Dose-dependent effects of intracoronary verapamil on systemic and coronaryhemodynamics

Citation
O. Oldenburg et al., Dose-dependent effects of intracoronary verapamil on systemic and coronaryhemodynamics, CARDIO DRUG, 14(6), 2000, pp. 651-655
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR DRUGS AND THERAPY
ISSN journal
09203206 → ACNP
Volume
14
Issue
6
Year of publication
2000
Pages
651 - 655
Database
ISI
SICI code
0920-3206(200012)14:6<651:DEOIVO>2.0.ZU;2-Z
Abstract
Calcium antagonists are used in interventional cardiology to prevent corona ry vasoconstriction or to overcome the no-reflow phenomenon. The aim of the current study was to evaluate the dose-dependent effects of intracoronary verapamil on systemic and coronary hemodynamics. In 20 patients scheduled f or routine coronary angiography, heart rate, blood pressure, and ECG record ings mere recorded continuously and intracoronary flow velocity was obtaine d by intracoronary Doppler measurements in angiographically normal vessels. The cross-sectional area, measured by quantitative coronary angiography, a llowed the calculation of coronary blood flow (CBF) and the coronary vascul ar resistance index (CVRI). Without premedication, increasing dosages of ve rapamil (0.01 mg, 0.1 mg, 1.0 mg, and 2.0 mg) were injected into the left c oronary artery. Intracoronary verapamil administration led to a decrease in systemic blood pressure only after administration of 1.0 mg or 2.0 mg (cha nge in mean arterial pressure: from 87.6 +/- 14.6 mmHg to 80.1 +/- 14.9 mmH g and 78.5 +/- 13.9 mmHg, respectively; both P < 0.05) without a change in heart rate. Epicardial diameters of the left coronary artery increased only at dosages of 1.0 mg and 2.0 mg (from 2.14 +/- 0.4 mm to 2.22 +/- 0.3 mm, P < 0.01), whereas the coronary blood flow velocity increased significantly at the smallest dosage of 0.01 mg (from 19.9 +/- 8.7 cm/s to 33.2 +/- 14.9 cm/s, P < 0.001) and was further enhanced with increasing dosages. CBF inc reased and CVRI decreased at every dosage of verapamil compared with baseli ne values. CBF increased also after 0.1 mg (from 13.5 +/- 6.5 mL/min to 19. 5 +/- 9.3 mL/min; P < 0.05), reaching a maximal effect after administration of 1.0 mg verapamil (26.3 +/- 16.1 mL/min, P < 0.05). Application of 2.0 m g did not further increase CBF compared with 1.0 mg. Intracoronary applicat ion of verapamil leads to a decrease in systemic blood pressure at higher d osages, whereas heart rate remains unchanged at any dosage. The maximal inc rease in coronary blood flow and decrease in vascular resistance can be rea ched by administration of 1.0 mg verapamil into the left; coronary artery.