Influence of calcium administration on the short-term hemodynamic and anti-ischemic effects of nifedipine

This prospective study investigated whether pretreatment with intravenously administered calcium would influence the effect of nifedipine on rest hemodynamics and treadmill performance in patients with ischemic heart disease. Seventeen patients were studied after undergoing a qualifying treadmill exercise test that revealed ST segment depression indicative of ischemic heart disease. Study subjects performed three additional treadmill tests as part of the protocol. One treadmill test was obtained from each patient to provide baseline measurements without a preceding intravenous infusion and in the absence of all antianginal drugs including nifedipine; two additional exercise tests were preceded by an infusion and 10 mg of bite-and-swallow nifedipine. The infusions, administered in a randomized, double-blind, crossover fashion, consisted of either 10 ml of 10% calcium chloride (13.6 mEq) in 50 ml of 5% dextrose in water or 5% dextrose in water alone. Rest systolic blood pressure (134 ± 4.6 mm Hg) was unchanged after placebo infusion (135 ± 4.6 mm Hg) but decreased to 124 ± 4.1 mm Hg (p < 0.01) 25 min after nifedipine administration. Rest systolic blood pressure increased after calcium infusion (from 139 ± 4.3 to 148 ± 4.8 mm Hg, p < 0.01) and then decreased significantly 25 min after nifedipine administration to 135 ± 4.2 mm Hg (p < 0.01). Despite a decrease at the time of peak nifedipine effect after either infusion, systolic blood pressure was significantly lower after administration of nifedipine alone than after administration of calcium and nifedipine (124 ± 4.1 vs. 135 ± 4.2 mm Hg, p < 0.01). Peak exercise systolic blood pressure was reduced after placebo and nifedipine (170 ± 7.5 mm Hg, p < 0.05), but not after calcium and nifedipine, in comparison with the value of 178 ± 8.2 mm Hg on the baseline treadmill test. Exercise duration was longer (p < 0.05) than baseline duration (365 ± 27 s) after placebo and nifedipine (409 ± 32 s) but was not significantly changed after calcium and nifedipine (391 ± 34 s). Maximal ST segment depression on baseline testing (1.35 ± 0.1 mm) was significantly reduced (p < 0.05) after administration of either nifedipine alone (0.79 ± 0.1 mm) or calcium and nifedipine (0.85 ± 0.2 mm). All 17 patients had ST segment depression on baseline exercise testing compared with only 12 of 17 subjects after nifedipine alone and only 10 after calcium and nifedipine. Conclusions: Calcium administration was associated with a significant increase in systolic blood pressure in patients with ischemic heart disease. Nifedipine reversed the increase in blood pressure induced by calcium but systolic pressure did not decrease below baseline values. By electrocardiographic criteria, treadmill performance was still improved compared with baseline values when administration of nifedipine was preceded by calcium.