Adverse hemodynamic and clinical effects of calcium channel blockade in pulmonary hypertension secondary to obliterative pulmonary vascular disease

M. Packer, N. Medina, M. Yushak

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Abstract

The hemodynamic and clinical responses to calcium channel blockade with verapamil and nifedipine were compared with those of hydralazine in 12 patients with pulmonary hypertension secondary to obliterative pulmonary vascular disease. All three drugs produced a marked and similar decrease in pulmonary vascular resistance; however, this was accompanied by a significant increase in cardiac index with hydralazine (+0.71 liter/min per m2, p < 0.01), no change in cardiac index with nifedipine and a significant decrease in cardiac index with verapamil (-0.25 liter/min per m2, p < 0.05). Mean pulmonary artery pressure decreased markedly with both calcium channel blockin drugs (-16.0 mm Hg with verapamil and -14.5 mm Hg with nifedipine, both p < 0.01), but this was associated with a concomitant increase in mean right arterial pressure (+6.2 mm Hg with verapamil and +4.4 mm Hg with nifedipine, both p < 0.01); neither variable changed after hydralazine. Hence, right ventricular performance (as reflected by right ventricular stroke work index) deteriorated during treatment with both calcium channel blocking drugs, despite the decrease in resistance to right ventricular ejection; in contrast, right ventricular stroke work index increased after hydralazine. The unfavorable hemodynamic effects of calcium channel blockade were accompanied by severe adverse clinical events, including profound hypotension and cardiogenic shock during acute drug administration and the exacerbation of right heart failure during long-term treatment. These deleterious responses to verapamil and nifedipine are likely the result of a direct depressant effect exerted by these drugs on right ventricular function independent of their pulmonary vasodilatory actions.

Original languageEnglish (US)
Pages (from-to)890-901
Number of pages12
JournalJournal of the American College of Cardiology
Volume4
Issue number5
StatePublished - 1984

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Calcium Channels
Nifedipine
Verapamil
Hydralazine
Vascular Diseases
Pulmonary Hypertension
Lung Diseases
Hemodynamics
Pharmaceutical Preparations
Stroke
Right Ventricular Function
Cardiogenic Shock
Calcium Channel Blockers
Vascular Resistance
Hypotension
Pulmonary Artery
Arterial Pressure
Heart Failure
Pressure
Lung

ASJC Scopus subject areas

  • Nursing(all)

Cite this

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title = "Adverse hemodynamic and clinical effects of calcium channel blockade in pulmonary hypertension secondary to obliterative pulmonary vascular disease",
abstract = "The hemodynamic and clinical responses to calcium channel blockade with verapamil and nifedipine were compared with those of hydralazine in 12 patients with pulmonary hypertension secondary to obliterative pulmonary vascular disease. All three drugs produced a marked and similar decrease in pulmonary vascular resistance; however, this was accompanied by a significant increase in cardiac index with hydralazine (+0.71 liter/min per m2, p < 0.01), no change in cardiac index with nifedipine and a significant decrease in cardiac index with verapamil (-0.25 liter/min per m2, p < 0.05). Mean pulmonary artery pressure decreased markedly with both calcium channel blockin drugs (-16.0 mm Hg with verapamil and -14.5 mm Hg with nifedipine, both p < 0.01), but this was associated with a concomitant increase in mean right arterial pressure (+6.2 mm Hg with verapamil and +4.4 mm Hg with nifedipine, both p < 0.01); neither variable changed after hydralazine. Hence, right ventricular performance (as reflected by right ventricular stroke work index) deteriorated during treatment with both calcium channel blocking drugs, despite the decrease in resistance to right ventricular ejection; in contrast, right ventricular stroke work index increased after hydralazine. The unfavorable hemodynamic effects of calcium channel blockade were accompanied by severe adverse clinical events, including profound hypotension and cardiogenic shock during acute drug administration and the exacerbation of right heart failure during long-term treatment. These deleterious responses to verapamil and nifedipine are likely the result of a direct depressant effect exerted by these drugs on right ventricular function independent of their pulmonary vasodilatory actions.",
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T1 - Adverse hemodynamic and clinical effects of calcium channel blockade in pulmonary hypertension secondary to obliterative pulmonary vascular disease

AU - Packer, M.

AU - Medina, N.

AU - Yushak, M.

PY - 1984

Y1 - 1984

N2 - The hemodynamic and clinical responses to calcium channel blockade with verapamil and nifedipine were compared with those of hydralazine in 12 patients with pulmonary hypertension secondary to obliterative pulmonary vascular disease. All three drugs produced a marked and similar decrease in pulmonary vascular resistance; however, this was accompanied by a significant increase in cardiac index with hydralazine (+0.71 liter/min per m2, p < 0.01), no change in cardiac index with nifedipine and a significant decrease in cardiac index with verapamil (-0.25 liter/min per m2, p < 0.05). Mean pulmonary artery pressure decreased markedly with both calcium channel blockin drugs (-16.0 mm Hg with verapamil and -14.5 mm Hg with nifedipine, both p < 0.01), but this was associated with a concomitant increase in mean right arterial pressure (+6.2 mm Hg with verapamil and +4.4 mm Hg with nifedipine, both p < 0.01); neither variable changed after hydralazine. Hence, right ventricular performance (as reflected by right ventricular stroke work index) deteriorated during treatment with both calcium channel blocking drugs, despite the decrease in resistance to right ventricular ejection; in contrast, right ventricular stroke work index increased after hydralazine. The unfavorable hemodynamic effects of calcium channel blockade were accompanied by severe adverse clinical events, including profound hypotension and cardiogenic shock during acute drug administration and the exacerbation of right heart failure during long-term treatment. These deleterious responses to verapamil and nifedipine are likely the result of a direct depressant effect exerted by these drugs on right ventricular function independent of their pulmonary vasodilatory actions.

AB - The hemodynamic and clinical responses to calcium channel blockade with verapamil and nifedipine were compared with those of hydralazine in 12 patients with pulmonary hypertension secondary to obliterative pulmonary vascular disease. All three drugs produced a marked and similar decrease in pulmonary vascular resistance; however, this was accompanied by a significant increase in cardiac index with hydralazine (+0.71 liter/min per m2, p < 0.01), no change in cardiac index with nifedipine and a significant decrease in cardiac index with verapamil (-0.25 liter/min per m2, p < 0.05). Mean pulmonary artery pressure decreased markedly with both calcium channel blockin drugs (-16.0 mm Hg with verapamil and -14.5 mm Hg with nifedipine, both p < 0.01), but this was associated with a concomitant increase in mean right arterial pressure (+6.2 mm Hg with verapamil and +4.4 mm Hg with nifedipine, both p < 0.01); neither variable changed after hydralazine. Hence, right ventricular performance (as reflected by right ventricular stroke work index) deteriorated during treatment with both calcium channel blocking drugs, despite the decrease in resistance to right ventricular ejection; in contrast, right ventricular stroke work index increased after hydralazine. The unfavorable hemodynamic effects of calcium channel blockade were accompanied by severe adverse clinical events, including profound hypotension and cardiogenic shock during acute drug administration and the exacerbation of right heart failure during long-term treatment. These deleterious responses to verapamil and nifedipine are likely the result of a direct depressant effect exerted by these drugs on right ventricular function independent of their pulmonary vasodilatory actions.

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