What is the pathophysiology of systolic dysfunction (HFrEF)?

• A. Cardiomyocyte loss leading to LV reduced pumping
• B. Structural and cellular alterations leading to LV inability to relax
• C. Myocardial edema causing electrical conduction block
• D. Increased afterload from valvular disease causing LV dilation

Answer: (A)

Systolic dysfunction with reduced ejection fraction centers on weakened contraction of the left ventricle due to loss or damage of cardiomyocytes, often with replacement fibrosis. When viable heart muscle cells are lost or their contractile function is impaired, the heart can’t generate normal force to eject blood with each beat. The result is a lower ejection fraction and reduced stroke volume, which is the defining problem in HFrEF. The ventricle may then dilate as a compensatory response to maintain output, but the core issue remains diminished contractile power from myocardial loss.

Choosing an alternative that emphasizes inability to relax describes diastolic dysfunction (HF with preserved EF), not the reduced pumping capacity characteristic of HFrEF. Edema and conduction block are features that can accompany heart failure or acute issues but do not represent the primary pathophysiology of reduced systolic function. Increased afterload from valvular disease can contribute to systolic dysfunction, but the fundamental mechanism for HFrEF is the loss/dysfunction of contractile myocardium itself.