EFFECT OF EXERCISE ON CORONARY PRESSURE-FLOW RELATIONSHIP IN HYPERTROPHIED LEFT-VENTRICLE

Left ventricular (LV) hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hyp operfusion and ischemia during exercise. The present study was perform ed to determine whether exercise causes alterations in minimum coronar y resistance or effective back pressure [coronary pressure at zero flo w (P-zf)] that limit maximum myocardial perfusion in the hypertrophied heart. Ascending aortic banding in 7 dogs increased the LV weight-to- body weight ratio to 7.7 +/- 0.3 g/kg compared with 4.6 +/- 0.2 g/kg i n 11 normal dogs (P < 0.01). Maximum coronary vasodilation was produce d by intracoronary infusion of adenosine. Under resting conditions, th e slope of the pressure-flow relationship (conductance) was significan tly lower in the LVH animals than in the normal dogs (7.2 +/- 0.8 vs. 11.9 +/- 0.8 x 10(-2) ml . min(-1). g(-1). mmHg(-1); P < 0.01); the sl ope correlated with the degree of hypertrophy (r = 0.74; P < 0.001). T he P-zf measured during total coronary artery occlusion (P-zf,P-measur ed) was significantly elevated in LVH compared with normal dogs (25.6 +/- 2.2 vs. 13.0 +/- 1.2 mmHg; P < 0.01); P-zf,P-measured was positive ly correlated (r = 0.78, P < 0.0005) with LV end-diastolic pressure me asured during total coronary artery occlusion (9.0 +/- 1.1 mmHg in nor mal dogs and 22.2 +/- 3.2 mmHg in LVH dogs; P < 0.01). Graded treadmil l exercise to maximum heart rates of 210 +/- 9 and 201 +/- 8 beats/min in normal and LVH animals, respectively, caused similar decreases in the slope of the pressure-flow relationship in LVH (from 7.7 +/- 0.9 t o 6.1 +/- 0.8 x 10(-2) ml . min(-1). g(-1). mmHg(-1); P < 0.01) and no rmal dogs (from 11.9 +/- 0.8 to 10.0 +/- 0.7 x 10(-2) ml . min(-1). g( -1). mmHg(-1); P < 0.01). However, exercise-induced increases in P-zf, P-measured were significantly greater in the LVH animals (from 25.6 +/ - 2.2 to 40.8 +/- 2.1 mmHg; P < 0.01) than in normal animals (from 13. 0 +/- 1.2 to 24 +/- 2.1 mmHg; P < 0.01) (P < 0.01 LVH vs. normal). The greater increase in P-zf paralleled a more pronounced increase in LV end-diastolic pressure in the LVH dogs (from 22.2 +/- 3.2 to 39.1 +/- 2.7 mmHg) than in normal dogs (from 9.0 +/- 1.1 to 14.2 +/- 2.0 mmHg). The results suggest that exaggerated increases in filling pressure du ring exercise in the hypertrophied left ventricles contributed to impa irment of myocardial perfusion during exercise by augmenting the back pressure, which opposes coronary flow. This could be of particular imp ortance because of the limited vasodilator reserve available to compen sate for increased effective back pressure in the hypertrophied heart and might contribute to increased vulnerability to ischemia during the high metabolic demands of exercise.