Inhibition of matrix metalloproteinase-9 activity by lisinopril after myocardial infarction in hamsters

We measured angiotensin-converting enzyme and matrix metalloproteinase-9 activities after myocardial infarction in hamsters and compared the effects of an angiotensin-converting enzyme inhibitor lisinopril with those of an angiotensin receptor blocker candesartan cilexetil after myocardial infarction. Angiotensin-converting enzyme activity was significantly increased 3 and 7 days, but not 1 day after myocardial infarction. Matrix metalloproteinase-9 activity was significantly increased 1 day after myocardial infarction. Lisinopril significantly inhibited both angiotensin-converting enzyme and matrix metalloproteinase-9 activities, but candesartan cilexetil did not. Angiotensin-converting enzyme inhibitors might directly inhibit matrix metalloproteinase-9 activity.     

阿托伐他汀对急性心肌梗死患者血清成分与水平的影响

目的探讨阿托伐他汀对急性心肌梗死(AMI)患者炎症因子和内皮功能的影响。方法选择我院急性心肌梗死患者120例,随机均分为治疗组与对照组,2组均给予常规溶栓、抗凝、扩冠、β2受体阻滞剂和血管紧张素转换酶抑制剂等药物治疗,治疗组另口服阿托伐他汀。治疗前、后对血清可溶性细胞间黏附分子(sICAM-1)、内皮素(ET)和肿瘤坏死因子-α(TNF-α)水平进行测定,并进行统计学比较。结果治疗前sICAM-1、ET和TNF-α水平2组差异无统计学意义。治疗后2组血清sICAM-1、ET和TNF-α水平均较治疗前有所下降(P<0.05),阿托伐他汀组sICAM-1、ET和TNF-α水平明显低于对照组水平(P<0.05)。结论阿托伐他汀对急性心肌梗死患者炎症因子和内皮功能有一定的影响。     

Effects of temocapril and olmesartan on myocardial sympathetic nervous activity and fatty acid metabolism in rats with chronic beta-adrenergic stimulation

We investigated the effects of an angiotensin-converting enzyme inhibitor (temocapril) and an angiotensin II type 1 receptor blocker (olmesartan) on changes in myocardial sympathetic nervous activity, fatty acid metabolism and myocardial blood flow using 131I-meta-iodobenzylguanidine, 125I-beta-methyl-iodophenyl pentadecanoic acid and 99mTc-tetrofosmin, respectively, in rats with isoproterenol-induced cardiac hypertrophy. Male Sprague-Dawley rats underwent isoproterenol administration (3 mg/kg per day) for 1 week by osmotic mini-pump. The hearts were excised and analyzed for the uptake of meta-iodobenzylguanidine. Beta-methyl-iodophenyl pentadecanoic acid and tetrofosmin in 11 segments in four groups; sham group (saline), isoproterenol group (isoproterenol alone), angiotensin-converting enzyme inhibitor group (isoproterenol and temocapril), and angiotensin II type 1 receptor blocker group (isoproterenol and olmesartan). Isoproterenol significantly increased the heart weight compared with the sham group, whereas it was significantly blunted in the angiotensin-converting enzyme inhibitor and angiotensin II type 1 receptor blocker groups. The ratio of the percent kilogram dose per gram of meta-iodobenzylguanidine to tetrofosmin, an index of myocardial sympathetic nervous activity, was significantly decreased in the isoproterenol group (0.18 +/- 0.01) compared with the sham group (0.41 +/- 0.03). Importantly, these changes were significantly improved in the angiotensin-converting enzyme inhibitor (0.28 +/- 0.01) and the angiotensin II type 1 receptor blocker groups (0.32 +/- 0.01). The ratio of the percent kilogram dose per gram of beta-methyl-iodophenyl pentadecanoic acid to tetrofosmin, an index of myocardial fatty acid metabolism, was significantly decreased in the isoproterenol group (1.30 +/- 0.03) compared with the sham group (1.60 +/- 0.10). In contrast, there were no significant differences in beta-methyl-iodophenyl pentadecanoic acid to tetrofosmin ratios between the sham and angiotensin-converting enzyme inhibitor groups, or the angiotensin II type 1 receptor blocker group. Cardiac hypertrophy induced by chronic beta-adrenergic stimulation is accompanied by impairment of sympathetic nervous activity and fatty acid metabolism. These abnormalities are effectively prevented by the angiotensin-converting enzyme inhibitor and the angiotensin II type 1 receptor blocker.     

Gene expression profile revealed different effects of angiotensin II receptor blockade and angiotensin-converting enzyme inhibitor on heart failure

Although recent clinical studies have indicated that angiotensin II receptor blocker is as effective in treating heart failure as an angiotensin-converting enzyme inhibitor, it is unknown whether their effects are different. Dahl salt-sensitive rats were treated with an angiotensin-converting enzyme inhibitor benazepril, and an angiotensin II receptor blocker candesartan from 11 weeks old. We examined cardiac geometry and function by echocardiography, and histology and gene expression by high-density oligonucleotide arrays using Affymetrix U34 (Affymetrix, Santa Clara, CA, U.S.A.). Dahl salt-sensitive rats fed a high salt diet showed a marked increase in blood pressure and developed concentric hypertrophy at 11 weeks, followed by left ventricle dilation and congestive heart failure by 20 weeks after birth. Although both medications had only a mild antihypertensive effect, they strongly suppressed the development of cardiac hypertrophy, fibrosis and heart failure to the same extent. Gene expression pattern examined by Affymetrix GeneChip (Affymetrix) is quite different between the two drug groups, indicating that angiotensin II receptor blocker and angiotensin-converting enzyme inhibitor prevent heart failure by different mechanisms.     

119例急性心肌梗死患者用药情况调查分析

目的:了解β受体阻滞药、血管紧张素转换酶抑制药、阿司匹林、他汀类药物在急性心肌梗死患者中的利用情况。方法:对重庆市江北区4所医院1999年～2004年诊断为急性心肌梗死的119例出院患者的资料进行回顾性分析。结果:β受体阻滞药与血管紧张素转换酶抑制药的适宜应用率分别为79.0%、85.7%,实际应用率分别为35.3%、43.7%,分别有55.3%、49.0%适宜应用β受体阻滞药和血管紧张素转换酶抑制药的患者未得到相应治疗;阿司匹林应用率较高,达84.9%;他汀类药物2002年后才逐步应用,应用率为15.1%。结论:除阿司匹林应用合理外,其它3种药物的应用与我国“急性心肌梗死诊断和治疗指南”的要求存在明显差距。但这种情况正在改变。     

Candesartan for the treatment of hypertension and heart failure

Candesartan is a selective angiotensin II Type I (AT(1)) receptor blocker which binds tightly to, and dissociates slowly from the receptor. It is an effective, long-acting antihypertensive agent with few or no side effects, when compared to placebo in hypertension trials. Several studies indicate that candesartan might prevent diabetes. A research programme of three prospective randomised outcome trials (the CHARM [Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity] programme) has shown that candesartan is of clinical value in a broad spectrum of patients with symptomatic heart failure, regardless of background therapy and ventricular function. There is a clear benefit of candesartan in patients unable to tolerate an angiotensin-converting enzyme inhibitor (ACEI) and this benefit is of a similar magnitude to that obtained with an ACEI. CHARM-Added shows that symptoms, morbidity and cardiovascular mortality are further reduced if an AT(1)-receptor blocker is added to an ACEI. This benefit is not only statistically significant but also clinically important. CHARM-Preserved indicate that candesartan can reduce hospital admission for heart failure in patients with preserved systolic function.     

Candesartan for the treatment of hypertension and heart failure

Candesartan is a selective angiotensin II Type I (AT₁) receptor blocker which binds tightly to, and dissociates slowly from the receptor. It is an effective, long-acting antihypertensive agent with few or no side effects, when compared to placebo in hypertension trials. Several studies indicate that candesartan might prevent diabetes. A research programme of three prospective randomised outcome trials (the CHARM [Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity] programme) has shown that candesartan is of clinical value in a broad spectrum of patients with symptomatic heart failure, regardless of background therapy and ventricular function. There is a clear benefit of candesartan in patients unable to tolerate an angiotensin-converting enzyme inhibitor (ACEI) and this benefit is of a similar magnitude to that obtained with an ACEI. CHARM-Added shows that symptoms, morbidity and cardiovascular mortality are further reduced if an AT₁-receptor blocker is added to an ACEI. This benefit is not only statistically significant but also clinically important. CHARM-Preserved indicate that candesartan can reduce hospital admission for heart failure in patients with preserved systolic function.     

Effects of early angiotensin-converting enzyme inhibition in a pig model of myocardial ischemia and reperfusion.

In a blind, randomized study, the effects of perindopril, a nonsulfhydryl-containing angiotensin-converting enzyme (ACE) inhibitor, were compared with those of placebo in a closed-chest pig model of myocardial infarction. In anesthetized pigs, myocardial ischemia and reperfusion were induced by inflation and deflation of a catheter balloon in the left anterior descending coronary artery (LAD), respectively. Thirty minutes after induction of ischemia and 15 min before reperfusion, a bolus injection of 0.06 mg/kg perindoprilat (n = 12), the active compound of perindopril, or placebo (n = 12) was administered in the pulmonary artery of these animals. After the acute phase of myocardial infarction, treatment with 12 mg/day perindopril or placebo was continued orally for 2 weeks. During the entire treatment period, 7 of 12 animals died in the placebo group versus 2 of 12 animals in the perindopril group (Fisher's exact test p less than 0.04). This beneficial effect of perindopril on mortality could not be attributed to salvage of myocardial tissue because the increases in creatine phosphokinase and coronary venous purine levels were similar in perindopril- and placebo-treated animals. Neither were there any significant between-treatment differences in the hemodynamic and (neuro)humoral parameters during the acute phase of myocardial infarction. The difference in mortality was observed within 24 h after myocardial infarction. Prevention of acute pump failure and, especially, life-threatening ventricular arrhythmias may explain this improvement in survival by perindopril. Retrospectively, logistic regression analysis showed that, irrespective of treatment, survival was inversely correlated to plasma renin activity (PRA) before induction of ischemia (r = -0.33; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of perindopril in the prevention of stroke

Stroke is one of the leading causes of disability and death worldwide and is a more common cause of cardiovascular morbidity and mortality than myocardial infarction among patients with hypertension. Identifying and modifying key risk factors is crucial to reduce morbidity and mortality from stroke. Hypertension is the most important modifiable risk factor for ischemic stroke, and antihypertensive treatment is of paramount importance to reduce the incidence of stroke mortality and morbidity. Perindopril is a third-generation long acting, once-daily lipophilic angiotensin-converting enzyme inhibitor with high tissue angiotensin-converting enzyme affinity, lowering angiotensin II and potentiating bradykinin. Its efficacy, safety and tolerability are well established in the treatment of hypertension and heart failure. The purpose of this article is to review the evidence from clinical trials as well as from recent patents that has been gathered in regard to perindopril, demonstrating not only its efficacy in reducing blood pressure, but also to other cardiovascular protective properties that act in addition to the obvious blood-pressure-lowering effect in the prevention of stroke in patients with essential hypertension, with particular attention paid to the results from the Perindopril Protection Against Recurrent Stroke Study (PROGRESS).     

Acute renal failure during lisinopril and losartan therapy for proteinuria

The use of combined therapy with an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II receptor blocker (ARB) for treatment of proteinuria has been gaining support. Limited data are available regarding this treatment in the pediatric population. This report describes a case of acute compromise of renal function associated with hypotension in a 7-year-old boy treated with the ACE inhibitor lisinopril and the ARB losartan. It emphasizes the need for close surveillance of renal function and blood pressure during such therapy even in patients with relative preservation of renal function. Further investigation into the utility and safety of dual therapy with an ACE inhibitor plus an ARB in pediatric patients is warranted. Key Words: renal failure, proteinuria, angiotensin-converting enzyme inhibitor, ACEI, angiotensin II receptor blocker, ARB.     

American Heart Association scientific sessions

The Annual Scientific Sessions of the American Heart Association is the leading scientific conference in the cardiovascular field, both for basic and clinical research in cardiology and related disclipines. This report covers the outcome of major clinical trials that were presented in the 'late-breaking' clinical trial sessions. The Valsartan in Acute Myocardial Infarction Trial (VALIANT) investigated the angiotensin receptor blocker valsartan, the angiotensin-converting enzyme inhibitor captopril, and their combination in 14,703 survivors of an acute myocardial infarction with a reduced left ventricular ejection fraction on clinical outcome. The study demonstrated that valsartan and captopril where equally effective, whereas the combination was associated with an increased risk of side effects without further benefit. VALIANT is a landmark trial because it was the first large study that compared the combination of an angiotensin receptor blocker with an angiotensin-converting enzyme inhibitor in the setting of acute myocardial infarction. Other trials that will be summarised in this report are the Na + /H + Exchange Inhibition to Prevent Coronary Events in Acute Cardiac Conditions Trial (EXPEDITION; cariporide in coronary artery bypass graft surgery), the Reversal of Atherosclerosis with Aggressive Lipid Lowering Trial (REVERSAL; atorvastatin and pravastatin for atherosclerosis reversal), the Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation V (SPORTIF V; ximelagatran and warfarin for stroke prevention in atrial fibrillation), the Prophylactic Amiodarone for the Prevention of Arrhythmias that Begin Early After Revascularisation (PAPABEAR; amiodarone for the prevention of postoperative atrial fibrillation), the Acute and Chronic Therapeutic Impact of a Vasopressin 2 Antagonist in Congestive Heart Failure (ACTIV in CHF; vasopressin 2 antagonist tolvaptan in congestive heart failure) and Prevention of Renal and Vascular Endstage Disease Intervention Trial (PREVEND IT; fosinopril and pravastatin in microalbuminuric subjects without hypertension or hypercholesterolemia).     

American Heart Association Scientific Sessions

The Annual Scientific Sessions of the American Heart Association is the leading scientific conference in the cardiovascular field, both for basic and clinical research in cardiology and related disclipines. This report covers the outcome of major clinical trials that were presented in the ‘late-breaking’ clinical trial sessions. The Valsartan in Acute Myocardial Infarction Trial (VALIANT) investigated the angiotensin receptor blocker valsartan, the angiotensin-converting enzyme inhibitor captopril, and their combination in 14,703 survivors of an acute myocardial infarction with a reduced left ventricular ejection fraction on clinical outcome. The study demonstrated that valsartan and captopril where equally effective, whereas the combination was associated with an increased risk of side effects without further benefit. VALIANT is a landmark trial because it was the first large study that compared the combination of an angiotensin receptor blocker with an angiotensin-converting enzyme inhibitor in the setting of acute myocardial infarction. Other trials that will be summarised in this report are the Na⁺/H⁺ Exchange Inhibition to Prevent Coronary Events in Acute Cardiac Conditions Trial (EXPEDITION; cariporide in coronary artery bypass graft surgery), the Reversal of Atherosclerosis with Aggressive Lipid Lowering Trial (REVERSAL; atorvastatin and pravastatin for atherosclerosis reversal), the Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation V (SPORTIF V; ximelagatran and warfarin for stroke prevention in atrial fibrillation), the Prophylactic Amiodarone for the Prevention of Arrhythmias that Begin Early After Revascularisation (PAPABEAR; amiodarone for the prevention of postoperative atrial fibrillation), the Acute and Chronic Therapeutic Impact of a Vasopressin 2 Antagonist in Congestive Heart Failure (ACTIV in CHF; vasopressin 2 antagonist tolvaptan in congestive heart failure) and Prevention of Renal and Vascular Endstage Disease Intervention Trial (PREVEND IT; fosinopril and pravastatin in microalbuminuric subjects without hypertension or hypercholesterolemia).     

Effects of angiotensin II type 1 receptor antagonist (candesartan) in preventing fatal ventricular arrhythmias in dogs during acute myocardial ischemia and reperfusion

Fatal arrhythmias may be prevented by long-term oral administration of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 (AT 1 ) receptor antagonists. However, there have been no studies evaluating the electrophysiologic changes that occur with the acute administration of AT 1 receptor antagonists during acute myocardial ischemia and reperfusion. This study aimed to evaluate the ability of candesartan to prevent fatal arrhythmias during acute myocardial ischemia and reperfusion. The left anterior descending (LAD) coronary artery was ligated for 10 min and then reperfused for 10 min in 45 adult mongrel dogs. Candesartan (1 mg/kg) or saline was administered intravenously 10 min before ligation of the LAD coronary artery (candesartan group [n = 20] and control group [n = 25], respectively). Changes in ventricular effective refractory period (ERP) and intramyocardial conduction time (ICT) in the risk area were compared during LAD occlusion and reperfusion. Ischemia-induced shortening of ERP was inhibited in the candesartan group compared with the control. There was a 4.7 +/- 5.8% increase in ERP in the candesartan group, compared with a 11.5 +/- 6.3% shortening in the control group (p < 0.01). Prolongation of ICT was inhibited in the candesartan group compared with the control group during both ischemia and reperfusion (maximal prolongation of ICT: 0.1 +/- 3.0% vs. 37.7 +/- 9.6%, respectively; p < 0.01). Incidence of ventricular fibrillation was lower in the candesartan group than in the control group (25% [5/20] vs. 72% [18/25], respectively; p < 0.01). Candesartan suppresses changes in ERP and ICT during acute myocardial ischemia and reperfusion, suggesting that candesartan can prevent the development of fatal arrhythmias.     

The prevention of myocardial ultrastructural changes by perindopril, atenolol and amlodipine in chronic alcohol administered rats.

The effects of perindopril, an angiotensin converting enzyme inhibitor, atenolol, a beta adrenergic receptor blocker and amlodipine, a calcium channel blocker were investigated in chronic alcohol administered rats. Adult male Wistar rats (240-320 g) were used in the present study. Alcohol was given to rats by a modified liquid diet for 21 days. Perindopril (2.5 and 5 mgkg(-1)), atenolol (5 and 10 mg kg(-1)) and amlodipine (5 and 10 mg kg(-1)) were injected to rats in different groups intraperitoneally for 21 days. Control rats were pair fed by an isocaloric liquid diet containing sucrose as a caloric substitute for alcohol. Saline was injected to control rats for 21 days. Rats were anesthetized with ether. Their hearts were removed and 1 mm3 samples from left ventricles were fixed. Five fields per heart were examined and photographed with transmission electron microscope. Blood alcohol levels were also measured spectrophotometrically. Daily alcohol consumption of the rats was in a range of 12.09-15.5 g kg(-1). Blood alcohol concentrations were found as 145.63 mg dl(-1) at 21st day of alcohol consumption. Chronic alcohol consumption caused some marked myocardial injuries. Perindopril and atenolol but not amlodipine produced some significant beneficial effects on alcohol-induced myocardial damages. Our results imply that perindopril and atenolol but not amlodipine have protective effects on heavy chronic alcohol consumption-induced myocardial injury in rats.     

Cardiovascular status following combined angiotensin-converting enzyme and AT1 receptor inhibition in conscious spontaneously hypertensive rats

1. Combined treatment of spontaneously hypertensive rats (SHR) with AT1 receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors has been shown to reduce mean arterial pressure (MAP) more than monotherapy with either agent. The aims of the present study were to investigate the effects of chronic dual renin-angiotensin system (RAS) inhibition using non-hypotensive doses of the AT1 receptor antagonist candesartan cilexetil and the ACE inhibitor perindopril on cardiovascular function and structure. 2. Adult male SHR, aged 15 weeks, were divided into four groups: (i) candesartan cilexetil (0.5 mg/kg per day in drinking water); (ii) perindopril (0.3 mg/kg per day in drinking water); (iii) combined treatment (dual RAS inhibition); or (iv) the appropriate vehicle (0.1% ethanol/0.1% polyethylene glycol/1.5 mmol/l sodium bicarbonate dissolved in water for candesartan cilexetil; distilled water for perindopril). Systolic blood pressure was measured weekly using the tail-cuff method and urinary microalbuminuria was measured fortnightly. 3. After 4 weeks, rats were instrumented for intravenous drug administration and measurement of MAP. At this time, the cardiovascular effects of angiotensin (Ang) I and AngII (5-20 ng) and sodium nitroprusside (SNP) and acetylcholine (ACh; 1-5 micro g) were assessed. In addition, left ventricular : bodyweight and media : lumen ratios were determined as indices of cardiac and vascular hypertrophy, respectively. 4. Candesartan cilexetil and perindopril alone had minimal effect on MAP when measured both directly and indirectly, whereas direct MAP was significantly decreased in the combined treatment group (131 +/- 6 mmHg; P < 0.05) compared with the vehicle group (156 +/- 9 mmHg). Pressor responses to AngI were significantly decreased in all groups compared with the vehicle-treated group and pressor responses to AngII were significantly decreased in the candesartan cilexetil-treated (P < 0.01) and combined treatment groups (P < 0.01) compared with the vehicle-treated group. Depressor responses to ACh and SNP were not significantly affected by any of the antihypertensive therapies compared with vehicle-treated SHR. 5. Vascular hypertrophy was significantly decreased in the candesartan cilexetil and combined groups compared with the vehicle-treated group, whereas cardiac hypertrophy was reduced, with the rank order of effect being: dual RAS inhibition > perindopril > candesartan cilexetil. Urinary albumin tended to decrease with dual RAS inhibition, but was not significantly affected by this short-term treatment. 6. These results demonstrate the efficacy of low-dose dual RAS inhibition as an antihypertensive modality, at least in SHR, not only in reducing arterial pressure, but also in improving cardiovascular structure.     

Additive improvement of left ventricular remodeling by aldosterone receptor blockade with eplerenone and angiotensin II type 1 receptor antagonist in rats with myocardial infarction

We investigated the effects of the aldosterone blocker eplerenone alone and in combination with angiotensin II type 1 receptor antagonist on ventricular remodeling in rats with left ventricular (LV) dysfunction after extensive myocardial infarction (MI). Adding an aldosterone antagonist to an ACE inhibitor reduces mortality and morbidity in heart failure. Starting 1 day after MI, rats were treated with placebo, eplerenone (100 mg/kg/day), the angiotensin type 1 receptor antagonist candesartan (1 mg/kg/day), or a combination of both for nine weeks. Both monotherapies attenuated the rise in LV end-diastolic dimension (LVDd) and LV end-diastolic volume (LVEDV) compared with placebo, whereas combined treatment further attenuated LVDd and LVEDV and significantly improved LV function. Increased collagen type I and III gene expressions in the noninfarcted LV myocardium from MI placebo rats was attenuated by candesartan, but almost completely prevented by eplerenone and eplerenone/candesartan. The addition of eplerenone to candesartan prevented the increases in LV gene expression of ANP and BNP more effectively than either monotherapy. The aldosterone blocker eplerenone improved LV remodeling in rats with LV dysfunction after extensive MI. Combination therapy with an candesartan substantially potentiates this effect by a complementary prevention of LV fibrosis, cardiac hypertrophy, and molecular alterations.     

Regulation of angiogenesis and angiogenic factors by cardiovascular medications

Coronary artery disease (CAD) is the most important cause of death in the industrialized world. After experimental myocardial infarction, numerous dilated vessels appear in the border zone between the infarct and noninfarct areas. Angiogenic therapy has been widely regarded as an attractive approach for both treating CAD and enhancing arterioprotective functions of the endothelium. In this report, we critically review the evidence supporting the regulation of angiogenesis and angiogenic factors by cardiovascular medications such as statins, cholesterol ester transfer protein inhibitor, angiotensin II type 1 receptor blocker, angiotensin-converting enzyme inhibitor and calcium channel blocker, etc. Furthermore, in patients with CAD, vascular growth (vasculogenesis), capillary network growth (angiogenesis) and collateral artery growth (arteriogenesis), may be important. Current evidence from clinical trials on these therapies suggests that the development of coronary collateral circulation is likely to be a viable therapeutic strategy for CAD, while adaptation to chronic coronary stenosis can proceed. Many studies have suggested that newly developed strategies which include the administration of angiogenic growth factors and the transplantation of bone marrow-derived angioblasts are beneficial for the ischemic heart. Our assessment of the evidence in this review leads us to conclude that the development of collateral circulation using conventional cardiovascular medications may also play a critical role and needs to be reconsidered in the treatment of patients with CAD.     

Clinical trials evaluating angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in the setting of acute myocardial infarction

There is strong evidence from controlled clinical trials that in the setting of acute myocardial infarction complicated by heart failure or isolated left ventricular dysfunction, angiotensin-converting enzyme inhibitors started late during hospitalisation and continued in the long term, significantly reduced mortality and improved the prognosis. On the other hand, administration of angiotensin-converting enzyme inhibitors during the first 24 h in unselected patients with acute myocardial infarction provided only a slight benefit in terms of mortality. Angiotensin-II receptor blockers have and are being examined in the setting of acute myocardial infarction with left ventricular dysfunction and can provide an alternative for patients who cannot tolerate angiotensin-converting enzyme inhibitors. In this article, an evidence-based review of these major trials and suggestions for clinical application are presented.     

ST段抬高心肌梗死818例临床资料对比分析

目的：探究2006年与2014年我院收治ST段抬高心肌梗死患者一般资料、主要用药、住院期间不良心血管事件发生率的变化情况。方法：将我院2006年和2014年全部ST段抬高心肌梗死患者分为2006年组（n=96例）和2014年组（n =722例）,对2组临床资料进行回顾性分析并比较。结果：2014年组与2006年组相比,合并吸烟史、氯吡格雷、血管紧张素转换酶抑制剂/血管紧张素受体拮抗剂（ACEI/ARB）/螺内酯应用及急诊冠脉介入治疗比例升高,住院期间再发心绞痛、心源性死亡比率下降,阿司匹林、他汀类药物使用率及发病到就诊时间、住院天数无明显变化。结论：吸烟与急性心肌梗死发病率升高关系密切。患者对急性心肌梗死知识仍然缺乏,医生对RAAS抑制剂重视程度不够。     

Clinical trials evaluating angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in the setting of acute myocardial infarction

There is strong evidence from controlled clinical trials that in the setting of acute myocardial infarction complicated by heart failure or isolated left ventricular dysfunction, angiotensin-converting enzyme inhibitors started late during hospitalisation and continued in the long term, significantly reduced mortality and improved the prognosis. On the other hand, administration of angiotensin-converting enzyme inhibitors during the first 24 h in unselected patients with acute myocardial infarction provided only a slight benefit in terms of mortality. Angiotensin-II receptor blockers have and are being examined in the setting of acute myocardial infarction with left ventricular dysfunction and can provide an alternative for patients who cannot tolerate angiotensin-converting enzyme inhibitors. In this article, an evidence-based review of these major trials and suggestions for clinical application are presented.