Effect of exercise on coronary pressure-flow relationship in hypertrophied left ventricle

D. J. Duncker, Jianyi J Zhang, T. J. Pavek, M. J. Crampton, Robert J Bache

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23 Scopus citations

Abstract

Left ventricular (LV) 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 (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 in 11 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 vs. 11.9 ± 0.8 x 10-2 ml · min-1 · g-1 · mmHg-1; P < 0.01); the slope correlated with the degree of hypertrophy (r = 0.74; P < 0.001). The P(zf) measured during total coronary artery occlusion (P(zf,measured)) was significantly elevated in LVH compared with normal dogs (25.6 ± 2.2 vs. 13.0 ± 1.2 mmHg; P < 0.01); P(zf,measured) was positively correlated (r = 0.78, P < 0.0005) 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 ± 0.8 x 10-2 ml · min- 1 · g-1 · mmHg-1; P < 0.01) and normal dogs (from 11.9 ± 0.8 to 10.0 ± 0.7 x 10-1 ml · min-1 · g-1 · mmHg-1; P < 0.01). However, exercise-induced increases in P(zf, 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 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.

Original languageEnglish (US)
Pages (from-to)H271-H281
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume269
Issue number1 38-1
DOIs
StatePublished - 1995

Keywords

  • adenosine
  • blood flow
  • coronary vasodilation
  • supravalvular aortic stenosis
  • vasodilator reserve

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