Cardiac muscle is one of the three types of muscle in the human body. Due to its vital function, it requires a highly specialised circulation, called the coronary circulation. This article will look at the coronary circulation, its adaptations, and clinical conditions related to coronary circulation.
Overview
Cardiac muscle has its own dedicated circulatory system: the coronary blood vessels. Cardiac muscle constantly undergoes phases of contraction and relaxation to pump blood around the body. As myocardial oxygen demand increases, coronary blood flow to the cardiac muscle must also increase to meet requirements.
Anything that prevents blood from passing through the coronary vessels, for example, atherosclerosis, will result in ischaemia and a consequent myocardial infarction.
Fig 1 – A brief overview of the coronary circulation.
Adaptations
Capillary density
One of the adaptations of the coronary circulation is that there are far more capillaries per mm2 in cardiac muscle than in skeletal muscle. This means there is a larger endothelial surface area for O2 delivery and removal of metabolic products.
Coronary vessel perfusion
Perfusion of the coronary arteries occurs during diastole. Blood enters the coronary arteries through the aortic sinuses, which are openings found behind the aortic valve leaflets. As the heart relaxes during diastole, the aortic valve shuts and blood fills the valve pockets, allowing blood flow into the coronary arteries to supply the cardiac muscle. The coronary arteries also send branches into the myocardium, which become compressed during systole. Therefore, when the muscle relaxes, myocardial blood flow is increased as there is less compression on these vessels. This creates an intermittent blood flow, where there is high flow during diastole, that gets interrupted during systole.
Metabolic products
Vasodilation of the coronary arteries helps maintain a high basal rate of blood flow. This vasodilation occurs as a result of nitric oxide (NO), which is released from endothelial cells. Moreover, the accumulation of metabolites such as adenosine, K+ ions and H+ ions also adds to this vasodilation. This phenomenon is known as reactive hyperaemia, and it occurs in tissues around the whole body as well as the heart.
Clinical Relevance
Myocardial Infarction
If the blood supply to the cardiac muscle is obstructed, for example by a thrombus, then the oxygen supply is reduced, leading to ischaemia (lack of adequate blood flow). Due to the high oxygen demand from this tissue, it cannot survive for very long without adequate oxygen supply. Prolonged periods of ischaemia result in infarction, which is the death of healthy cardiac myocytes. This causes the classic symptom of central crushing chest pain, which may also radiate to the left upper limb and jaw.
The diagnosis of a myocardial infarction involves using an electrocardiogram (ECG) or biomarkers in the blood, such as troponins or creatine kinase-MB (CK-MB). The initial management of a myocardial infarction involves pain relief e.g. morphine, glyceryl trinitrate (GTN) spray and antiplatelets such as aspirin and clopidogrel. Definitive treatment is via a Percutaneous Coronary Intervention (PCI) if possible within 12 hours of symptom onset. However, if PCI is not available, thrombolysis can be used.
Fig 2 – The progressive narrowing of an artery leading to occlusion and potential myocardial infarction.
