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Preoperative therapy with ACE inhibitors has an influence on renal functions. This study demonstrates that administration of ACE inhibitors provides better renal protection after cardiac surgery.
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In patients who reported angina (n = 111) during the three months preceding MI, LV volume change was -0.73 +/- 2.6 ml over the 90-day post-MI period, compared with 6.8 +/- 2.6 ml for patients (n = 172) without angina (p = 0.017). In contrast, there were no differences in changes in ejection fraction based on prior angina. Maximal creatine kinase was significantly lower in patients with prior angina (2,119 +/- 1,729 vs. 2,701 +/- 2,088, p = 0.016). In a multivariate model, prior angina remained protective for ventricular remodeling after adjusting for age, gender, baseline ejection fraction, Killip class, baseline end-diastolic volume, and drug treatment group (p = 0.042). However, the protective effect of pre-infarction angina appeared to be attenuated in diabetic patients.
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Treatment with ramipril resulted in reduced primary end point rates (11.3% vs. 14.9% in the placebo arm; relative risk [RR] 0.77, 95% confidence interval [CI] 0.62 to 0.96; p = 0.019), fewer strokes (3.1% vs. 4.8%; RR 0.64, 95% CI 0.43 to 0.96; p = 0.029) and fewer CV deaths (4.2% vs. 6.9%; RR 0.62, 95% CI 0.44 to 0.88; p = 0.0068). There were trends toward reduced rates of myocardial infarction, heart failure and all-cause death. The beneficial effect of ramipril was similar in women and men.
We investigated the acute effect of the new long-acting ACE-inhibitor ramipril on angina-limited exercise tolerance and exercise-induced ST-depression in 18 normotensive patients with angiographically confirmed coronary artery disease in a double-blind, placebo-controlled study. Patients underwent a repeat exercise ECG 24 hours following either 5 mg ramipril p.o. or placebo. Plasma-ACE activity (nmol/min x ml) in the ramipril-group (n = 8) was significantly reduced 24 hours after 5 mg ramipril compared to placebo (n = 10): 14.0 +/- 2.0 vs 87.2 +/- 13.5, p less than 0.001. Exercise-induced ST-segment depression was not different before and after ramipril or placebo. Heart rate at rest and during angina-limited exercise was not different between the first exercise-ECG and that after ramipril or placebo, nor between the groups. Systolic arterial pressure (mmHg) was slightly, but insignificantly, lower after than before ramipril at rest (113.8 +/- 5 vs 125 +/- 6.8) and at maximal exercise, 1.5 watt/kg (150 +/- 9.4 vs 158.3 +/- 13.3). In the placebo group, blood pressure at rest and during exercise was not different before and after placebo: 126 +/- 4.7 vs 125.5 +/- 7.5 and 157.5 +/- 3.8 vs 158 +/- 3.6. Rate-pressure-product (mmHg/min x 1000) at rest prior to (8.42 +/- 0.83 and 8.95 +/- 0.51) and after ramipril or placebo (8.00 +/- 0.94 and 8.93 +/- 0.71) showed no significant difference. Similarly, rate-pressure-product at maximal exercise was equal among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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ACE inhibition and AT1 receptor blockade have beneficial effects in remodeling processes during cardiac pressure overload. There are small differences between the 2 therapeutical approaches, but the combination therapy has no additional benefit.
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Thee results showed that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (AT1ras) provide marked decreases in proteinuria, making their use indisputable in patients with glomerulonephritis. Carvedilol was not found to be as effective as ACEIs and AT1ras in decreasing proteinuria and preserving renal function.
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On the basis of recent evidence that the cyclooxygenase-2 (COX-2) gene promoter contains functional binding sites for the nuclear factor of activated T cells (NFAT) and that COX-2 is expressed in a regulated fashion in the kidney, this study aimed to assess the effect of immunosuppressants on COX-2 expression in the kidney. Therefore, Wistar-Kyoto rats were treated with cyclosporine A (CsA; 15 mg/kg per day) or tacrolimus (5 mg/kg per day) for 7 d each. Both drugs markedly lowered COX-2 expression while COX-1 expression remained unaltered. Furthermore, CsA blunted the increase of renocortical COX-2 expression in response to low salt intake or a combination of low-salt diet with the ACE inhibitor ramipril (10 mg/kg per day), which strongly stimulates renocortical COX-2 expression. At the same time, calcineurin inhibitors moderately enhanced basal as well as stimulated renin secretion and renin gene expression. These findings suggest that inhibition of calcineurin could be a crucial determinant for the regulated expression of COX-2 in the kidney. Inhibition of COX-2 expression may therefore at least in part account for the well-known adverse effects of immunosuppressants in the kidney. Moreover, our data suggest that the stimulation of the renin system by low salt and by ACE inhibitors is not essentially mediated by COX-2 activity.
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Treatment with ramipril has a significant impact on plasma fibrinolytic variables during the recovery phase after acute MI. The renin-angiotensin system appears to play an important role in the regulation of vascular fibrinolysis, and interruption of this regulatory pathway may contribute to the clinical benefits of ACE inhibitors.
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Urinary excretion of albumin and N-acetyl-beta-D-glucosaminidase decreased in 13 patients (group 1), but increased in the remaining five patients (group 2). Blood pressure clearly decreased in group 1, but remained constant in group 2. In terms of clinical and biochemical data, the group 2 patients differed from those in group 1, having a lower age, a shorter history of diabetes and higher hemoglobin A1c levels despite higher doses of insulin.
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Up to seven in every 1000 patients experience angioedema from angiotensin-converting enzyme (ACE) inhibitors, even after many years of use. In 2003, every 20th Norwegian used an ACE inhibitor.
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It is well-known that patients with terminal renal insufficiency are at increased risk for a future cardiovascular event. A relevant relationship also appears to apply to the early stages of renal insufficiency. The HOPE study has shown that the incidence of myocardial infarction, apoplexy and cardiovascular mortality in patients with incipient renal insufficiency is significantly raised. The study also found that the incidence of cardiovascular events is in direct proportion to the level of serum creatinine. Against this background, patients at risk can be readily identified. The HOPE study documents a considerable cardiovascular risk for patients with incipient renal insufficiency and concomitant uncomplicated hypertension, atherosclerosis or diabetes. In view of this, the use of ACE inhibitors in patients with moderate renal insufficiency should now be introduced. In the HOPE subjects, ramipril was found not only to lower the cardiovascular risk, but also to improve renal insufficiency.
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Cognitive and functional decline are important consequences of atrial fibrillation, even in the absence of overt stroke.
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The mechanism by which bradykinin induces catecholamine release from neural tissues was investigated in two experimental models of rat origin. The rat phaeochromocytoma cell line PC12 was used to identify the subtype of bradykinin receptors involved in the stimulation of noradrenaline secretion and to compare the effects of three different B2-antagonists. An increase of catecholamine release induced by bradykinin in vivo could be confirmed by measuring plasma levels in pithed spontaneously hypertensive rats (SHR) during electric preganglionic stimulation of the spinal cord. In this whole animal model, the effects of inhibition of both uptake and alpha 2-adrenoceptors on plasma levels of noradrenaline and adrenaline were studied as well as the potentiation of exogenous bradykinin by inhibition of angiotensin I-converting enzyme and neutral endopeptidase. The receptor subtypes involved (i.e. B1 or B2) were characterized by application either of HOE 140 or desArg9-[Leu8]-bradykinin respectively. In PC12 cells bradykinin provoked a prominent increase of noradrenaline release at low concentrations (concentration required for 50% of the maximum response 1 nM), whereas the B1-agonist desArg9-bradykinin was only effective at concentrations higher than 30 microM. The effects of both kinins could be blocked by the B2-specific antagonist HOE 890307 which, like HOE 140, exerted no agonistic effect of its own. As has been shown in other neural cells, the B2-specific antagonist [Thi5,8, D-Phe7]-bradykinin only acted as a low-affinity agonist without any antagonistic effects. In experiments where the intention was to induce B1-receptor expression either by angiotensin I-converting enzyme inhibition or lipopolysaccharide application, no alteration of the secretory response of PC12 cells to bradykinin or desArg9-bradykinin could be shown. In pithed SHR, infusion of bradykinin (up to 1200 ng/min/kg) did not enhance stimulation-dependent release of noradrenaline or adrenaline. After pretreatment of the rats with ramipril bradykinin became effective and its effects were further potentiated by the concomitant application of phosphoramidon. B2-antagonism by HOE 140 abolished the bradykinin-induced release of noradrenaline and reduced the effect on plasma adrenaline. The B1-specific antagonist desArg9-[Leu8]-bradykinin was unable to diminish the stimulatory effects of bradykinin and instead brought about an increase of plasma adrenaline levels. In conclusion, bradykinin stimulates release of catecholamines from PC12 cells, peripheral sympathetic neurons and chromaffine cells by activation of ganglionic or presynaptic B2-receptors. The adrenal medulla and PC12 cells appear to be highly susceptible not only to stimulation by bradykinin, but also to non-specific stimulatory effects of certain kinin-antagonists.
Angiotensin converting enzyme inhibitors are effective in the treatment of hypertension and congestive heart failure. Within the past two years, four new agents in this class-benazepril, fosinopril, quinapril and ramipril--have been approved in the United States for use in the treatment of hypertension. These agents have been shown to be as effective as the older angiotensin converting enzyme inhibitors in treating hypertension and, in limited trials, congestive heart failure. The side effect profiles of the new agents are similar to those of other agents in this class that do not contain a sulfhydryl group. Fosinopril has a unique route of elimination that may make it the preferred agent in patients with renal failure. Otherwise, the new angiotensin converting enzyme inhibitors have no proven clinical advantages over other available agents. However, at moderate to high doses, the new agents may be substantially less expensive.
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Immobilization stress induces vascular oxidative stress by activating the angiotensin II/AT(1) receptor signaling pathway, thereby provoking endothelial dysfunction which can contribute to the development of atherosclerosis and hypertension.
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We studied cardiovascular and catecholamine responses for 3 days in three groups of patients undergoing abdominal hysterectomy. The night before surgery and again 2 h before induction of anaesthesia, patients received the ACE inhibitor, ramipril, the beta 1 blocker, metoprolol, or placebo. In the actively treated groups, mean diastolic pressure was reduced during surgery and increases in heart rate and arterial pressure after surgical incision were attenuated. During operation, stroke volume (SV) and cardiac output (CO) were significantly higher in the ramipril group. In contrast, beta 1, adrenergic block caused no significant changes in SV or CO. The concentration of noradrenaline in plasma and urine indicated that ACE inhibition caused attenuated release of noradrenaline. The results support the concept that angiotensin II facilitates release of noradrenaline from sympathetic nerves and that ACE inhibition inhibits this release.
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A total of 77 patients were analyzed. The median highly sensitive C-reactive protein concentration at baseline was 2.17 mg/l (interquartile interval 0.97-4.54); whereas in post-treatment, the median was 1.70 mg/l (interquartile interval 0.88-3.41), P=0.0009. Patients were stratified according to risk level determined by baseline highly sensitive C-reactive protein levels: low-risk (<1 mg/l), intermediate risk (1-3 mg/l) and high risk (>3 mg/l) The reduction in highly sensitive C-reactive protein occurred at the expense of the high-risk group (baseline 5.02 mg/l, post-treatment 3.3 mg/l, P<0.0001), with no differences in the other groups. In multiple regression analysis, the reduction observed in the high-risk group could not be explained by baseline treatment or change in any of the variables analyzed.
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In adult hypertensive patients, treatment with aliskiren plus ARB was associated with significantly better compliance/persistence and fewer hospitalizations and ER visits compared with ACEI plus ARB therapy. Reductions in total healthcare costs were non-significantly different between patients treated with aliskiren plus ARB versus ACEI plus ARB, despite the increased prescription costs associated with aliskiren plus ARB therapy.
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In this high-risk cohort, ramipril reduced the risk of MI, worsening and new angina, and the occurrence of coronary revascularizations.
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C57B1/6 mice received either the ACEI ramipril (2.5 mg/kg body weight), the ARB telmisartan (20 mg/kg body weight), or the combination. In all groups, pressure overload was induced by transverse aortic constriction (TAC). Cardiac hypertrophy (heart weight/tibia length) induced by TAC was reduced in all 3 treatment groups, with the most pronounced effect in the telmisartan group. The cardiomyocyte short-axis diameter and cardiac fibrosis were increased by TAC and similarly reduced by ACEI, ARB, and the combination therapy. The TAC-induced increase in the number of proliferating Ki67(pos) cardiomyocytes and noncardiomyocytes was reduced more potently by ACEI than by ARB. Four days of drug treatment induced a significant increase in Scal(pos)/VEGFR1(pos) endothelial progenitor cells (EPCs) in all animals in the treated SHAM groups. After 1 day of aortic constriction, only ramipril increased EPC numbers; after 5 weeks, telmisartan monotherapy did not change the EPC levels compared to vehicle or the combination therapy but raised it compared to ramipril. Neither TAC nor one of the therapies changed the number of cardiac capillaries per cardiomyocytes.
Local inhibition of angiotensin-converting enzyme (ACE, kininase II) produces both-attenuation of angiotensin II generation and of bradykinin degradation. To delineate the participation of bradykinin in the cardioprotective actions of ACE inhibitors, experiments were performed in rats and dogs with cardiac ischemia-reperfusion injuries. In isolated perfused working rat hearts with regional myocardial ischemia, bradykinin in concentrations as low as 1 x 10(-9) M increases coronary flow and reduces the incidence and duration of reperfusion ventricular fibrillation. In addition, enzyme activities of lactate dehydrogenase and creatine kinase as well as lactate output were decreased in the venous effluent of bradykinin-perfused hearts, which also showed improved cardiodynamic and metabolic parameters. Even concentrations of bradykinin lower than 1 x 10(-10) M, which were without influence on coronary flow, exerted comparable beneficial metabolic effects connected with reduced incidence and duration of ventricular fibrillation. Combined perfusions with threshold concentrations of bradykinin (1 x 10(-12) M) and the ACE inhibitor ramiprilat (2,58 x 10(-9) M), which were ineffective given alone, resulted in a marked cardioprotective effect. Perfusion with angiotensin II (1 x 10(-9) M) aggravated reperfusion arrhythmias and worsened myocardial metabolism. Bradykinin perfusion prevented this deterioration in a concentration-dependent manner. The bradykinin antagonist D-Arg-[Hyp2, Thi5,8, D-Phe7]-bradykinin (1 x 10(-5)) completely abolished the cardioprotective effects of bradykinin or the ACE inhibitor. However, higher concentrations of bradykinin (1 x 10(-7) M) or ramiprilat (2,58 x 10(-5) M) reversed these properties of the bradykinin antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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Quantitative data for prediction of incidence and progression of early CKD are scarce in individuals with type 2 diabetes. Therefore, two risk prediction models were developed for incidence and progression of CKD after 5.5 years and the relative effect of predictors were ascertained.