Genesis of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an anatomical or dynamic event?

ABSTRACT

To determine the relative role of both the anatomical and dynamic components involved in the determination of systolic anterior motion (SAM) of the mitral valve, we studied 53 selected patients with hypertrophic cardiomyopathy (HCM) by M-mode and cross-sectional echocardiography (CSE). Recordings of high quality for quantitative analysis were a precondition for the inclusion in the study. Twelve of these patients had no SAM, 14 had SAM of the anterior mitral leaflet (AML), six had SAM of the posterior mitral leaflet (PML), and 21 had SAM of both the AML and PML. The length of both the AML and PML, the left ventricular outflow tract (LVOT) area and the percentage of thickening of the left ventricular posterior wall (%LVPW) were measured in 18 control subjects (group I), in patients with AML-SAM (group II), in patients with AML+ PML-SAM (Group III), in patients with PML-SAM (group IV) and in patients with HCM but without SAM (group V). The length of AML in group I (23 +/- 1.5 mm) was significantly different compared with that in groups III (28 +/- 2 mm) and IV (29 +/- 2 mm), P less than 0.001. Significant differences were present in the PML-length between group I (14 +/- 1 mm) and groups III (20 +/- 3 mm) and IV (25 +/- 4 mm), respectively (P less than 0.001), between group II (14 +/- 2 mm) and groups III and IV, respectively (P less than 0.001), and also between group V (14 +/- 1 mm) and groups III and IV (P less than 0.001). Differences were found when the %LVPW of groups II (76 +/- 17%), III (77 +/- 11%) and IV (83 +/- 19%) were compared, respectively, with groups I (42 +/- 12%) and V (54 +/- 7%), P less than 0.001; a significant difference was also found between groups I and V, P less than 0.001. The mean LVOT area was significantly reduced in groups II (3.5 +/- 1.3 cm2), III (3 +/- 1 cm2) and IV (3 +/- 1 cm2) when compared with group V (5.9 cm2), P less than 0.001. We conclude that the induction and maintenance of SAM in HCM is multifactorial, mainly depending on the length of both the AML and/or PML, the LVOT area and on the increased contractility of the LVPW.