scholarly journals Influence of tissue affinity of angiotensin-converting enzyme inhibitors on left ventricular remodeling after myocardial infarction

1998 ◽  
Vol 21 (4) ◽  
pp. 277-285 ◽  
Author(s):  
M. Konermann ◽  
C. Altmann ◽  
F. Laschewski ◽  
W. Josephs ◽  
H. J. Odenthal ◽  
...  
2000 ◽  
Vol 8 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Yi Zhun Zhu ◽  
How Sung Lee

Myocardial infarction was the underlying event in the majority of deaths from cardiovascular disease in Western countries in the past quarter-century. The introduction of angiotensin-converting enzyme inhibitors to the treatment of heart failure following myocardial infarction was a major advance in the last 10 years. However, the role of cardiac angiotensin-converting enzyme during postinfarction cardiac remodeling remains to be elucidated. Experimental studies demonstrated that angiotensin-converting enzyme inhibitors administered one week before myocardial infarction could limit infarct size, improve cardiac function, and prevent cardiac hypertrophy. Numerous large-scale clinical trials have shown that angiotensin-converting enzyme inhibitors are safe and can reduce mortality and the occurrence of severe left ventricular dysfunction after myocardial infarction. This review focuses on the effects of these inhibitors in experimental studies and in multicenter clinical trials.


2010 ◽  
Vol 1 (1) ◽  
pp. 62-64
Author(s):  
A. S Galyavich

The paper analyzes the use of angiotensin-converting enzyme (ACE) inhibitors in patients after prior myocardial infarction. It presents the data of controlled studies, which indicate that it is warranted to use ACE inhibitors to improve prognosis in patients. It is concluded that it is unreasonable for a physician not to prescribe ACE inhibitors to post-myocardial infarction patients with obvious or asymptomatic left ventricular dysfunction and to diabetic patients (if no contraindications).


2006 ◽  
Vol 291 (5) ◽  
pp. H2021-H2025 ◽  
Author(s):  
Marc A. Pfeffer ◽  
Edward D. Frohlich

The expanding clinical indications for the use of angiotensin-converting enzyme (ACE) inhibitors during the past three decades to reduce cardiovascular morbidity and mortality across a broad spectrum of cardiovascular diseases have been the consequence of impressively productive interchanges between basic science and clinical medicine. In some areas, the initial discovery from animal investigations produced the hypotheses that were confirmed and expanded in patients with specific disease processes. In the development of ACE inhibitors, there are also important examples where an unexpected discovery from clinical trials spurred a host of laboratory investigations that uncovered novel mechanisms to underpin the clinical observations. Although developed as an antihypertensive agent, these effective interchanges, termed “translational research,” have collectively produced convincing data to demonstrate that ACE inhibitors can and should be used to slow progression of renal disease, prevent and treat heart failure, attenuate adverse left ventricular remodeling after myocardial infarction and improve prognosis, reduce atherosclerotic complications in patients with coronary artery disease, and, even more recently, reduce the incidence of Type II diabetes.


1995 ◽  
Vol 73 (7) ◽  
pp. 827-831 ◽  
Author(s):  
Yï-Chun Zhu ◽  
Harald M. Stauss ◽  
Gang Bao ◽  
Peter Gohlke ◽  
Yi-Zhun Zhu ◽  
...  

Angiotensin converting enzyme inhibitors (ACEIs) not only reduce angiotensin II synthesis but also potentiate endogenous kinins. In addition to their antihypertensive actions, accumulated evidence has demonstrated an improvement by ACEIs of cardiac function, cardiac structural and metabolic status, and myocardial blood flow in conditions such as cardiac ischemia, left ventricular hypertrophy, and myocardial infarction. The mechanisms underlying the antihypertensive and cardioprotective actions of ACEIs are under intensive investigation. A reduction of angiotensin II synthesis is undoubtedly responsible for a major part of the antihypertensive effects of ACEIs. However, in experimental renal hypertension but not in genetic hypertension, bradykinin potentiation has been shown to partially mediate the acute and chronic antihypertensive actions of these drugs. In addition, experimental observations suggest that bradykinin potentiation plays a pivotal role in the cardioprotective effects of ACEIs.Key words: angiotensin converting enzyme inhibitors, antihypertension, cardiac function, myocardial infarction, tissue blood flow, bradykinin, angiotensin II.


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