This study suggests that high doses of calcium-channel blockers in patients with primary pulmonary hypertension who respond with reductions in pulmonary-artery pressure and pulmonary vascular resistance may improve survival over a five-year period.
Neurohormonal activation occurs in patients with isolated right ventricular failure and inherently normal left ventricles and appears to be related to the overall severity of cardiopulmonary derangements. The elevation in endothelin levels is consistent with its release in response to pulmonary hypertension.
Forty-seven patients with primary pulmonary hypertension were evaluated with a dose titration protocol utilizing nifedipine (20 mg orally) or diltiazem (60 mg orally) given every hour until maximal effectiveness was achieved. Of the patients tested, 15 (32%) had a greater than 20% reduction in pulmonary artery pressure (mean 36.2 +/- 8%, p less than 0.01) and pulmonary vascular resistance (mean 50.2 +/- 7%, p less than 0.01) (pressure responders). Nineteen (40%) had a greater than 20% reduction in pulmonary vascular resistance (mean 25.2 +/- 12%, p less than 0.01), with less than a 20% decrease in pulmonary artery pressure (resistance responders). Ten had no significant change in pulmonary artery pressure or pulmonary vascular resistance (nonresponders), and three were unable to tolerate the calcium channel blocking agents. No hemodynamic profile allowed prediction of the type of response to these agents. No mortality or serious morbidity was associated with the drug testing. These findings indicate that calcium channel blockers, when titrated to maximally effective doses, may cause substantial reductions in pulmonary artery pressure and pulmonary vascular resistance in patients with primary pulmonary hypertension. Testing with hemodynamic monitoring is necessary to ascertain which patients will respond. Patients with primary pulmonary hypertension are able to tolerate short-term administration of high doses of calcium channel blockers.
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