Cardiac hypertrophy
Also known as: myocardial hypertrophy, hypertrophy of the heart
Cardiac hypertrophy is an increase in heart muscle mass caused by enlargement of individual cardiac myocytes. It develops as an adaptation to chronic pressure or volume overload and, when pathologic, predisposes to heart failure and arrhythmia.
Cardiac myocytes are terminally differentiated and cannot divide meaningfully in adults, so a heart facing a sustained increase in workload responds by enlarging existing cells rather than adding new ones. Each myocyte synthesizes additional sarcomeres, raising wall thickness or chamber size and increasing total heart weight.
The pattern depends on the stimulus. Pressure overload — chronic hypertension or aortic stenosis — adds sarcomeres in parallel, thickening the wall inward while the chamber cavity stays the same or shrinks. This is concentric hypertrophy, and it produces a stiff ventricle with impaired filling, the hallmark of diastolic dysfunction. Volume overload — aortic or mitral regurgitation, chronic anemia, or a left-to-right shunt — adds sarcomeres in series, lengthening myocytes so the chamber dilates with a proportionally smaller increase in wall thickness. This is eccentric hypertrophy, and it tends toward systolic dysfunction.
Not all hypertrophy is harmful. Physiologic hypertrophy from endurance or resistance training, sometimes called athlete's heart, increases mass without fibrosis and largely reverses when training stops. Pathologic hypertrophy is different: the enlarged muscle outgrows its capillary supply and raises myocardial oxygen demand, promoting ischemia, interstitial fibrosis, and electrical remodeling that raises arrhythmia risk and eventually leads to heart failure. Hypertrophic cardiomyopathy is a distinct genetic disorder caused by sarcomere protein mutations, classically producing asymmetric septal thickening and a recognized cause of sudden cardiac death in young athletes.
USMLE Step 1 tests cardiac hypertrophy in cardiovascular pathology, expecting you to match a hemodynamic stimulus to concentric versus eccentric remodeling, apply the law of Laplace to wall stress, distinguish physiologic from pathologic hypertrophy, and separate hypertrophic cardiomyopathy from hypertrophy secondary to pressure overload.
Key takeaways
- Cardiac hypertrophy is growth of the heart by myocyte enlargement, not by cell division.
- Pressure overload adds sarcomeres in parallel, producing concentric hypertrophy and diastolic dysfunction.
- Volume overload adds sarcomeres in series, producing eccentric hypertrophy with chamber dilation.
- Physiologic hypertrophy from training lacks fibrosis and is largely reversible; pathologic hypertrophy leads to ischemia, fibrosis, and heart failure.
- Hypertrophic cardiomyopathy is a genetic sarcomere disorder and a cause of sudden death in young athletes.