Abstract 19277: Late Systolic Central Hypertension as a Predictor of Incident Heart Failure: the Multi-Ethnic Study of Atherosclerosis
Background: Experimental studies demonstrate that high aortic pressure in late systole relative to early systole, causes greater myocardial remodeling and dysfunction, for any given absolute peak systolic pressure.
Methods: We tested the hypothesis that late systolic hypertension, defined as the ratio of late (last 1/3 of systole) to early (first 2/3 of systole) pressure-time integrals (PTI) of the aortic pressure waveform, independently predicts incident heart failure (HF) in the general population. Aortic pressure waveforms were derived from a generalized transfer function applied to the radial pressure waveform recorded non-invasively from 6,124 adults. The late/early systolic PTI ratio (L/ESPTI) was assessed as a predictor of incident heart failure (HF) during median 8.5 years of follow-up.
Results: The L/ESPTI was predictive of incident HF (hazard ratio per 1% increase=1.22; 95%CI=1.15-1.29; P<0.0001) even after adjustment for established risk factors for HF (HR=1.23; 95%CI=1.14-1.32: P<0.0001). In a multivariate model that included brachial systolic and diastolic blood pressure and other standard risk factors of HF, L/ESPTI was the modifiable factor associated with the greatest improvements in model performance. A high L/ESPTI was more predictive of HF than the presence of hypertension. After adjustment for each other and various predictors of HF, the HR associated with hypertension was 1.39 (95%CI=0.86-2.23; P=0.18) whereas the HR associated with a high L/E was 2.31 (95%CI=1.52-3.49; P<0.0001). Cumulative hazard curves for HF among participants stratified according to the presence or absence of hypertension (prevalence=45%) or a high L/ESPTI (set empirically to an identical prevalence of 45% based on E/LSPTI) are shown in the figure.
Conclusions: Independently of the absolute level of peak pressure, late systolic hypertension is strongly associated with incident HF in the general population.
Author Disclosures: J.A. Chirinos: None. P. Segers: None. D.A. Duprez: None. L. Brumback: None. D. Bluemke: Other Research Support; Modest; Siemens Medical Systems, Philips Medical Systems. R. Kronmal: None. D. Vaidya: None. P. Ouyang: None. R. Townsend: None. D.R. Jacobs: None.
- © 2014 by American Heart Association, Inc.