Related Experiment Video

Updated: May 25, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

Impact of renin-angiotensin-aldosterone system gene polymorphisms on left ventricular dysfunction in coronary artery

Avshesh Mishra1, Anshika Srivastava, T Mittal

  • 1Department of Genetics, Sanjay Gandhi Post Graduate Institute of Medical Sciences (SGPGIMS), Lucknow, India.

Disease Markers
|February 3, 2012
PubMed

Insights

The angiotensin II type 1 receptor (AT1) A1166C variant is linked to increased susceptibility to left ventricular dysfunction (LVD) in coronary artery disease patients. This finding highlights a potential genetic marker for LVD risk.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Cardiology
  • Genetic Epidemiology

Background:

  • Left ventricular dysfunction (LVD) and reduced cardiac output are significant complications in some coronary artery disease (CAD) patients.
  • The renin-angiotensin-aldosterone system (RAAS) is activated in LVD, leading to vasoconstriction and fluid retention.
  • Genetic variations in RAAS components may influence LVD susceptibility.

Purpose of the Study:

  • To investigate the association between single nucleotide polymorphisms (SNPs) in ACE (rs4340), AT1 (rs5186), and CYP11B2 (rs1799998) and LVD in CAD patients.
  • To identify genetic markers that confer risk for developing LVD.

Main Methods:

  • Two cohorts of CAD patients and healthy controls were studied.
  • Genotyping for ACE I/D, AT1 A1166C, and CYP11B2 T-344C polymorphisms was performed using PCR.
  • Left ventricular ejection fraction (LVEF) was assessed to categorize patients with LVD (LVEF ≤ 45).

Main Results:

  • The ACE I/D polymorphism was associated with CAD but not LVD.
  • The AT1 A1166C variant showed a significant association with LVD in both primary (p=0.013; OR=3.69) and replication (p=0.020; OR=5.20) cohorts.
  • No significant association was found between CYP11B2 (rs1799998) and either CAD or LVD.

Conclusions:

  • The AT1 A1166C polymorphism plays a crucial role in susceptibility to left ventricular dysfunction.
  • This genetic variant may serve as a predictive marker for LVD in patients with coronary artery disease.
Abstract

More Related Videos

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats07:41

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...