Ischemic heart disease

Ischemic (coronary) heart disease (IHD)- define as acute and chronic heart damage, caused due to diminishing or stopping blood delivery to myocardium. Disease of the coronary arteries is almost always due to atheroma and its complications, particularly thrombosis.

Etiology and pathogenesis

Atherosclerosis of coronary arteries; the degree of its expression is different -from small wall affection to complete occlusion of vessel.

Spasm of coronary arteries develops, as a rule, on a background of atherosclerosis of coronary arteries. The physical overloading, mental stress provokes the development of clinical features of IHD.

The main pathophysiological mechanism of IHD is imbalance between the demand myocardium in oxygen and possibilities of coronary arteries satisfied the myocardium by adequate amount of blood.

The followings mechanisms are involved in pathological process:

• mechanical occlusion of coronary arteries due to an atherosclerotic process;

• dynamic occlusion of coronary arteries due to coronarospasm;

• activation of thrombocytes aggregation with development of microagregates in microcirculation;

• promotion of production the pro-coagulating factors, insufficiently level of prostacyclin and endothelin- derived relaxing factor;

• increasing of demand myocardium in oxygen under influencing of the intensive physical loading, mental stress, resulting in the high level catecholamines in blood caused cardiotoxic action;

• insufficiency of collateral circulation of blood;

• activation of the lipid peroxidation;

• activation of immune mechanisms.

Thus the pathological substrate of IHD is almost atheroma narrowing of the coronary arteries. Atheroma or atherosclerosis is a focal disease of the arterial intima. There are some stages of evolution of atherosclerotic process. Initial stage is fatty streaks, which develop as circulating monocytes migrate into the intima take up oxidized low density lipoprotein from the plasma and become lipid foam cells. As these foams cells die extracellular lipid pools appear. Smooth muscle cells then migrate into and proliferate within the plaque. A mature fibrinolipid plaque has a core extracellular lipid, separated from the lumen by a thick cap of a collagen-rich fibrous tissue. Such plaque may narrow the lumen of the vessel and often precipitate local vasospasm and thrombosis. The luminal diameter of a coronary artery must be decreased by at least 50 % to 70 % before blood flows becomes inadequate to meet the metabolic demands of the heart during exercise or stress.

The evolution of the atheromatous plague corresponds with clinical forms of IHD. The principal cause of stable angina is atherosclerosis involving at least one large epicardial artery that limited coronary flow under some condition. Stable angina is related to a fixed obstruction and it is usually precipitated by an increase in myocardial oxyden demand (demanded ischemia).

Unstable angina is defined as an obstruction of at least one major epicardial artery that occupies at least 70 % of the artery's cross-sectional diameter or an obstruction of the left main coronary artery that occupies at last 50 % of its diameter. Episodes of myocardial ischemia are due to abrupt reduction in coronary blood flow results from plaque rupture, rapid growth of the lesion or incomplete occlusion of the vessel. Unstable angina is a transitory condition. A platelet rich thrombus forms rapidly around the site of the rupture, reducing, but not usually occluding the blood flow in the vessel.

Myocardial infarction is almost always due to the formation of occlusive thrombus at the site of rupture of an atheromatous plaque in a coronary artery. The affected artery is more commonly completely occluded, usually by a fibrin-rich "red" thrombus.

Sudden death in most cases is attributable to IHD and is usually due to arrhitmia or asystole (ventricular fibrillation, sinoatrial block, complete AV-block) related to acute coronary syndrome, heart failure or scarring from a previous myocardial infarction.