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Original Contribution
September 5, 2012

Aortic Stiffness, Blood Pressure Progression, and Incident Hypertension

Author Affiliations

Author Affiliations: National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Massachusetts (Drs Kaess, Rong, Levy, Benjamin, and Vasan); Klinik und Poliklinik für Innere Medizin II, University Hospital Regensburg, Regensburg, Germany (Dr Kaess); Department of Mathematics and Statistics (Dr Larson), Department of Biostatistics, School of Public Health (Dr Larson), Sections of Preventive Medicine and Epidemiology and Cardiology (Drs Benjamin and Vasan), Evans Department of Medicine and Whitaker Cardiovascular Institute, School of Medicine (Drs Hamburg, Vita, Benjamin, and Vasan), Boston University, Boston, Massachusetts; National Heart, Lung, and Blood Institute, Bethesda, Maryland (Dr Levy); and Cardiovascular Engineering Inc, Norwood, Massachusetts (Dr Mitchell).

JAMA. 2012;308(9):875-881. doi:10.1001/2012.jama.10503

Context Vascular stiffness increases with advancing age and is a major risk factor for age-related morbidity and mortality. Vascular stiffness and blood pressure pulsatility are related; however, temporal relationships between vascular stiffening and blood pressure elevation have not been fully delineated.

Objective To examine temporal relationships among vascular stiffness, central hemodynamics, microvascular function, and blood pressure progression.

Design, Setting, and Participants Longitudinal community-based cohort study conducted in Framingham, Massachusetts. The present investigation is based on the 2 latest examination cycles (cycle 7: 1998-2001; cycle 8: 2005-2008 [last visit: January 25, 2008]) of the Framingham Offspring study (recruited: 1971-1975). Temporal relationships among blood pressure and 3 measures of vascular stiffness and pressure pulsatility derived from arterial tonometry (carotid-femoral pulse wave velocity [CFPWV], forward wave amplitude [FWA], and augmentation index) were examined over a 7-year period in 1759 participants (mean [SD] age: 60 [9] years; 974 women).

Main Outcome Measures The primary outcomes were blood pressure and incident hypertension during examination cycle 8. The secondary outcomes were CFPWV, FWA, and augmentation index during examination cycle 8.

Results In a multivariable-adjusted regression model, higher FWA (β, 1.3 [95% CI, 0.5-2.1] mm Hg per 1 SD; P = .002) and higher CFPWV (β, 1.5 [95% CI, 0.5-2.6] mm Hg per 1 SD; P = .006) during examination cycle 7 were jointly associated with systolic blood pressure during examination cycle 8. Similarly, in a model that included systolic and diastolic blood pressure and additional risk factors during examination cycle 7, higher FWA (odds ratio [OR], 1.6 [95% CI, 1.3-2.0] per 1 SD; P < .001), augmentation index (OR, 1.7 [95% CI, 1.4-2.0] per 1 SD; P < .001), and CFPWV (OR, 1.3 [95% CI, 1.0-1.6] per 1 SD; P = .04) were associated with incident hypertension during examination cycle 8 (338 cases [32%] in 1048 participants without hypertension during examination cycle 7). Conversely, blood pressure during examination cycle 7 was not associated with CFPWV during examination cycle 8. Higher resting brachial artery flow (OR, 1.23 [95% CI, 1.04-1.46]) and lower flow-mediated dilation (OR, 0.80 [95% CI, 0.67-0.96]) during examination cycle 7 were associated with incident hypertension (in models that included blood pressure and tonometry measures collected during examination cycle 7).

Conclusion In this cohort, higher aortic stiffness, FWA, and augmentation index were associated with higher risk of incident hypertension; however, initial blood pressure was not independently associated with risk of progressive aortic stiffening.