Pulse wave velocity (PWV) is a reliable measurement of arterial stiffness. Our study assesses the association between body mass index (BMI) and brachial-ankle PWV (baPWV) in a healthy cohort and seeks to explain possible mechanisms associated with the obesity paradox. A cross-sectional study was conducted in 578 normal individuals. The mean age was 48.3 ± 14.6 years, and 468 (81.0%) were men. 288 subjects (49.8%) were overweight and obese. baPWV and ankle-brachial index (ABI) were performed to evaluate arterial stiffness and atherosclerosis respectively. Normal weight was defined as 18.5 < BMI <25 kg/m2, overweight as 25 ≤ BMI < 28 kg/m2 and obesity as BMI ≥28 kg/m2. The overweight/obese subjects had significantly higher baPWV than the normal-weight group (1490.0 ± 308.0/1445.2 ± 245.2 cm/s vs 1371.2 ± 306.4 cm/s, P < .001). For the whole cohort, baPWV showed a significant positive correlation with BMI (r = 0.205, P < .001). However, baPWV was significantly lower as BMI increased: 1490.0 ± 308.0 cm/s (overweight); 1445.2 ± 245.2 cm/s (obese); P < .001) when adjusted for age, gender, heart rate, mean blood pressure, and cardiovascular risk factors (glucose, cholesterol, triglyceride, and low-density lipoprotein). For the whole cohort BMI was negatively associated with baPWV (β = −0.06, P = .042). ABI showed no relationship with BMI. In a middle-age healthy Chinese population, arterial stiffness measured as baPWV increased with BMI. Evidence of reduced arterial stiffness with increasing BMI when accounting for all other cardiovascular risk factors may contribute to underlying factors involved in the obesity paradox that becomes more prominent with increasing age.
Arterial stiffness is an important predictor of cardiovascular events, independent of traditional risk factors. Stiffening of arteries, though an adaptive process to hemodynamic load, results in substantial increase in the pulsatile hemodynamic forces that detrimentally affects the microcirculation perfusing the vital organs such as the brain, heart and kidneys. Studies have proposed that arterial stiffness precedes and may contribute to the development of hypertension in individuals with obesity. Our study sought to determine the gender-based effects on arterial stiffening in obesity which may predispose to the development of hypertension. We found female sex is associated with higher susceptibility of weight-related arterial stiffening and rise in blood pressure in obesity. Women had significantly higher carotid-femoral pulse wave velocity (CF-PWV) with higher body mass index (BMI) status (normal: 7.9 ± 2 m/s; overweight: 9.1 ± 2 m/s; obese: 9 ± 2 m/s, p < 0.001), whereas it was similar in males across all BMI categories. The linear association between arterial stiffness and BMI following adjustment for age and brachial systolic and diastolic blood pressure (BP), remained significant in females (β = 0.06; 95% CI 0.01 to 0.1; p < 0.05) but not in males (β = 0.04; 95% CI −0.01 to 0.1; p > 0.05). The mean CF-PWV values increased by 0.1 m/s for every 1 kg/m2 increase in BMI in the female subjects in the age adjusted linear model, while such effect was not seen in the male subjects. In line with arterial stiffening, the overweight and obese females demonstrated significantly higher systolic brachial BP. (BP difference: ΔBP 9−11 mmHg, p < 0.01) and central systolic pressure (ΔBP 8−10 mmHg, p < 0.05) compared to their lean counterparts, unlike the male subjects. Our results suggest that female gender is associated with higher susceptibility of weight-related arterial stiffening and rise in blood pressure.
ObjectivesThe aim of this study was to explore the risk of target organ damage (TOD) in different groups based on carotid-femoral pulse wave velocity (cfPWV) and central aortic blood pressure (CBP) in different populations.MethodsThe study cohort was divided into four groups according to the status of cfPWV and CBP [Group (cfPWV/CBP): high cfPWV and high CBP; Group (cfPWV): high cfPWV and normal CBP; Group (CBP): normal cfPWV and high CBP; Group (control): normal cfPWV and normal CBP]. TOD was determined by the assessment of carotid intima-media thickness (CIMT) abnormality, chronic kidney disease (CKD), microalbuminuria, and left ventricular hypertrophy (LVH).ResultsA total of 1,280 patients (mean age 53.14 ± 12.76 years, 64.1% male patients) were recruited in this study. Regarding Group (control) as reference, LVH was significantly higher in Group (cfPWV) and Group (CBP) [OR 2.406, 95% CI (1.301–4.452), P < 0.05; OR 2.007, 95% CI (1.335–3.017), P < 0.05]; microalbuminuria was significantly higher in Group (cfPWV/CBP) and Group (CBP) [OR 3.219, 95% CI (1.630–6.359), P < 0.05; OR 3.156, 95% CI (1.961–5.079), P < 0.05]. With age stratified by 60 years, the risk of CKD was significantly higher in Group (cfPWV/CBP) [OR 4.019, 95% CI (1.439–11.229), P < 0.05].ConclusionDifferent phenotypes based on the status of cfPWV and CBP were associated with different TOD. Individuals with both cfPWV and CBP elevated have a higher risk of microalbuminuria.
Objectives: Arterial stiffness is widely accepted as an important predictor of cardiovascular disease (CVD) development. While obesity is generally associated with increased CVD risk, there is evidence that overweight patients with existing CVD may have better clinical outcomes than their lean counterparts. Our study sought to observe any potential association between brachial–ankle pulse wave velocity (BAPWV), a marker of arterial stiffness related to CVD risk, and Body Mass Index (BMI), a crude and widely used measure of obesity. Methods: Adult individuals (n = 857) assessed for routine CV risk were included and grouped according to their BMI (<25 kg/m2: normal; 25–30 kg/m2: overweight, ≥30 kg/m2: obese). Their anthropometric parameters, brachial cuff pressures, and BAPWV were measured. Results: Brachial pressure was significantly higher as BMI increased. BAPWV showed a positive linear association with systolic (r = 0.66, p < 0.01), mean (r = 0.60, p < 0.01), diastolic (r = 0.51, p < 0.01), and pulse (r = 0.53, p < 0.01) pressures. However, a linear relationship between BMI and BAPWV was only apparent in males aged <50 years (p = 0.01) and in females aged ≥50 years (p < 0.01). In individuals with similar brachial systolic pressure, BAPWV was higher in normal-weight subjects compared to overweight–obese ones. Conclusions: This conflicting finding is attributed to an overestimation of the degree of arterial stiffness as a measure of CVD risk in individuals with a less ‘healthy’ BMI. This suggests that BMI may not the appropriate obesity indicator to assess CV risk. Our finding emphasizes the importance of establishing a non-linear relationship between CVD risk, age, and BMI, taking into account apparent sex differences, to predict future CV events. While this finding may suggest a lower degree of stiffness in large arteries of overweight–obese subjects compared to their normal-weight counterparts, the potential implications for individuals with higher BMI need be explored further.
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