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Related Experiment Video

Updated: Jun 12, 2026

Model of Ischemic Heart Disease and Video-Based Comparison of Cardiomyocyte Contraction Using hiPSC-Derived Cardiomyocytes

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AGT*M235T polymorphism in acute ischemic cardiac dysfunction: the gisca project.

Claudia Guerra Murad Saud¹, Amália Faria Dos Reis, Arlisa Monteiro de Castro Dias

¹Universidade Federal Fluminense, Rio de Janeiro, RJ, Brasil. cgsaud@cardiol.br

Arquivos Brasileiros De Cardiologia

|June 16, 2010

Summary

The AGT*M235T polymorphism, specifically the absence of the *235T allele, may reduce the risk of cardiac dysfunction after acute coronary syndrome (ACS). This genetic factor appears protective in patients hospitalized for ACS.

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Published on: February 22, 2022

Area of Science:

Cardiovascular Genetics
Molecular Cardiology
Genetics of Cardiovascular Disease

Background:

The AGT*M235T polymorphism is linked to elevated angiotensinogen levels, hypertension, and cardiac dysfunction (CD).
Understanding genetic predispositions to CD post-acute coronary syndrome (ACS) is crucial for risk stratification.

Purpose of the Study:

To investigate the association between the AGT*M235T polymorphism and the risk of developing cardiac dysfunction following ACS.
To determine if specific genotypes influence cardiac outcomes in patients hospitalized for ACS.

Main Methods:

A cohort of 363 patients hospitalized for ACS was analyzed.
Genetic analysis of the AGT*M235T polymorphism was performed.
Clinical data and genotype distributions were compared between patients who developed CD (cases) and those who did not (controls).

Main Results:

A significant difference in genotype distribution was observed in women, with the *235T allele more prevalent in the cardiac dysfunction group.
Logistic regression indicated that anterior wall myocardial infarction and unstable angina were associated with increased CD risk.
Absence of the *235T allele, controlled blood glucose, beta-blocker use, and specific heart rate ranges were associated with a lower risk of CD.

Conclusions:

The absence of the AGT *235T allele appears to be a protective factor against cardiac dysfunction after ACS.
Genetic variations in the angiotensinogen gene may play a role in cardiovascular outcomes post-ACS.