Abstract 19660: Time-resolved Wall Stress Assessments Reveal Marked Late Systolic Load in Heart Failure with Reduced Ejection Fraction (HFREF)
Background: Systolic myocardial wall stress (MWS) quantifies myocardial afterload. MWS has historically been assessed only in end-systole, but recent time-resolved assessments in subjects with normal LV EF demonstrate that peak stress occurs in early systole, followed by a marked shift in the pressure-stress relation that reduces late systolic stress in normal hearts. This shift is dependent on progressive geometric changes during ejection.
Hypothesis: HFREF is associated with an abnormal time course of LV MWS.
Methods: We compared 18 subjects with HFREF (mean age=56; mean BMI=30 kg/m2; mean LV EF=34%) to controls matched for age, body size and arterial load. We assessed time-resolved LV geometry and central pressure with cardiac MRI and carotid tonometry, respectively. We computed MWS throughout ejection (Arts method).
Results: Peak MWS (736 vs. 735 kdynes/cm2;P=0.99) and mean MWS throughout ejection (633 vs. 580 kdynes/cm2; P=0.38) were not significantly different between the groups. However, subjects with HFREF demonstrated a delay in the time to peak stress (103 msec vs. 79 msec into ejection; P<0.0001). Furthermore, despite similar wave reflection magnitude (0.50 vs. 0.49; P=0.91) and late systolic pressure augmentation between the groups, subjects with HFREF demonstrated a pronounced increase in the ratio of late (second half of ejection) vs. early (first half of ejection) MWS-time integral (0.91 vs. 0.75; P<0.0001), which was due to a markedly blunted mid-systolic shift in the pressure-stress relation (145 vs. 285 kdynes/cm2; P<0.0001), resulting in a failure to reduce late systolic wall stress for any given pressure (Figure).
Conclusions: HFREF is associated with marked abnormalities in the systolic loading sequence due to an intrinsically abnormal pressure-stress relation during ejection. For any given arterial load, this exposes the myocardium to excessive late systolic stress and may promote a vicious circle of adverse LV remodeling and failure.
Author Disclosures: J.A. Chirinos: None. P. Konda: None. A. Dunde: None. D. Rawath: None. P. Zamani: None. N. Vadde: None. V. Panchal: None. P. Shiva-Kumar: None. V. Ferrari: None. P. Segers: None. S. Akers: None.
- © 2014 by American Heart Association, Inc.