Temporal coupling between papillary muscle strain and left ventricular untwisting during diastole

Left ventricular (LV) untwisting is classically considered a passive recoil phenomenon. However, during conditions of shortened diastole, passive mechanisms alone may be insufficient to ensure effective diastolic suction. We hypothesized that both anterolateral papillary muscle (APM) and posteromedial papillary muscle (PPM) contribute actively, alongside passive elastic recoil, to LV untwisting during diastole.

In this prospective study, individuals with normal transthoracic echocardiograms underwent two-dimensional speckle-tracking imaging. Longitudinal strain of APM and PPM was obtained, alongside LV torsion measurements. Functional data analysis and penalized function-on-function regression were used to model the temporal association between papillary muscle strain and LV untwisting. A total of 75 patients were enrolled in the study, with a mean age of 37.2 ± 14.9 years. Of these, 16 (21.3%) were female. Hypertension was present in 12 (16%) patients while 7 (9.3%) patients had diabetes. The mean peak torsion measured 25 ± 10 degrees. Maximum contractions of APM and PPM were -17 ± 3.8% and -17 ± 3.7%, respectively. The mean peak LV torsion occurred at 41% of the cardiac cycle and peak global longitudinal strain at 43%, while peak APM and PPM contractions occurred significantly later, at 51% (P < 0.001). Functional regression revealed a significant, time-dependent relationship between papillary muscle contraction and untwisting. Greater APM and PPM contraction was associated with enhanced LV untwisting, during early and mid-diastole.

Papillary muscles actively contract during diastole and are associated with LV untwisting in a temporally coordinated manner.