Ventricular remodeling

Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume.

Pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles.

The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process.

This thin, weakened area is unable to withstand the pressure and volume load on the heart in the same manner as the other healthy tissue.

These consequences also led to the increase in oxidative stress on the heart, causing the proliferation of fibroblasts, activation of metalloproteinases, and induction of apoptosis, which would be explained below.

[7] Several signal pathways such as Angiotensin II, Transforming growth factor beta (TGF-beta), and Endothelin 1 are known to trigger synthesis and degradation of collagen fibres in the heart.

Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload.

[9] Carvedilol, a 3rd generation beta blocker, may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function.

[10][11] Cardiac resynchronization therapy (CRT) has shown the ability to reverse left ventricular remodeling in some patients.