Ischemic heart disease: causes and risk factors

Causes and pathophysiology of coronary heart disease

Usually IHD develops due to the appearance of atheromatous plaques in the intima of coronary arteries of large and medium caliber, less often due to spasm of coronary arteries. Rare causes of coronary heart disease include coronary thromboembolism, lamination, aneurysm (eg, in Kawasaki's disease) and vasculitis (eg, in systemic lupus erythematosus, syphilis).

Atherosclerosis of the coronary arteries is more often distributed unevenly, typical places are places of turbulent blood flow (for example, branching of blood vessels). Progressive narrowing of the arterial lumen leads to ischemia (manifested by angina pectoris). The degree of stenosis that can lead to ischemia depends on the need for oxygen.

Sometimes an atheromatous plaque ruptures or breaks. The causes are unclear, but probably an inflammatory process that softens the plaque is important. As a result of the rupture of the plaque, thrombogenic substances activate platelets and the process of coagulation, which leads to acute thrombosis and ischemia. The consequences of acute ischemia, combined in the concept of acute coronary syndrome (ACS), depend on the localization and severity of vascular obstruction and range from unstable angina to transmural myocardial infarction.

Spasm of the coronary artery - a transient local increase in the tone of the vessel, leading to a noticeable narrowing of its lumen and a decrease in blood flow; the result can be symptomatic myocardial ischemia ("Variant angina"). Significant narrowing can lead to the formation of a thrombus, which causes myocardial infarction. Spasm can occur in arteries with or without atherosclerotic lesions. In arteries not affected by atherosclerosis, there is probably an initial increase in vascular tone and a hyperergic response to vasoconstrictor effects. The exact mechanism of variant angina has not been clarified, however, the role of an anomaly in the synthesis of nitric oxide or an imbalance between endothelium-narrowing and dilating factors is suggested. In arteries, altered atherosclerotic, atheromatous plaque can lead to increased contractility; The proposed mechanisms include the resulting loss of sensitivity to natural vasodilators (eg, acetylcholine) and increased formation of vasoconstrictors (such as angiotensin II, endothelium, leukotrienes, serotonin, thromboxane) in the area of atherosclerotic plaque. Repeated spasms can damage the inner shell of the artery, leading to the formation of an atherosclerotic plaque. The use of substances that have a vasoconstrictive effect (for example, cocaine, nicotine), can cause a spasm of the coronary artery.

[1], [2], [3], [4], [5], [6], [7], [8], [9]

Risk factors for coronary heart disease

The risk factors for IHD are the same as for atherosclerosis: high LDL cholesterol and lipoprotein a, low HDL cholesterol in the blood, diabetes mellitus (especially type 2), smoking, overweight and hypodynamia. Smoking is the most powerful factor predisposing to the development of myocardial infarction in women (especially up to 45 years). A certain role is played by genetic predisposition and some diseases (such as AH, hypothyroidism). An important risk factor is the high content of apoprotein B, which may indicate a risk of atherosclerosis in cases where the amount of total cholesterol or LDL is normal.

A high concentration of C-reactive protein in the blood is a sign of instability of atherosclerotic plaque and inflammation, which is more likely to indicate a risk of ischemia than an elevated LDL level. A large number of triglycerides and insulin in the blood (reflecting insulin resistance) can also be a risk factor, but this fact is less well understood. The risk of CHD increases in smokers who eat high-fat foods and calories, low in plant fiber (found in fruits and vegetables) and vitamins C and E, a relatively low content of a-3 (n-3) polyunsaturated fatty acids (PUFAs), at least in some people, as well as with low resistance to stress.

Anatomy

The right and left coronary arteries originate from the right and left coronary sinuses in the root of the aorta, just above the aortic valve aperture. The venous arteries are divided into large and medium arteries that are located on the surface of the heart (epicardial coronary arteries) and then give smaller arterioles to the myocardium. The left coronary artery begins as the left main artery and is quickly divided into the left anterior descending and envelope arteries. The left anterior descending artery is usually located in the anterior interventricular groove and (in some people) extends to the apex of the heart. This artery supplies the anterior part of the septum, including the proximal parts of the conductive system and the anterior wall of the left ventricle (LV). The envelope artery, which is usually smaller than the left anterior descending, supplies the lateral wall of the left ventricle. Most people note the predominance of right blood flow: the right coronary artery passes through the atrioventricular sulcus on the right side of the heart; it supplies the sinus node (in 55% of cases), the right ventricle, and (usually) the atrioventricular node and the lower wall of the myocardium. Approximately 10 to 15% of people have a predominance of left-sided blood flow: the envelope artery is somewhat larger and, continuing along the posterior atrioventricular sulcus, supplies the posterior wall and the AV node.

[10], [11], [12], [13], [14], [15], [16]