Discussion
This case was the first to report the ”reverse redistribution” of local myocardial perfusion during ATP stress MCE. Previous reports showed that coronary vessels with spastic trend were often in a slight contraction state, and radionuclide myocardial perfusion was delayed. When vasodilators were used, myocardial perfusion was significantly improved. This phenomenon was called ”reverse redistribution”, which was related to coronary vasospasm, but it also existed in other diseases, such as stunned myocardium, scar myocardium, etc. [2-3]. The decrease of coronary flow reserve also indicates the dysfunction of myocardial microcirculation in these areas [4]. Chest pain, expansion of delayed myocardial perfusion areas, increase of distal coronary flow spectrum resistance and decrease of blood flow volume all showed local myocardial microvascular contraction during recovery period. Cases of ATP-induced coronary vasospasm have been reported, but the exact mechanism of ATP-induced coronary vasospasm was not clear, which could be related to the damage of vascular endothelial cells, the decrease of endothelium-dependent relaxation and the enhancement of reactive contraction [5-6]. The factors leading to vasospasm mainly included smoking, drinking, damage to vascular endothelium, excessive contraction of smooth muscle cells, autonomic nerve regulation disorder , inflammation and so on[7-8]. This patient also had risk factors of smoking and drinking. In the past, ATP-induced coronary spasm was considered as a side effect of ATP. In fact, ATP-induced coronary spasm was not the spasm of the whole coronary artery, and this patient was only limited to the delayed myocardial perfusion of some segments of the left ventricular wall. Therefore, it could be inferred that there were certain lesions or dysfunction in myocardial micro vessels in areas with delayed perfusion. When these regional myocardial micro vessels were stimulated by risk factors, they could induce spasm and chest pain. This case needed to be distinguished from the large coronary spasm of the left anterior descending artery. In the resting state, the coronary angiography did not find a slight contraction of the large coronary artery, the delayed areas of myocardial perfusion were inconsistent with the distribution areas of the coronary artery, and the coronary blood flow did not accelerate significantly. Therefore, it was considered that it was not caused by the large coronary spasm.
There were few cases of ATP-induced coronary micro vasospasm reported in the past. The main reasons were as follows. On the one hand, myocardial micro vasospasm had no characteristic changes in ECG, 2D ultrasound, CT and coronary angiography. On the other hand, the characteristics of myocardial perfusion and coronary flow spectrum were ignored in recovery period.
Conclusion The ”reverse redistribution” areas of ATP stress MCE were the prone areas of myocardial microvascular spasm, and the areas of delayed myocardial perfusion in the recovery period were the areas of ATP-induced myocardial microvascular spasm. Therefore, ATP stress MCE could provide a valuable reference for clinicians to seek chest pain caused by myocardial microvascular spasm.