Verapamil therapy: a new approach to the pharmacologic treatment of hypertrophic cardiomyopathy. I. Hemodynamic effects.

Rosing, Douglas R.; Kent, Kenneth M.; Borer, J. S.; Seides, Stuart F.; Maron, B J; Epstein, Stephen E.

doi:10.1161/01.cir.60.6.1201

Cited by 189 publications

(20 citation statements)

References 25 publications

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“…i5 The question of the importance of disarray is still under discussion. [6][7][8] A summary of the subject states that disarray, at both histological and electronmicroscopical levels, is indicative but not pathognomonic of hypertrophic cardiomyopathy, and additional features such as gross asymmetric hypertrophy of the left ventricle must also be present. 19 The process of disarray must, however, start somewhere, and these events will first become evident at the electronmicroscopical level.…”

Section: Discussionmentioning

confidence: 99%

Role of calcium in the induction of cardiac hypertrophy and myofibrillar disarray. Experimental studies of a possible cause of hypertrophic cardiomyopathy.

Pearce¹,

Hawkey²,

Symons³

et al. 1985

Heart

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SUMMARY The role of calcium in the pathogenesis of hypertrophic cardiomyopathy was investigated experimentally. For this purpose the calcium antagonist verapamil and the calcium ionophore A23187 were administered to pregnant rats together with triac in order to observe their effect on triac induced myocardial disarray and hypertrophy in developing rat hearts. At a low dose verapamil reduced both the level of disarray and hypertrophy, but a higher dose produced hypertrophy when given alone. A23187 did not appreciably potentiate the actions of triac when given in combination but when administered alone produced both disarray and hypertrophy. Verapamil prevents the inward movement of calcium ions to the myocardial cell, whereas A23187 increases the inflow of calcium ions. The results suggest that the actions of triac in producing myocardial disarray and hypertrophy are attributable to an increased concentration of intracellular calcium.Hypertrophic cardiomyopathy, in common with all other cardiomyopathies, is of unknown aetiology.' It has been established that myofibrillar disarray is characteristic of hypertrophic cardiomyopathy,2 and it is likely that other cardiac muscle abnormalities, which permit firm morphological diagnosis,3 develop subsequently. Quantifiable ultrastructural changes, mimicking those seen in patients with hypertrophic cardiomyopathy, can be produced in the heart muscle of developing rats by administering triiodothyroacetic acid during pregnancy.4 This model, which was developed from observations that hypertrophic cardiomyopathy. can be associated with covert or overt hyperthyroidism,56 has been used to show that the deleterious effect of triac is due to an increase in cell membrane permeability.7 This study therefore suggested that an increased entry of calcium into the myocardial cells may be at least Requests for reprints to Dr E G J Olsen,

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Section: Discussionmentioning

confidence: 99%

Role of calcium in the induction of cardiac hypertrophy and myofibrillar disarray. Experimental studies of a possible cause of hypertrophic cardiomyopathy.

Pearce¹,

Hawkey²,

Symons³

et al. 1985

Heart

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“…An inappropriate calcium reuptake rate into the SR could therefore delay sarcomer relaxation (Gulch et ul., 1978;Nayler and Berry, 1975;Suko et al, 1970). This might explain the beneficial effect of calcium-entry blockers in improving relaxation and thereby early filling in HCM (Andersson et al, 1984;Bonow et al, 1981 b;Hess et al, 1983;Kaltenbach et ul., 1979;Rosing et al, 1979;Tendera, 1983). These drugs would reduce the amount of calcium entering the sarcolemma in systole, thereby also reducing the amount of calcium for reuptake into the SR in diastole.…”

Section: Dcm (mentioning

confidence: 99%

Noninvasive findings in patients with hypertrophic and dilative cardiomyopathy: A combined echocardiographic and radionuclide angiographic study

Bryhn

Persson

1986

Clinical Cardiology

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Summary: Fifteen patients with hypertrophic (HCM) and 15 with dilative cardiomyopathy (DCM) were examined with radionuclide angiography and M-mode echocardiography to evaluate the combination of two noninvasive methods for measuring left ventricular performance. The patients with HCM had delayed myocardial relaxation and rapid filling time with preserved peak rate of early ventricular filling. DCM patients, on the contrary, had low values of left ventricular systolic performance and low peak filling rate. Myocardial relaxation and rapid filling time, however, were short, indicating compensatory mechanisms in the failing ventricle improving rapid filling.

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“…[1][2][3] The impairment of left ventricular diastolic function in patients with HCM is closely related to intracellular Ca 2+ overload and is also known to be frequency dependent. 4 Therefore, calcium antagonists are a rational choice for the treatment of HCM and many studies have reported improvement of diastolic function with these agents.…”

mentioning

confidence: 99%

Antiarrhythmic Drug, Cibenzoline, can Directly Improve the Left Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

et al. 2001

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ypertrophic cardiomyopathy (HCM) is functionally characterized by normal or supernormal left ventricular systolic function and impaired left ventricular diastolic function, and the severity of left ventricular diastolic dysfunction is related to exercise capacity, clinical symptoms and even prognosis. [1][2][3] The impairment of left ventricular diastolic function in patients with HCM is closely related to intracellular Ca 2+ overload and is also known to be frequency dependent. 4 Therefore, calcium antagonists are a rational choice for the treatment of HCM and many studies have reported improvement of diastolic function with these agents. However, the effect of calcium antagonists is often insufficient in many patients with HCM.The class Ia antiarrhythmic drug, cibenzoline, is known to have a calcium channel-blocking property, 5,6 and it has recently been reported that cibenzoline can attenuate the left ventricular pressure gradient (LVPG) and also improve the transmitral Doppler flow patterns in patients with hypertrophic obstructive cardiomyopathy (HOCM). [7][8][9] However, it is unknown whether this beneficial effect on left ventricular diastolic function is due to a direct effect of cibenzoline or the result of attenuation of the LVPG. We therefore investigated whether cibenzoline directly improves Methods Study PatientsNineteen patients with HCM were enrolled after giving informed consent, and were divided into 12 cases of HOCM and 7 of HNCM (Table 1). The diagnosis of HCM was made by echocardiography based on the World Health Organization/International Society and Federation of Cardiology definition of cardiomyopathies. 10 HOCM was diagnosed when the HCM patient had a LVPG more than 30 mmHg without provocation. The LVPG, which was determined by the Doppler approach with the Bernoulli equation, 11 ranged between 41 and 154 mmHg. The level of obstruction was in the subaortic region in 9 patients and in the mid-left ventricular cavity in 3. One patient with a midventricular obstruction participated in this study after giving informed consent. Patients who had systemic hypertension, significant valvular heart disease, or any other systemic conditions that might cause cardiac hypertrophy were excluded. Study ProtocolEchocardiographic, mechanocardiographic and gated radionuclide angiographic studies were performed with 30

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Verapamil therapy: a new approach to the pharmacologic treatment of hypertrophic cardiomyopathy. I. Hemodynamic effects.

Cited by 189 publications

References 25 publications

Role of calcium in the induction of cardiac hypertrophy and myofibrillar disarray. Experimental studies of a possible cause of hypertrophic cardiomyopathy.

Role of calcium in the induction of cardiac hypertrophy and myofibrillar disarray. Experimental studies of a possible cause of hypertrophic cardiomyopathy.

Noninvasive findings in patients with hypertrophic and dilative cardiomyopathy: A combined echocardiographic and radionuclide angiographic study

Antiarrhythmic Drug, Cibenzoline, can Directly Improve the Left Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

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