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.


RESULTS
We tested the hypothesis that late systolic hypertension, defined as the ratio of late (last one third of systole) to early (first two thirds 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 noninvasively from 6124 adults. The late/early systolic PTI ratio (L/E(SPTI)) was assessed as a predictor of incident HF during median 8.5 years of follow-up. The L/E(SPTI) was predictive of incident HF (hazard ratio per 1% increase=1.22; 95% CI=1.15 to 1.29; P<0.0001) even after adjustment for established risk factors for HF (HR=1.23; 95% CI=1.14 to 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/E(SPTI) was the modifiable factor associated with the greatest improvements in model performance. A high L/E(SPTI) (>58.38%) 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 to 2.23; P=0.18), whereas the HR associated with a high L/E was 2.31 (95% CI=1.52 to 3.49; P<0.0001).


CONCLUSIONS
Independently of the absolute level of peak pressure, late systolic hypertension is strongly associated with incident HF in the general population.
Division of Cardiovascular, School of Medicine, University of Pennsylvania, Philadelphia, PA (J.A.C., P.Z.).
Julio A
JA
Chirinos
Biofluid, Tissue, and Solid Mechanics for Medical Applications, IBiTech, iMinds Future Health Department, Ghent University, Ghent, Belgium (P.S.).
Patrick
P
Segers
Division of Cardiology, School of Medicine, University of Minnesota, Minneapolis, MN (D.A.D.).
Daniel A
DA
Duprez
Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA (L.B., R.K.).
Lyndia
L
Brumback
Radiology and Imaging Sciences, National Institutes of Health (NIH) Clinical Center, Bethesda, MD (D.A.B.).
David A
DA
Bluemke
Division of Cardiovascular, School of Medicine, University of Pennsylvania, Philadelphia, PA (J.A.C., P.Z.).
Payman
P
Zamani
Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA (L.B., R.K.).
Richard
R
Kronmal
Johns Hopkins School of Medicine, Baltimore, MD (D.V., P.O.).
Dhananjay
D
Vaidya
Johns Hopkins School of Medicine, Baltimore, MD (D.V., P.O.).
Pamela
P
Ouyang
Division of Nephrology/Hypertension, School of Medicine, University of Pennsylvania, Philadelphia, PA (R.R.T.).
Raymond R
RR
Townsend
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN (D.R.J.) Department of Nutrition, University of Oslo, Norway (D.R.J.).
David R
DR
Jacobs
D000368:Aged; D000369:Aged, 80 and over; D001011:Aorta / Q000503:physiopathology*; D062186:Arterial Pressure; D001916:Brachial Artery / Q000503:physiopathology; D003971:Diastole; D005260:Female; D006333:Heart Failure / Q000175:diagnosis / Q000208:ethnology* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000208:ethnology* / Q000503:physiopathology; D015994:Incidence; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011379:Prognosis; D016016:Proportional Hazards Models; D012307:Risk Factors; D013599:Systole; D013997:Time Factors; D014481:United States / Q000453:epidemiology; D016277:Ventricular Function, Left
arterial hemodynamics; heart failure; late systolic load; left ventricular afterload