Angiotensin Converting Enzyme Inhibition in Heart, Kidney, and Serum Studied Ex Vivo after Administration of Zofenopril, Captopril, and Lisinopril (original) (raw)
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Journal of the American …, 2005
This study was designed to identify all randomized clinical trial data evaluating angiotensinconverting enzyme inhibitors or angiotensin receptor blockers for the prevention of atrial fibrillation (AF), to estimate the magnitude of this effect and to identify patient subgroups most likely to benefit. BACKGROUND Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reduce morbidity and mortality in patients with heart failure, vascular disease, and hypertension. Several reports suggest that they may also prevent the development of AF.
Journal of The American College of Cardiology, 2005
This study was designed to identify all randomized clinical trial data evaluating angiotensinconverting enzyme inhibitors or angiotensin receptor blockers for the prevention of atrial fibrillation (AF), to estimate the magnitude of this effect and to identify patient subgroups most likely to benefit. BACKGROUND Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reduce morbidity and mortality in patients with heart failure, vascular disease, and hypertension. Several reports suggest that they may also prevent the development of AF.
American heart journal, 2004
The renin-angiotensin-aldosterone system has a pivotal role in the short- and long-term regulation of blood pressure through its principal mediator, angiotensin II. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II-receptor blockers (ARBs) decrease the deleterious effects of angiotensin II on the vasculature and heart, but have different mechanisms of action. Although the blood pressure-lowering effect of ACE inhibitors and ARBs is equivalent to that of most other antihypertensive agents, emerging data suggest that these drug classes may have a greater effect on decreasing cardiovascular morbidity and mortality rates in specific patient populations. We reviewed large (approximately > or =5000 patients) hypertension clinical trials using ACE inhibitors and ARBs and with cardiovascular morbidity/mortality end points. Six trials of ACE inhibitors and 5 trials of ARBs (3 completed, 2 ongoing) were selected for this analysis. Data from these hypertension mega-trials su...
Journal of the renin-angiotensin-aldosterone system : JRAAS, 2008
Introduction. Angiotensin-converting enzyme (ACE) inhibitors reduce cardiovascular events in patients with established vascular disease and heart failure (HF). ACE-inhibitors have important effects on fibrinolytic balance, which may be the underlying mechanism for a reduction in cardiovascular events.Although angiotensinreceptor blockers (ARBs) offer greater tolerability than ACE-inhibitors, the major ARB trials have demonstrated a lack of reduction in myocardial infarction (MI) occurrence and mortality in contrast to ACE-inhibitors. In this study, we investigated the combined effects of ARBs and ACE-inhibitors on fibrinolytic and inflammatory parameters in patients with uncontrolled hypertension. Methods. Twenty-four patients with uncontrolled hypertension despite taking adequate doses of ACE-inhibitor therapy were selected. Patients were started on Candesartan 16 mg once a day. Plasma plasminogen activator inhibitor (PAI-1) antigen (Ag), tissue plasminogen activator (t-PA) Ag, thrombin-activatable fibrinolysis inhibitor (TAFI) % activity and high sensitivity C-reactive protein (hsCRP) levels, were measured during low salt intake at baseline and two weeks after therapy with an ARB. Results. Addition of ARB to the regimen reduced systolic (155±17 vs. 139±13, p<0.001), and diastolic (91±9 vs. 81±8, p<0.001) blood pressures (BP). No significant changes were observed in PAI-1 Ag (66±51 vs. 68±52, p=0.9), t-PA Ag (12.6±5.3 vs. 13.3±4.7, p=0.3),TAFI % activity (119±30 vs. 118±32, p=0.9) and hsCRP (3.9±3.4 vs. 3.6±3.6, p=0.7) levels after adding an ARB. Conclusions. Combined ARB and ACE-inhibitor use provide better BP control without any detrimental effect in plasma inflammatory and fibrinolytic parameters.
Abstract The renin–angiotensin–aldosterone system plays a major role in the pathophysiology of hypertension and closely related cardio- and cerebrovascular events. Although both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor antagonists (angiotensin receptor blockers; ARBs) are equally important in the treatment of hypertension, according to the results of recent years, there might be substantial differences in their cardiovascular protective effects, and these differences might be explained by our increasing knowledge of their nonoverlapping mechanisms of action. The number of studies investigating how ACE inhibitors and ARB agents differ will certainly be increasing in the future. ACE inhibitors are the safe therapeutic opportunity for hypertensive patients at high risk, with a cardiological comorbidity.
The renin angiotensin aldosterone system (RAAS) plays a central role in the pathophysiology of hypertension and vascular disease. Angiotensin converting enzyme inhibitors (ACEis) suppress angiotensin II (ANG II) concentrations, whereas angiotensin receptor blockers (ARBs) block the binding of ANG II to AT 1 receptors. ACEis and ARBs are both effective anti-hypertensive agents and have similar risk reductions in stroke — a blood pressure dependent phenomenon. ACEis also reduce the risk of myocardial infarction (MI) and mortality in high risk hypertensive patients, as well as in diabetics, the elderly, those with vascular disease, and in congestive heart failure. ARBs, in contrast, do not reduce the risk of MI or death in clinical trials where the comparator has been another active therapy or even a placebo. Systematic reviews of ARBs that include meta-analyses or meta-regression analyses confirm that ARBs lack the cardiovascular protective effects of ACEis, which in part are " independent " of blood pressure lowering. Practice guidelines, especially those in high risk hypertensive patients, should reflect the evidence that ACEis and ARBs have divergent cardiovascular effects — ACEis reduce mortality, whereas ARBs do not. ACEis should be the preferred RAAS inhibitor in high risk patients. Angiotensin converting enzyme inhibitors (ACEis) and angioten-sin II type 1 (AT 1) receptor blockers (ARBs) are anti-hypertensive (HTN) agents that modulate the renin angiotensin aldosterone system (RAAS) by targeting angiotensin II (ANG II), each with a unique mode of action. ACEis suppress the production of ANG II, whereas ARBs block the ANG II stimulation of the AT 1 receptor; therefore each is a unique therapeutic class. ACEis and ARBs do have similar blood pressure (BP) lowering effects, with a positive impact on stroke, 1 diabetic kidney disease, 2 symptoms of congestive heart failure (HF), 3 and at least in post hoc analyses of large clinical trials, reduce the incidence of diabetes mellitus(DM) and atrial fibrillation. 4 This shared efficacy has led to the conclusions in many practice guidelines that ACEis and ARBs are equivalent, interchangeable, and alternative
Hypertension, 2005
Some evidence suggests that long-term angiotensin-converting enzyme (ACE) inhibition may become less effective, thereby increasing angiotensin II levels, which could be inhibited by the addition of an angiotensin receptor blocker. We conducted a meta-analysis of randomized trials with searches of MEDLINE, EMBASE, and Cochrane databases. Overall, the combination of an ACE inhibitor and an angiotensin receptor blocker reduced ambulatory blood pressure by 4.7/3.0 mm Hg (95% confidence interval [CI], 2.9 to 6.5/1.6 to 4.3) compared with ACE inhibitor monotherapy and 3.8/2.9 mm Hg (2.4 to 5.3/0.4 to 5.4) compared with angiotensin receptor blocker monotherapy. Clinic blood pressure was reduced by 3.8/2.7 mm Hg (0.9 to 6.7/0.8 to 4.6) and 3.7/2.3 mm Hg (0.4 to 6.9/0.2 to 4.4) compared with ACE inhibitor and angiotensin receptor blocker, respectively. However, the majority of these studies used submaximal doses or once-daily dosing of shorter-acting ACE inhibitors and, when a larger dose of shorter-acting ACE inhibitor was given or a longer-acting ACE inhibitor was used, there was generally no additive effect of the angiotensin receptor blocker on blood pressure. Proteinuria was reduced by the combination compared with ACE inhibitor and angiotensin receptor blocker monotherapy, an effect that was independent of blood pressure in several studies, suggesting that the combination could have benefits in proteinuric nephropathies. None of the studies was of sufficient size and duration to determine whether there may be safety concerns. In conclusion, although there is a small additive effect on blood pressure with an ACE inhibitor-angiotensin receptor blocker combination, the routine use of this combination in uncomplicated hypertension is not recommended until more carefully controlled studies are performed. (Hypertension. 2005;45:880-886.)