We have previously reported that chronic bradycardial pacing increases both capillary density/ mm2(CD) and maximal work output in normal rabbit hearts. This technique has now been applied to rabbits with volume-overload hypertrophy due to lesion of the aortic valve. Four groups of animals were studied: controls (C), paced (P), valve-lesioned (VL), and paced valve-lesioned (PVL). The aortic valve was lesioned 8 weeks before the acute experiments; pacing was started 4 weeks before the acute experiments, and thus, the PVL group had developed hypertrophy before pacing was started. The degree of hypertrophy was similar in VL hearts whether paced or not: heart wt/body wt ratio increased by 33.5±8.9percent; (mean±SEM) in VL and 25.2±8.2percent; in PVL versus control animals of similar body weight (p<0.001). The hearts of the PVL animals showed a higher CD (2,277±107) than VL hearts (1,383±43), CD in C hearts of similar weights being 1,595±103, and in P hearts 2,350±194. Thus, CD was lower by 14percent; in VL and higher by 43percent; in PVL than in C hearts. Valve-lesioning had a significant effect in reducing maximal cardiac minute work (p<0.001), whereas pacing significantly unproved maximal cardiac minute work (p<0.001) to 2.467±0.206 J/gX10-4in the P group versus 1.609±0.105 in the C group. In the valve-lesioned hearts, work levels were normal after pacing (1.613±0.152 J/ gX10-4) compared with the lower maximal cardiac minute work in hypertrophy alone (1.102±0.162). Chronic bradycardial pacing, therefore, reversed what was a small deficit in capillary density to a substantial increase and significantly unproved maximal cardiac minute work performance in hypertrophied hearts.