Which histologic feature is associated with diastolic dysfunction?

Which histologic feature is associated with diastolic dysfunction?

• A. Thinner, elongated cardiomyocytes and fibrosis
• B. Cardiac myocyte atrophy and apoptosis
• C. Cardiomyocyte hypertrophy, inflammation, and fibrosis
• D. Myocardial edema with neutrophil infiltration

Answer: (C)

Diastolic dysfunction is about a stiff ventricle that doesn’t relax well to allow proper filling. The histologic pattern that best fits this problem is cardiomyocyte hypertrophy with interstitial fibrosis, often accompanied by inflammatory remodeling. Hypertrophy thickens the ventricular wall, while fibrosis makes the heart muscle more rigid; together they reduce compliance and raise filling pressures despite a preserved ejection fraction. This combination directly explains why filling during diastole is impaired. Other patterns don’t align as well with diastolic dysfunction. Thinner, elongated cardiomyocytes with fibrosis suggest a remodeling style more typical of dilated or systolic failure, where the chamber is less able to generate pressure and the walls may be thinner. Myocyte atrophy and apoptosis imply loss of myocardial mass rather than stiffening. Myocardial edema with neutrophil infiltration points to acute inflammation or injury rather than the chronic remodeling that characterizes diastolic dysfunction.

Diastolic dysfunction is about a stiff ventricle that doesn’t relax well to allow proper filling. The histologic pattern that best fits this problem is cardiomyocyte hypertrophy with interstitial fibrosis, often accompanied by inflammatory remodeling. Hypertrophy thickens the ventricular wall, while fibrosis makes the heart muscle more rigid; together they reduce compliance and raise filling pressures despite a preserved ejection fraction. This combination directly explains why filling during diastole is impaired.

Other patterns don’t align as well with diastolic dysfunction. Thinner, elongated cardiomyocytes with fibrosis suggest a remodeling style more typical of dilated or systolic failure, where the chamber is less able to generate pressure and the walls may be thinner. Myocyte atrophy and apoptosis imply loss of myocardial mass rather than stiffening. Myocardial edema with neutrophil infiltration points to acute inflammation or injury rather than the chronic remodeling that characterizes diastolic dysfunction.