Left ventricular remodeling

Pressure overload seen in hypertension and aortic stenosis leads to left ventricular hypertrophy, and the heart undergoes pathologic molecular, cellular, and tissue changes in the myocardium.

The left ventricular remodeling includes reactivation of the fetal gene program, induction of fibrosis, and dilation, that ultimately contribute to the development of heart failure.

Pressure overload induced LVH differs between men and women: left ventricular remodeling is more concentric in women, with less LV dilation and wall thinning.

There is higher level of fibrosis related genes and male hearts compared with female hearts.

Beneficial effects of angiotensin converting enzyme inhibitors and beta blockers are associated with their effects on left ventricular remodeling.

Surgical left ventricular reconstruction for heart failure with left ventricular remodeling caused by coronary artery disease attempts to reduce the left ventricular volume, increase the ejection fraction and improve left ventricular function.

Comparing coronary artery bypass graft surgery to coronary artery bypass surgery combined with surgical ventricular reconstruction in patients with coronary artery disease and left ventricular systolic dysfunction revealed the addition of the later surgery resulted in significantly greater reduction in left ventricular volume than achieved by CABG alone (Jones RH)

Surgical left ventricular reconstruction with CABG does improve left ventricle volume, but does not improve outcome in patients so treated compared to patients treated with CABG alone: no improvement in death or cardiac hospitalization or in any other clinical outcome (Jones RH).