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.