Key result
Higher Body Mass Index is independently associated with augmented central arterial stiffness (cfPWV B = 0.303, p < 0.001) and reduced subendocardial perfusion, but not with coronary artery disease.
Why the study?
It was not yet fully known whether obesity causes an independent increase in central arterial stiffness.
Is higher Body Mass Index associated with increased arterial stiffness prior to target organ damage?
Cross-Sectional (n=133)
No
Is higher Body Mass Index associated with increased arterial stiffness prior to target organ damage?
Effect estimate: B = 0.303
p-value: p=<0.001
Increased BMI is independently associated with augmented central arterial stiffness and reduced subendocardial perfusion, suggesting early vascular changes prior to target organ damage.
May warrant stiffness monitoring in higher-BMI patients; hypothesis-generating for causal and interventional studies.
BACKGROUND: Obesity is associated with several neurohumoral changes that play an essential role in organ damage. Increased arterial stiffness causes functional vessel wall changes and can therefore lead to accelerated target organ damage as well. Whether obesity causes an independent increase in central arterial stiffness is, however, not yet fully known. METHODS: One hundred thirty-three patients (63.2% male) were included. Body Mass Index (BMI) was defined as body weight in kilograms, divided by the square of body height in meters. Chronic Kidney Disease Epidemiology Collaboration creatinine 2009 equation was used to estimate the glomerular filtration rate (eGFR). Non-invasive applanation tonometry was used for arterial stiffness measurements (Sphygmocor Atcor Medical, Sydney, Australia). All patients underwent coronarography. RESULTS: and ankle-brachial index (ABI) 1.0 ± 0.1. Their arterial stiffness measurements showed mean carotid-femoral pulse wave velocity (cfPWV) 10.3 ± 2.7 m/s, subendocardial viability ratio (SEVR) 164.4 ± 35.0%, and pulse pressure (PP) 47.8 ± 14.5 mmHg. Spearman's correlation test revealed a statistically significant correlation between BMI and SEVR (r = -0.193; p = 0.026), BMI and cfPWV (r = 0.417; p < 0.001) and between BMI and PP (r = 0.227; p = 0.009). Multiple regression analysis confirmed an independent connection between BMI and cfPWV (B = 0.303; p < 0.001) and between BMI and SEVR (B = -0.186; p = 0.040). There was no association between BMI and kidney function, ABI, or coronary artery disease. CONCLUSION: Increased BMI is independently associated with augmented central arterial stiffness and reduced subendocardial perfusion but not with coronary artery disease, kidney function, or ABI.
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Piko et al. (2023) conducted a cross-sectional in High cardiovascular risk (planned elective coronarography) (n=133). Higher Body Mass Index vs. Lower Body Mass Index was evaluated on Central arterial stiffness measured by carotid-femoral pulse wave velocity (cfPWV) (B = 0.303, p=<0.001). Higher Body Mass Index is independently associated with augmented central arterial stiffness (cfPWV B = 0.303, p < 0.001) and reduced subendocardial perfusion, but not with coronary artery disease.
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