R. J. Kim Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., December 18, 2002; 40(12): 2156 - 2164. [Abstract] [Full Text] [PDF]
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S. L. Van Driest, M. J. Ackerman, S. R. Ommen, R. Shakur, M. L. Will, R. A. Nishimura, A. J. Tajik, and B. J. Gersh Prevalence and Severity of "Benign" Mutations in the {beta}-Myosin Heavy Chain, Cardiac Troponin T, and {alpha}-Tropomyosin Genes in Hypertrophic Cardiomyopathy Circulation, December 10, 2002; 106(24): 3085 - 3090. [Abstract] [Full Text] [PDF]
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C. Autore, M. R. Conte, M. Piccininno, P. Bernabo, G. Bonfiglio, P. Bruzzi, and P. Spirito Risk associated with pregnancy in hypertrophic cardiomyopathy J. Am. Coll. Cardiol., November 20, 2002; 40(10): 1864 - 1869. [Abstract] [Full Text] [PDF]
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S. Sharma, B. J. Maron, G. Whyte, S. Firoozi, P. M. Elliott, and W. J. McKenna Physiologic limits of left ventricular hypertrophy in elite junior athletes: Relevance to differential diagnosis of athlete's heart and hypertrophic cardiomyopathy J. Am. Coll. Cardiol., October 16, 2002; 40(8): 1431 - 1436. [Abstract] [Full Text] [PDF]
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M. Arad, J.G. Seidman, and C. E. Seidman Phenotypic diversity in hypertrophic cardiomyopathy Hum. Mol. Genet., October 1, 2002; 11(20): 2499 - 2506. [Abstract] [Full Text] [PDF]
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B. J. Maron Hypertrophic Cardiomyopathy: A Systematic Review JAMA, March 13, 2002; 287(10): 1308 - 1320. [Abstract] [Full Text] [PDF]
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M. J. Eriksson, B. Sonnenberg, A. Woo, P. Rakowski, T. G. Parker, E. D. Wigle, and H. Rakowski Long-term outcome in patients with apical hypertrophic cardiomyopathy J. Am. Coll. Cardiol., February 20, 2002; 39(4): 638 - 645. [Abstract] [Full Text] [PDF]
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B. J. Maron, I. Olivotto, P. Bellone, M. R. Conte, F. Cecchi, B. P. Flygenring, S. A. Casey, T. E. Gohman, S. Bongioanni, and P. Spirito Clinical profile of stroke in 900 patients with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., January 16, 2002; 39(2): 301 - 307. [Abstract] [Full Text] [PDF]
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S. G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, J. A. Camm, R. Cappato, S. M. Cobbe, C. Di Mario, et al. TASK FORCE ON SUDDEN CARDIAC DEATH, EUROPEAN SOCIETY OF CARDIOLOGY: Summary of Recommendations Europace, January 1, 2002; 4(1): 3 - 18. [Abstract] [PDF]
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I. Olivotto, F. Cecchi, S. A. Casey, A. Dolara, J. H. Traverse, and B. J. Maron Impact of Atrial Fibrillation on the Clinical Course of Hypertrophic Cardiomyopathy Circulation, November 20, 2001; 104(21): 2517 - 2524. [Abstract] [Full Text] [PDF]
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Guidelines for the management of patients with atrial fibrillation. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to develop guidelines for the management of patients with atrial fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology Eur. Heart J., October 2, 2001; 22(20): 1852 - 1923. [PDF]
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V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology J. Am. Coll. Cardiol., October 1, 2001; 38(4): 1266 - 1266. [Full Text] [PDF]
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D. V. Exner, G. J. Klein, and E. N. Prystowsky Primary Prevention of Sudden Death With Implantable Defibrillator Therapy in Patients With Cardiac Disease: Can We Afford to Do It? (Can We Afford Not To?) Circulation, September 25, 2001; 104(13): 1564 - 1570. [Full Text] [PDF]
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S.G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, A.J. Camm, R. Cappato, S.M. Cobbe, C. Di Mario, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology Eur. Heart J., August 2, 2001; 22(16): 1374 - 1450. [PDF]
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