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Treatment of Primary Pulmonary Hypertension with Nifedipine: A Hemodynamic and Scintigraphic Evaluation

[+] Article, Author, and Disclosure Information

Grant support by grants MOI-RR00633, ROIHL27950, and Ischemia SCOR grant HL-17669 from the National Institutes of Health; and the Betty Crossman Marcus Memorial Fund for Pulmonary Research. Dr. Hillis is an Established Investigator of the American Heart Association.

▸Requests for reprints should be addressed to Lewis J. Rubin, M.D.; Pulmonary Division 111F, Dallas Veterans Administration Medical Center, 4500 South Lancaster Road; Dallas, TX 75216.

Dallas, Texas

© 1983 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1983;99(4):433-438. doi:10.7326/0003-4819-99-4-433
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To evaluate the potential value of nifedipine treatment for primary pulmonary hypertension, hemodynamic and scintigraphic measurements were made before and 15 to 30 minutes after nifedipine, 10 to 20 mg, was given sublingually to nine patients. Nifedipine treatment increased cardiac output (mean ± SD, 3.6 ± 1.7 to 5.3 ± 2.8 L/min, p < 0.001) and decreased mean aortic pressure (99 ± 19 to 85 ± 12 mm Hg, p < 0.001) and total pulmonary and total systemic resistances (1605 ± 787 to 1025 ± 540 dyn · s · cm-5 and 2761 ± 1557 to 1591 ± 823 dyn · s · cm-5, respectively; p < 0.005). Heart rate and mean pulmonary arterial pressure did not change significantly. Right ventricular end-diastolic volume decreased 10% (p = 0.01), end-systolic volume decreased 15% (p < 0.01), and right ventricular ejection fraction increased 18% (p < 0.05) in eight patients. After 4 to 14 months (mean, 7.3 ± 3.8) of treatment with nifedipine, 40 to 120 mg/d, in six patients, cardiac output increased (3.6 ± 2.0 to 5.0 ± 1.8 L/min, p < 0.01) and total pulmonary resistance decreased (1572 ± 730 to 987 ± 586 dyn · s · cm-5, p = 0.025), whereas pulmonary arterial pressure remained unchanged (59 ± 23.2 to 55 ± 28.6 mm Hg, p > 0.05) compared with baseline values. We conclude that nifedipine therapy may be useful in the chronic management of patients with primary pulmonary hypertension.





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