Reduction of cerebral blood flow with induced tachycardia in rats and in patients with coronary artery disease and premature ventricular contractions.

A reduction of cerebral blood flow (CBF) was observed in experimental studies in rats immediately after the onset of parasystolic rhythm or with stable, but haemodynamically compromising, tachycardias. Based on these data and with a view to studying the effects of premature ventricular contractions (PVCs) on the cerebral circulation in humans, CBF was measured using the 133-Xenon inhalation method in 24 age matched human controls (group A1: age 58.5 +/- 6.2 years; group A2: 52.2 +/- 7.8 years) in nine coronary artery disease (CAD) patients without PVCs (B), in 11 CAD patients with frequent PVCs (> 300.h-1) (C) and in nine patients, after exclusion of CAD by angiography, also with frequent PVCs (> 300.h-1) (D). Holter monitoring was performed during the CBF measurement. CBF determined in the human control groups A1 and A2 was 79.9 +/- 9.9 ml.100 g.-1 min-1 and 81.5-13.0 ml. 100 g-1 min-1, respectively. CBF was 74.1 +/- 13.6 ml . 100 g.-1 min-1 (P = 0.267 vs A1) in group B, 65.8 +/- 11.8 ml.100 g-1 min-1 (P = 0.004 vs A1) in group C and 74.2 +/- 15.6 ml.100 g.-1 min-1 (P = 0.218 vs A2) in group D. The significant reduction of CBF in CAD patients with frequent PVCs suggests that arrhythmias have a significant impact on CBF. Non-CAD patients with frequent PVCs did not show significant CBF decreases in comparison with controls. One can hypothetize that an impairment of electrical postextrasystolic potentiation, due to premature ventricular depolarization, and hence myocardial dysfunction leads to CBF reduction in CAD patients. The CBF reduction with CAD could also reflect concomitant coronary and cerebral arteriosclerosis.