Acute Mitral Regurgitation Resulting from Ruptured or Elongated Chordae Tendineae<subtitle>AUSCULTATORY AND PHONOCARDIOGRAPHIC FINDINGS</subtitle>

Abstract

Eighteen patients with severe acute mitral regurgitation requiring operation have been described. The history, physical signs and phonocardiographic findings were compared with the anatomical findings at operation. Fourteen had ruptured chordae tendineae (five anterior leaflet: eight posterior leaflet: one both leaflets) and four had elongated chordae with prolapsing leaflets. The commonest auscultatory finding was an apical pan-systolic murmur with a mid-systolic crescendo which was often propagated to the base and into the neck thus simulating aortic stenosis. The mid-systolic crescendo appeared to be due to the regurgitant flow of a high velocity jet through a relatively small regurgitant orifice. The basal propagation was due to the regurgitant jet being directed forwards and medially against the atrial septum in the region of the aortic root. This type of murmur was found in patients with either anterior or posterior leaflet chordal rupture and also in some patients with elongated chordae. It was therefore of no help in differentiating these lesions. A plateau shaped pan-systolic murmur was never found in patients with ruptured chordae to the posterior leaflet. A loud first heart sound was often present particularly in the presence of an intact anterior leaflet. All patients had third heart sounds and all but one of those in sinus rhythm had an atrial sound which was often associated with a palpable atrial impulse and a tall ‘A’ wave on the apexcardiogram. The clinical findings therefore did not readily distinguish between the different groups of patients. Left ventricular cine-angiography was the best method of determining the site of leaflet prolapse. Although an underlying cause was found for ruptured chordae in most of the Group IA patients, the aetiology was obscure in the remainder. The Group II patients with elongated chordae and voluminous leaflets clearly had degeneration of the valve tissues but whether this was acquired or due to an inherited anomaly remains unknown.