Hemodynamic effects of nisoldipine, a highly specific calcium antagonist, in patients with acute myocardial infarction

Wilson, J. H. P.; Pj, Commerford; Rs, Millar

doi:10.1007/bf00050916

Cited by 7 publications

(1 citation statement)

References 11 publications

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“…Although it has long been proposed that myocardial calcium overload can cause reperfusion damage after myocardial ischaemia, only recently has it been shown that some of this damage can specifically be inhibited by calcium channel antagonists added only at the time of reperfusion 171 . Some of this protection may be mediated by the newly described antioxidant properties of calcium channel antagonists' 81 . As will be discussed later, these properties must still be shown to be clinically relevant.…”

Section: Decreased Reperfusion Injury In Animal Modelsmentioning

confidence: 99%

Mechanisms whereby calcium channel antagonists may protect patients with coronary artery disease

Opie

1997

European Heart Journal

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Calcium antagonists have multiple mechanisms whereby they are able to protect against myocardial ischaemia. Recently questions have been posed about the long-term safety of this group of agents. This article is a selective rather than a complete review of the problems. Fears have largely centred around rapidly acting nifedipine when inappropriately used. This agent remains useful in Prinzmetal's angina, a condition in which there are no long-term comparative outcome studies. Current evidence is that verapamil is as safe and as effective as the beta-blocker in effort angina and that non-dihydropyridines (verapamil and diltiazem) are efficacious in the follow up of non-Q wave infarct. Verapamil post-infarct is safe and reduces reinfarction, provided that clinical heart failure is first excluded.

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Section: Decreased Reperfusion Injury In Animal Modelsmentioning

confidence: 99%

Mechanisms whereby calcium channel antagonists may protect patients with coronary artery disease

Opie

1997

European Heart Journal

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Acute effects of intravenous nisoldipine on left ventricular function after acute myocardial infarction

Wall

Chin

Pauwels³

et al. 1994

Cardiovasc Drug Ther

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Nisoldipine is a calcium antagonist with potent coronary vasodilating effects in patients with chronic stable angina pectoris. In an initial study we showed that intravenous nisoldipine, given 24-72 hours after uncomplicated myocardial infarction, was a safe and feasible intervention that had beneficial effects on global and regional myocardial function. We subsequently studied the acute effects of nisoldipine in six patients within 24 hours (mean 14 +/- 4 hours) after the onset of myocardial infarction. Nisoldipine was administered as a 4.5 micrograms/kg intravenous bolus over 3 minutes, followed by intravenous infusion of 0.2 microgram/kg over 60 minutes. Radionuclide angiography, cardiac output, and intraarterial blood pressure measurements were performed before and during nisoldipine. Left ventricular ejection fraction increased from 48.3 +/- 10.3% to 55.3 +/- 11.8% (p = 0.034) during nisoldipine infusion. Regional wall motion score changed during nisoldipine infusion from 3.3 +/- 2.5 to 1.8 +/- 2.6 (p = 0.027). Cardiac output increased from 5.5 +/- 1.0 to 7.3 +/- 1.3 l/min (p = 0.0001). Heart rate increased from 78 +/- 12 to 88 +/- 11 min-1 (p = 0.004). Mean arterial blood pressure decreased from 92 +/- 20 to 79 +/- 13 mmHg (p = 0.038). The rate-pressure product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine improves global and regional left ventricular function in patients with acute myocardial infarction within the first 24 hours.

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Effects of blood pressure reduction on the elastic profile of the aortic tree in patients with coronary heart disease

Heintz¹,

Dahl²,

Roeber³

et al. 1995

Am J Hypertens

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Decreased arterial compliance of large arteries in coronary heart disease has been reported. Using intravascular ultrasound it was demonstrated that arterial compliance decreases with increasing distance from the heart. Until now changes in the elastic profile have not been investigated after a stepwise blood pressure (BP) reduction induced by antihypertensive agents. The local viscoelastic properties of the aortic tree were analyzed before and after a mean arterial BP reduction of about 5 and 15 mm Hg below baseline by the steady-state infusion of increasing doses of nisoldipine in 15 patients with coronary artery disease. Intravascular ultrasound imaging combined with arterial pressure measurements were performed at five sites along the aortic tree to determine the viscoelastic profile before nisoldipine administration and again after the 5 and 15 mm Hg nisoldipine-induced blood pressure reductions. The elasticity parameters varied depending on the distance from the heart and on the BP level. At both BP reduction levels nisoldipine infusion led to an increase in arterial compliance at the abdominal aorta and at the aortic bifurcation. A dissociation between the 5 and the 15 mm Hg BP reduction was found at the common iliac artery and at the external iliac artery. Our results provide direct quantitative evidence that stepwise BP reductions exhibit different and, in part, contrary effects on the elastic profile, depending on the aortic tree location. The results also suggest that nisoldipine infusion can significantly ameliorate local viscoelastic properties at the abdominal aorta and at the aortic bifurcation, an effect that was associated or caused by a change in BP attributable to a decrease in peripheral resistance.

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Hemodynamic effects of nisoldipine, a highly specific calcium antagonist, in patients with acute myocardial infarction

Cited by 7 publications

References 11 publications

Mechanisms whereby calcium channel antagonists may protect patients with coronary artery disease

Mechanisms whereby calcium channel antagonists may protect patients with coronary artery disease

Acute effects of intravenous nisoldipine on left ventricular function after acute myocardial infarction

Effects of blood pressure reduction on the elastic profile of the aortic tree in patients with coronary heart disease

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