Pressure and volume overload results in concentric and eccentric hypertrophy of cardiac ventricular chambers with, respectively, parallel and series replication of sarcomeres. These divergent patterns of hypertrophy were related 40 years ago to disparate wall stresses in both conditions, with systolic wall stress eliciting parallel replication of sarcomeres and diastolic wall stress, series replication. These observations are relevant to clinical practice, as they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients with aortic stenosis. Stress-sensing mechanisms in cardiomyocytes and activation of cardiomyocyte death by elevated wall stress continue to intrigue cardiovascular scientists.
William Grossman, Walter J. Paulus
Schematic overview of the development of concentric hypertrophy with the parallel addition of sarcomeres in pressure overload and of eccentric hypertrophy with a series addition of sarcomeres in volume overload.
Chamber enlargement increases systolic wall stress in volume overload (dashed black arrow indicates positive feedback). Wall thickening induces concentric hypertrophy in pressure overload and contributes to eccentric hypertrophy in volume overload (blue arrow). Concentric hypertrophy reduces systolic wall stress in pressure overload, and eccentric hypertrophy reduces diastolic wall stress in volume overload (dashed red lines indicate negative feedback).