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angiotensin/infarkt

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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
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
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:
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
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
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
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
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
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
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
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
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,
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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