**6. Pathological physiology (by the example of aortic stenosis)**

Hemodynamic manifestations of aortic stenosis develop with a decrease in the area of the aortic ostium less than 1 cm<sup>2</sup> , which is usually combined with a pressure gradient between the LV and aorta of 50 mm Hg. Art. The "critical" area of the Aorta opening, corresponding to the picture of a sharp aortic stenosis, is 0.5– 0.7 cm<sup>2</sup> with an aortic systolic gradient of 100–150 mm Hg. Art. To ensure adequate cardiac output, the LV during systole must develop a pressure of 200–250 mm Hg. Art. Possessing powerful compensatory capabilities, hypertrophied LV intensifies contractions and copes with the defect for a long time. Gradually, the amount of "residual" blood in the cavity of the left ventricle increases and diastolic filling increases. The cavity of the left ventricle expands, and tonogenic dilatation occurs. Additional mobilization of the myocardium occurs due to the activation of the Frank- Starling mechanism. When a further increase in the length of muscle fibers ceases to be accompanied by an increase in contraction, the so-called myogenic dilation occurs; LV decompensation gives rise to a phase of general heart failure. Long-term existence of AV stenosis and compensatory hyperfunction leads to the development of LV myocardial hypertrophy, the mass of which can reach 1200 g or more (at a rate of 250–300 g). The consequence of this is relative coronary insufficiency. In addition, in patients with aortic stenosis, there may be an absolute deterioration in coronary blood flow due to a sharp increase in intraventricular and intramyocardial pressure, as well as a drop in pressure at the base of the aorta (blood is ejected into the aorta in a thin and strong jet), making it difficult to fill the coronary arteries during diastole. For these reasons, in patients with aortic stenosis, angina pectoris occurs in 70% of cases, although only half of the patients have coronary atherosclerosis. Due to developing myocardial ischemia in this category of patients, the risk of sudden death is high [3, 27, 28]. When stenosis is combined with aortic valve insufficiency (more often with a bicuspid aortic valve), an increase in "preload" is added to the increased "afterload" of the LV, which leads to greater stress in the LV wall and a decrease in effective stroke volume.
