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Effect of treadmill exercise on transmural distribution of blood flow in hypertrophied left ventricle
D J Duncker1, Y Ishibashi, R J Bache
1Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
Insights
Pressure-overload left ventricular hypertrophy (LVH) impairs blood flow during exercise due to increased extravascular forces. This study shows exercise exacerbates subendocardial hypoperfusion in LVH hearts, highlighting the role of external compression on coronary vessels.
Area of Science:
- Cardiovascular Physiology
- Cardiac Hypertrophy Research
Background:
- Pressure-overload left ventricular hypertrophy (LVH) increases vulnerability to subendocardial hypoperfusion during exercise.
- Abnormal perfusion in LVH may stem from inadequate coronary vessel growth or increased extravascular forces on intramural vessels.
Purpose of the Study:
- To assess the contribution of extravascular forces to abnormal myocardial blood flow distribution in LVH.
- To examine the effect of exercise on blood flow distribution when coronary vasomotor tone is abolished with adenosine.
Main Methods:
- Ascending aortic banding was performed in six dogs to induce LVH.
- Myocardial blood flow was measured at rest and during exercise with and without maximal coronary vasodilation induced by adenosine.
- Transmural distribution of blood flow was assessed using subendocardial-to-subepicardial (Endo-to-Epi) ratios.
Main Results:
- LVH hearts showed significantly increased LV-to-body weight ratio compared to normal hearts.
- During adenosine infusion, exercise caused a more pronounced redistribution of blood flow away from the subendocardium in LVH hearts (Endo-to-Epi ratio 0.35) compared to normal hearts (Endo-to-Epi ratio 0.76).
- The exaggerated decrease in subendocardial blood flow in LVH during exercise was attributed to increased extravascular compressive forces, reduced diastolic duration, and elevated LV end-diastolic pressure.
Conclusions:
- Increased extravascular compressive forces significantly contribute to exercise-induced subendocardial hypoperfusion in pressure-overload LVH.
- Abnormalities in diastolic function and elevated LV filling pressures exacerbate impaired myocardial perfusion during physical exertion in LVH.
Abstract:
Pressure-overload left ventricular (LV) hypertrophy (LVH) is associated with increased vulnerability to subendocardial hypoperfusion during exercise. Abnormal perfusion could be the result of failure of the coronary vessels to grow in proportion to the degree of myocyte hypertrophy or could be due to increased extravascular forces acting on the intramural coronary vasculature. This study assessed the contribution of extravascular forces by examining the effect of exercise on the distribution of myocardial blood flow when coronary vasomotor tone was abolished with a maximal vasodilating dose of intracoronary adenosine. One year after ascending aortic banding in six dogs, the LV-to-body weight ratio was 7.80 +/- 0.38 g/kg compared with 4.57 +/- 0.20 g/kg in nine normal dogs (P < 0.01). Under awake resting conditions blood flow in LVH hearts increased from 1.17 +/- 0.27 ml . min-1 . g-1 during basal conditions to 5.78 +/- 1.06 ml . min-1 . g-1 during adenosine (at a coronary pressure of 100 +/- 6 mmHg), whereas in normal dogs blood flow increased from 1.22 +/- 0.17 to 5.26 +/- 0.71 ml . min-1 . g-1 (at a coronary pressure of 62 +/- 4 mmHg). At rest the transmural distribution of blood flow during adenosine was not different between hypertrophied and normal hearts, with subendocardial-to-subepicardial (Endo-to-Epi) blood flow ratios of 1. 01 +/- 0.09 and 1.14 +/- 0.13, respectively (P = not significant). During adenosine infusion, treadmill exercise to produce heart rates of 200-220 beats/min caused redistribution of blood flow away from the subendocardium that was much more marked in LVH (Endo-to-Epi blood flow ratio = 0.35 +/- 0.04) than in normal hearts (Endo-to-Epi blood flow ratio = 0.76 +/- 0.09, P < 0.05 vs. LVH). In comparison with normal, the exaggerated decrease in subendocardial blood flow produced by exercise in LVH hearts resulted from abnormally increased extravascular compressive forces, including a greater decrease in diastolic duration and an increase in LV end-diastolic pressure.