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| Bicuspid Aortic Valve |
| Etiology •Congenital |
| Pathogenesis •Unknown for the congenital lesion. •Acquired subsequent calcific stenosis attributed to "wear and tear" mechanisms with hemodynamic changes attributed to deformities., |
| Epidemiology •Affects 1-2% of the population. |
| General Gross Description •The two cusps are about equal in size. One of the two cusps is bisected into two deformed cusps by a thick fold extending from the annulus to the free margin, as if there were 3 cusps at first, one large and two smaller ones with fusion of the commissure between the two small ones. •Fibrosis and extensive calcification may ensue causing a severe aortic stenosis. The resulting calcific deposits and excrescences can be very deforming. |
| General Microscopic Description •Fibrosis, hyalinization, and calcified amorphous matter are noted. The pathology is not that of arteriosclerosis or usual dystrophic calcification, which is not usually deforming. |
| Clinical Correlation •Asymptomatic until orifice area reduced to 1/3 normal. •Blood pressure normal while asymptomatic. Reduced pulse pressure thereafter. •Characteristic palpable thrill and murmur. •Angina pectoris, exertional dyspnea, and syncope, are cardinal symptoms. •Sudden death occurs in 10-20% of cases at average age of 60, presumably due to arrhythmia. •Death occurs in 7th and 8th decades. •Average survivals after onset of following manifestations are as follows: congestive heart failure - 1.5-2 yrs.; dyspnea - 2 yrs.; angina pectoris or syncope - 3yrs. •Valve replacement indicated when any of the 3 cardinal symptoms appear. •Asymptomatic diagnosed cases require careful followup. |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 545. |
| Bicuspid Aortic Valve |
| Synopsis by: J Hasson, MD (T39000M24570)[367] |
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