Interrelations Between Arterial Stiffness, Target Organ Damage, and Cardiovascular Disease Outcomes
Year: 2019
Type: article
Study design: Observational Study
Abstract: Background Excess transmission of pressure pulsatility caused by increased arterial stiffness may incur microcirculatory damage in end organs (target organ damage [TOD] ) and, in turn, elevate risk for cardiovascular disease ( CVD ) events. Methods and Results We related arterial stiffness measures (carotid-femoral pulse wave velocity, mean arterial pressure, central pulse pressure) to the prevalence and incidence of TOD (defined as albuminuria and/or echocardiographic left ventricular hypertrophy) in up to 6203 Framingham Study participants (mean age 50±15 years, 54% women). We then related presence of TOD to incident CVD in multivariable Cox regression models without and with adjustment for arterial stiffness measures. Cross-sectionally, greater arterial stiffness was associated with a higher prevalence of TOD (adjusted odds ratios ranging from 1.23 to 1.54 per SD increment in arterial stiffness measure, P<0.01). Prospectively, increased carotid-femoral pulse wave velocity was associated with incident albuminuria (odds ratio per SD 1.28, 95% CI, 1.02-1.61; P<0.05), whereas higher mean arterial pressure and central pulse pressure were associated with incident left ventricular hypertrophy (odds ratio per SD 1.37 and 1.45, respectively; P<0.01). On follow-up, 297 of 5803 participants experienced a first CVD event. Presence of TOD was associated with a 33% greater hazard of incident CVD (95% CI , 0-77%; P<0.05), which was attenuated upon adjustment for baseline arterial stiffness measures by 5-21%. Conclusions Elevated arterial stiffness is associated with presence of TOD and may partially mediate the relations of TOD with incident CVD . Our observations in a large community-based sample suggest that mitigating arterial stiffness may lower the burden of TOD and, in turn, clinical CVD .
Institutions: Boston University, Framingham Heart Study, University of Turku, Turku University Hospital, Finnish Institute for Health and Welfare, University of California, Davis, Cedars-Sinai Medical Center, Cedars-Sinai Smidt Heart Institute, The University of Texas at San Antonio Health Science Center
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,750
Awards: G1008083287, UC Davis Alzheimer's Disease Core Center, G250621538, G278200998, Microglial, Inflammatory and Omics Markers of Cerebral Small Vessel Disease in the CHARGE Consortium, G3405256882, ADSP Follow-up in Multi-Ethnic Cohorts via Endophenotypes, Omics & Model Systems, Inflammatory Mediators, Cardiovascular Health, and Longevity in Women, G4976486911, Temporal Trends, Novel Imaging and Molecular Characterization of Preclinical and Clinical Alzheimer's Disease in the Framingham Cohorts, Biomarkers of Ventricular and Vascular Remodeling, Aortic Dysfunction, Pulsatile Stress and Target Organ Damage in Framingham, The Framingham Heart Study, Vascular Function in the Framingham Third Generation, Ventricular Vascular Coupling: Correlates and Prognosis, Vascular Stiffness as a Precursor of Hypertension in a Middle-aged Cohort, ENDOTHELIAL VASAMOTOR FUNCTION IN THE FRAMINGHAM STUDY, Genetics of Oxidative Stress in Ventricular Remodeling, Cognitively Healthy Nonagenarians in the Cross Cohort Collaboration (CCC), Cardiac microstructure and the immune-inflammatory response to SARS-CoV-2, Precursors of Stroke Incidence and Prognosis, South Texas Alzheimer's Disease Center
OpenAlex ID: W2956803505