Comparison of the acute hemodynamic response to intravenous nisoldipine (bay k 5552) and intravenous nifedipine for left ventricular dysfunction secondary to myocardial infarction

The acute effects on left ventricular function of nisoldipine were studied in six patients 56 +/- 12 hours (range 44 to 72 hours) after the onset of uncomplicated acute myocardial infarction. Nisoldipine was administered as a 4.5 micrograms/kg intravenous bolus over 3 minutes followed by an infusion of 0.2 microgram/kg during 60 minutes. Radionuclide angiography and two-dimensional echocardiography were performed before and during infusion with nisoldipine. The left ventricular ejection fraction increased significantly from 38% +/- 10% to 49% +/- 10% (P = 0.028) during nisoldipine infusion. Regional wall motion index was determined both by radionuclide and by two-dimensional echocardiography and showed a significant change during nisoldipine infusion from 1.9 +/- 0.3 to 1.5 +/- 0.3 (p = 0.028, radionuclide angiography) and from 0.7 +/- 0.2 to 0.3 +/- 0.2 (p = 0.043, two dimensional echocardiography). Heart rate increased significantly from 78 +/- 12 min-1 to 92 +/- 13 min-1 (p = 0.028), but mean double product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine significantly improves global and regional left ventricular function in patients shortly after acute myocardial infarction. This beneficial effect may, however, be partially offset by an increase in heart rate. Since mean double product did not change, it is suggested that nisoldipine may improve coronary blood flow in patients with acute myocardial infarction.

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

See 1 more Smart Citation

The acute effects of intravenous nisoldipine on left ventricular function 24 to 72 hours after uncomplicated acute myocardial infarction

Nooijer

Wall

Cats

et al. 1988

“…In this respect, nisotdipine is 100 times more vascular selective than nifedipine and is the most vascular selective of the currently available CCBs [11]. Nisoldipine, therefore, has the capacity to lower blood pressure without affecting the functioning of either the myocardium or skeletal muscle and does not produce the negative inotropic effects that occur with some other CCBs, such as nifedipine [12,13]. There is some evidence from in vitro studies, particularly using porcine artery preparations, that nisoldipine preferentially acts on the coronary rather than the peripheral vasculature, especially when the former is in a depolarized state, such as occurs during periods of ischemia [12,14,15].…”

Section: Nisoldipinementioning

confidence: 99%

Nisoldipine CC: Efficacy and tolerability in hypertension and ischemic heart disease

1997

Nisoldipine is a second-generation dihydropyridine calcium channel blocker (CCB). It is the most vascular selective of the currently available CCBs, and thus has the capacity to lower blood pressure without affecting the functioning of the myocardium and skeletal muscle, and without producing any negative inotropic effects. Nisoldipine coat core (CC) is an extended-release formulation that allows nisoldipine to be released gradually over 24 hours, minimizing fluctuations in plasma concentration and providing a good trough/peak ratio. It has a slow onset and long duration of action, and ambulatory blood pressure monitoring has demonstrated that its antihypertensive effect is maintained over 24 hours with no evidence of reflex tachycardia, hypotension, or sympathetic neurohormonal activation and no effects on circadian variation. Studies in patients with hypertension have shown that nisoldipine CC provides reductions in blood pressure that are at least equivalent to those seen with diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, and other CCBs, without deleterious effects on metabolic parameters. In particular, it has been found to be effective in elderly patients and in black patients with severe hypertension. The DEFIANT studies have demonstrated that nisoldipine CC improves cardiac function and exercise tolerance in patients recovering from acute myocardial infarction, without increasing the risk of mortality compared with placebo. It also improves exercise performance in patients with stable angina pectoris. Nisoldipine CC is well tolerated in all groups of patients, with the most frequently reported side effects being headache and peripheral edema, which are usually mild and transient.

“…However, the effects of nisoldipine on myocardial contractility in isolated systems are controversial [6]. In clinical studies nisoldipine proved to be effective in the treatment of coronary artery disease [7,8]; in heart failure, however, favorable effects of nisoldipine were not found by all investigators [9][10][11].Vasodilation of epicardial coronary stenoses is regarded as an important antianginal mechanism [12, 13]; stenosis dilation has already been documented in several studies with nifedipine [14,15]. The present study investigates the influence of intravenous administration of two different doses of nisoldipine on angiographically normal and stenotic epicardial coronary arteries.…”

mentioning

confidence: 99%

Vasodilatory effects of nisoldipine on coronary arteries—Correlation with plasma levels

Jost

Rafflenbeul

Mogwitz

et al. 1990

Vasomotion of angiographically normal and stenotic epicardial coronary arteries was analyzed up to 15 minutes after the onset of an intravenous infusion (4 minutes) of 0.5 mg (13 patients, group A) or 1 mg nisoldipine (13 patients, group B). After both doses the maximal increase of the mean diameters of normal coronary segments was achieved not before the 15th minute, averaging 11 +/- 6% in group A (p less than 0.001) and 18 +/- 9% in group B (p less than 0.001). Eleven of 15 and 8 of 9 coronary stenoses in groups A and B dilated to 5-80% and 15-70%, respectively. The nisoldipine concentration reached maximal levels at the end of the infusion (fourth minute) with an average of 8 +/- 4 ng/ml and 17 +/- 7 ng/ml in groups A and B, respectively. A significant correlation between nisoldipine plasma levels and dilation of normal coronary segments was obtained only with the individual maxima of these parameters and only in group A (p less than 0.01). The hysteresis of the coronary dilation in relation to the drug plasma levels may be due to the high receptor affinity of nisoldipine. In either group nisoldipine provoked a persistent increase in coronary sinus oxygen saturation (p less than 0.01) and a substantial and prolonged drop in systolic and diastolic aortic pressure (p less than 0.001). Both doses of nisoldipine induced a rise in heart rate (p less than 0.01) and a slight drop in the rate-pressure product (p less than 0.05).