Over the past 10 years, several clinical studies have concluded that, in patients already receiving conventional therapies, angiotensin-converting enzyme (ACE) inhibitors further reduce the risk of death following myocardial infarction (MI). Post-MI ACE inhibitors have proven to be effective as long term therapy in high risk patients as well as when used for much shorter periods in a broad patient population. However, while considerable mortality data have been collected, the effects of ACE inhibitors post-MI on other cardiovascular outcomes have not been as well documented. In addition, a number of issues regarding the most effective use of these agents remain unresolved. This paper, the second of two parts, focuses on the clinical issues and controversies surrounding the use of ACE inhibitors following acute MI. The effects of ACE inhibitors on the outcomes of sudden death, nonsudden death, recurrent angina, mitral regurgitation and left ventricular dysfunction are reviewed and potential mechanisms of action are proposed. In addition, ACE inhibitor therapy is discussed in terms of patient selection criteria, choice of agent, optimal dosing regimen, concomitant use of other therapies and relative costs of treatment. Finally, potential mechanisms of action of ACE inhibitors are proposed for each of the outcomes examined.
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FEBS J
January 2025
Department of Life Sciences, University of Bath, UK.
Angiotensin-1-converting enzyme (ACE) is a zinc-dependent carboxypeptidase of therapeutic interest for the treatment of hypertension, inflammation and fibrosis. It consists of two homologous N and C catalytic domains, nACE and cACE, respectively. Unfortunately, the current clinically available ACE inhibitors produce undesirable side effects due to the nonselective inhibition of these domains.
View Article and Find Full Text PDFInt J Cardiol Cardiovasc Risk Prev
March 2025
Department of Public and Occupational Health, Amsterdam Public health Research Institute, Amsterdam university Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Background: Chronic inflammation is a well-recognized contributor to hypertension pathogenesis. However, the role of targeting inflammation in hypertension treatment, particularly through modulation of inflammatory markers like interleukin-6 (IL-6), remains less understood. We investigated the effects of antihypertensive medications with and without IL-6-lowering properties on long-term blood pressure (BP) control in a multi-ethnic cohort in the Netherlands.
View Article and Find Full Text PDFJACC Adv
January 2025
Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA.
Background: Patients with systemic right ventricle (SRV), either d-transposition of the great arteries following an atrial switch procedure or congenitally corrected transposition of the great arteries, develop severe right ventricular dysfunction, prompting appropriate medical therapy. However, the efficacy of beta-blockers and angiotensin receptor blockers or angiotensin-converting enzyme inhibitors (ACEI) in SRV patients is unproven.
Objectives: The objective of this study was to determine the effects of ACEI/ARB and beta-blockers on outcomes in SRV patients after accounting for likely cofounders affecting their use.
J Prev Med Hyg
September 2024
Department of Cardiology, School of Medicine, Health Management and Economics Research Center, Hazrat-e Rasool General Hospital, Iran University of Medical Sciences, Tehran, Iran.
Background: There is evidence supporting the efficacy of Sacubitril /Valsartan for improving left heart failure, but few studies have examined its effects on right ventricular (RV) dysfunction. The current study aimed to investigate the effects of Sacubitril /Valsartan on RV dysfunction in patients with right heart failure.
Methods: The current study was a randomized and parallel clinical trial study.
Curr Med Chem
January 2025
3rd Department of Cardiology, General Hospital of Thoracic Diseases 'Sotiria', National and Kapodistrian University of Athens, School of Medicine, Athens, Greece.
Arterial hypertension is a silent and progressive disease with deleterious vascular implications on all target organs, including the heart, the brain, the kidneys, and the eyes. Oxidative stress, defined as the overproduction of Reactive Oxygen Species (ROS) over antioxidants, is capable of deteriorating not only the normal endothelial but also the cellular function with further cardiovascular implications. Xanthine oxidase activity, NADPH oxidase overexpression, and ROS production lead to hypertension and high arterial tone, culminating in end-organ damage.
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