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Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
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IntroductionThe mitral valve, one of the heart's four valves, regulates blood flow. These valves have flaps that open and close to direct blood properly through the heart and body. During each heartbeat, the flaps open for blood to pass through and seal shut to prevent backflow. Specifically, the mitral valve opens to allow blood flow from the heart's upper left chamber to the lower left chamber. It then closes securely as the lower left chamber contracts to pump blood to the body, preventing...
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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...
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Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...
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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
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Related Experiment Video

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Genetic predisposition to left ventricular dysfunction: a multigenic and multi-analytical approach.

Avshesh Mishra1, Anshika Srivastava1, Tulika Mittal2

  • 1Department of Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow 226014, UP, India.

Gene
|May 31, 2014
PubMed
Summary
This summary is machine-generated.

Genetic variants in AT1, MMP9, and NFKB1 pathways significantly increase the risk of left ventricular dysfunction (LVD) in coronary artery disease (CAD) patients. These gene interactions highlight key factors contributing to LVD susceptibility.

Keywords:
Genetic predispositionHigher order gene–gene interactionLVDLeft ventricular ejection fraction (LVEF)MDR

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Area of Science:

  • Cardiovascular Genetics
  • Molecular Cardiology
  • Genetic Epidemiology

Background:

  • Left ventricular dysfunction (LVD) is a complex condition influenced by mechanical, neurohormonal, and genetic factors.
  • Previous research linked renin-angiotensin-aldosterone system (RAAS), matrix metalloproteinases (MMPs), and inflammatory pathway genes to LVD.
  • Understanding genetic contributions is crucial for identifying LVD susceptibility in coronary artery disease (CAD) patients.

Purpose of the Study:

  • To identify specific genetic variants and their interactions contributing to LVD susceptibility in CAD patients.
  • To investigate the combined effects of RAAS, MMPs, and inflammatory gene polymorphisms on LVD risk.
  • To elucidate the genetic basis of LVD in the context of established coronary artery disease.

Main Methods:

  • Analysis of 11 polymorphisms in RAAS, MMPs, and inflammatory pathways in 510 CAD patients and 230 controls.
  • Categorization of patients into LVD (n=162, LVEF≤45%) and non-LVD groups.
  • Application of single locus analysis, classification and regression tree (CART), and multifactor dimensionality reduction (MDR) for gene-gene interaction analysis.

Main Results:

  • Single locus analysis identified AT1 A1166C, MMP9 R668Q, and NFKB1-94 ATTG ins/del polymorphisms as independently associated with LVD.
  • High-order interaction analysis revealed that AT1 A1166C and NFKB1-94 ATTG ins/del polymorphisms significantly increased LVD risk (OR=8.55).
  • A four-factor model (AT1 A1166C, MMP7 A-181G, MMP9 R668Q, NFKB1-94 ATTG ins/del) demonstrated the highest predictive accuracy for LVD risk.

Conclusions:

  • The AT1 A1166C polymorphism plays a significant independent role in LVD susceptibility.
  • Interactions between AT1 A1166C, MMP9 R668Q, and NFKB1-94 ATTG ins/del polymorphisms substantially contribute to genetic susceptibility to LVD in CAD patients.
  • These genetic findings provide insights into the complex etiology of LVD in the context of coronary artery disease.