angiotensin/infarction

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Brain renin-angiotensin system blockade with orally active aminopeptidase A inhibitor prevents cardiac dysfunction after myocardial infarction in mice.

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Brain renin-angiotensin system (RAS) hyperactivity has been implicated in sympathetic hyperactivity and progressive left ventricular (LV) dysfunction after myocardial infarction (MI). Angiotensin III, generated by aminopeptidase A (APA), is one of the main effector peptides of the brain RAS in the

Association of angiotensin I-converting enzyme gene polymorphism with myocardial ischemia and patency of infarct-related artery in patients with acute myocardial infarction.

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OBJECTIVE We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction. BACKGROUND The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has

D allele of the angiotensin-converting enzyme gene is a risk factor for secondary cardiac events after myocardial infarction.

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We retrospectively examined the relationship between the genotype of the angiotensin-converting enzyme (ACE) gene or the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, and the secondary cardiac events after myocardial infarction. The study population consisted of 176 patients (ACE genotype:

The genotype of the angiotensin-converting enzyme gene and global left ventricular dysfunction after myocardial infarction.

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We examined the relation between the genotype of the angiotensin-converting enzyme (ACE) gene and the development of left ventricular dysfunction, as assessed by biplane left ventriculograms, after myocardial infarction. Seventy-nine patients (deletion homozygote [DD] = 13; insertion/deletion

Deletion-type allele of the angiotensin-converting enzyme gene is associated with progressive ventricular dilation after anterior myocardial infarction. Captopril and Thrombolysis Study Investigators.

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OBJECTIVE This study sought to determine whether patients who are homozygous for the deletion (D)-type allele of the angiotensin-converting enzyme gene display augmented ventricular dilation after myocardial infarction. BACKGROUND Recent evidence suggests that the deletion-type allele of the

Synergistic effects of angiotensin-converting enzyme and angiotensin-II type 1 receptor gene polymorphisms on risk of myocardial infarction.

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We reported from our previous multicentre case-control study that the deletion (D) polymorphism of the gene encoding angiotensin-converting enzyme (ACE) was associated with increased risk of myocardial infarction. The main function of ACE is to convert angiotensin I into angiotensin II, which exerts

Angiotensin-converting enzyme gene polymorphism interacts with left ventricular ejection fraction and brain natriuretic peptide levels to predict mortality after myocardial infarction.

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OBJECTIVE The goal of this study was the exploration of the associations between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and post-myocardial infarction (MI) outcomes, especially any interaction with the accepted clinical prognostic markers brain natriuretic

Effect of angiotensin-converting enzyme gene polymorphism on left ventricular remodeling after anteroseptal infarction.

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OBJECTIVE Genetic influence on cardiac remodeling is uncertain. The purpose of this study is to determine the effects of polymorphism of the angiotensin-converting enzyme (ACE) gene on cardiac remodeling after myocardial infarction. METHODS The subjects were 43 patients with old anteroseptal

The relationship between angiotensin-converting enzyme (insertion/deletion) gene polymorphism and left ventricular remodeling in acute myocardial infarction.

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BACKGROUND The development of left ventricular remodeling after acute myocardial infarction is a predictor of heart failure and mortality. The genetic influence on cardiac remodeling in the early period after acute myocardial infarction, is however, unclear. The aim ofthis study was to investigate

Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Myocardial Infarction Patients With Renal Dysfunction.

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BACKGROUND There is no consensus whether angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blocker (ARB) should be used for secondary prevention in all or in only high-risk patients after an acute myocardial infarction (AMI). OBJECTIVE This study sought to investigate whether

Insertion/deletion polymorphism in the angiotensin-converting enzyme gene in myocardial infarction survivors.

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BACKGROUND Insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene influenced the plasma concentration of the ACE, and is D allele have been repetitively suggested as a risk factor for myocardial infarction (MI). METHODS Two hundert thirty six male myocardial infarction

Renin-angiotensin system and associated gene polymorphisms in myocardial infarction in young South African Indians.

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The renin-angiotensin system plays an important role in cardiovascular regulation. Abnormalities in genetic components of this system, such as the angiotensin-converting enzyme (ACE) gene, angiotensin II type 1 (AT1) receptor gene and angiotensinogen (AGT) gene, may cause a variety of adverse

A peptide vaccine targeting angiotensin II attenuates the cardiac dysfunction induced by myocardial infarction.

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A peptide vaccine targeting angiotensin II (Ang II) was recently developed as a novel treatment for hypertension to resolve the problem of noncompliance with pharmacotherapy. Ang II plays a crucial role in the pathogenesis of cardiac remodeling after myocardial infarction (MI), which causes heart

Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation.

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Myocardial infarction (MI) triggers a local inflammatory response which orchestrates cardiac repair and contributes to concurrent neuroinflammation. Angiotensin-converting enzyme (ACE) inhibitor therapy not only attenuates cardiac remodeling by interfering with the neurohumoral system,

Renin-angiotensin system inhibitors in patients with or without ischaemic mitral regurgitation after acute myocardial infarction.

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UNASSIGNED Little is known about the long-term effects of renin-angiotensin system inhibitors (RASI) on cardiovascular events in patients after acute myocardial infarction (AMI) with ischaemic mitral regurgitation (IMR). The purpose of this study was to investigate the association of RASI with the

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