1.2 Structure of the Coronary Circulation

Structure of the coronary circulation

• Coronary circulation arises from the ascending aorta just above the aortic valve (at the left and right aortic sinuses)

• Two main coronary arteries:

  • Left coronary artery (LCA)

  • Right coronary artery (RCA)

• Coronary arteries are functional end arteries: Limited collateral supply, limited amount of anastomoses

• Perfusion occurs mainly during diastole and not systole

• Autonomic innervation

Coronary arteries and regions

Left coronary artery (LCA)

• Origin: Left aortic sinus

• Course: Between posterior pulmonary trunk and left auricle

• Branches:

  1. Left anterior descending (LAD) / anterior interventricular artery

  • Descends in anterior interventricular groove

  • Supplies: 

    • Anterior 2/3 of the interventricular septum

    • Anterior walls of both ventricles

    • Apex

  2. Circumflex artery

     • Courses in left atrioventricular (coronary) sulcus

     • Supplies:

       • Left atrium

       • Lateral and posterior LV

       • May give posterior LV branch

     • Gives off left marginal artery (to lateral LV wall)

  3. SA nodal branch (in ~40% of people)

Right coronary artery (RCA)

• Origin: Right aortic sinus

• Course: Between rigth auricle and pulmonary trunk, runs in right coronary sulcus

• Branches

  1. Right marginal artery, supplies right ventricle

  2. Posterior interventricular artery (PDA) / right posterior descending artery

     • Supplies:

       • Posterior 1/3 of the interventricular septum

       • Inferior walls of both ventricles

  3. SA nodal branch (in ~60% of people)

  4. AV nodal branch (in ~80% of people)

Dominance patterns (Myocardial regional supply)

• Determined by the artery that gives rise to the posterior interventricular artery (PDA)

Venous drainage of the heart

Coronary sinus system (65% drainage)

• Main venous collector, drains into right atrium

• Tributaries:

  • Great cardiac vein (runs with LAD)

  • Middle cardiac vein (runs with PDA)

  • Small cardiac vein (with RCA)

  • Posterior vein of the LV

  • Left marginal vein

• Thebesian valve guards entry into right atrium

• AV node lies close to coronary sinus opening

Anterior cardiac veins (~35%)

• Drain anterior RV directly into RA, bypassing the coronary sinus

Thesbesian veins (venae cordis minimae)

• microscopic veins draining directly into all chambers (mostly RA and RV)

Physiological control of coronary arteries

Coronary perfusion

• occurs during diastole due to compression during systole

• Coronary perfusion pressure (CPP) = Aortic Diastolic pressure - Left ventricular end-diastolic pressure (LVEDP)

  • Aortic diastolic pressure: Supplies the “push” into coronary arteries

  • LVEDP: Back pressure within the LV that opposes perfusion

Autonomic regulation

Sympathetic nervous system

• Origin:

  • Preganglionic fibres arise from the lateral horn of spinal cord segments T1 to T5

  • Postganglionic fibres originate in the cervical sympathetic ganglia (superior, middle, and inferior) and the thoracic sympathetic chain

• Pathway:

  • Postganglionic fibres travel as cardiopulmonary splanchnic nerves to the heart

• Effects:

  • Sinoatrial (SA) and atrioventricular (AV) nodes: increase heart rate and conduction velocity

  • Ventricular myocardium: increase contractility

  • Coronary arteries:

    • Beta-2 receptor stimulation causes vasodilation

    • Alpha-1 receptor stimulation causes vasoconstriction, which becomes more dominant in disease states

Parasympathetic nervous system

• Origin:

  • Preganglionic fibres arise from the brainstem, specifically the nucleus ambiguus and dorsal motor nucleus

  • They travel via the vagus nerve (cranial nerve X)

  • Postganglionic fibres originate in the cardiac plexus

• Effects:

  • SA and AV nodes: reduce heart rate and conduction velocity

  • Coronary arteries: cause mild vasodilation, primarily in atrial tissue

Endothelial factors

• Nitric Oxide (NO): Vasodilation

• Endothelin-1: Vasoconstriction

• Prostacyclin: Vasodilation, platelet inhibition

Metabolic and endocrine factors

• Adenosine, K+, CO₂, H⁺, low O₂: → local vasodilation

• Hormones (e.g., adrenaline): can vasodilate via β2 or vasoconstrict via α1

Physical factors

• External compression during systole limits flow

• Mechanical shear stress influences endothelial function