Summary of Coronary Artery Regulation

• In heath:

  • On exercise myocardial oxygen demands increase and sympathetically mediated vasodilation via beta-2 receptors together with an increased production of metabolites by the myocardium plus an increased synthesis of NO etc.. by the coronary artery endothelium ensures that adequate vasodilation occurs resulting in the necessary increase in blood flow to the myocardium
• Unhealthy coronary arteries pt1:

  • unable to fully vasodilate due to the loss of endothelial derived vasodilators including NO and the presence of obstructive atheroma
  • This means that when myocardial activity rises and therefore myocardial demand for O2 rises, the diseased coronary arteries may not be able to meet demands
• Unhealthy coronary arteries pt2:

  • In addition, an “unfit” heart has a reduced aerobic capacity so is unable to extract and utilise O2 efficiently in order to manufacture ATP to “fuel” cardiac function including contraction
  • This means that at all levels of activity; rest and exercise, the myocardium of an unfit heart needs a higher blood flow than a fitter (more aerobically efficient) heart
• Unhealthy coronary arteries and unhealthy body pt1:

  • Inadequate physical activity is a major driver (risk factor) for atheroma development
  • So, we can safely imagine the majority of the atherosclerotic population to be inadequately active
  • Inadequate activity reduces VO2 max primarily through type 1 skeletal muscle atrophy and reduced aerobic efficiency
  • On activity, deconditioned skeletal muscles place huge demands on the heart to increase blood flow
  • This is necessary to compensate for the fact the deconditioned muscles are poor at extracting O2 from blood
• Unhealthy coronary arteries and unhealthy body pt2:

  • so, to get more o2, deconditioned muscles need more blood
  • Needing more blood requires the heart to work hard (increase heart rate & stroke volume) and pushes up the myocardium’s own demands for oxygenated blood from the coronary arteries
  • Diseased coronary arteries with a limited vasodilation capacity and obstructive atheroma(s) in situ may not be able to meet this demand, resulting in inadequate myocardial perfusion and the risk of hypoxia / ischaemia