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Preservation of left ventricular performance with reduced ischemic dysfunction by intravenous nisoldipine
B P Kimball1, K R Watson, S Bui
1Cardiovascular Investigation Unit, Toronto Hospital, Ontario, Canada.
Insights
Intravenous nisoldipine improved cardiac performance in patients with coronary artery disease by reducing blood pressure and preventing myocardial ischemia during rapid atrial pacing. This calcium channel blocker maintained ventricular function through vasodilation and ameliorating ischemic dysfunction.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Coronary artery disease (CAD) poses significant challenges to cardiac performance, particularly during increased cardiac demand.
- Myocardial ischemia, often induced by rapid atrial pacing, can impair ventricular function.
- Nisoldipine, a calcium channel blocker, is investigated for its potential to mitigate these effects.
Purpose of the Study:
- To evaluate the effect of intravenous nisoldipine on cardiac performance in patients with CAD during pacing-induced ischemia.
- To assess whether nisoldipine's benefits stem from afterload reduction or prevention of myocardial ischemia.
- To analyze the drug's impact on both global and regional myocardial function.
Main Methods:
- The study involved 14 patients with coronary artery disease.
- Cardiac performance was assessed during pacing-induced ischemia before and after intravenous administration of nisoldipine.
- Load-independent global (peak-systolic pressure/end-systolic volume) and regional (peak-systolic pressure/end-systolic radial length) contractile indexes were utilized.
Main Results:
- Nisoldipine significantly decreased aortic pressure and prevented the rise in left ventricular end-diastolic pressure during rapid atrial pacing.
- Resting cardiac index and left ventricular ejection fraction increased post-nisoldipine administration.
- Nisoldipine prevented the deterioration of left ventricular ejection fraction and fractional radial shortening during pacing, preserving myocardial function.
Conclusions:
- Intravenous nisoldipine effectively maintains ventricular performance in patients with CAD during rapid atrial pacing.
- The drug achieves this by a combination of systemic vasodilation and amelioration of ischemic myocardial dysfunction.
- Nisoldipine demonstrates a protective effect against pacing-induced ischemia, improving overall cardiac function.
Abstract:
The effect of intravenous nisoldipine on cardiac performance was examined during pacing-induced ischemia in 14 patients with coronary artery disease. The relative contributions of afterload reduction or prevention of myocardial ischemia were assessed using load-independent global (peak-systolic pressure/end-systolic volume) and regional (peak-systolic pressure/end-systolic radial length) "contractile" indexes. Nisoldipine decreased aortic pressure (predrug, 109 +/- 14 vs postdrug, 88 +/- 13 mm Hg, p less than 0.01) and prevented elevation of left ventricular end-diastolic pressure during rapid atrial pacing (predrug, 7.9 +/- 5.7 vs postdrug, -0.5 +/- 4.9 mm Hg, p less than 0.001). Resting cardiac index (predrug, 3.3 +/- 0.6 vs postdrug, 4.2 +/- 0.7 liters/min/m2, p less than 0.05), and left ventricular ejection fraction (predrug, 68.1 +/- 9.0 vs postdrug, 74.2 +/- 9.4%, p less than 0.05) increased after nisoldipine, which also prevented the deterioration in left ventricular ejection fraction (predrug, -8.1 +/- 7.9 vs postdrug, -1.0 +/- 3.7%, p less than 0.05) and fractional radial shortening (predrug, -8.7 +/- 13.1 vs postdrug, 3.7 +/- 16.4%, p less than 0.01) during rapid atrial pacing. Under these conditions, nisoldipine preserved myocardial function, as determined by global peak-systolic pressure/end-systolic volume (predrug, -0.82 +/- 0.39 vs postdrug, 0.17 +/- 1.54 mm Hg/ml, p less than 0.05) and regional (peak-systolic pressure/end-systolic radial length, predrug, -23.8 +/- 36.1 vs postdrug, 12.7 +/- 36.3 mm Hg/cm, p less than 0.01) "contractile" indexes. Intravenous nisoldipine maintains ventricular performance during rapid atrial pacing via a combination of systemic vasodilation and amelioration of ischemic myocardial dysfunction.