Circulation, Vol 76, 135-141, Copyright © 1987 by American Heart Association
S Rich and BH Brundage
In an attempt to produce substantial reductions in pulmonary arterial
pressure and pulmonary vascular resistance in patients with primary
pulmonary hypertension, a new treatment strategy using high doses of
calcium channel-blocking drugs was developed. Thirteen patients were given
an initial test dose of 60 mg diltiazem or 20 mg nifedipine followed by
consecutive hourly doses until a 50% fall in pulmonary vascular resistance
and 33% fall in pulmonary arterial pressure was achieved or untoward side
effects developed. The initial drug challenges failed to produce
significant reductions in mean pulmonary arterial pressure or pulmonary
vascular resistance. In eight of 13 patients, continued hourly doses
produced a reduction in mean pulmonary arterial pressure of 48% (61 to 35
mm Hg, p less than .01) and a reduction in pulmonary vascular resistance of
60% (15 to 6 units, p less than .01). These patients were discharged on
high-dose (up to 720 mg/day diltiazem or 240 mg/day nifedipine) calcium
channel-blocking drugs as long-term therapy. Five patients have returned
for restudy after 1 year. In four of five the reductions in pulmonary
arterial pressure and pulmonary vascular resistance were sustained and were
associated with regression of right ventricular hypertrophy as assessed by
electrocardiography and echocardiography. One patient who reduced her dose
to a conventional level had a return of her pulmonary arterial pressure and
pulmonary vascular resistance toward previous levels. We conclude that
substantial reductions in pulmonary arterial pressure and pulmonary
vascular resistance that are associated with regression of right
ventricular hypertrophy are possible in some patients with primary
pulmonary hypertension by use of calcium channel-blocking drugs.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
High-dose calcium channel-blocking therapy for primary pulmonary hypertension: evidence for long-term reduction in pulmonary arterial pressure and regression of right ventricular hypertrophy
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