[Evaluation of coronary hemodynamics and exercise 201Tl-myocardial scintigraphy in patients with vasospastic angina].
K Matsumura, Emiko Nakase, T Haiyama, Akira Hasegawa, Tomiyoshi Saito
Abstract
K Matsumura, Emiko Nakase, T Haiyama, Akira Hasegawa, Tomiyoshi Saito
Abstract
To clarify the coronary hemodynamics and myocardial perfusion in patients with vasospastic angina, we performed exercise-201Tl-myocardial scintigraphy (planar and SPECT) in 72 patients and left coronary digital subtraction angiography (DSA) in 37 patients without significant organic coronary artery stenosis. Coronary artery spasm was documented by coronary angiography in all patients. Fifty-four patients (75%) developed exercise-induced 201Tl-myocardial perfusion defect on SPECT. 201Tl pulmonary uptake (L/H) was significantly increased in patients with vasospastic angina. Especially, L/H was higher in patients with multiple small perfusion defect on 201Tl-SPECT, so that exercise-induced left ventricular dysfunction existed in patients with vasospastic angina and especially in cases with multiple small perfusion defect on 201Tl-SPECT. The left coronary circulation time (CCT) was prolonged in patients with vasospastic angina. The mechanism of prolonged CCT is still unknown, but we suspected that prolonged CCT was induced by increased peripheral coronary vascular resistance in patients with vasospastic angina. It was concluded that the peripheral coronary circulation was disturbed in patients with vasospastic angina, but its abnormal coronary circulation had no relation to location of spasm-induced vessels. We concluded that impaired coronary microcirculation was taken a part of pathophysiology in vasospastic angina.
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To clarify the coronary hemodynamics and myocardial perfusion in patients with vasospastic angina, we performed exercise-201Tl-myocardial scintigraphy (planar and SPECT) in 72 patients and left coronary digital subtraction angiography (DSA) in 37 patients without significant organic coronary artery stenosis. Coronary artery spasm was documented by coronary angiography in all patients. Fifty-four patients (75%) developed exercise-induced 201Tl-myocardial perfusion defect on SPECT. 201Tl pulmonary uptake (L/H) was significantly increased in patients with vasospastic angina. Especially, L/H was higher in patients with multiple small perfusion defect on 201Tl-SPECT, so that exercise-induced left ventricular dysfunction existed in patients with vasospastic angina and especially in cases with multiple small perfusion defect on 201Tl-SPECT. The left coronary circulation time (CCT) was prolonged in patients with vasospastic angina. The mechanism of prolonged CCT is still unknown, but we suspected that prolonged CCT was induced by increased peripheral coronary vascular resistance in patients with vasospastic angina. It was concluded that the peripheral coronary circulation was disturbed in patients with vasospastic angina, but its abnormal coronary circulation had no relation to location of spasm-induced vessels. We concluded that impaired coronary microcirculation was taken a part of pathophysiology in vasospastic angina.
Key concepts: Medicine, Cardiology, Internal medicine, Angina, Perfusion, Coronary circulation, Artery, Hemodynamics