<unk> circulation confers a protective blood supply to the myocardium jeopardized by ischemia.  During embryological development, an extensive overlay of inter coronary anastomoses derives from endothelial precursor cells which, in response to local signals, migrate and differentiate into new vessels in a process termed vasculogenesis.  With progressive luminal encroachment of atheromatous plaque,<unk> vasculature is remodeled to reduce overall resistance to the epicardial coronary flow which entails a decrease in the number of conduits and an increase in the caliber from 10–200 μm to 100–800 μm.  Following total or subtotal occlusion of an epicardial artery, arteriogenesis (recruitment of preexisting<unk> channels) occurs conjointly with angiogenesis (sprouting of new vessels) to salvage the ischemic myocardium by shunting the blood from nonjeopardized territories.  The mechanism responsible for modulating the processes of coronary vasculogenesis, arteriogenesis, and angiogenesis remains elusive.  In the setting of myocardial infarction, the presence of well-developed<unk> zation is associated with a reduced infarct size, mitigated QT prolongation, lessened post-infarct ventricular dilatation, and decreased mortality.  However, further prospective studies are warranted to determine whether therapeutic promotion of<unk> growth translates into favorable cardiovascular outcomes.
Coronary collaterals
Coronary artery bifurcation
Coronary artery trifurcation
Left ventricular aneurysm pathophysiology
Coronary artery dual ostia
Coronary artery dominance
Coronary artery irregularity
No-reflow phenomenon