Original Article
Clinical Course and Prognosis of Hypertrophic Cardiomyopathy in an Outpatient Population
N Engl J Med 1989; 320:749-755March 23, 1989DOI: 10.1056/NEJM198903233201201
- Abstract
- Abstract
Hypertrophic cardiomyopathy has been investigated mainly at referral institutions. Thus, the clinical history of the disease that emerges from published studies could be influenced by a bias in patient selection. In the present study, we compared the clinical features of an outpatient population of 25 patients who had hypertrophic cardiomyopathy with those reported in 78 studies published during the past five years.
In the 25 study patients, age, sex, and the extent of left ventricular hypertrophy, as well as the prevalence of diastolic filling abnormalities, subaortic obstruction, and ventricular arrhythmias, were similar to those in patients described in the literature. Cardiac symptoms, however, were much less severe in the study patients. Eighteen patients (72 percent) were asymptomatic, six
(24 percent) had mild symptoms, and only one (4 percent) had moderate-to-severe symptoms. Of 24 patients followed for a mean period of 4.4 years (range, 2.9 to 5.7), none died or had clinical deterioration. Of 3404 patients described in the 78 studies we reviewed, 2483 (73 percent) came from only two referral institutions. Of the 1721 patients in whom severity of symptoms was reported, 757 (44 percent) had moderate-to-severe symptoms. However, 727 (96 percent) of these patients were studied at one of the same two referral institutions.
We conclude that the natural history of hypertrophic cardiomyopathy may be more benign than can be inferred from published reports. (N Engl J Med 1989; 320: 749–55.)
Media in This Article
Table 1
Clinical, Morphologic, and Functional Features of Hypertrophic Cardiomyopathy in an Outpatient Population and in 78 Published Studies.*Table 2
Doppler Diastolic Indexes in 20 Outpatients with Hypertrophic Cardiomyopathy and 20 Normal Control Subjects.*Article Activity
- Article
MOST of our knowledge of the clinical features and natural history of hypertrophic cardiomyopathy comes from observations derived from hospital-based study populations and investigations performed at referral institutions. Thus, the clinical picture of hypertrophic cardiomyopathy that emerges from published studies may be influenced by a bias in patient referrals. We studied the morphologic, functional, and clinical features of a population of outpatients with hypertrophic cardiomyopathy. These patients had a substantially more favorable clinical course than is usually described in the literature.
Methods
Selection of Patients
The department of cardiology at our hospital was opened in March 1983. At that time, because of our interest in hypertrophic cardiomyopathy, we decided to assemble a population of patients with this disease. We identified an initial group of 20 patients with hypertrophic cardiomyopathy by reviewing the registers of the echocardiography laboratories run privately in the Genoa metropolitan area and not associated with hospitals. In the subsequent two years, five additional patients who had previously been found to have a cardiac murmur, an abnormal electrocardiogram (ECG), or both, were given a diagnosis of hypertrophic cardiomyopathy in our laboratory. These circumstances afforded us the opportunity to investigate a group of outpatients with hypertrophic cardiomyopathy.
Routine screening of students and workers, including electrocardiography, is part of the health care system in Italy. Since more than 80 percent of patients with hypertrophic cardiomyopathy have abnormal ECGs,1 the reason for the initial echocardiogram was an abnormal ECG in 17 (68 percent) of our 25 study patients. The first echocardiographic examination was performed because of cardiac murmur in five patients, dyspnea on mild exertion in one, and palpitations in one. In the remaining patient, the first echocardiogram was obtained during a screening of the first-degree relatives of a proband with hypertrophie cardiomyopathy.
In each of the 25 patients, the diagnosis of hypertrophic cardiomyopathy was established by echocardiographic demonstration of a hypertrophied, nondilated left ventricle in the absence of another cardiac or systemic disease that could produce comparable left ventricular hypertrophy.2 The presence of obstruction to the left ventricular outflow under basal conditions was assessed from the M-mode echocardiogram on the basis of the magnitude and duration of systolic anterior motion of the mitral valve.3 , 4 In each study patient, a clinical assessment of symptoms, echocardiographic measurements of the extent of hypertrophy, and Doppler measurements of diastolic function were obtained by the same investigator. Four study patients had mild systemic hypertension, which was not considered sufficiently severe to produce left ventricular hypertrophy of the magnitude observed.5 Follow-up data were available in all 25 study patients. In 24 patients, the period of follow-up ranged from 2.9 to 5.7 years (mean, 4.4). The remaining patient died of carcinoma of the pancreas five months after the initial echocardiographic examination.
During the period of the study (March 1983 to December 1985), five additional patients who had previously received a diagnosis of hypertrophic cardiomyopathy were referred to our cardiology department for additional clinical evaluation and treatment. Since these patients represented a hospital-referral population, they were excluded from the present investigation.
Echocardiography
The echocardiographic studies were performed with an Advanced Technology Laboratory Mark 300 mechanical sector scanner or a Hewlett–Packard 77020ACI phased-array sector scanner. The thickness of the anterior ventricular septum and the posterior free wall and the diastolic dimension of the left ventricular cavity were measured according to criteria described elsewhere.6 The overall extent and distribution of left ventricular hypertrophy were assessed with use of two-dimensional echocardiographic indexes reported elsewhere.7 8 9 Serial M-mode and two-dimensional echocardiographic measurements were obtained at the time of the initial and the most recent clinical examination in 24 of the 25 study patients.
The Doppler echocardiographic studies were recorded in 20 of the study patients with use of a Hewlett–Packard 77020ACI ultrasound imaging system. At the time of the Doppler study, 16 patients were taking no cardioactive medications or had discontinued such medications at least 48 hours before the examination; the remaining 4 patients were taking beta-blockers (2 patients) or calcium antagonists (2 patients). The 20 patients ranged in age from 18 to 75 years (mean ±SD, 44±14). None of the patients had a clinical history of systemic arterial hypertension. Blood pressure, measured by cuff sphygmomanometry at the time of the Doppler examination, was within the normal range in each patient. The Doppler transmitral flow-velocity profile was recorded simultaneously with a Lead II electrocardiogram and phonocardiogram, and the following measurements were obtained as described elsewhere10: duration of isovolumic relaxation,11 peak early diastolic flow velocity, rate of decrease of flow velocity in early diastole, peak late diastolic flow velocity, and ratio between the early and late peaks of flow velocity. These Doppler diastolic indexes have been shown previously to have satisfactory reproducibility.10 , 12 The results were compared with data obtained in 20 normal control subjects of similar age (mean age, 44±14 years; range, 16 to 73).13 The pattern of diastolic filling in a given patient was judged to be abnormal if one or more Doppler diastolic indexes exceeded the 95 percent confidence limits obtained in the control group.14
Ambulatory Electrocardiography
Continuous 24-to-48-hour ECG recordings were obtained in 21 of the 25 study patients (24-hour recordings were obtained in 8 patients and 48-hour recordings in 13). All cardioactive medications were discontinued at least 48 hours before ECG monitoring in 19 patients. The remaining 2 patients were taking medications at the time of the ECG recordings (1 was taking beta-blockers and the other was taking calcium antagonists). The ECG recordings were obtained with use of a portable tape recorder and modified V1 and V5 leads, and were analyzed with an American Edwards Laboratories 5000 system. Supraventricular or ventricular tachycardia was defined as three or more premature complexes in succession.
Review of the Literature
To compare the clinical features of our study population with the clinical picture of hypertrophic cardiomyopathy in the cardiology literature, we reviewed all articles on hypertrophic cardiomyopathy published between January 1983 and December 1987 in four cardiology journals (Circulation, the Journal of the American College of Cardiology, the American Journal of Cardiology, and the British Heart Journal) (see Appendix). Editorials, case reports, autopsy and surgical studies, and laboratory investigations were excluded from the analysis. We examined the remaining 78 studies and identified the following variables: the institution at which the study originated; the number, age, and sex of the patients studied; the prevalence of moderate-to-severe cardiac symptoms (New York Heart Association functional Class III or IV); the prevalence of subaortic obstruction under basal conditions, defined as a basal gradient of 30 mm Hg or more at cardiac catheterization, or prolonged mitral–septal contact during systole on M-mode echocardiography3 , 4; the thickness of the ventricular septum and posterior free wall; and the diastolic dimension of the left ventricular cavity (as assessed with M-mode echocardiography).
Statistical Methods
Data were expressed as means ±SD. The mean values for age and the echocardiographic measurements reported in the published studies were pooled and compared with those obtained in our study population. Differences between continuous variables were determined with use of the unpaired Student t-test. Differences between proportions were determined with use of the chi-square test or Fisher's exact test, as appropriate.
Results
Findings in the Study Population (Table 1Table 1
Clinical, Morphologic, and Functional Features of Hypertrophic Cardiomyopathy in an Outpatient Population and in 78 Published Studies.*)Clinical Findings
The age and sex distributions in our 25 study patients were similar and not significantly different from those reported in the literature. Cardiac symptoms were substantially less severe, however. Eighteen patients (72 percent) were asymptomatic, 6 (24 percent) had mild symptoms (New York Heart Association functional Class II), and only 1 patient (4 percent) had moderate-to-severe symptoms (Class III). Among the mildly symptomatic patients, the most common limiting symptom was dyspnea after moderate exertion (six patients). Less frequent symptoms included palpitations, chest pain, and presyncope. None of the patients had episodes of syncope. The only patient with severe symptoms was a 51-year-old woman with chronic atrial fibrillation and symptoms of fatigue and dyspnea after mild exertion. Subaortic obstruction under basal conditions, as assessed from M-mode echocardiography, was present in five study patients (20 percent). Three of these patients had mild cardiac symptoms, and two were asymptomatic.
Follow-up data were available in all 25 study patients. One patient died of carcinoma of the pancreas shortly after the diagnosis of hypertrophic cardiomyopathy was made. None of the others died or had clinical deterioration during a mean follow-up period of 4.4 years (range, 2.9 to 5.7). Of the six patients with mild symptoms (Class II), two improved to Class I with medical treatment (atenolol or verapamil), and four remained in Class II. The only patient who was severely symptomatic was in atrial fibrillation at the initial examination. This patient reverted to sinus rhythm and showed substantial improvement (to Class II) when therapy was changed from propranolol to amiodarone. The patient was still in sinus rhythm at the most recent examination.
Left Ventricular Morphology
At the initial examination, the septal and posterior free-wall thickness in our study patients did not differ significantly from the mean values reported in the literature (Table 1), whereas the diastolic dimension of the left ventricular cavity was greater than the mean published values (45±5 and 40±4 mm, respectively; P<0.001). Two-dimensional echocardiography was used to assess the overall extent and distribution of left ventricular hypertrophy.7 8 9 The maximal thickness of the left ventricular wall was 23±4 mm (range, 15 to 39), and the left ventricular wall-thickness index — a quantitative measurement of the extent of left ventricular hypertrophy derived from the sum of the wall thicknesses of the anterior septum, posterior septum, posterior free wall, and lateral free wall — was 71±18 mm. Both values are comparable to the mean values (21 and 65 mm, respectively) reported for these indexes in two previous studies performed at the National Heart, Lung, and Blood Institute in a total of 158 patients with hypertrophic cardiomyopathy.9 , 15 In the 24 study patients in whom serial echocardiograms were available, the cardiac dimensions at the most recent examination were not significantly different from those obtained initially. However, when the serial echocardiograms were analyzed with regard to individual patients, one patient did have a substantial increase in wall thickness (10 mm) in two of the four segments into which the left ventricle had been divided.16 The progression of hypertrophy occurred between the ages of 16 and 19; the patient remained asymptomatic throughout the period of follow-up. None of the remaining patients had an increase or a decrease in the left ventricular wall thickness of 5 mm or more.8
Left Ventricular Filling Patterns
The mean values for the Doppler diastolic indexes in 20 patients and 20 normal controls are shown in Table 2Table 2
Doppler Diastolic Indexes in 20 Outpatients with Hypertrophic Cardiomyopathy and 20 Normal Control Subjects.*. Because of the large standard deviation of the Doppler measurements in the patients with hypertrophic cardiomyopathy and the relatively small number of patients, none of the differences between the two groups attained statistical significance. However, when the data on individual patients were analyzed, one or more Doppler diastolic indexes in 12 of the 20 patients (60 percent) exceeded the 95 percent confidence limits obtained in the normal controls (Table 2). The most common diastolic abnormalities were prolonged isovolumic relaxation (six patients) and increased velocity of transmitral flow during atrial systole (six patients) — indicating, respectively, an impairment of the early phase of diastole and an increase in the atrial contribution to ventricular filling.10 , 14 The prevalence of abnormal Doppler patterns of diastolic filling in our patients was not significantly different from the 82 percent prevalence reported in a recent study of 111 patients with hypertrophic cardiomyopathy, in which the same Doppler diastolic indexes and criteria for normality were used.14 Ambulatory Electrocardiographic Findings
Of the 21 study patients in whom ambulatory ECG recordings were obtained, 7 (33 percent) had brief, asymptomatic episodes of supraventricular tachycardia (3 to 15 consecutive beats). Five patients (24 percent) had ventricular tachycardia (3 to 8 beats; mean, 4). Four of these five patients had a single run, and one had two runs. Each episode was asymptomatic and terminated spontaneously. The patients with only one run of ventricular tachycardia were not treated with antiarrhythmic medications. In the patient with two runs, ventricular tachycardia was abolished with flecainide (200 mg per day), as assessed on 48-hour ambulatory ECG recordings. None of the five patients with documented ventricular tachycardia died during a mean follow-up of four years (range, 3.2 to 5 years). The prevalence of ventricular tachycardia identified in our study population (24 percent) was similar to the prevalence reported in two leading studies (19 and 28 percent).17 , 18
Demographic Findings
An echocardiographic survey of all first-degree relatives in the families of the 25 patients was not performed. However, five of our patients had at least one first-degree relative who had been identified as having hypertrophic cardiomyopathy on the basis of clinical and echocardiographic findings.
Review of the Literature
From January 1983 to December 1987, 78 clinical studies of a total of 3404 patients with hypertrophic cardiomyopathy were published in Circulation, the Journal of the American College of Cardiology, the American Journal of Cardiology, and the British Heart Journal (Appendix and Table 1). Thirty-five of the 78 studies (45 percent), involving 2483 of the 3404 patients (73 percent), were performed at two centers: the National Heart, Lung, and Blood Institute (Bethesda, Md.) and the Royal Postgraduate Medical School (Hammersmith, London) (Table 3Table 3
Clinical Features of Patients with Hypertrophic Cardiomyopathy at Two Referral Centers* and Other Institutions, as Reported between January 1983 and December 1987 in Four Cardiology Journals.†). Of 1721 patients in whom data on the severity of cardiac symptoms were reported, 757 (44 percent) were severely symptomatic (New York Heart Association Class III or IV). However, 727 (96 percent) of these patients were studied at one of the same two referral institutions. Additional clinical, morphologic, and functional features of the patients with hypertrophic cardiomyopathy described in the 78 studies reviewed are summarized in Table 3.Discussion
Hypertrophic cardiomyopathy is a complex disease, characterized by a broad spectrum of morphologic and functional abnormalities.19 20 21 22 23 Although some patients with hypertrophic cardiomyopathy may be severely symptomatic or require surgical treatment,24 25 26 many others remain asymptomatic and unaware of their disease. In such patients, the diagnosis of hypertrophic cardiomyopathy is often first made in the course of routine examinations. Whenever the clinical presentation of a disease shows such great variability, patterns in patient referral and selection biases may have a major influence on the investigational findings. This may be particularly true in the case of hypertrophic cardiomyopathy, a disease that has been investigated mainly at referral institutions.
The present study reports the clinical, morphologic, and functional findings in a population of outpatients with hypertrophic cardiomyopathy. Although the age and sex distributions in our study patients were similar to those reported in the literature, their clinical presentation was substantially more favorable than that described in hospitalized study populations. More than 70 percent of the patients were asymptomatic, about 25 percent had mild symptoms, and only one patient had moderate-to-severe symptoms. None of the study patients died of cardiac causes or had clinical deterioration during a mean follow-up period of four years. This benign course contrasted with the clinical deterioration and 2-to-4-percent annual mortality rate reported in major clinical investigations.27 28 29 30 Despite this milder clinical presentation, the magnitude of left ventricular hypertrophy in our study patients was comparable to that described in the literature. The only morphologic difference was the presence of a larger left ventricular diastolic cavity — a factor that may have played a part in determining the lower severity of symptoms in our patients.
The pattern of left ventricular diastolic filling was abnormal in about 60 percent of our patients — a percentage similar to that reported recently in more than 100 patients with hypertrophic cardiomyopathy.14 This relatively high prevalence of diastolic abnormalities should not be considered inconsistent with the low prevalence of symptoms of cardiac failure observed in our study population, since diastolic abnormalities are frequently identified in asymptomatic patients with hypertrophic cardiomyopathy.14 Subaortic obstruction under basal conditions was present in 20 percent of our study patients, and ventricular tachycardia was identified during ambulatory ECG monitoring in 25 percent. Both figures are similar to those reported in the literature17 , 18 (and Appendix).
Although our outpatient population was small, our patients were carefully characterized, and their morphologic features, as well as the prevalence of diastolic filling abnormalities, subaortic obstruction, and complex ventricular arrhythmias, were similar to those reported in the literature. With regard to their clinical presentation, however, our study patients would seem to represent the mild end of the disease spectrum. Although the clinical features of outpatients with hypertrophic cardiomyopathy have not previously been described, the favorable clinical course identified in our patients is perhaps not surprising, since in many clinical disorders outpatient populations may have more favorable clinical features than the corresponding inpatient populations. Nevertheless, our findings raise the important question of how many patients with hypertrophic cardiomyopathy are never hospitalized and remain free of severe cardiac symptoms and functional limitation.
We reviewed the 78 clinical studies of hypertrophic cardiomyopathy published in four leading cardiology journals from 1983 through 1987 (Appendix). A total of 3404 patients were studied. However, almost 50 percent of the studies and over 70 percent of the patients came from one of two centers — the National Heart, Lung, and Blood Institute and the Royal Post-graduate Medical School. Severe cardiac symptoms were described in about 1700 patients, but more than 90 percent of these patients came from the same two referral institutions. In addition, given the large number of patients (almost 2500) described in the studies published over a relatively short period by these two institutions, it is possible that many patients were reported on more than once.
A large genetic study of almost 300 relatives of patients with hypertrophic cardiomyopathy31 provides indirect but convincing support for our hypothesis that the clinical features of the overall population of patients with this disease may be milder than those reported in the literature. More than 70 percent of the affected relatives in that study were asymptomatic, a figure that matches the percentage of asymptomatic patients identified in our outpatient population. On the other hand, more than 80 percent of the probands had cardiac symptoms and functional limitation. In conclusion, whereas the large body of studies performed at major referral institutions has undoubtedly increased our understanding of the pathophysiology of hypertrophic cardiomyopathy, our analysis suggests that patient-selection biases have probably led to misleading conclusions about the severity of the disease. Our findings in an outpatient population suggest that many such patients may have a better clinical course and prognosis than could be inferred from the current literature.
Source Information
From the Divisione di Cardiologia, Ente Ospedaliero Ospedali Galliera, Genoa, Italy. Address reprint requests to Dr. Spirito at the Divisione di Cardiologia, Ente Ospedaliero Ospedali Galliera, Via Volta 8, Genoa 16128, Italy.
Appendix
The 78 clinical studies of hypertrophic cardiomyopathy published in four leading cardiology journals from January 1983 through December 1987 are listed here in order of publication according to journal.
Circulation
1983
Spicer RL, Rocchini AP, Crowley DC, Vasiliades J, Rosenthal A. Hemodynamic effects of verapamil in children and adolescents with hypertrophic cardiomyopathy. 67:413–20.
Spirlto P, Maron BJ. Significance of left ventricular outflow tract cross-sectional area in hypertrophie cardiomyopathy: a two-dimensional echocardiographic assessment. 67:1100–8.
Ciró E, Nichols PF III, Maron BJ. Heterogeneous morphologic expression of genetically transmitted hypertrophic cardiomyopathy: two-dimensional echocardiographic analysis. 67:1227–33.
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. 68:282–93.
Bonow RO, Ostrow HG, Rosing DR, et al. Effects of verapamil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy: pressure-volume analysis with a nonimaging scintillation probe. 68:1062–73.
TenCate JF, Serruys PW, Mey S, Roelandt J. Effects of short-term administration of verapamil on left ventricular relaxation and filling dynamics measured by a combined hemodynamic-ultrasonic technique in patients with hypertrophic cardiomyopathy. 68:1274–9.
1984
Pollick C, Rakowski H, Wigle ED. Muscular subaortic stenosis: the quantitative relationship between systolic anterior motion and the pressure gradient. 69:43–9.
1985
Keren G, Belhassen B, Sherez J, et al. Apical hypertrophic cardiomyopathy: evaluation by noninvasive and invasive techniques in 23 patients. 71:45–56.
Cannon RO III, Rosing DR, Maron BJ, et al. Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. 71:234–43.
Spirito P, Maron BJ, Chiarella F, et al. Diastolic abnormalities in patients with hypertrophic cardiomyopathy: relation to magnitude of left ventricular hypertrophy, 72:310–6.
Bonow RO, Dilsizian V, Rosing DR, Maron BJ, Bacharach SL, Green MV. Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects. 72:853–64.
Betocchi S, Cannon RO III, Watson RM, et al. Effects of sublingual nifedipine on hemodynamics and systolic and diastolic function in patients with hypertrophic cardiomyopathy. 72:1001–7.
1986
Cannon RO III, Schenke WH, Bonow RO, Leon MB, Rosing DR. Left ventricular pulsus alternans in patients with hypertrophic cardiomyopathy and severe obstruction to left ventricular outflow. 73:276–85.
Hess OM, Murakami T, Krayenbuehl HP. Does verapamil improve left ventricular relaxation in patients with myocardial hypertrophy? 74:530–43.
Paulus WJ, Nellens P, Heyndrickx GR, Andries E. Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy. 74:544–54.
1987
O'Gara PT, Bonow RO, Maron BJ, et al. Myocardial perfusion abnormalities in patients with hypertrophic cardiomyopathy: assessment with thallium-201 emission computed tomography. 76:1214–23.
Journal of the American College of Cardiology
1983
Kaul S, Tei C, Shah PM. Interventricular septal and free wall dynamics in hypertrophic cardiomyopathy. 1:1024–30.
Shapiro LM, McKenna WJ. Distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy: a two-dimensional echocardiographic study. 2:437–44.
Kawai C, Yui Y, Hoshino T, Sasayama S, Matsumori A. Myocardial catecholamines in hypertrophic and dilated (congestive) cardiomyopathy: a biopsy study. 2:834–40.
Paulus WJ, Lorell BH, Craig WE, Wynne J, Murgo JP, Grossman W. Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation? 2:879–86.
1984
Alvares RF, Shaver JA, Gamble WH, Goodwin JF. Isovolumic relaxation period in hypertrophic cardiomyopathy. 3:71–81.
1985
Newman H, Sugrue D, Oakley CM, Goodwin JF, McKenna WJ. Relation of left ventricular function and prognosis in hypertrophic cardiomyopathy: an angiographic study. 5:1064–74.
Maron BJ, Gottdiener JS, Arce J, Rosing DR, Wesley YE, Epstein SE. Dynamic subaortic obstruction in hypertrophic cardiomyopathy: analysis by pulsed Doppler echocardiography. 6:1–15.
1986
Betocchi S, Bonow RO, Bacharach SL, Rosing DR, Maron BJ, Green MV. Isovolumic relaxation period in hypertrophic cardiomyopathy: assessment by radionuclide angiography. 7:74–81.
Takenaka K, Dabestani A, Gardin JM, et al. Left ventricular filling in hypertrophic cardiomyopathy: a pulsed Doppler echocardiographic study. 7:1263–71.
Louie EK, Maron BJ. Hypertrophic cardiomyopathy with extreme increase in left ventricular wall thickness: functional and morphologic features and clinical significance. 8:57–65.
Gidding SS, Snider AR, Rocchini AP, Peters J, Farnsworth R. Left ventricular diastolic filling in children with hypertrophic cardiomyopathy: assessment with pulsed Doppler echocardiography. 8:310–6.
Spirito P, Maron BJ, Bonow RO, Epstein SE. Severe functional limitation in patients with hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy. 8:537–44.
Yock PG, Hatte L, Popp RL. Patterns and timing of Doppler-detected intracavitary and aortic flow in hypertrophic cardiomyopathy. 8:1047–58.
1987
Fighali S, Krajcer Z, Edelman S, Leachman RD. Progression of hypertrophic cardiomyopathy into a hypokinetic left ventricle: higher incidence in patients with midventricular obstruction. 9:288–94.
Spirito P, Maron BJ. Absence of progression of left ventricular hypertrophy in adult patients with hypertrophic cardiomyopathy. 9:1013–7.
Iwase M, Sotobata I, Takagi S, Miyaguchi K, Jing HX, Yokota M. Effects of diltiazem on left ventricular diastolic behavior in patients with hypertrophic cardiomyopathy: evaluation with exercise pulsed Doppler echocardiography. 9:1099–105.
Bonow RO, Vitale DF, Maron BJ, Bacharach SL, Frederick TM, Green MV. Regional left ventricular asynchrony and impaired global left ventricular filling in hypertrophic cardiomyopathy: effect of verapamil. 9:1108–16.
Cannon RO III, Schenke WH, Maron BJ, et al. Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy. 10:53–62.
Maron BJ, Spirito P, Green KJ, Wesley YE, Bonow RO, Arce J. Noninvasive assessment of left ventricular diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy. 10:733–42.
Watson RM, Liberati Schwartz J, Maron BJ, Tucker E, Rosing DR, Josephson ME. Inducible polymorphic ventricular tachycardia and ventricular fibrillation in a subgroup of patients with hypertrophic cardiomyopathy at high risk for sudden death. 10:761–74.
American Journal of Cardiology
1983
Maron BJ, Wolfson JK, Ciro E, Spirito P. Relation of electrocardiographic abnormalities and patterns of left ventricular hypertrophy identified by 2-dimensional echocardiography in patients with hypertrophic cardiomyopathy. 51:189–94.
Bonow RO, Frederick TM, Bacharach SL, et al. Atrial systole and left ventricular filling in hypertrophic cardiomyopathy: effect of verapamil. 51:1386–91.
Hanrath P, Schluter M, Sonntag F, Diemert J, Bleifeld W. Influence of verapamil therapy on left ventricular performance at rest and during exercise in hypertrophic cardiomyopathy. 52:544–8.
Pouleur H, Rousseau MF, van Eyll C, Brasseur LA, Charlier AA. Force-velocity-length relations in hypertrophic cardiomyopathy: evidence of normal or depressed myocardial contractility. 52:813–7.
1984
Ciró E, Maione S, Giunta A, Maron BJ. Echocardiographic analysis of ventricular septal dynamics in hypertrophic cardiomyopathy and other diseases. 53:187–93.
Maron BJ, Nichols PF III, Pickle LW, Wesley YE, Mulvihill JJ. Patterns of inheritance in hypertrophic cardiomyopathy: assessment by M-mode and two-dimensional echocardiography. 53:1087–94.
Suzuki Y, Kadota K, Nohara R, et al. Recognition of regional hypertrophy in hypertrophic cardiomyopathy using thallium-201 emission-computed tomography: comparison with two-dimensional echocardiography. 53:1095–102.
Ciró E, Maron BJ, Bonow RO, Cannon RO, Epstein SE. Relation between marked changes in left ventricular outflow tract gradient and disease progression in hypertrophic cardiomyopathy. 53:1103–9.
Frank MJ, Watkins LO, Prisant LM, Stefadouros MA, Abdulla AM. Potentially lethal arrhythmias and their management in hypertrophic cardiomyopathy. 53:1608–13.
Spicer RL, Rocchini AP, Crowley DC, Rosenthal A. Chronic verapamil therapy in pediatric and young adult patients with hypertrophic cardiomyopathy. 53:1614–9.
McKenna WJ, Harris L, Rowland E, et al. Amiodarone for long-term management of patients with hypertrophic cardiomyopathy. 54:802–10.
Spirito P, Maron BJ. Patterns of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography. 54: 1039–46.
Suwa M, Hirota Y, Kawamura K. Improvement in left ventricular diastolic function during intravenous and oral diltiazem therapy in patients with hypertrophic cardiomyopathy: an echocardiographic study. 54:1047–53.
Sugrue DD, Dickie S, Myers MJ, Lavender JP, McKenna WJ. Effect of amiodarone on left ventricular ejection and filling in hypertrophic cardiomyopathy as assessed by radionuclide angiography. 54:1054–8.
1985
Higgins CB, Byrd BF III, Stark D, et al. Magnetic resonance imaging in hypertrophic cardiomyopathy. 55:1121–6.
Cokkinos DV, Krajcer Z, Leachman RD. Coronary artery disease in hypertrophic cardiomyopathy. 55:1437–8.
Gardin JM, Dabestani A, Glasgow GA, Butman S, Burn CS, Henry WL. Echocardiographic and Doppler flow observations in obstructed and nonobstructed hypertrophic cardiomyopathy. 56:614–21.
1986
Mulrow JP, Healy MJ, McKenna WJ. Variability of ventricular arrhythmias in hypertrophic cardiomyopathy and implications for treatment. 58:615–8.
Grose R, Strain J, Spindola-Franco H. Angiographic and hemodynamic correlations in hypertrophic cardiomyopathy with intracavitary systolic pressure gradients. 58:1085–92.
1987
Hada Y, Sakamoto T, Amano K, et al. Prevalence of hypertrophic cardiomyopathy in a population of adult Japanese workers as detected by echocardiographic screening. 59:183–4.
Unverferth DV, Schmidt WR II, Fertel RH. Cyclic nucleotide analysis of myocardial biopsies in hypertrophic cardiomyopathy. 59:185–6.
Bryg RJ, Pearson achéal, Williams GA, Labovitz AJ. Left ventricular systolic and diastolic flow abnormalities determined by Doppler echocardiography in obstructive hypertrophic cardiomyopathy. 59:925–31.
Nair CK, Kudesia V, Hansen D, et al. Echocardiographic and electrocardiographic characteristics of patients with hypertrophic cardiomyopathy with and without mitral anular calcium. 59:1428–30.
Spirito P, Maron BJ, Bonow RO, Epstein SE. Occurrence and significance of progressive left ventricular wall thinning and relative cavity dilatation in hypertrophic cardiomyopathy. 60:123–9.
Spirito P, Watson RM, Maron BJ. Relation between extent of left ventricular hypertrophy and occurrence of ventricular tachycardia in hypertrophic cardiomyopathy. 60:1137–42.
Theard MA, Bhatia SJ, Plappert T, St. John Sutton MG. Doppler echocardiographic study of the frequency and severity of aortic regurgitation in hypertrophic cardiomyopathy. 60:1143–7.
British Heart Journal
1983
Nagata S, Nimura Y, Beppu S, Park YD, Sakakibara H. Mechanism of systolic anterior motion of mitral valve and site of intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy. 49:234–43.
Thompson DS, Wilmshurst P, Juul SM, et al. Pressure-derived indices of left ventricular isovolumic relaxation in patients with hypertrophic cardiomyopathy. 49:259–67.
Emanuel R, Marcomichelakis J, Withers R, O'Brien K. Asymmetric septal hypertrophy and hypertrophic cardiomyopathy. 49:309–16.
Kinoshita N, Nimura Y, Okamoto M, Miyatake K, Nagata S, Sakakibara H. Mitral regurgitation in hypertrophic cardiomyopathy: non-invasive study by two dimensional Doppler echocardiography. 49:574–83.
Shapiro LM, Zezulka A. Hypertrophic cardiomyopathy: a common disease with a good prognosis: five year experience of a district general hospital. 50:530–3.
1984
Anderson DM, Raff GL, Ports TA, Brundage BH, Parmley WW, Chatterjee K. Hypertrophic obstructive cardiomyopathy: effects of acute and chronic verapamil treatment on left ventricular systolic and diastolic function. 51:523–9.
Stone DL, Petch MC, Verney GI, Dixon AK. Computed tomography in patients with hypertrophic cardiomyopathy. 52:136–9.
Sugrue DD, McKenna WJ, Dickie S, et al. Relation between left ventricular gradient and relative stroke volume ejected in early and late systole in hypertrophic cardiomyopathy: assessment with radionuclide cineangiography. 52:602–9.
1985
Siegel RJ, Criley JM. Comparison of ventricular emptying with and without a pressure gradient in patients with hypertrophic cardiomyopathy, 53:283–91.
Domenicucci S, Lazzeroni E, Roelandt J, et al. Progression of hypertrophic cardiomyopathy: a cross sectional echocardiographic study. 53:405–11.
McKenna WJ, Oakley CM, Krikler DM, Goodwin JF. Improved survival with amiodarone in patients with hypertrophic cardiomyopathy and ventricular tachycardia. 53:412–6.
Been M, Kean D, Smith MA, Douglas RH, Best JJ, Muir AL. Nuclear magnetic resonance in hypertrophic cardiomyopathy. 54:48–52.
Symons C, Fortune F, Greenbaum RA, Dandona P. Cardiac hypertrophy, hypertrophic cardiomyopathy, and hyperparathyroidism — an association. 54:539–42.
1986
Haugland H, Ohm OJ, Boman H, Thorsby E. Hypertrophic cardiomyopathy in three generations of a large Norwegian family: a clinical, echocardiographic, and genetic study. 55:168–75.
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Gherardo Finocchiaro, Bruno Pinamonti, Marco Merlo, Francesca Brun, Giulia Barbati, Gianfranco Sinagra. (2012) Prognostic role of clinical presentation in symptomatic patients with hypertrophic cardiomyopathy. Journal of Cardiovascular Medicine 13:12, 810-818
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Marina Di Domenico, Rita Casadonte, Pietroantonio Ricci, Mario Santini, Giacomo Frati, Antonietta Rizzo, Caterina Romano Carratelli, Monica Lamberti, Elvira Parrotta, Barbara Quaresima, Concetta M. Faniello, Francesco Costanzo, Giovanni Cuda. (2012) Cardiac and skeletal muscle expression of mutant β-myosin heavy chains, degree of functional impairment and phenotypic heterogeneity in hypertrophic cardiomyopathy. Journal of Cellular Physiology 227:10, 3471-3476
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Daniel Jacoby, William J. McKenna. (2012) Support for Routine Use of Metabolic Stress Testing in Hypertrophic Cardiomyopathy. The American Journal of Cardiology 109:10, 1534-1535
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Ronald E. Ross, Mark V. Sherrid, Mairead M. Casey, Daniel G. Swistel, Sandhya K. Balaram. (2012) Does Surgical Relief of Obstruction Improve Prognosis for Hypertrophic Cardiomyopathy?. Progress in Cardiovascular Diseases 54:6, 529-534
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Bernard J. Gersh, Barry J. Maron, Robert O. Bonow, Joseph A. Dearani, Michael A. Fifer, Mark S. Link, Srihari S. Naidu, Rick A. Nishimura, Steve R. Ommen, Harry Rakowski, Christine E. Seidman, Jeffrey A. Towbin, James E. Udelson, Clyde W. Yancy, Alice K. Jacobs, Sidney C. Smith, Jeffrey L. Anderson, Nancy M. Albert, Christopher E. Buller, Mark A. Creager, Steven M. Ettinger, Robert A. Guyton, Jonathan L. Halperin, Judith S. Hochman, Harlan M. Krumholz, Frederick G. Kushner, Rick A. Nishimura, E. Magnus Ohman, Richard L. Page, William G. Stevenson, Lynn G. Tarkington, Clyde W. Yancy. (2011) 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: Executive summary. The Journal of Thoracic and Cardiovascular Surgery 142:6, 1303-1338
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Bernard J. Gersh, Barry J. Maron, Robert O. Bonow, Joseph A. Dearani, Michael A. Fifer, Mark S. Link, Srihari S. Naidu, Rick A. Nishimura, Steve R. Ommen, Harry Rakowski, Christine E. Seidman, Jeffrey A. Towbin, James E. Udelson, Clyde W. Yancy, Alice K. Jacobs, Sidney C. Smith, Jeffrey L. Anderson, Nancy M. Albert, Christopher E. Buller, Mark A. Creager, Steven M. Ettinger, Robert A. Guyton, Jonathan L. Halperin, Judith S. Hochman, Harlan M. Krumholz, Frederick G. Kushner, Rick A. Nishimura, E. Magnus Ohman, Richard L. Page, William G. Stevenson, Lynn G. Tarkington, Clyde W. Yancy. (2011) 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy. The Journal of Thoracic and Cardiovascular Surgery 142:6, e153-e203
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Bernard J. Gersh, Barry J. Maron, Robert O. Bonow, Joseph A. Dearani, Michael A. Fifer, Mark S. Link, Srihari S. Naidu, Rick A. Nishimura, Steve R. Ommen, Harry Rakowski, Christine E. Seidman, Jeffrey A. Towbin, James E. Udelson, Clyde W. Yancy. (2011) 2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy. Journal of the American College of Cardiology
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Bernard J. Gersh, Barry J. Maron, Robert O. Bonow, Joseph A. Dearani, Michael A. Fifer, Mark S. Link, Srihari S. Naidu, Rick A. Nishimura, Steve R. Ommen, Harry Rakowski, Christine E. Seidman, Jeffrey A. Towbin, James E. Udelson, Clyde W. Yancy. (2011) 2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: Executive Summary. Journal of the American College of Cardiology
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Tomoko Tani, Toshikazu Yagi, Takeshi Kitai, Kitae Kim, Hitomi Nakamura, Toshiko Konda, Yoko Fujii, Junichi Kawai, Atsushi Kobori, Natsuhiko Ehara, Makoto Kinoshita, Shuichiro Kaji, Atsushi Yamamuro, Shigefumi Morioka, Toru Kita, Yutaka Furukawa. (2011) Left atrial volume predicts adverse cardiac and cerebrovascular events in patients with hypertrophic cardiomyopathy. Cardiovascular Ultrasound 9:1, 34
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Toru Kubo, Hiroaki Kitaoka, Makoto Okawa, Yoshihisa Matsumura, Nobuhiko Hitomi, Naohito Yamasaki, Takashi Furuno, Jun Takata, Masanori Nishinaga, Akinori Kimura, Yoshinori L. Doi. (2005) Lifelong Left Ventricular Remodeling of Hypertrophic Cardiomyopathy Caused by a Founder Frameshift Deletion Mutation in the Cardiac Myosin-Binding Protein C Gene Among Japanese. Journal of the American College of Cardiology 46:9, 1737-1743
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Franco Cecchi, Iacopo Olivotto, Sandro Betocchi, Claudio Rapezzi, Maria Rosa Conte, Gianfranco Sinagra, Elisabetta Zachara, Antonello Gavazzi, Roberto Rordorf, Gianfranco Carnemolla, Maurizio Porcu, Stefano Nistri, Paolo Gruppillo, Simona Giampaoli. (2005) The Italian registry for hypertrophic cardiomyopathy: A nationwide survey. American Heart Journal 150:5, 947-954
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