Abstract 16790: A Step Forward to Our Understanding of the Mitral Valve Mechanics and Role in Patients With Hypertrophic Cardiomyopathy: a Real-time Three-dimensional Transesophageal Study
Introduction/Purpose: There is growing evidence that the mitral apparatus in hypertrophic cardiomyopathy (HCM) has primary structural abnormalities. The objective of this study was the assessment of the mitral valve in patients (pts) with HCM, both non-obstructive and obstructive, using Real-Time Three-Dimensional Transesophageal Echocardiography (RT3DTEE).
Methods: Complete transthoracic and RT3DTEE study focused on the mitral valve, was performed in 55 HCM pts with asymmetrical septal hypertrophy and 28 controls. The HCM pts were divided in two groups: Group I included 37 patients with the non-obstructive pattern, while group II included 18 patients with LVOT obstruction. The study population was in sinus rhythm and had intact mitral valves. The mitral valve 3D datasets were analyzed offline with dedicated quantification software.
Results: Group I (mean age 46 ± 17 years, 25 males), Group II (mean age 50 ± 15 years, 10 males), control group (mean age 49 ± 12 years, 13 males). The mean interventricular septum width was significantly higher 19.3±3.42 mm in Group I, 21.06±4.04 mm in Group II compared to control group 9.1±1.08 mm, p<0.05. The peak LVOT pressure gradient in Group II was 58±25 mmHg. The results of the RT3DTEE study are shown in the table.
Conclusion: The mitral valve in pts with HCM appears to have unique anatomic characteristics, such as larger annular height and narrower aortomitral angle. Furthermore the anterior displacement of the coaptation line in patients with obstruction combined with a larger tenting height of the leaflets in the left ventricle in systole seems to contribute to the systolic traction of the anterior leafllet towards the intervetnricular septum that causes the LVOT obstruction. These primary changes of the mitral valve, as illustrated by RT3DTEE, offer new data on the pathophysiology of the disease.
Author Disclosures: E. Venieri: None. C. Aggeli: None. A. Anastasakis: None. C. Ritsatos: None. I. Felekos: None. D. Tousoulis: None.
- © 2016 by American Heart Association, Inc.