Rest and exercise hemodynamic effects of oral hydralazine in patients with coronary artery disease and left ventricular dysfunction.
Author(s) -
Michael C. Hindman,
David Slosky,
Robert H. Peter,
G E Newman,
Robert H. Jones,
A G Wallace
Publication year - 1980
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.61.4.751
Subject(s) - medicine , hydralazine , afterload , cardiology , arteriovenous oxygen difference , cardiac output , hemodynamics , ejection fraction , coronary artery disease , angina , stroke volume , blood pressure , heart failure , myocardial infarction
To determine the hemodynamic effects of afterload reduction at rest and during upright exercise in patients with coronary artery disease and left ventricular dysfunction, 12 patients were studied before and after taking 50-75 mg of oral hydralazine every 6 hours for 48 hours. Oxygen consumption and heart rate were unchanged from control both at rest and during two work loads on a bicycle ergometer. Cardiac output was significantly increased at rest and during both workloads. The arteriovenous oxygen difference was significantly reduced at rest and during exercise. Pulmonary capillary wedge pressure was also significantly lower at rest and during exercise. Systemic vascular resistance was reduced at rest, and exercise-induced vasodilation was augmented by the administration of hydralazine. Left ventricular end-diastolic volume and ejection fraction assessed by radionuclide angiocardiography were not significantly changed at rest or during exercise after hydralazine. Seven of the 12 patients have maintained clinical improvement during a follow-up of 6-12 months. Hemodynamic improvement provided by oral hydralazine at rest is maintained during moderate exertion in patients with coronary artery disease and left ventricular dysfunction. In selected patients, chronic afterload reduction with oral hydralazine may result in increased cardiac reserve, decreased pulmonary congestion or decreased myocardial oxygen demands, thereby improving or abolishing resting or exertional dyspnea or angina.
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