TY - JOUR
T1 - Use of calcium-channel blocking drugs in hypertrophic cardiomyopathy
AU - Rosing, Douglas R.
AU - Idänpään-Heikkilä, Ulla
AU - Maron, Barry J.
AU - Bonow, Robert O.
AU - Epstein, Stephen E.
N1 - Funding Information:
From the National Heart, Lung, and Blood Instiie, the National Institutes of Health, Bethesda, Maryland.
PY - 1985/1/25
Y1 - 1985/1/25
N2 - Verapamil exerts a wide spectrum of hemodynamic effects in patients with hypertrophic cardiomyopathy (HC), and its administration offers an important alternative to β-receptor blocker therapy in such patients. The intravenous administration of verapamil to 62 patients in the catheterization laboratory decreased systolic blood pressure from 118 ± 17 to 102 ± 17 mm Hg (p <0.001). It had no significant effect on heart rate, mean pulmonary artery wedge pressure, left ventricular (LV) end-diastolic pressure or cardiac output; however, LV outflow gradient in the basal state decreased from 62 ± 34 to 29 ± 34 mm Hg (p <0.05). These findings demonstrate a decrease in LV outflow tract obstruction. Radionuclide angiography indicated the major action responsible for the reduction in obstruction appears to be an improvement in LV diastolic function. Short-term nifedipine administration to patients with HC produced no significant effect on LV outflow tract gradients and early diastolic filling. Short-term double-blind studies showed that verapamil improved exercise time by 26 ± 35% (p <0.005) compared with placebo, whereas propranolol improved it by 21 ± 35% (p <0.025). In a separate study, verapamil improved exercise duration by 38 ± 58% (p = 0.02) compared with placebo, whereas nifedipine improved it by 20 ± 47% (difference is not significant). Verapamil resulted in a more beneficial s ubjective symptomatic response than propranolol or nifedipine when compared with placebo. Long-term verapamil therapy was instituted in 227 patients; 133 of these patients have continued taking the medication for an average of 25 ± 13 months because their quality of life improved compared with what they experienced with their former therapy (usually β blocker). Improved exercise capacity of 40% has been maintained in 32 patients for 2 years. A decrease in ventricular septal thickness of 1.5 ± 2.6 mm was also found in 32 patients studied after 39 ± 8 months of verapamil therapy. Nine patients died during follow-up study, but it is unclear whether the drug increased survival or, conversely, whether any of the deaths could be attributed to verapamil administration. Significant adverse electrophysiologic and hemodynamic effects were seen in 59 instances. The electrophysiologic events, atrioventricular block and sinus arrest, were definitely verapamil-related, but it is uncertain how many of the hemodynamic problems of hypotension and pulmonary congestion were drug-related. It was necessary to discontinue verapamil in only 7% of patients because of adverse effects. These studies indicate that verapamil offers an important alternative to β-blocker therapy in selected patients with HC.
AB - Verapamil exerts a wide spectrum of hemodynamic effects in patients with hypertrophic cardiomyopathy (HC), and its administration offers an important alternative to β-receptor blocker therapy in such patients. The intravenous administration of verapamil to 62 patients in the catheterization laboratory decreased systolic blood pressure from 118 ± 17 to 102 ± 17 mm Hg (p <0.001). It had no significant effect on heart rate, mean pulmonary artery wedge pressure, left ventricular (LV) end-diastolic pressure or cardiac output; however, LV outflow gradient in the basal state decreased from 62 ± 34 to 29 ± 34 mm Hg (p <0.05). These findings demonstrate a decrease in LV outflow tract obstruction. Radionuclide angiography indicated the major action responsible for the reduction in obstruction appears to be an improvement in LV diastolic function. Short-term nifedipine administration to patients with HC produced no significant effect on LV outflow tract gradients and early diastolic filling. Short-term double-blind studies showed that verapamil improved exercise time by 26 ± 35% (p <0.005) compared with placebo, whereas propranolol improved it by 21 ± 35% (p <0.025). In a separate study, verapamil improved exercise duration by 38 ± 58% (p = 0.02) compared with placebo, whereas nifedipine improved it by 20 ± 47% (difference is not significant). Verapamil resulted in a more beneficial s ubjective symptomatic response than propranolol or nifedipine when compared with placebo. Long-term verapamil therapy was instituted in 227 patients; 133 of these patients have continued taking the medication for an average of 25 ± 13 months because their quality of life improved compared with what they experienced with their former therapy (usually β blocker). Improved exercise capacity of 40% has been maintained in 32 patients for 2 years. A decrease in ventricular septal thickness of 1.5 ± 2.6 mm was also found in 32 patients studied after 39 ± 8 months of verapamil therapy. Nine patients died during follow-up study, but it is unclear whether the drug increased survival or, conversely, whether any of the deaths could be attributed to verapamil administration. Significant adverse electrophysiologic and hemodynamic effects were seen in 59 instances. The electrophysiologic events, atrioventricular block and sinus arrest, were definitely verapamil-related, but it is uncertain how many of the hemodynamic problems of hypotension and pulmonary congestion were drug-related. It was necessary to discontinue verapamil in only 7% of patients because of adverse effects. These studies indicate that verapamil offers an important alternative to β-blocker therapy in selected patients with HC.
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U2 - 10.1016/0002-9149(85)90630-7
DO - 10.1016/0002-9149(85)90630-7
M3 - Article
C2 - 3881913
AN - SCOPUS:0021905610
SN - 0002-9149
VL - 55
SP - B185-B195
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 3
ER -