Clinical InvestigationAcute Ischemic Heart DiseaseEffects of early angiotensin-converting enzyme inhibition in patients with non–ST-elevation acute anterior myocardial infarction
Section snippets
Subjects
The SMILE Study included 1556 patients admitted to 154 Italian coronary care units who were randomized to study treatment with an ACE inhibitor or placebo in addition to recommended pharmacological treatment. Details of the study protocol have been published elsewhere.7 Main SMILE Study inclusion criteria were the following: (1) male or female sex, (2) age 18 to 80 years, (3) admittance to the intensive care unit within 24 hours of the onset of chest pain typically associated with
Patients
A total of 526 (33.8%) of the 1556 patients included in the main SMILE Study had NSTEMI with chest pain. Mean treatment duration was 5.1 ± 0.4 weeks (median 5.4 weeks), whereas average follow-up time was 52 ± 2 weeks.
The number of NSTEMI patients was well balanced between the two treatment arms: 273 patients (51.9% of the NSTEMI patients) were assigned to placebo and 253 (48.1%) to zofenopril. As reported in Table I, the two treatment groups were homogeneous for baseline clinical
Discussion
The results of this post hoc analysis of the SMILE Study7 demonstrate that a 6-week treatment period with zofenopril is effective in reducing death and severe refractory CHF in non-thrombolysed NSTEMI patients9 and represent the first evidence of a prognostic benefit of early ACE inhibition in these patients. In addition to these clinically relevant observations, our study highlights the beneficial effect of short-term treatment with zofenopril on long-term survival after withdrawal of
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Cited by (19)
Peripheral neutrophils and naive CD4 T cells predict the development of heart failure following acute myocardial infarction: A bioinformatic study
2021, Revista Portuguesa de CardiologiaCitation Excerpt :Acute myocardial infarction (AMI), which may lead to cardiac dysfunction, is a common cause of HF. Studies have demonstrated that 14-36% of AMI patients will eventually develop HF.5,6 Early and reliable prediction of HF and appropriate intervention following AMI are considered an effective strategy to prevent the development of HF.
(E)-N’-(1-(3-oxo-3H-benzo[f]chromen-2-yl)ethylidene)benzohydrazide protecting rat heart tissues from isoproterenol toxicity: Evidence from in vitro and in vivo tests
2020, European Journal of PharmacologyCitation Excerpt :Previous studies have reported that ACE inhibitors were widely used in treatment of myocardial infarction to prevent left ventricular remodeling process (Mnafgui et al., 2016; Daoud et al., 2017). In fact, the inhibition of ACE activity inactivated expression of cytokine transforming growth factor (TGF-β1), a major mediator of the remodeling process and fibrosis tissues (Border and Noble, 1994; Borghi et al., 2006). An electrocardiogram (ECG) is a medical test that detects infarction by measuring the electrical activity generated by the heart as it contracts (Daoud et al., 2017).
2018 Guidelines of the Taiwan Society of Cardiology, Taiwan Society of Emergency Medicine and Taiwan Society of Cardiovascular Interventions for the management of non ST-segment elevation acute coronary syndrome
2018, Journal of the Formosan Medical AssociationCitation Excerpt :In patients with acute MI, early administration of angiotensin converting enzyme inhibitors (ACEIs) have beneficial effects on total mortality reduction60,61 The survival benefit of ACEIs was consistent in MI patients with left ventricular dysfunction or heart failure.62–64 In NSTEMI patients, post-hoc analysis of the Survival of Myocardial Infarction Long-term Evaluation (SMILE) study demonstrated zofenopril treatment significantly reduced one year mortality rate.65 A meta-analysis also proved the survival improvement in acute MI patients with early use of ACEI within 36 h of disease attack.66
Cardiopreventive effect of ethanolic extract of Date Palm Pollen against isoproterenol induced myocardial infarction in rats through the inhibition of the angiotensin-converting enzyme
2017, Experimental and Toxicologic PathologyCitation Excerpt :The myocardial infarction induced by isoproterenol is often underwent a significant rise in ACE activity associated with elevation in heart weight ratio indicative of ventricular remodeling process. This mechanism improves the dilation of the non-infarcted left ventricular, the infarct expansion as well as the compensatory reactive hypertrophy (Mnafgui et al., 2016a,b; Borghi et al., 2006). The increase in the ACE activity certainly report the inhibition of cardiac remodeling process by reducing the expression of cytokine transforming growth factor (TGF-β1) which is a mediator of the remodeling process and fibrosis tissues (Mnafgui et al., 2016a,b).
Acute Coronary Syndromes and Acute Myocardial Infarction
2008, Critical Care Medicine: Principles of Diagnosis and Management in the AdultACE inhibitors after myocardial infarction: close-up on zofenopril
2007, Annales de Cardiologie et d'Angeiologie
- a
See Appendix A.