Effect of intravenous and intracoronary nifedipine on coronary blood flow and myocardial oxygen consumption

Schanzenbächer, P.; Liebau, G.; Deeg, P; Kochsiek, K

doi:10.1016/s0002-9149(83)80120-9

Cited by 53 publications

(10 citation statements)

References 12 publications

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“…At the end of the period of taking the combination of atenolol and nifedipine, 11 patients had a negative exercise test and it was stopped due to fatigue. Twelve patients had positive tests; three stopped due to chest pain, four due to shortness of breath and five due to silent ST segment depression > 2 mm.…”

Section: Effect Of the Fixed Combination Of Atenolol And Nifedipinementioning

confidence: 99%

Optimal control of myocardial ischaemia: the benefit of a fixed combination of atenolol and nifedipine in patients with chronic stable angina

El-Tamimi

Davies

1992

Heart

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Objective-To study the effects on myocardial ischaemia of 50 mg of atenolol, 20 mg of slow release nifedipine, and their fixed combination given 12 hourly.Design-A treadmill exercise test and 24 hour ambulatory electrocardiographic monitoring were carried out after a period of five days off treatment (control) and at the end of three weeks of each treatment period.Patients-23 patients with stable angina pectoris, documented coronary artery disease, and a positive exercise test were randomised in a double blind, three way, cross over study.Results-Compared with the control, nifedipine significantly induced an increase in resting heart rate of (mean (SEM)) 14 (2) beats/min whereas atenolol and the combination significantly reduced it by 24 (2) and 20 (1) beats/min respectively. The number of exercise tests rendered negative after each intervention was five for nifedipine, nine for atenolol, and 11 for the combination. Compared with the control the time to the start of myocardial ischaemia (1 mm ST segment depression) during exercise significantly increased by 3-2 (0-6) min after nifedipine, by 4-6 (0 4) min after atenolol, and by 4-6 (0 5) min after the combination; rate-pressure product (beats/min. mm Hg) at 1 mm ST segment depression increased by 2824 (970) after nifedipine but fell by 4436 (900) and 4501 (719) after atenolol and the combination. The weekly frequency of angina was reduced from a mean of five while taking nifedipine, to three while taking atenolol, and to two while taking the combination. The total ischaemic time during ambulatory monitoring was significantly reduced from 69 (17) min during control to 37-5 (9-8) min during nifedipine, to 15-6 (5-5) min during atenolol, and to 6-5 (2-7) min during the combination.Conclusion-The undesirable effect ofa high basal heart rate induced by nifedipine was neutralised by its combination with atenolol. Whereas atenolol and the combination were equally efficacious in controiling exercise induced ischaemia, the combination was more effective in reducing total ischaemic burden. (Br Heart J 1992;68:291-5) In most patients with chronic stable angina, both an increase in myocardial oxygen consumption and a decrease in myocardial blood flow contribute to the development of ischaemia, whether symptoms occur at rest or during exercise.' 2 3 Blockers relieve ischaemia primarily by decreasing myocardial oxygen demand, and calcium channel blockers do so by improving myocardial oxygen supply. By acting on these different determinants of myocardial ischaemia, the combination of both drugs could provide better control of myocardial ischaemia.We have investigated the anti-ischaemic effects of a calcium antagonist (nifedipine) and a ,B blocker (atenolol) singly and in a fixed combination on symptoms, and exercise induced and ambulatory ischaemia.Patients and methods Thirty patients were enrolled, but only 23 completed the study: 19 men and four women, aged 40 to 72 (mean 56-2) years, who had stable exertional angina of eight to 156 months duration (mean 56.2). T...

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Section: Effect Of the Fixed Combination Of Atenolol And Nifedipinementioning

confidence: 99%

Optimal control of myocardial ischaemia: the benefit of a fixed combination of atenolol and nifedipine in patients with chronic stable angina

El-Tamimi

Davies

1992

Heart

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“…In clogs, nisoldipine enhanced coronary collateral flow to poststenotic regions with a comparable distribution to the epicardial and endocardial layers [37 I. Whereas in previous clinical studies with intravenous nifedipine coronary blood flow was increased for only a couple of minutes [38,39], in the present study both dosages of nisoldipine caused a prolonged rise in coronary venous oxygen satm'ation, probably clue to a slower dissociation of nisoldipine fl'om the binding site [30,31].…”

Section: Discussionmentioning

confidence: 46%

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

Jost

Rafflenbeul

Mogwitz

et al. 1990

Cardiovasc Drug Ther

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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).

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“…The effects of nifedipine on myocardial oxygen consumption vary with the route of administration, and are related to effects on loading conditions, heart rate, and contractility. Following intravenous administration, studies in both humans (26,30) and experimental animals (3) have found no changes in resting myocardial oxygen consumption and either no change or transient minimal reductions in ventricular function (28,33). Following intracoronary administration, however, a significant decrease in regional myocardial oxygen consumption has been noted in both humans (26,29) and experimental animals (35).…”

Section: Discussionmentioning

confidence: 99%

Effect of nifedipine on the myocardial and vascular response to myocardial ischemia

et al. 1986

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Nifedipine reduces reactive hyperemia following brief coronary artery occlusions. To determine whether this is related to improvement in collateral blood flow to ischemic myocardium or alterations in myocardial oxygen consumption, ten chloralose anesthetized dogs were instrumented with coronary sinus catheters, circumflex artery flowmeters, and ultrasonic microcrystals for measurement of myocardial segment shortening. Myocardial oxygen consumption and circumflex coronary artery flow were determined at rest and during incremental infusions of isoproterenol. Myocardial blood flow measured with microspheres and segmental function were assessed during and following 30- and 60-second coronary artery occlusions. Thirty minutes after the intravenous administration of nifedipine, 10 micrograms/kg iv, all measurements were repeated. Nifedipine did not alter myocardial oxygen consumption or the relationship between oxygen consumption and circumflex coronary artery flow either at rest or during isoproterenol infusion. Following 60-second coronary occlusions, nifedipine reduced peak circumflex coronary artery flow (176 +/- 99 vs. 128 +/- 68 cc/min) and reactive hyperemia debt repayment (221 +/- 84 vs. 158 +/- 66%; p less than 0.01). Nifedipine did not alter flow to ischemic segments during coronary artery occlusions (0.16 +/- 0.10 vs. 0.19 +/- 0.13 ml/min/g mean transmural flow). Furthermore, nifedipine did not affect the severity of ischemic segment dysfunction, nor the rate of recovery of ischemic segment function following release of coronary artery occlusion. We conclude that the reduction in reactive hyperemia induced by nifedipine was not related to alterations in the severity of hypoperfusion in ischemic areas, or alterations in myocardial oxygen consumption. Reductions in reactive hyperemia produced by nifedipine did not impair recovery of mechanical function in postischemic myocardium.

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Effect of intravenous and intracoronary nifedipine on coronary blood flow and myocardial oxygen consumption

Cited by 53 publications

References 12 publications

Optimal control of myocardial ischaemia: the benefit of a fixed combination of atenolol and nifedipine in patients with chronic stable angina

Optimal control of myocardial ischaemia: the benefit of a fixed combination of atenolol and nifedipine in patients with chronic stable angina

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

Effect of nifedipine on the myocardial and vascular response to myocardial ischemia

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