ventricular remodeling
When a building is repeatedly stressed, its structure slowly changes shape — sometimes for the worse. The heart does something similar. Ventricular remodeling is the progressive change in the size, shape, and wall structure of the ventricle in response to injury or chronic overload. After a heart attack or under long-standing strain, the chamber can enlarge, stretch, and become more spherical, and its muscle composition shifts.
At the cellular level, remodeling involves the heart-muscle cells lengthening or thickening, scar tissue (fibrosis) accumulating, and harmful neurohormonal signals (such as the renin-angiotensin and sympathetic systems) being switched on. Although these changes begin as an attempt to compensate, they often become self-reinforcing: an enlarging, more spherical ventricle pumps less efficiently, which drives further remodeling — a vicious cycle that underlies the progression of heart failure.
Crucially, remodeling can go both ways. Effective treatment — heart-failure medications, restoring blood flow, fixing a leaking valve, or resynchronising contraction — can sometimes partly reverse the process, shrinking the chamber and improving function, which is called reverse remodeling. Tracking ventricular size and ejection fraction over time is one way clinicians judge whether a heart is deteriorating or recovering.
Months after starting optimal heart-failure therapy, a patient's dilated ventricle has shrunk and ejection fraction risen from 25% to 40% — an example of reverse remodeling.
A shrinking chamber and rising ejection fraction on therapy illustrate reverse remodeling.
Several heart-failure drugs are valued precisely because they slow or partly reverse adverse remodeling.