Related Experiment Video

Updated: Aug 19, 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

Renin-angiotensin system and haemostasis gene polymorphisms and outcome after coronary artery bypass graft surgery

Henry Völzke1, Volker Kleine, Daniel M Robinson

  • 1Department of Epidemiology and Social Medicine, Ernst Moritz Arndt University, Walther Rathenau Str. 48, D-17487 Greifswald, Germany. voelzke@uni-greifswald.de

International Journal of Cardiology
|January 29, 2005
PubMed

Insights

Gene polymorphisms in the renin-angiotensin system interact with age to influence outcomes after coronary artery bypass graft surgery. Other clotting factor gene polymorphisms showed no association with patient survival or cardiac events.

Area of Science:

  • Cardiovascular Genetics
  • Surgical Outcomes Research
  • Pharmacogenomics

Background:

  • Coronary artery bypass graft (CABG) surgery carries significant 2-year mortality risks.
  • Renin-angiotensin system (RAS) gene polymorphisms may influence hypertension and cardiovascular disease.
  • Previous studies identified angiotensin I-converting enzyme DD genotype as a predictor of CABG outcomes.

Purpose of the Study:

  • To investigate associations between RAS gene polymorphisms (angiotensinogen 235 M/T, angiotensin II type 1 receptor 1166 A/C) and clotting system gene polymorphisms (glycoprotein IIIa PlA1/PlA2, factor V Leiden 1691 G/A) and outcomes after CABG.
  • To determine if these genetic factors impact total mortality, cardiac mortality, or need for revascularization within two years post-surgery.

Main Methods:

  • Follow-up of 247 patients for 2 years post-CABG.
  • Primary endpoint: total mortality. Secondary endpoint: cardiac mortality or need for myocardial revascularization.
  • Genotyping performed using polymerase chain reaction and restriction fragment length polymorphism techniques.

Main Results:

  • Older age and non-use of internal mammary artery grafts predicted primary endpoint (total mortality).
  • Reduced left ventricular ejection fraction predicted secondary endpoint (cardiac mortality/revascularization).
  • No direct association found between the studied genetic polymorphisms and CABG outcomes in main regression models. However, angiotensin II type 1 receptor 1166 A/C and angiotensinogen 235 M/T polymorphisms modulated the effect of age on outcomes.

Conclusions:

  • Interactions exist between angiotensin II type 1 receptor 1166 A/C and angiotensinogen 235 M/T gene polymorphisms and age regarding CABG outcomes.
  • Glycoprotein IIIa PlA1/PlA2 and factor V Leiden 1691 G/A gene polymorphisms were not associated with mid-term mortality or cardiac morbidity after CABG.
Abstract

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...
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,...
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...
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
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...