Angina affects the coronaries, therefore, in this article I will describe the anatomy of these arteries and how they can be effected by atheromas. I will explain the pathogenesis of atherosclerosis.
Anatomy of coronary arteries
Understanding the coronary arteries of the heart is important because angina is due to the occlusion of these vessels. Additionally, if surgery is required, then the vessel in question will need to be operated on. The coronary circulation is involved in supplying the heart with oxygenated blood. The right and left coronary arteries which both arise from the base of the aorta circle the heart within the coronary sulcus.
What is atherosclerosis?
Atherosclerosis is the process where the artery walls thicken due to deposition of fatty materials such as cholesterol. It is possible that atherosclerosis begins in patient during childhood. Fatty lipid deposits were likely to have been seen as streaks in the arterial intimas of larger arteries if they were dissected. Over the years, the fatty streaks would have developed into atherosclerotic plaques in areas where arteries branch or bifurcate such as the aorta, coronaries, internal carotid arteries and the circle of Willis due to turbulent blood flow.
How atherosclerosis occurs
Low density lipoproteins(LDL)are heavily involved in the pathogenesis of an atherosclerotic plaque. A diet rich in fats and cholesterol causes high levels of cholesterol to be transported by LDL to the inner arterial walls. LDLs become oxidised by free radicals from products such as cigarette smoke. Oxidised LDL promotes endothelial cell damage and increases the expression of adhesion molecules on endothelial cell surfaces allowing circulating monocytes to attach. The monocytes then penetrate through the single layered endothelial cell into the tunica intima where they mature into macrophages. It is important to also note that endothelial cell damage can also be brought about by high blood pressure, poorly controlled diabetes and smoking.
Oxidised LDL also acts as a chemotactic factor to attract macrophages. Macrophages inside the intima ingest oxidised LDL through scavenger receptors. Normally LDL intake is highly regulated because a negative feedback mechanism exists due to the presence of the protein, apoliprotein b100. However, with oxidised LDL, macrophages are unable to control intake because apoliprotein b100 is absent on their receptors. This causes macrophages to become loaded with cholesterol to form a foam cell that will become a fatty streak on the vessel. Stimulation of the macrophages and endothelial cells by oxidised LDL causes secretions of cytokines and growth factors. These factors act on the smooth muscles in the tunica media to cause smooth muscle cells to migrate into the intima so that they can proliferate and secrete collagen and other connective tissue proteins. An advanced plaque usually resides in the arterial wall that has thickened due to smooth muscle proliferation and there is often a fibrous connective tissue cap surrounding the foam cells that have died. Recent research has suggested consuming blueberries can increase antioxidant enzymes in the body to reduce the plaque size.
Types of angina and their causes
Angina exists in three forms: stable, unstable and variant. Stable angina also known as exertional angina occurs when blood flow through coronary arteries is reduced by at least 70% due to the presence of atheromas. During resting conditions, the heart’s oxygen demand is low and therefore patients do not present with symptoms even with coronary vessel stenosis. However, when one ‘exerts’ themselves such as when exercising the heart’s oxygen demand increases because the heart needs to pump more blood around the body in order to deliver oxygen and nutrients to the rapidly respiring cells in the body. The heart responds by increasing heart rate and blood pressure. As a result of this the heart needs to increase blood flow to itself because oxygen demand has increased. In healthy individuals, the heart responds by dilation of coronary arteries to increase blood flow. However, the presence of atheromas prevents increased blood flow through the vessels because they become fixed and non-dilatable. Failure of the heart to meet oxygen demands leads to the development of ischaemia in the subendocardium and chest pain because the heart is producing reduced amounts of creatine phosphate and ATP. This leads to impaired ventricular contraction and diastolic relaxation in the affected area. Symptoms are often the result of decreased cardiac output, pulmonary congestion and activation of the sympathetic nervous system.
Unstable angina causes myocardial ischaemia and necrosis due to sudden occlusion of coronary vessels due to sudden rupture of an atherosclerotic plaque which leads to platelet aggregation and formation of an intracoronary thrombus. Occlusion of coronaries may also be due to the release of vasoconstricting agents released during platelet aggregation and endothelial damage. The less common variant angina, also known as vasospastic or Prinzmetal angina occurs due to transient occlusive spasms of the coronary arteries. It is interesting to note that 30% of these patients show no signs of atherosclerotic coronary plaques. In patients who do have plaques, the spasms are most likely to occur near to these sites. It has been thought the spasms occur because of a particular part of the coronary artery becoming overly reactive to vasoconstricting agents such as noradrenalin or serotonin.
Signs and symptoms of angina
Signs and symptoms of angina are caused by the imbalance between myocardial oxygen demand and amount of oxygen being supplied. Common symptoms which patients complain of include ‘heavy’, ‘tight’ or ‘gripping’ pain usually over the left side of the chest that may radiate to the jaws or arms. There are chemosensitive sympathetic fibres present in the left ventricle which are sensitive to pH drops caused by accumulation of lactic acid, adenosine, bradykinin and prostaglandin build up due to ischaemia of the myocardium. These sympathetic fibres then converge up the spinothalamic tract which converge onto the somatic afferents which may explain why patients get referred pain in the arm and jaw. Other signs and symptoms patients may experience during an angina attack include breathlessness, nausea, fatigue, dizziness, belching and restlessness. Stable angina is triggered as a result of physical activity or stress while unstable and variant angina can develop when resting. Attacks of unstable angina can last longer than five minutes and may not respond to treatment with glyceryl trinitrate. Variant angina can occur during the early mornings and can be exacerbated by smoking and cocaine use.