Is increased arterial stiffness an additional link between obesity and organ damage?

Abstract Background. Obesity is associated with several neurohumoral changes that play an important 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. 133 patients (63.2% male) were included. BMI was defined as body weight in kilograms, divided by the square of body height in meters. Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine 2009 equation was used to estimate glomerular filtration rate (eGFR). Non-invasive applanation tonometry was used for arterial stiffness measurements (Sphygmocor Atcor Medical, Sydney, Australia). All patients underwent coronarography. Results. The mean age of our patients was 65.0 ± 9.2 years. Their mean BMI was 28.5 ± 4.4 kg/m 2 , eGFR 75.5 ± 17.2 ml/min/1.73 m 2 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 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.