Hemodynamic and coronary effects of molsidomine at basal state, during atrial pacing, and during cold pressor test in patients with stable angina pectoris

Abstract

Heart rate (HR), cardiac output (CO), coronary sinus blood flow (CSF), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), mean arterial (MAP), and coronary arteriovenous difference for oxygen (AVDcO 2) were measured in patients with stable angina pectoris without cardiac failure before and 40 to 60 minutes after administration of 2 or 3 mg of molsidomine. In 20 patients these measurements were made in basal state during spontaneous rhythm. In eight of these patients (including three receiving beta blockers) the measurements were made during atrial pacing. In eight other patients, all receiving long-term beta-blocker therapy, the measurements were made during cold pressor test. At the basal state in spontaneous rhythm, a gradual reduction in the LVSP to 70% or less of its initial value was observed in four patients receiving 3 mg of molsidomine (two of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In the 16 other patients molsidomine decreased LVSP, LVEDP, MAP, CO, and double product (DP = LVSP × HR). The AVDcO 2 was unchanged. CSF and myocardial oxygen uptake index (MV̇O 2 = CSF × AVDcO 2) were decreased. During atrial pacing, hemodynamic and coronary effects were similar to those seen in the basal state. During the cold pressor test, the increases in LVSP, MAP, and LVEDP were significantly reduced by molsidomine. The variations in CSF and coronary resistance ( MAP CSF ) were also significantly different after administration of molsidomine, with better metabolic regulation of the coronary circulation. These results suggest that in patients with stable coronary insufficiency without cardiac failure the improvement in ventricular load induced by molsidomine may reduce the metabolic requirements of the myocardium both in spontaneous rhythm and during atrial pacing. There is a risk of hypotension that does not appear to be related to the association with beta blockers. Molsidomine can help to preserve the predominance of physiologic regulation of the coronary circulation in conditions in which it is threatened.