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Published on: August 2, 2024
Pulsatile Load Components, Resistive Load and Incident Heart Failure: The Multi-Ethnic Study of Atherosclerosis
Payman Zamani1, Scott M Lilly2, Patrick Segers3
1Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Perelman School of Medicine. Philadelphia, Pennsylvania.
Background:
Left ventricular (LV) afterload is composed of systemic vascular resistance (SVR) and components of pulsatile load, including total arterial compliance (TAC), and reflection magnitude (RM). RM, which affects the LV systolic loading sequence, has been shown to strongly predict HF. Effective arterial elastance (Ea) is a commonly used parameter initially proposed to be a lumped index of resistive and pulsatile afterload. We sought to assess how various LV afterload parameters predict heart failure (HF) risk and whether RM predicts HF independently from subclinical atherosclerosis.
Methods:
We studied 4345 MESA participants who underwent radial arterial tonometry and cardiac output (CO) measurements with the use of cardiac MRI. RM was computed as the ratio of the backward (Pb) to forward (Pf) waves. TAC was approximated as the ratio of stroke volume (SV) to central pulse pressure. SVR was computed as mean pressure/CO. Ea was computed as central end-systolic pressure/SV.
Results:
During 10.3 years of follow-up, 91 definite HF events occurred. SVR (P = .74), TAC (P = .81), and Ea (P = .81) were not predictive of HF risk. RM was associated with increased HF risk, even after adjustment for other parameters of arterial load, various confounders, and markers of subclinical atherosclerosis (standardized hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.18-1.88; P = .001). Pb was also associated with an increased risk of HF after adjustment for Pf (standardized HR 1.43, 95% CI 1.17-1.75; P = .001).
Conclusions:
RM is an important independent predictor of HF risk, whereas TAC, SVR, and Ea are not. Our findings support the importance of the systolic LV loading sequence on HF risk, independently from subclinical atherosclerosis.
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