The QUinapril Ischemic Event Trial (QUIET) design and methods: Evaluation of chronic ACE inhibitor therapy after coronary artery intervention

Texter, Michele; Lees, Robert S.; Pitt, Bertram; Dinsmore, Robert E.; Uprichard, Andrew

doi:10.1007/bf00878518

Cited by 38 publications

(15 citation statements)

References 39 publications

(39 reference statements)

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“…The risk reduction was Ϸ24% in the Studies of Left Ventricular Dysfunction (SOLVD) 4,49,50 and Survival and Ventricular Enlargement (SAVE) 3 trials and Ϸ37% in the Survival of Myocardial Infarction Long-Term Evaluation (SMILE) study 51 ; also, there was a 25% reduction in sudden death in the Trandolapril Cardiac Evaluation (TRACE). 52 Several long-term clinical trials were initiated to evaluate the potential clinical benefits of ACE inhibition in patients with coronary artery disease without left ventricular dysfunction; these trials were as follows: the Quinapril Ischemic Events Trial (QUIET), 53,54 Heart Outcomes Prevention Evaluation (HOPE), 3 Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 55 Prevention of Events with Angiotensin-Converting Enzyme Inhibition (PEACE), 56 and the European Trial on Reduction of Cardiac Events With Perindopril in Stable Coronary Artery Disease (EUROPA). 57 Of these, the QUIET and HOPE studies have been completed.…”

Section: Tissue Ace As a Therapeutic Targetmentioning

confidence: 99%

Tissue Angiotensin and Pathobiology of Vascular Disease

2001

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Abstract-There is increasing evidence that direct pathobiological events in the vessel wall play an important role in vascular disease. An important mechanism involves the perturbation of the homeostatic balance between NO and reactive oxygen species. Increased reactive oxygen species can inactivate NO and produce peroxynitrite. Angiotensin II is a potent mediator of oxidative stress and stimulates the release of cytokines and the expression of leukocyte adhesion molecules that mediate vessel wall inflammation. Inflammatory cells release enzymes (including ACE) that generate angiotensin II. Thus, a local positive-feedback mechanism could be established in the vessel wall for oxidative stress, inflammation, and endothelial dysfunction. Angiotensin II also acts as a direct growth factor for vascular smooth muscle cells and can stimulate the local production of metalloproteinases and plasminogen activator inhibitor. Revolutions, 1970 S ince its discovery a century ago, the role of the renin-angiotensin system as an endocrine system involved in blood pressure and fluid electrolyte regulation has been well established. 1 Disorders of this system contribute importantly to the pathophysiology of hypertension, renal disease, and congestive heart failure. The recent discoveries of the tissue actions of angiotensin II (Ang II) have revolutionized our thinking of the role of this peptide in cardiovascular disease. Evidence indicates that Ang II is more than a hormone that exerts hemodynamic and renal actions but that it is also a local, biologically active mediator that has direct effects on endothelial and smooth muscle cells. 2 It plays a key role in the initiation and amplification of pathobiological events that lead to vascular disease. Indeed, recent clinical trials of ACE inhibitors have consistently documented the salutary effects of this class of agents in treating and preventing cardiovascular disease, with impressive reductions in coronary and cerebral vascular events despite a modest effect on blood pressure lowering. [3][4][5] These data suggest that ACE inhibitors may also exert direct actions on the blood vessel beyond their hemodynamic effects. The present article reviews the evidence for the direct tissue actions of Ang II, the cellular signaling pathways, and the interactions of Ang II with other local mediators. It is hypothesized that these tissue effects are important in the process of vascular disease and may mediate the additional nonhemodynamic actions of ACE inhibitors in treating cardiovascular conditions, such as coronary artery disease. Endothelium, Oxidative Stress, and Vascular DiseaseTo understand the effect of Ang II on vascular pathobiology, we must first examine the role of the endothelium. Ang II is synthesized by and has a key action on the endothelium: it exerts direct influence on endothelial function. The endothelium is well recognized as having a pivotal role in maintaining normal vascular function and structure. 6 The endothelium presents a thromboresistant surface to blood and f...

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Section: Tissue Ace As a Therapeutic Targetmentioning

confidence: 99%

Tissue Angiotensin and Pathobiology of Vascular Disease

2001

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“…Enalapril did not show any lipid lowering effect. Thus, modulation of ACE in the vasculature may be another target for the anti-atherosclerotic, as presumed with findings that ACE inhibitors reduce the incidence of myocardial infarction in patients with asymptomatic left ventricular dysfunction (The SOLVD Investigators, 1992) and presumably the progression of atherosclerosis (Texter et al, 1993 (Bernini et al, 1995). The mechanism for enalapril-induced attenuation of lipid peroxidation remains to be determined with respect to the common characteristics of ACE or kininase II inhibitors and to the linkage between the converting enzyme and activation of NADPH oxidase.…”

Section: Ace Activitiesmentioning

confidence: 99%

Inhibitory effects of fluvastatin, a new HMG‐CoA reductase inhibitor, on the increase in vascular ACE activity in cholesterol‐fed rabbits

Mitani¹,

Bandoh²,

Ishikawa³

et al. 1996

British J Pharmacology

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1 The effects of fluvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the vascular angiotensin converting enzyme (ACE) activity in hyperlipidaemic rabbits were compared with those of enalapril, an ACE inhibitor. 2 Rabbits were fed a 1.5% cholesterol containing diet or normal diet for 16 weeks and treated with either fluvastatin or enalapril in the diet at the respective doses of 2 and 10 mg kg-' day-'. The total cholesterol, triglyceride and phospholipid levels in serum were significantly increased in rabbits fed the high cholesterol diet. Treatment with fluvastatin but not enalapril resulted in a decrease in serum lipids. 3 The vascular ACE activities assessed via the cleavage rate from synthetic substrate in the aortic arches and upper thoracic aortae were increased by 8 to 10 times when the rabbits were made hyperlipidaemic. Fluvastatin as well as enalapril significantly lowered the tissue ACE in the aortae. 4 The ACE activities in serum did not alter in hyperlipidaemic rabbits either in the presence or absence of fluvastatin. The serum ACE activity was lowered by enalapril. 5 The lipid peroxide in serum as well as the plaque area in the thoracic aorta was significantly increased in the cholesterol diet-fed rabbits. Treatment with fluvastatin or enalapril reduced both serum lipid peroxide and plaque formation. The relaxant responses to acetylcholine (ACh) were significantly suppressed in the cholesterol-fed rabbits. Treatment with fluvastatin or enalapril significantly reversed the suppression of ACh-induced relaxation. 6 It seems that the reduction of vascular ACE is not coupled to lipids and ACE activity in serum, but rather to lipid peroxidation. Thus, the decrease in vascular ACE activity by fluvastatin as well as the lipid-lowering effect may reduce the risk of atherosclerosis progression in the vasculature.

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“…Several studies are now under way and the first of these to report will be the Quinapril Ischaemic Event Trial (QUIET), a prospective double-blind, placebo-controlled study to assess the effects of quinapril in patients with CAD [42]. Again, because quinapril binds particularly strongly to tissue ACE, it may be well suited to modification of any endothelial and intireal changes that are driven by angiotensin II and form part of the atherosclerotic process.…”

Section: Current Trialsmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitors and coronary artery disease

Sayer

1996

Cardiovasc Drug Ther

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The renin-angiotensin system and angiotensin converting enzyme (ACE) are increasingly being implicated in the pathogenesis of coronary artery disease and its sequelae. Genetic studies of ACE gene polymorphism hint at an association between the ACE genotype and atherosclerosis. Animal studies have demonstrated the potential beneficial effects of ACE inhibition at a variety of sites, including improvement of endothelial function, inhibition of platelet aggregation, reduction of atherosclerosis, and inhibition of myointimal proliferation. Although these have not all been validated in human studies, the reduction of ischemic events in studies of ACE inhibition in left ventricular dysfunction cannot be explained solely by improved hemodynamics, and it is possible that actions on the endothelium, the atherosclerotic process, and platelets are at least in part responsible. The results of studies in humans looking more directly at the influence of ACE inhibitors on atherosclerosis and ischemic heart disease are awaited.

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The QUinapril Ischemic Event Trial (QUIET) design and methods: Evaluation of chronic ACE inhibitor therapy after coronary artery intervention

Cited by 38 publications

References 39 publications

Tissue Angiotensin and Pathobiology of Vascular Disease

Tissue Angiotensin and Pathobiology of Vascular Disease

Inhibitory effects of fluvastatin, a new HMG‐CoA reductase inhibitor, on the increase in vascular ACE activity in cholesterol‐fed rabbits

Angiotensin-converting enzyme inhibitors and coronary artery disease

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