There are two coronary arteries, right and left, both of them arise from the coronary ostium which is located in the first part of the aorta, called the ascending aorta. The right coronary artery arises from the anterior sinus of Valsalva and follows the groove between the right atrium and right ventricle. It supplies the SA node, AV node, bundle of His, right ventricle and the inferior part of the left ventricle. The left coronary artery arises from the left sinus of Valsalva, and is divided into anterior descending and circumflex branches. The former courses along the anterior interventricular groove while the latter passes along the atrioventricular groove between the left atrium and ventricle. The arteries divide to form arterioles and capillaries and ultimately venules and veins are formed which drain into the coronary sinus.

The blood flow is dependent on the systemic pressure head and on the peripheral resistance. As the blood vessels are compressed during systole by. the active contraction of the myocardium, the vascular resistance is increased and forward flow of blood is impeded. Therefore, coronary flow occurs mainly during the diastole and this is again dependent on the aortic diastolic pressure. Dilatation of lumen of the coronary artery also increases the coronary flow. Unlike other tissues myocardium completely takes out oxygen of the arterial blood and hence venous blood is completely desaturated. In face of excessive demand, the coronary arteries should dilate resulting in more blood flow. The most potent coronary dilator is oxygen lack. Ischaemic heart disease is occlusive coronary arterial disease mostly due to atherosclerosis producing relative or complete impairment of blood supply to the heart. Apart from occlusive coronary arterial disease, myocardial ischaemia may result from the following conditions | ISCHAEMIC HEART DISEASE

  1. Severe anemia.
  2. Tachyarrhythmia.
  3. Heart failure
  4. Other conditions associated with low cardiac output, e.g. Mitral stenosis, Aortic stenosis.
  1. Cardiac hypertrophy from various causes (relative ischaemia). But these are not the common causes of myocardial ischaemia in the vast majority of the cases.
  2. Again one should remember that though there are several causes leading to occlusive coronary disease atherosclerotic occlusion is by far the commonest and most important cause of ischaemic heart disease. Occlusive coronary arterial disease may result from.

  1. Atherosclerosis– commonest cause.
  2. Subendothelial haemorrhage.
  3. Coronary vasospasm.
  4. Polyarteritis nodosa and giant cell arteritis.
  5. Coronaritis.
  6. Coronary embolism from various causes
  7. Coronary arteriovenous fistula.
  8. Syphilitic coronary osteitis.


The factors responsible for development of atherosclerotic coronary artery (ASCAD) can be grouped under the following three headings. But it is not clear how these factors operate for its production.


Major risk factors

  1. Hypertension: It has been observed that high blood pressure appears to aggravate ASCAD and is more pronounced with advancing years. In hypertensive patients atherosclerotic complication is the most common cause of death. Hypertension increases the filtration of lipid material from the blood to the intimal cells, particularly in presence of elevated plasma lipids. This results intimal injury leading to aggregation of platelets and proliferation of smooth muscles of intima.
  2. Smoking: There is a strong association between smoking habits and ASCAD. Smoking results in 70% greater chance of ASCAD amongst smokers than non-smokers. It precipitates arrhythmia resulting in sudden death in patients with ASCAD. Smoking is associated with reduced HDL cholesterol which is one of the mechanism of its adverse effect. Risk of smoking is independent of other factors. Incidence of sudden death is definitely greater in smokers. When smoking is stopped the risk is markedly reduced. Chewing tobacco, cigar and pipe smoking are less important.
  3. Hyperlipidaemia: From population survey high mean serum cholesterol level has been found to be associated with premature ischaemic heart disease and vice-versa. Though high serum cholesterol and LDL cholesterol are important, yet a decrease in HDL cholesterol is thought to be more important. Again the ratio of HDL cholesterol to total cholesterol (<0.15) is thought to be a better predictor of ASCAD than either level alone or apoprotein A, B or E. Decreased HDL impairs the clearance of cholesterol from the arterial wall.
  4. Diabetes Mellitus: Diabetes is associated with increased incidence of ASCAD in men and women to the extent of 50% and 100% respectively. Even asy’mptomatic hyperglycaemia in adults may be a risk factor. This is possible due to increased serum cholesterol, decreased HDL cholesterol, platelet adhesiveness, microangiopathy and cardiomyopathy. This is true for both type 1 and type 2 diabetes mellitus. The mortality rate from ASCAD has been found to be double in comparison to normal glycaemic subjects. The role of serum glucose and serum insulin is not definitely known. However, the severity of diabetes cannot be correlated with the severity of ASCAD.
  5. Sex: ASCAD is common in men than in women. This is very much marked in premenopausal women. In young menstruating women coronary disease is rare in comparison to men of same age. However, with menopause (particularly surgical induced) there is an unexplained increase of ASCAD. In general ASCAD is five times more common in men than in women in the age group of fifty years.
  6. Family History: The disease may run in several members of the same family possibly due to:
  7. a) Genetic predisposition to the development of diabetes, hypertension or hyperlipidaemia.
  8. b) Environmental influence from the lifestyle, stress and others.
  9. c) Protective genetic influence from HDL cholesterol involvement.
  10. Diet: Excess fat in the diet is responsible for ischaemic heart disease. Saturated fat is more harmful. 8. Coagulation factors: High serum fibrinogen level is a strong independent risk factor. Coagulation cascade, platelet aggregation endothelial dysfunction, smooth muscle cell proliferation etc. are related to it. Various polymorphism of factor VII gene may be associated with increase risk of coronary thrombosis.
  11. Hyperhomocysteinemia: This has come out as a major risk factor of ASCAD in recent times or is related to endothelial dysfunction.
  12. Infection: Herpes virus, Cmv, H. pylori clamydia pneumoneae have been detected in atherosclerotic plaque.

Minor risk factors

  1. Oral contraceptives: There is increased incidence of myocardial infarction among women taking oral contraceptives for more than 5 years. It has been found that there is three to four fold increase in the incidence of infarction in women under 50 years of age in comparison to women who have never used the pills.
  2. Prostaglandins: Endothelial cells synthesize prostacyclin (PGI,). This factor is a vasodilator and prevents platelet aggregation. Blood platelets synthesize thromboxane (TXA2 ) which is a vasoconstrictor and aggregator of platelets. These two factors TXA2 and PGI2 are produced locally and their imbalance will produce vasoconstriction and platelet aggregation.
  3. Age: Incidence of ASCAD increases with advancing age. However, in young age group it is not uncommon (Pecocious ischaemic heart disease).
  4. C-Reactive protein: This has been linked with future CAD.

Factors of doubtful importance

  1. Physical inactivity: This may produce obesity which may predispose to diabetes and hypertension. Exercise may lead. to dilatation of coronary arteries and increase their anastomosis. However, National Exercise and Heart Disease project, Ontario Exercise Heart Collaborative study could not be corroborated. But it is worthwhile to note that the Framingham Heart study has found an inverse relationship between physical activity and cardiovascular and coronary disease mortality.
  2. Personality, Socio-cultural and Psycho-social factors are also controversial.
  3. Obesity, Hypertriglyceridaemia, Gout, Arcus senilis, Diagnonal ear lobe crease, mannesium and chromium deficiency, excessive sugar consumption, drinking soft water alcohol excess have all been seen to be commonly associated with ASCAD.
  4. Endothelial factors: Endothelium may produce a relaxing factor which may increase endothelial permeability and endothelial damage. There may be other vasoactive substances from endothelial cells. All these may be responsible for coronary arterial constriction.


Excessive intake of saturated fat and cholesterol backed by a genetic predisposition sets the atherosclerotic process in motion. The first step is the accumulation of sub endothelial lipid and lipid laden monocytes. This is called ‘fatty streak formation. LDL is the major atherogenic lipid which undergoes oxidation in situ by the protective lipids HDL when they are difficult to mobilize. Moreover, these oxidized LDL are locally cytotoxic. Gradually there will be altered endothelial function due to less production of EDRF (Endothelium derived relaxing factor) leading to disruption of endothelium. This leads to adherence of platelets and release of PDGF (Platelet derived Growth factor) and other growth factors, The local cells undergo proliferation and thus a ‘mature’ fibrous plaque is finally formed. This results in coronary arterial obstruction and various syndromes described below.


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