Table 3. Microvascular obstruction triggers: analysis of clinical data.

Hypothetical trigger	Disease	Effect	Ref.
AMI: acute myocardial infarction; CBF: coronary blood flow; CRP: C-reactive protein; MVO: microvascular obstruction; NSTEMI: non-ST-elevation myocardial infarction; NPY: neuropeptide Y; PCI: percutaneous coronary intervention; SA: stable angina; STEMI: ST-elevation myocardial infarction; TIMI: thrombolysis in myocardial infarction.
Microembolization and microthrombi	STEMI + PCI	The content of microparticles in the coronary artery was associated with MVO	[87]
Platelet aggregation	STEMI + PCI	Correlations were found between the frequency of MVO and ADP-induced platelet aggregation/ aggregation of neutrophil platelets/aggregation of monocyte platelets	[88]
	STEMI + PCI	MVO was more frequently observed in the high platelet reactivity group	[90]
Disturbance of blood viscosity	STEMI/NSTEMI/SA + PCI	Whole blood viscosity was higher in patients with MVO	[30]
Inflammation	STEMI + PCI	Microvascular obstruction score positively correlated with the CRP level and leukocytes. The CRP level was a predictor of MVO in patients with STEMI. The high interleukin-6 level was a predictor of MVO. Patients with MVO had a higher serum level of interleukin-18	[12,30,96–97]
Ca2+ overload	STEMI + PCI	The L-type Ca2+ channel blockers induced endothelium-independent vasodilation of coronary arteries, Verapamil alleviated MVO in patients with STEMI	[98–99]
	STEMI + PCI	Plasma endothelin-1 on admission was accompanied by MVO and increased long-term mortality	[100]
Diabetes	AMI + diabetes	Hyperglycemia was associated with MVO	[110]