Coronary and systemic hemodynamic effects of clevidipine, an ultra-short-acting calcium antagonist, for treatment of hypertension after coronary artery surgery

Citation
N. Kieler-jensen et al., Coronary and systemic hemodynamic effects of clevidipine, an ultra-short-acting calcium antagonist, for treatment of hypertension after coronary artery surgery, ACT ANAE SC, 44(2), 2000, pp. 186-193
Citations number
29
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ACTA ANAESTHESIOLOGICA SCANDINAVICA
ISSN journal
00015172 → ACNP
Volume
44
Issue
2
Year of publication
2000
Pages
186 - 193
Database
ISI
SICI code
0001-5172(200002)44:2<186:CASHEO>2.0.ZU;2-I
Abstract
Background: The aim was to evaluate the use of clevidipine, a new vascular selective, ultra-short-acting calcium antagonist for blood pressure control after coronary artery bypass grafting (CABG). Methods: The effects of clevidipine on central hemodynamics, myocardial blo od flow and metabolism were studied at two different phases after CABG. In phase 1 (n=13), the hypertensive phase, the effects of clevidipine were com pared to those of sodium nitroprusside (SNP) when used to control postopera tive hypertension. In phase 2 (n=9), the normotensive phase, a clevidipine dose-response relationship was established, Results: At a target mean arterial pressure (MAP) of 75 mmHg, systemic vasc ular resistance (SVR) and heart rate (HR) were lower, preload, stroke volum e (SV) and pulmonary vascular resistance (PVR) were higher, while there wer e no differences in myocardial lactate metabolism or oxygen extraction with clevidipine compared to SNP. In the normotensive phase, clevidipine induce d a dose-dependent decrease in MAP (-19%), SVR (-27%) and PVR (-15%), accom panied by an increase in SV (10%), but no reflex increase in HR or changes in cardiac preload. Clevidipine caused a direct coronary vasodilation, as i ndicated by a decrease in myocardial oxygen extraction from 54% to 45%. Myo cardial lactate metabolism was unaffected by clevidipine. The blood clearan ce of clevidipine was 0.05 l.min(-1).kg(-1), the volume of distribution at steady state was 0.08 l.kg(-1) and the initial and terminal half-lives were <1 min and 4 min, respectively. Conclusions: Clevidipine rapidly reduced MAP and induced a systemic, pulmon ary and coronary vasodilation with no effect on venous capacitance vessels or HR. Clevidipine caused no adverse effects on myocardial lactate metaboli sm. Clevidipine thus appears suitable to control blood pressure after CABG.