Transesophageal echocardiographic recognition of subaortic complications in aortic valve endocarditis. Clinical and surgical implications.

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Abstract
BACKGROUND: Secondary involvement of the mitral-aortic intervalvular fibrosa and the anterior mitral leaflet (subaortic structures) can occur in patients with aortic valve endocarditis. The secondary involvement of these structures occurs as a result of direct extension of the infection from the aortic valve or as a result of an infected aortic regurgitant jet striking the ventricular surfaces of the mitral-aortic intervalvular fibrosa and the anterior mitral leaflet. The abscess of mitral-aortic intervalvular fibrosa can expand to form an aneurysm. Subsequently, this mitral-aortic intervalvular fibrosa aneurysm can develop a perforation and communicate with the left atrium, resulting in the systolic regurgitation of blood from the left ventricular outflow tract into the left atrium. Secondary infection can also occur on the ventricular surface of the anterior mitral leaflet and result in the formation of an aneurysm or perforation of anterior mitral leaflet. METHODS AND RESULTS: This study examines the utility of transesophageal echocardiography in the detection of these subaortic complications in 55 consecutive patients with aortic valve endocarditis. A total of 24 patients (44%) had involvement of subaortic structures, including four with an abscess in the mitral-aortic intervalvular fibrosa, four with mitral-aortic intervalvular fibrosa aneurysm, seven with perforation of the mitral-aortic intervalvular fibrosa with communication into the left atrium, two with an aneurysm of the anterior mitral leaflet, and seven with perforation of the anterior mitral leaflet. The transesophageal echocardiographic findings were confirmed at surgery in 20 patients and at necropsy in two. By comparison, transthoracic echocardiography visualized these lesions in five of 24 patients (21%), including none of four with mitral-aortic intervalvular fibrosa abscesses, two of four with mitral-aortic intervalvular fibrosa aneurysms, one of seven with mitral-aortic intervalvular fibrosa perforations, one of two with anterior mitral leaflet aneurysms, and one of seven anterior mitral leaflet perforations. Eccentric mitral regurgitation-type systolic jets were noted in eight additional patients by transthoracic color flow imaging, and this finding suggested the possibility of these unusual subaortic complications. If these patients are included, then transthoracic echocardiography suggested the presence of these subaortic complications in 13 of 24 patients (54%). CONCLUSIONS: The results indicate that 1) involvement of the subaortic structures in patients with aortic valve endocarditis may be more common than previously recognized, 2) patients with aortic valve endocarditis and eccentric jets of mitral regurgitation on transthoracic echocardiography should undergo further evaluation by transesophageal echocardiography to exclude these unusual complications, 3) precise recognition of these complications is of value in the optimal medical and surgical management of these patients, and 4) these complications may be responsible for unexplained congestive heart failure and hemodynamic deterioration in some patients with aortic valve endocarditis.

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