[Assessment of left ventricular twist mechanics by two-dimensional strain in severe aortic stenosis with preserved ejection fraction].

UNLABELLED: Left ventricular (LV) twist is increased in aortic stenosis (AS) and the hypothesis of a compensatory mechanism is suggested but not established. Our aim was to assess LV twist mechanics in severe AS (<1cm(2) or 0.6cm(2)/m(2)) with preserved LV ejection fraction (LVEF>50%), and to analyze its relationship with LV systolic longitudinal function, early impaired in this setting, LV diastolic function, and symptomatic status.

METHODS: Forty-five consecutive patients with severe AS and preserved LVEF (mean age 73±11 years, 47% female, LVEF 68±11%, 67% symptomatic) underwent a transthoracic echocardiography including a bidimensional strain analysis by speckle tracking method, and were compared to a control group matched for age and sex (n=15). Global longitudinal strain (GLS) was measured using the four, two, and three apical views, and LV twist mechanics from the basal and apical short axis views. LV twist was defined as the net difference between apical and basal rotation, and LV twisting and untwisting rate (in°/s) were derived from twist curves.

RESULTS: Peak apical rotation, LV twist (25±8° vs 20±6), as well as peak systolic and diastolic apical rotation rate, and peak LV twisting rate were significantly higher in patients with AS when compared to controls (all, P<0.05), whereas, the other parameters of LV twist mechanics including basal rotation, were not significantly different between groups. By contrast, the GLS was significantly lower in patients with AS when compared to controls (-17.9±4 vs -20.5±2%, P<0.01). In addition, the GLS was significantly correlated to LV torsion (r=-0.42, P<0.01). Moreover, LV twist progressively impaired with the worsening of diastolic dysfunction and with symptoms onset.

CONCLUSION: LV twist is increased in severe AS with preserved LVEF, compensating the impairment of systolic longitudinal function. However, above a certain threshold LV twist deteriorates, attesting the failure of the compensatory mechanisms, leading to advanced diastolic dysfunction and symptom onset.