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Pathology - Valvular cardiac pathology
Aortic stenosis
• The predominant valve pathology. • Primarily results from calcification of a structurally normal tricuspid valve in the elderly (senile calcific aortic stenosis). Bicuspid aortic valves undergo calcification at an earlier age. Chronic rheumatic illness can potentially lead to aortic stenosis. • Prolonged turbulent blood flow through the valve is believed to result in damage, subsequently leading to calcification. • Exhibits chest discomfort, syncope, and dyspnea.
Aortic regurgitation
• Aortic regurgitation (AR) can result from disorders that induce dilation of the aortic root, such as Marfan syndrome and ankylosing spondylitis. • Congenital anomalies of the valve leaflets may also contribute to AR. • Dilation of the aortic root exerts tension on the annulus of the aortic valve, hindering complete closure of the leaflets. • Symptoms include dyspnea and palpitations.
Mitral Stenosis
Mitral stenosis is typically a consequence of persistent rheumatic valvular heart disease. • The constriction of the valve obstructs the unobstructed flow of blood from the left atrium to the left ventricle during ventricular diastole. • The increase in left atrial pressure is conveyed to the pulmonary venous system, resulting in pulmonary edema and dyspnea. • The left atrium enlarges and becomes susceptible to atrial fibrillation. • Stenotic mitral valves exhibit significant thickening of the valve leaflets and the associated chordae tendineae. The fusion of the leaflets results in the characteristic 'fish mouth' appearance.
Mitral regurgitation
• Typically results from mitral valve prolapse or ischemic heart disease. • In mitral valve prolapse, the abnormal valve leaflets bulge into the left atrium during ventricular systole. • In ischemic heart disease, regurgitation arises from a combination of ischemic papillary dysfunction and the dilation of the mitral valve annulus due to left ventricular enlargement. • Patients may stay asymptomatic for a period as the left ventricle and left atrium hypertrophy to accommodate the additional volume; however, decompensation and the onset of left ventricular failure will ultimately occur.
Aortic stenosis
• The predominant valve pathology. • Primarily results from calcification of a structurally normal tricuspid valve in the elderly (senile calcific aortic stenosis). Bicuspid aortic valves undergo calcification at an earlier age. Chronic rheumatic illness can potentially lead to aortic stenosis. • Prolonged turbulent blood flow through the valve is believed to result in damage, subsequently leading to calcification. • Exhibits chest discomfort, syncope, and dyspnea.
Aortic regurgitation
• Aortic regurgitation (AR) can result from disorders that induce dilation of the aortic root, such as Marfan syndrome and ankylosing spondylitis. • Congenital anomalies of the valve leaflets may also contribute to AR. • Dilation of the aortic root exerts tension on the annulus of the aortic valve, hindering complete closure of the leaflets. • Symptoms include dyspnea and palpitations.
Mitral Stenosis
Mitral stenosis is typically a consequence of persistent rheumatic valvular heart disease. • The constriction of the valve obstructs the unobstructed flow of blood from the left atrium to the left ventricle during ventricular diastole. • The increase in left atrial pressure is conveyed to the pulmonary venous system, resulting in pulmonary edema and dyspnea. • The left atrium enlarges and becomes susceptible to atrial fibrillation. • Stenotic mitral valves exhibit significant thickening of the valve leaflets and the associated chordae tendineae. The fusion of the leaflets results in the characteristic 'fish mouth' appearance.
Mitral regurgitation
• Typically results from mitral valve prolapse or ischemic heart disease. • In mitral valve prolapse, the abnormal valve leaflets bulge into the left atrium during ventricular systole. • In ischemic heart disease, regurgitation arises from a combination of ischemic papillary dysfunction and the dilation of the mitral valve annulus due to left ventricular enlargement. • Patients may stay asymptomatic for a period as the left ventricle and left atrium hypertrophy to accommodate the additional volume; however, decompensation and the onset of left ventricular failure will ultimately occur.
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