Rupture of chordae tendineae leads to mitral regurgitation, with rheumatic mitral valvulitis appearing to be the most common etiology at present.
The text introduces the etiology and context of mitral regurgitation secondary to ruptured chordae tendineae, though the abstract is truncated.
THE chordae tendineae serve an essential anchoring function in the mechanics of mitral-valve closure during ventricular systole. Rupture of one or more of these fibrous structures usually leads to mitral regurgitation, the severity of which is related to the location and number of chordae tendineae involved1 as well as the presence of prior disease of the mitral valve itself. Although active bacterial endocarditis was probably the major cause of ruptured chordae tendineae in the preantibiotic era,2 rheumatic mitral valvulitis, often with healed bacterial endocarditis, appears to be the most common etiology at present.3 4 5 However, a significant number of cases have . . .
Sanders et al. (1967) studied Mitral regurgitation secondary to ruptured chordae tendineae. Surgical treatment was evaluated. Rupture of chordae tendineae leads to mitral regurgitation, with rheumatic mitral valvulitis appearing to be the most common etiology at present.