Coronary Vascular Physiology
Overview
The coronary circulation is unique in its dependence on local metabolic autoregulation to continuously match myocardial oxygen supply with demand. Unlike other vascular beds, coronary flow occurs predominantly in diastole (when the myocardium is relaxed and not compressing intramyocardial vessels).
Coronary Arterial Anatomy
- Left Main Coronary Artery (LMCA): Arises from the left aortic sinus. Divides into the LAD and LCx. Average 1-2 cm length.
- Left Anterior Descending (LAD): Supplies anterior LV wall (Segments 1-7), interventricular septum, and apex. 'Widow maker' - largest territory.
- Left Circumflex (LCx): Supplies the lateral and posterior LV wall. In 15% of people is 'dominant' (supplies the PDA).
- Right Coronary Artery (RCA): Dominant in 85% of people — supplies the PDA, inferior LV, and AV node.
Autoregulation and Vasodilatory Mechanisms
Coronary autoregulation matches flow to metabolic demand:
- Hypoxia: The most potent direct coronary vasodilator.
- Adenosine: Released during ATP breakdown. Causes profound coronary vasodilation. Basis of pharmacological stress testing.
- Nitric Oxide (NO): Endothelium-derived; maintains basal coronary tone and mediates flow-mediated dilation.
WarningCoronary Steal Phenomenon
In patients with significant stenoses, adenosine-induced maximal vasodilation can cause 'coronary steal' — flow is diverted away from fixed-stenosis territories (which cannot further dilate) to normal beds. This creates reversible perfusion deficits on MPS, revealing ischaemia.
High Yield Facts
LightbulbFRCR / MD Prep Pearl
On myocardial perfusion scintigraphy (MPS): a reversible perfusion defect (stress-only, normal at rest) = ischaemia. A fixed defect (both stress and rest) = infarction/scar. The 17-segment AHA model maps perfusion territories to coronary arteries. CTCA can directly visualise stenoses and plaques non-invasively.