Abstract
Cardiovascular diseases are one of the leading causes of death in developing countries, generally originating as coronary artery disease (CAD) or hypertension. In later stages, many CAD patients develop left ventricle dysfunction (LVD). Left ventricular ejection fraction (LVEF) is the most prevalent prognostic factor in CAD patients. LVD is a complex multifactorial condition in which the left ventricle of the heart becomes functionally impaired. Various genetic studies have correlated LVD with dilated cardiomyopathy (DCM). In recent years, enormous progress has been made in identifying the genetic causes of cardiac diseases, which has further led to a greater understanding of molecular mechanisms underlying each disease. This progress has increased the probability of establishing a specific genetic diagnosis, and thus providing new opportunities for practitioners, patients, and families to utilize this genetic information. A large number of mutations in sarcomeric genes have been discovered in cardiomyopathies. In this review, we will explore the role of the sarcomeric genes in LVD in CAD patients, which is a major cause of cardiac failure and results in heart failure.
Highlights
Cardiac diseases are one of the main causes of death these days, generally originating as coronary artery disease (CAD) or hypertension
CAD patients with severe left ventricle dysfunction (LVD) have a higher mortality than those with preserved LV function, and this mortality rate is proportional to the severity of LVD
We review the role of common sarcomeric genes (MYBPC3, TNNT2, TTN, Myospryn) and their genetic variants with LVD in CAD patients
Summary
Cardiac diseases are one of the main causes of death these days, generally originating as coronary artery disease (CAD) or hypertension. In LV dilation, the chamber volume of the left ventricle gets enlarged when the walls are either normal or thinned. These two conditions are associated with specific hemodynamic variations. Only diastolic relaxation is impaired, while in the dilated condition, systolic functions are diminished. This results in a change of heart shape from an elliptical to a more spherical form, which causes considerable mechanical inefficiency and deterioration, resulting in CHF [3,6]. We review the role of common sarcomeric genes (MYBPC3, TNNT2, TTN, Myospryn) and their genetic variants with LVD in CAD patients
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