Pathophysiological evaluation and treatment of coronary microvessel disorders in humans

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We investigated coronary microvessel disorder (CMD) in terms of 1) how to detect ischemic evidence, 2) coronary hemodynamic characteristics, 3) adenosine dynamics, 4) endothelium-dependent relaxation (EDR), 5) lipid metabolism, and 6) pharmacological treatment against ischemia-induced mechanism. Results were as follows.1) Persistent decrease in coronary venous oxygen saturation (>5%) during rapid atrial pacing was an early sign of ischemia in the CMD patients. 2) The CMD patients had hypokinetic wall motion on effort in the apical area of the left ventricle and showed patchy enhancement of sonicated albumin in the left ventricular myocardium during dipyridamole-induced ischemia, suggesting coronary steal phenomenon. 3) There were no differences in arterial and venous adenosine concentrations during ischemia between CMD and control subjects. 4) The EDR of coronary microvessels in the CMD patients was significantly lower than that in the control subjects, although coronary conduit EDR was similar in these 2 groups. 5) There were no differences in T-chol, HDL-chol and LDL-chol between CMD and control subjects. Howeber, serum oxidized LDL was significantly higher in the CMD than in the control subjects. 6) Aminophylline and ACE inhibitor lessened ECG ST-dep during exercise in the CMD patients. Especially, a long-term administration (3 months) of ACE inhibitor appeared to reduce not only ECG ST-dep but also subjective complaints in the CMD patients. These results imply that oxidized LDL may impair endothelium of coronary prearteriolar vessel specifically, resulting in microvascular ischemia via coronary steal phenomenon. In conclusion, we assume that ACE inhibitor is effective for treatment of the patients with CMD.