Workshop on nisoldipine in coronary artery diseases and myocardial infarction
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Workshop on nisoldipine in coronary artery diseases and myocardial infarction papers presented at a workshop held in London, April 8, 1992, during the International Conference on Acute Myocardial Infarction by Workshop on Nisoldipine in Coronary Artery Diseases and Myocardial Infarction (1992 London)

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Published by Raven Health Care Communications in New York .
Written in English


  • Nisoldipine -- Congresses.,
  • Coronary heart disease -- Chemotherapy -- Congresses.,
  • Myocardial infarction -- Chemotherapy -- Congresses.

Book details:

Edition Notes

Includes bibliographical references.

Statementchairman, J. J. Kellermann.
ContributionsKellermann, Jan J.
LC ClassificationsRC684.C34 W67 1992
The Physical Object
Paginationvii, 35 p. :
Number of Pages35
ID Numbers
Open LibraryOL1459913M
LC Control Number93116405

Download Workshop on nisoldipine in coronary artery diseases and myocardial infarction


Coronary artery disease (CAD) and its primary complication, myocardial infarction, is a polygenic disease that remains a leading cause of death and disability worldwide. Recent progress in genomics has provided us with a golden opportunity to dissect the genetic basis of this condition paving the way for the development of novel methods to Author: Themistocles L. Assimes. A single left coronary artery was found in an asymptomatic year-old man who initially had electrocardiographic and vectorcardiographic evidence of anterolateral myocardial infarction. The single left coronary artery, which supplied the distribution of both the left and right coronary arteries, was free of disease at by: Increased frequency, duration, and/or severity of angina, as well as acute myocardial infarction, have rarely developed during initiation or dosage increase of calcium channel blockers (CCBs), particularly in patients with severe obstructive coronary artery disease . Summary. 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 by: 1.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is defined as non-obstructive (Cited by: 1. After nisoldipine, anginal symptoms were clearly reduced during the ischemic phase in the majority of patients. These findings suggest that intracoronary pretreatment with nisoldipine leads to a regional protection of ischemic myocardium without any appreciable effect on Cited by: 7. IN this issue, Vincent et al. report a tantalizing and well-documented account of a young woman who had a myocardial infarction despite angiographically normal coronary arteries. 1 The sequence of Cited by: sodium nitroprusside on mortality rate in acute myocardial infarction complicated by left ventricular failure: results of a Veterans Administration cooperative study. N Engl J Med ;– 7. Danish Study Group on Verapamil in Myocardial Infarction (DAVIT-I). Verapamil in acute myocardial infarction. Eur Heart J ;– Size: 46KB.

and who were suspected of having coronary artery disease were studied at the time of cardiac catheterization. Eleven patients were men and mean age of the patients was 57 years (range 44 to 69). Significant coronary artery disease was defined as at least . reported an insignificant increase in myocardial lactate uptake after nicardipine administration, from 15 +30 to 19 +31 gmol min1 (NS). In the study by Pepine et al. (), the lactate extraction fraction wasunchanged after nicardi-pine infusion in patients with coronary artery disease ( to %). Since this unchanged lactate extraction Cited by:   Abstract. Objective: The aim was to determine if long term treatment with nifedipine or nisoldipine affects structural remodelling of cardiac myocytes and is effective in attenuating or preventing reparative and reactive myocardial fibrosis in essential s: Five and a half month old male spontaneously hypertensive rats and Wistar Kyoto (WKY) rats received either ppm Cited by: of myocardial infarction, proven angiographic coronary artery disease, or a positive exercise test or perfusion defect. The left ventricular ejection fraction had to be at least 40%. Selection criteria and definitions have been previously described in detail elsewhere.7 The starting dose of nifedipine GITS or placebo was 30 mg once.