Open AccessComparative effects of intravenous dipyridamole and sublingual nitroglycerin on coronary hemodynamics and myocardial metabolism at rest and during atrial pacing in patients with coronary artery disease
Author(s) -
Arrotti J.,
Gunnar R. M.,
Ward J.,
Loeb H. S.
Publication year - 1980
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960030602
Subject(s) - medicine , nitroglycerin (drug) , dipyridamole , cardiology , coronary artery disease , sublingual administration , hemodynamics , rest (music) , anesthesia
The effects of intravenous dipyridamole (20 mg) and sublingual nitroglycerin (0.6 mg) were compared at rest and during rapid atrial pacing in patients with significant coronary obstruction. Dipyridamole, which had no significant effect on resting systolic blood pressure, caused a significant increase in coronary sinus flow (CSF) and reduction of coronary vascular resistance (CVR) and arterial‐coronary sinus oxygen difference (AO 2 ‐CSO 2 δ), whereas nitroglycerin reduced resting systolic pressure but had no significant effect on CSF, CVR, or AO 2 ‐CSO 2 °. Although these effects of dipyridamole and nitroglycerin on resting systolic pressure, CSF, CVR, and AO 2 ‐CSO 2 ° were qualitatively similar during rapid atrial pacing, the onset of chest pain and ischemic ECG changes occurred at a lower heart rate following dipyridamole (136±5 beats/min) than following nitroglycerin (149±6 beats/min, p<0.01). However, maximal double product and myocardial oxygen consumption achieved during pacing were similar following both dipyridamole and nitroglycerin and were less than control pacing values. Coronary dilatation following dipyridamole appears to reduce tolerance to pacing‐induced ischemia probably by maldistribution of coronary flow away from ischemic myocardium. Nitroglycerin differs from dipyridamole by improving tolerance to pacing; however, this difference appears to be due to systemic vasodilator effects of nitroglycerin rather than to enhancement of flow to ischemic myocardium.