היצרות מיטרלית I: מבוא

Mitral stenosis is most commonly caused by rheumatic endocarditis, which results from inadequately treated streptococcal infections. Less common causes include congenital malformations, autoimmune disorders like rheumatoid arthritis, radiation therapy to the chest, and severe mitral annular calcification in older adults.

Rheumatic endocarditis causes inflammation and scarring of the mitral valve leaflets and chordae tendineae. This leads to thickening, calcification, and fusion of valve structures, creating a characteristic fish-mouth appearance. These deformities narrow the valve orifice and obstruct blood flow from the left atrium to the left ventricle during diastole.

When the mitral valve narrows, blood backs up in the left atrium, increasing residual blood volume. Over time, this elevated pressure causes left atrial hypertrophy and dilation. The enlarged atrium becomes prone to arrhythmias like atrial fibrillation, which decreases cardiac efficiency and further compromises blood circulation.

Mitral stenosis causes blood to back up into the pulmonary veins, leading to pulmonary congestion and edema. The increased pressure in the pulmonary circulation can cause pulmonary hypertension and place excessive strain on the right ventricle, potentially leading to right ventricular hypertrophy and eventual heart failure.

An increased heart rate shortens the diastolic phase, reducing the time available for blood to flow from the left atrium into the left ventricle. This causes more blood to back up into the pulmonary veins, further reducing cardiac output and increasing pulmonary pressures, exacerbating the condition's hemodynamic effects.

Mitral stenosis reduces cardiac output through two mechanisms: decreased ventricular filling due to the narrowed valve orifice, and reduced forward blood flow into the left ventricle. This decreased cardiac output compromises the heart's ability to deliver oxygen-rich blood to body tissues, affecting overall cardiovascular function.

The thickened, fused, and calcified mitral valve leaflets create an obstruction that prevents normal blood flow during diastole. This obstruction generates a significant pressure differential between the left atrium and left ventricle, forcing the atrium to work harder to push blood through the narrowed valve opening.