The study by Grossman, Jones, and McLaurin investigates the patterns of left ventricular (LV) hypertrophy in response to chronic pressure and volume overload. The researchers measured LV wall stresses throughout the cardiac cycle in 30 patients, including 6 with pressure overload, 18 with volume overload, and 6 healthy controls. They found that pressure overload led to concentric hypertrophy, characterized by increased wall thickness and an increased h/R ratio (wall thickness to radius ratio), while volume overload resulted in eccentric hypertrophy, with a normal h/R ratio. Peak systolic wall stress was similar in all groups, but end diastolic wall stress was significantly higher in volume-overloaded patients. The study suggests that hypertrophy develops to normalize systolic wall stress, with increased systolic tension leading to fiber thickening, and increased diastolic tension causing fiber elongation. This hypothesis is supported by the findings that pressure overload leads to concentric hypertrophy, while volume overload results in eccentric hypertrophy. The study also validates the use of a combined hemodynamic-ultrasonic technique for measuring LV wall stress, showing good agreement with angiographic data.The study by Grossman, Jones, and McLaurin investigates the patterns of left ventricular (LV) hypertrophy in response to chronic pressure and volume overload. The researchers measured LV wall stresses throughout the cardiac cycle in 30 patients, including 6 with pressure overload, 18 with volume overload, and 6 healthy controls. They found that pressure overload led to concentric hypertrophy, characterized by increased wall thickness and an increased h/R ratio (wall thickness to radius ratio), while volume overload resulted in eccentric hypertrophy, with a normal h/R ratio. Peak systolic wall stress was similar in all groups, but end diastolic wall stress was significantly higher in volume-overloaded patients. The study suggests that hypertrophy develops to normalize systolic wall stress, with increased systolic tension leading to fiber thickening, and increased diastolic tension causing fiber elongation. This hypothesis is supported by the findings that pressure overload leads to concentric hypertrophy, while volume overload results in eccentric hypertrophy. The study also validates the use of a combined hemodynamic-ultrasonic technique for measuring LV wall stress, showing good agreement with angiographic data.