Angiotensin-converting enzyme inhibition to enhance vascular health--clinical and research models (original) (raw)
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Ischemic heart disease: the next target for the angiotensin-converting enzyme inhibitors
ACE in Ischemic Heart Disease
ngiotensin-converting enzyme (ACE) inhibitors exhibit important cardioprotective and vasculoprotective properties. It is believed that these are mediated by their inhibition of both angiotensin-II generation and bradykinin degradation. Animal and human experimental studies demonstrate that ACE inhibitors are effective blood pressure-lowering agents, reduce cardiac hypertrophy, favorably influence ventricular remodeling following myocardial infarction, can lead to coronary vasodilatation, and decrease sympathetic tone. Additionally, ACE inhibitors can restore or improve endothelial function, antagonize angiotensin II-mediated vascular smooth muscle cell growth and proliferation, decrease macrophage migration and function, have antioxidant properties, and decrease thrombotic activity, by both inhibition of platelet aggregation and enhancement of endogenous fibrinolysis. 1,2 These multiple mechanisms of action contribute to the benefits associated with the use of ACE inhibitors in hypertension, myocardial infarction, and heart failure, and suggest that they may be effective agents in a wider range of ischemic syndromes. The main purpose of this article is to review the clinical data that support the role of ACE inhibitors in the prevention of ischemic events in a wider range of patients with established cardiovascular disease and to briefly summarize the major ongoing trials addressing this issue.
Pleiotropic benefits and utility of angiotensin converting enzyme inhibitors in current practice
International Journal of Research in Medical Sciences, 2021
The renin-angiotensin-aldosterone system (RAAS) is responsible for maintaining hemodynamic stability and thereby impacts multiple organ systems, such as the central nervous system, heart, and kidneys. Angiotensin II (ang II) is the main effector of the RAAS. However, overactivity of the RAAS can give rise to cardiovascular disorders, stroke, and nephrosclerosis. Unfavorable effects on cardiovascular system are attributed to ang II. RAAS activation also results in release and increased activity of several hormonal and inflammatory mediators, trigger formation of a number of secondary messengers and/or activate pathways, which negatively affects blood vessels and tissue. RAAS inhibitors, such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and calcium channel blockers can protect various organs from damage by blocking the protean manifestation of RAAS activity, either in its circulating or its locally tissue-active form. This review explains ...
The American Journal of Cardiology, 2001
Angiotensin-converting enzyme (ACE) is primarily localized (>90%) in various tissues and organs, most notably on the endothelium but also within parenchyma and inflammatory cells. Tissue ACE is now recognized as a key factor in cardiovascular and renal diseases. Endothelial dysfunction, in response to a number of risk factors or injury such as hypertension, diabetes mellitus, hypercholesteremia, and cigarette smoking, disrupts the balance of vasodilation and vasoconstriction, vascular smooth muscle cell growth, the inflammatory and oxidative state of the vessel wall, and is associated with activation of tissue ACE. Pathologic activation of local ACE can have deleterious effects on the heart, vasculature, and the kidneys. The imbalance resulting from increased local formation of angiotensin II and in-
The American Journal of Medicine, 1998
Angiotensin-converting enzyme (ACE) inhibitors have shown unexpected benefits in the prevention of ischemic events in patients with hypertension and congestive heart failure. In addition to these clinical observations, there is a growing body of knowledge about the molecular and cellular effects of ACE inhibitors. For example, ACE inhibition prevents stimulation of smooth muscle cell angiotensin II receptors, thereby blocking both contractile and proliferative actions. Angiotensin II blockade also diminishes the production of superoxide anion, which inactivates ambient nitric oxide. ACE inhibition of kininase II inhibits the breakdown of bradykinin, a direct stimulant of nitric oxide release from the intact endothelial cell. Thus, at the cellular level within the vasculature, ACE inhibition shifts the balance of ongoing mechanisms in favor of those promoting vasodilatory, antiaggregatory, antithrombotic, and antiproliferative effects. These effects underlie the potential benefits of ACE inhibition in the therapy of ischemia and atherosclerosis. Some data is available in humans to show that these effects can be sustained for months, thereby maintaining improved endothelial function and, presumably, allowing the initiation of steps that might alter the progression of atherosclerosis. Definitive information is not yet available in humans to show that ACE inhibition clearly alters the progression of atherosclerosis or diminishes coronary events in uncomplicated coronary disease. This promising area of investigation is, however, the subject of multiple clinical trials, which should provide clarification of this important question in coming years.
Angiotensin-Converting–Enzyme Inhibition in Stable Coronary Artery Disease
New England Journal of Medicine, 2004
ace inhibition in coronary disease 2059 Exclusion criteria Current use of or a current condition requiring use of an ACE inhibitor or a contraindication to ACE inhibitors Current use of an angiotensin II-receptor antagonist Hospitalization for unstable angina within the preceding 2 mo Valvular heart disease deemed to require surgical intervention Coronary-artery bypass grafting or percutaneous transluminal angioplasty within the preceding 3 mo Planned elective coronary revascularization Serum creatinine >2.0 mg/dl (177 µmol/liter) Serum potassium >5.5 mmol/liter Limited chance of 5-yr survival Psychosocial condition precluding long-term adherence Unable or unwilling to give consent Female sex and of childbearing potential and not using contraception Current use in a research trial of medication not approved by the U.