Treatment of hypertrophic obstructive cardiomyopathy with verapamil.

Kaltenbach, M.; Hopf, R.; Kober, G.; Bussmann, W.‐D.; Keller, Michael; Petersen, Yvonne

doi:10.1136/hrt.42.1.35

Cited by 198 publications

(20 citation statements)

References 8 publications

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“…Reduction of left ventricular hypertrophy, as is evidenced on ECG, chest X-ray and cineangiography, has been reported as an effect of prolonged verapamil treatment.18), 19) The effect may be mediated through the drug action to reduce outflow gradient.57) In the present series, however, CTR increased markedly in 1 of the 4 patients with verapamil (Fig. 3).…”

Section: Discussionsupporting

confidence: 55%

Long-term Clinical Effect of Calcium Inhibitors in Hypertrophic Cardiomyopathy Compared to the Effect of Beta-blocking Agents

et al. 1981

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SUMMARYLong-term clinical effects of beta-blockers (propranolol in most cases) and calcium inhibitors (nifedipine in most cases) were studied in 16 patients with hypertrophic cardiomyopathy.On overall subjective symptoms, beta-blockers were effective in 50% of symptomatic patients, while calcium inhibitors were effective in only 33%. On angina pectoris, however, calcium inhibitors were superior to beta-blockers in our patients. Blood pressure decreased with each drug, and the decrease was significant with nifedipine. Otherwise there was no change in physical findings with either drug.Long-term (more than 6 months) use of beta-blockers resulted in an increase in cardiothoracic ratio on chest X-ray, a decrease in left ventricular ejection fraction on echocardiogram and more pronounced ST-T change on electrocardiogram. Prolonged use of nifedipine resulted in a slight decrease in cardiothoracic ratio, but no systematic change on echocardiogram and on electrocardiogram.

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Section: Discussionsupporting

confidence: 55%

Long-term Clinical Effect of Calcium Inhibitors in Hypertrophic Cardiomyopathy Compared to the Effect of Beta-blocking Agents

et al. 1981

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“…In the 1970s, calcium antagonists, mainly verapamil were used for the treatment of patients with HOCM. Kaltenbach et al reported that the long-term use of verapamil improved the clinical symptoms and LV function in patients with HOCM [50]. It is acknowledged that verapamil improves LV diastolic function in the early diastolic phase [51][52][53].…”

Section: Calcium Antagonistsmentioning

confidence: 99%

Advances in medical treatment of hypertrophic cardiomyopathy

Hamada

Ikeda

Shigematsu

2014

Journal of Cardiology

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We reviewed the natural history of patients with hypertrophic cardiomyopathy (HCM). The effect of medical treatments on natural history, left ventricular (LV) functions and LV remodeling was also evaluated. Sudden cardiac death and end-stage heart failure are the most serious complications of HCM. Age <30 years and a family history of sudden premature death are risk factors for sudden cardiac death in HCM patients. End-stage heart failure is not a specific additional phenomenon observed in patients with HCM, but is the natural course of the disease in most of those patients. After the occurrence of heart failure, the progression to cardiac death is very rapid. Young age at diagnosis, a family history of HCM, and greater wall thickness are associated with a greater likelihood of developing end-stage heart failure. Neither beta-blockers nor calcium antagonists can prevent this transition. The class Ia antiarrhythmic drugs, disopyramide and cibenzoline are useful for the reduction of LV pressure gradient. Unlike disopyramide, cibenzoline has little anticholinergic activity; therefore, this drug can be easily adapted to long-term use. In addition to the reduction in LV pressure gradient, cibenzoline can improve LV diastolic dysfunction, and induce regression of LV hypertrophy in patients with HCM. A decrease in intracellular Ca(2+) concentration through the activation of the Na(+)/Ca(2+) exchanger associated with cibenzoline therapy is likely to be closely related with the improvement in HCM-related disorders. It is possible that cibenzoline can prevent the progression from typical HCM to end-stage heart failure.

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“…Calpain activity may be elevated in cardiomyocytes with raised intracellular Ca 2+ . The fact that the cardioselective Ca 2+ entry blocker, verapamil, 29 or long‐acting, third generation dihydropyridine Ca 2+ entry blocker, amlodipine, is beneficial for DCM treatment, 30 confirms the adverse effect of elevated Ca 2+ concentration in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 94%