Acute electrophysiologic, hemodynamic and left ventricular effects of nifedipine and beta-blocker interactions Maintenance of global and regional left ventricular wall motion

Abstract

To assess potential cardiac effects of nifedipine and β-blocker interactions, 10 men receiving chronic β-blocker therapy for angina underwent hemodynamic, electrophysiologic and left ventricular (LV) functional analyses at the time of cardiac catheterization before and after buccal administration of 10 mg of nifedipine. Although this combination is usually well tolerated, there have been occasional reports suggesting that the combination of nifedipine and β-blocking agents may increase the likelihood of congestive heart failure, severe hypotension or exacerbation of angina. All patients had class II or III stable angina pectoris and were receiving at least 160 to 240 mg/day of propranolol or equivalent doses of β-blocker therapy. Nifedipine produced no acute electrophysiologic changes, including heart rate, PR interval, AH interval, HV interval, sinus node recovery time or heart rate at which atrioventricular nodal block occurred. Hemodynamic effects included no significant change in mean right atrial pressure (7 ± 1 vs 5 ± 1 mm Hg), while mean pulmonary artery pressure decreased significantly (20 ± 2 vs 17 ± 1 mm Hg, p ≤0.05). In addition, LV end-diastolic pressure decreased significantly from 16 ± 2 to 10 ± 1 mm Hg (p ≤50.05), with a nonsignificant decrease in mean aortic pressure from 93 ± 5 to 86 ± 4 mm Hg. Likewise, no significant change occurred in cardiac index (3.2 ± 0.4 vs 3.0 ± 0.4 liters/min/m2) or systemic vascular resistance (1,157 ± 247 vs 1,170 ± 236 dynes/s/cm 5). Left ventricular ejection fraction (EF) was the same before and after nifedipine (73 ± 2 % vs 74 ± 2%). Segmental EF (5-segment area method) showed no differences in function when jeopardized segments (supplied by a coronary artery with ≥50% stenosis) were compared with nonjeopardized (normal blood supply) segments. Jeopardized segmental EF was 53 ± 3 % before and 56 ± 3 % after nifedipine, while nonjeopardized segments revealed a 58 ± 3 % EF before nifedipine and a 58 ± 3 % EF after the drug. Conversely, analysis by segmental function revealed significant improvement in depressed segments (EF ≤ 45 % ) after nifedipine from 38 ± 2 % to 47 ± 3 % (p ≤50.05) compared with normal segments (EF >45 %) from 60 ± 2 % to 59 ± 1 % (difference not significant). It is concluded that nifedipine and β-blocker interactions produced no significant adverse effects on electrophysiologic, hemodynamic or LV functional parameters in patients with normal LV function at rest. Furthermore, depressed segments appeared to normalize after the addition of nifedipine.