APStracts 2:0041H, 1995.

Effect of exercise on the coronary pressure-flow relationship in the hypertrophied left ventricle. Duncker, Dirk J., Jianyi Zhang, Todd J. Pavek, Melanie J. Crampton, Robert J. Bache. Cardiovascular Division, Department of Medicine University of Minnesota Medical School, Minneapolis, Minnesota.

APStracts 2:0041H, 1995.

Left ventricular hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during exercise. The present study was performed to determine whether exercise causes alterations in minimum coronary resistance or effective back pressure (coronary pressure at zero flow: Pzf) which limit maximum myocardial perfusion in the hypertrophied heart. Ascending aortic banding in seven dogs increased the LV to body weight ratio to 7.7+/-0.3 g/kg compared to 4.6+/-0.2 g/kg in 13 normal dogs (p<0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. Under resting conditions, the slope of the pressure-flow relationship (conductance) was significantly lower in the LVH animals than in the normal dogs (7.2+/-0.8 versus 11.9+/-0.8 x10-2(ml/min/g)/mmHg; p<0.01); the slope correlated with the degree of hypertrophy (r=0.74; p<0.001). The pressure at zero flow measured during total coronary artery occlusion (Pzfmeasured) was significantly elevated in LVH compared to normal dogs (25.6+/-2.2 mmHg vs 13.0+/-1.2 mmHg; p<0.01); Pzfmeasured was positively correlated (r=0.83, p<0.0001) with LV end-diastolic pressure measured during total coronary artery occlusion (9.0+/-1.1 mmHg in normal dogs and 22.2+/-3.2 mmHg in LVH dogs; p<0.01). Graded treadmill 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 to 6.1+/-0.8x10-2(ml/min/g)/mmHg; p<0.01) and normal dogs (from 11.9+/-0.8 to 10.0+/-0.7x10-2 (ml/min/g)/mmHg; p<0.01). However, exercise-induced increases in Pzfmeasured 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 Pzf 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 during exercise in the hypertrophied left ventricles contributed to impairment of myocardial perfusion during exercise by augmenting the back pressure which opposes coronary flow. This could be of particular importance because of the limited vasodilator reserve available to compensate for increased effective back pressure in the hypertrophied heart, and might contribute to increased vulnerability to ischemia during the high metabolic demands of exercise.

Received 14 July 1994; accepted in final form 6 February 1995.
APS Manuscript Number H621-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.