Abstract 2698: Left Ventricular Apical Endocardial Rotation, But Not Epicardial Rotation, Is Increased In Patients With Hypertension: Insight Into The Mechanism Of Augmented Twist In Hypertensive Heart.
Background: Left ventricular (LV) twist increases with an increase in apical rotation in hypertrophied LV. There are two explanations:
the loss of counteraction of contraction of endocardial clockwise fibers because of endocardial depressed circumferential strain (CS), and
equalization of sarcomere shortening between endocardial and epicardial layers of the thick wall.
Novel 2-dimensional speckle tracking echocardiography (2DT, Toshiba) allows us to measure rotation and CS at the endocardium and epicardium.
Methods: 20 patients with hypertension (HT) and 20 age-matched normals (NL) underwent 2DT. By tracing endocardial and epicardial borders of the basal and apical short-axis LV, we measured endocardial and epicardial rotational angles and CS. LV twist was defined as apical rotation relative to the base.
Results: Apical peak endocardial rotation was significantly higher in HT than in NL, whereas epicardial rotation was not different. Basal peak rotation showed no difference between two groups in both layers. Consequently, endocardial twist was larger in HT than in NL (14.5±3.6 vs. 10.6±5.1°, p<0.01), whereas epicardial twist was not different (7.6±4.1 vs. 8.1±3.2°, p=ns). CS did not differ significantly between HT and NL at both layers at both planes (basal endocardium, -30.3±4.5 vs. -28.2±7.8, epicardium, -12.6±2.4 vs. -13.5±4.2; apical endocardium, -32.8±9.1 vs. -32.7±7.8, epicardium, -13.8±3.9 vs. -13.6±3.9).
Conclusion: Augmented apical endocardial rotation contributed to increased LV twist in HT. In HT with preserved CS, the increase in LV twist may be a physiologic response to equalize sarcomere shortening between endocardial and epicardial layers.