Echocardiographic Measurement of the Left Ventricular Outflow Gradient in Idiopathic Hypertrophic Subaortic Stenosis

Wl, Henry; Ce, Clark; Dl, Glancy; Se, Epstein

doi:10.1056/nejm197305102881903

Cited by 199 publications

(34 citation statements)

References 17 publications

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“…"2 13 In addi-tion, a certain number of patients affected by VSD and free of all symptoms may not be recognized or may avoid seeing physicians, and thus escape medical statistics. 3 This study endeavors to give further information about this late evolution.…”

Section: Discussionmentioning

confidence: 99%

Hypercontractile cardiac states simulating hypertrophic cardiomyopathy.

Come¹,

Bulkley²,

Goodman³

et al. 1977

Circulation

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SUMMARY Hypertrophic cardiomyopathy (HCM) or idiopathic hypertrophic subaortic stenosis (IHSS) has been defined as an autosomal dominant myocardial disease characterized by specific physical findings, echocardiographic features, asymmetric septal hypertrophy and disordered myocardial architecture. Echocardiographic and scintiphotographic studies failed to reveal evidence of asymmetric septal hypertrophy in four patients with systolic anterior movement of the mitral valve and the typical auscultatory and HYPERTROPHIC CARDIOMYOPATHY (HCM) or idiopathic hypertrophic subaortic stenosis (IHSS) has been defined by certain physical findings," 2 and characteristic hemodynamic," 2 angiographicl'3 and pathologic abnormalities.1' 2, 4-7 Echocardiography provides a valuable noninvasive means of recognizing HCM and, in many institutions, has replaced catheterization as a means of confirming clinical diagnoses. Major echocardiographic features of HCM include abnormal thickness8" of the interventricular septum which is asymmetrically hypertrophied relative to the left ventricular free wall,9-1" systolic anterior movement of the mitral valve'2, '3 and reduction of systolic septal thickening and amplitude of systolic septal excursion.8 Myocardial imaging with a radioactive tracer, thallium 201,'4 has also demonstrated the presence of disproportionate septal thickness and appears to be an additional noninvasive means of diagnosing HCM, particularly when adequate echocardiographic definition of the interventricular septum is not feasible technically.A unified concept of hypertrophic cardiomyopathy as an autosomal dominant myocardial disease characterized by asymmetric septal hypertrophy and disordered myocardial architecture has been proposed.2'" This paper reports four patients with typical physical findings of HCM and echocardiographic documentation of systolic anterior movement of the mitral valve in whom a combination of echocardiographic and scintiphotographic studies and, in one instance, postmortem examination failed to demonstrate asymmetric septal hypertrophy. Systolic anterior movement of the mitral valve and the auscultatory and peripheral pulse abnormalities characteristic of HCM do not therefore appear to be specific for the autosomal dominant myocardial dis- ease characterized by asymmetric septal hypertrophy and abnormal septal histology. Materials and Methods Echocardiographic StudiesThe echocardiographic examinations were performed with a Smith-Kline Ekoline 20 A Ultrasonoscope using a 0.5 inch diameter, 2.25 MHz transducer focused at 7.5 cm. The echocardiograms were recorded on a Cambridge strip chart recorder or Honeywell direct writing recorder (patient 3). Standard techniques were employed to record tracings from the anterior and posterior mitral leaflets and from the septum and posterior wall just below the mitral leaflets. Systolic and end-diastolic cavity dimensions and septal and posterior wall thicknesses were measured at this level,"5 and the ratio of end-diastolic septal to posterior wall thickness calc...

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Section: Discussionmentioning

confidence: 99%

Hypercontractile cardiac states simulating hypertrophic cardiomyopathy.

Come¹,

Bulkley²,

Goodman³

et al. 1977

Circulation

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“…Because of the lack of important symptoms, the patients did not routinely undergo cardiac catheterization as part of this protocol. The presence of left ventricular outflow obstruction was assessed at cardiac catheterization in three patients and from the M-mode echocardiogram, based on the magnitude and duration of systolic anterior motion of the mitral valve, 14,15 in the other 26 patients. Eleven patients (38%) had evidence of resting left ventricular outflow obstruction.…”

Section: Patient Selectionmentioning

confidence: 99%

“…Thus, the verapamil dosage at the time of repeat study ranged from 240 to 480 mg/day (mean, 453), and this dosage was maintained for a mean of 6.7 days (range, 2-56) before the repeat study. The verapamil studies were performed [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] weeks (mean, 6±5) after the initial control studies.…”

Section: Study Protocolmentioning

confidence: 99%

Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy.

et al. 1989

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Recent studies indicate that reversible 201Tl perfusion defects, compatible with silent myocardial ischemia, commonly develop during exercise in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy (HCM). To determine whether this represents a dynamic process that may be modified favorably by medical therapy, we studied 29 asymptomatic or minimally symptomatic patients with HCM, aged 12-55 years (mean, 28), with exercise 201Tl emission computed tomography under control conditions and again after 1 week of oral verapamil (mean dosage, 453 mg/day). Treadmill time increased slightly during verapamil (21.0 +/- 3.6 to 21.9 +/- 2.7 minutes, p less than 0.005), but peak heart rate-blood pressure product was unchanged (26.3 +/- 6.0 X 10(3) compared with 25.0 +/- 6.4 X 10(3). Two midventricular short-axis images per study were divided into five regions each, and each of these 10 regions was then analyzed on a 0-2 scale by three observers blinded with regard to the patients' therapy. Average regional scores of 1.5 or less were considered to represent perfusion defects, and a change in regional score of 0.5 or more was considered to constitute a significant change. During control studies, 15 patients (52%) developed perfusion defects with exercise (average, 3.7 regions per patient). In 14 of these patients, all perfusion defects completely reversed after 3 hours of rest; one patient had fixed defects. After administration of verapamil, exercise perfusion scores improved in 10 of the 14 patients (71%) with reversible defects; there was overall improvement in 34 of 50 (68%) regions with initially reversible perfusion defects.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Hence, to include a meaningful number of study patients, we relied on echocardiographic identification of systolic anterior motion (SAM) of the anterior mitral leaflet to confirm the hemodynamic results in those patients in whom cardiac catheterization was carried out more than 2.5 years before monitoring, and to include an additional 33 patients in the study who were not catheterized, but in whom the mitral valve could be adequately recorded by echocardiography to determine the presence or absence of SAM. The magnitude of obstruction was estimated by previously described echocardiographic methods based on the degree of approximation of the anterior mitral leaflet to the ventricular septum.3 9 Mean age of the patients with and without obstruction was the same (38 + 2 years (SEM), ranges 9-65 and 12-64 years, respectively). None of the patients had undergone cardiac operation before electrocardiographic monitoring.…”

mentioning

confidence: 99%

Prevalence of arrhythmias during 24-hour electrocardiographic monitoring and exercise testing in patients with obstructive and nonobstructive hypertrophic cardiomyopathy.

Savage¹,

Seides²,

Maron³

et al. 1979

Circulation

229

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SUMMARY Many patients with hypertrophic cardiomyopathy die suddenly and unexpectedly, a significant number perhaps due to arrhythmia. Of 100 patients initially evaluated for signs or symptoms suggestive of heart disease or a family history of hypertrophic cardiomyopathy, 51 were selected solely because they met the echocardiographic criteria for the disease, and 49 patients were selected primarily because they had: 1) normal sinus rhythm despite left atrial enlargement, 2) a history of syncope, 3) a family history of premature death, or 4) a history of paroxysmal atrial fibrillation. All 100 patients were studied by 24-hour ambulatory electrocardiographic monitoring and 74 of them also underwent treadmill exercise testing. More than 50% of patients in all subgroups (with or without symptoms or left ventricular outflow tract obstruction) had multiform or repetitive ventricular premature depolarizations, including 19% who had ventricular tachycardia. Monitoring was superior to exercise testing for exposing these arrhythmias. Two patients experienced cardiac arrest within 2 months of monitoring; in each, monitoring had revealed ventricular tachycardia. Two patients with paroxysms of supraventricular tachycardia during monitoring developed fixed atrial fibrillation within 1 year. These preliminary observations suggest that monitoring may help identify patients at increased risk for significant arrhythmic events.MANY SYMPTOMATIC PATIENTS with hypertrophic cardiomyopathy die suddenly and unexpectedly during the course of their disease.'`' We have identified several people with hypertrophic cardiomyopathy in whom sudden death was the initial manifestation of disease.5 Despite the clinical importance of this problem and the likelihood that many of these sudden deaths are arrhythmic in origin,6 surprisingly little is known about the propensity of patients with hypertrophic cardiomyopathy to develop arrhythmias.In the present investigation we used 24-hour ambulatory electrocardiographic monitoring and treadmill exercise testing to examine the frequency and types of arrhythmias that occur in a large population of patients with hypertrophic cardiomyopathy. We sought to determine whether subgroups of patients with this disease are particularly susceptible to the development of arrhythmias. We also compared the sensitivity of 24-hour ambulatory electrocardiographic monitoring with that of treadmill exercise testing in detecting arrhythmias. Finally, we made a preliminary attempt to determine whether any electrocardiographic findings were predictive of subsequent mortality.From the Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20014. Presented in part at the 50th Annual Scientific Sessions, American Heart Association, Miami Beach, Florida, November, Methods Patient PopulationOne hundred patients with hypertrophic cardiomyopathy (asymmetric septal hypertrophy (ASH)) were studied after informed consent was secured. ASH was defined echocardiographically by a ven...

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Echocardiographic Measurement of the Left Ventricular Outflow Gradient in Idiopathic Hypertrophic Subaortic Stenosis

Cited by 199 publications

References 17 publications

Hypercontractile cardiac states simulating hypertrophic cardiomyopathy.

Hypercontractile cardiac states simulating hypertrophic cardiomyopathy.

Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy.

Prevalence of arrhythmias during 24-hour electrocardiographic monitoring and exercise testing in patients with obstructive and nonobstructive hypertrophic cardiomyopathy.

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