Obesity Is Associated with Dysfunctional Cardiac Hemodynamic Indices and Increased Vascular

Obesity is associated with dysfunctional cardiac hemodynamic indices and increased vascular resistance in pre-dialysis CKD patients

Introduction: Obesity is a key independent risk factor for cardiovascular disease.In chronic kidney disease (CKD) patients, obesity may worsen disease progression by increasing metabolic renal demands. Obese patients are known to have higher rates of coronary artery disease and cardiomyopathy than non-obese patients and are also more likely to suffer a cardiovascular related death. Obesityalso leads to increased peripheral vascular resistancewhich contributes to systemichypertension and endothelial dysfunction; both hasten decline in renal function and cardiovascular health. Non-invasive estimates of cardiac hemodynamics may provide a simpleindication of cardiac performancein patients withCKD.To our knowledge, this is the first study to explore the cardiac hemodynamic indices ofobese pre-dialysis CKD patients compared to non-obese patients.

Methods:35 patients (mean age: 60.2±11.7 years) with moderately severe CKD (3b-5, mean eGFR: 24.4±8.5 [9-41] ml/min/1.73m2) were analysed. Body composition (fat mass (FM) (kg) and body fat (BF%)) was assessed using bioelectric impedance analysis.Obesity was defined usingage, sex, and ethnicity-based BF% ranges,rather than body mass index (BMI) cut-offs. Cardiac hemodynamic indices were measured using a ‘Non-invasive Hemodynamic and Cardiac Output Monitor’(CHEETAH NICOM) device. Measures of resting blood pressure (BP), mean arterial pressure (MAP), total peripheral resistance index (TPRI), cardiac output (CO), CO index (COI), stroke volume index (SVI), and cardiac power index (CPI) were recorded. Controlling for age, sex, and ethnicity, statistical differences between ‘normal’, ‘overweight’ and ‘obese’ groups were analysed by ANCOVA.

Results: 71% of patients were either ‘overweight’ (n=6, 17%; mean FM: 24.4±5.4kg; BMI: 27.1±3.6 kg/m2; BF%: 34.8±7.7%) or ‘obese’ (n=19, 54%; mean FM: 36.1±8.9kg;BMI: 31.6±5.3 kg/m2; BF%: 41.8±6.1%). The remaining were classified within ‘normal’ BF% ranges (n=10, 29%; mean FM: 16.7±5.3kg;BMI: 24.3±4.1 kg/m2; BF%: 23.6±4.5%). In the ‘obese’ group, we observed significantly lower COI (‘obese’: 3.0±0.3 versus ‘normal’: 3.8±0.3, and ‘overweight’ 3.2±0.5 L/min/m2, P<.001); higher TPRI (‘obese’: 2830.0±504.2 versus ‘normal’: 2235.3±283.8, and ‘overweight’ 2682.0±671.4 dynes-sec/cm2, P= .022); lower SVI (‘obese’: 45.2±4.7 versus ‘normal’: 56.0±8.1, and ‘overweight’ 49.9±7.7 ml/m2/beat, P= .001); and lower CPI (‘obese’: 0.75±0.16 versus ‘normal’: 0.88±0.11, and ‘overweight’ 0.70±0.08W/m2, P= .011). There wereno significant differences in CO (P= .083), systolic BP (P= .625), diastolic BP (P= .492), or MAP (P= .825) between the groups. No differences in estimated glomerular filtration rate(eGFR) were observed (P= .859).

Conclusion: Obesity results in poorer cardiac hemodynamic measures, specifically those indicative of impaired cardiac function (i.e. reduced COI, SVI, and CPI). Reductions in cardiac circulatoryperformance may be caused by obesity-related changes to heart structure (i.e. cardiomyopathy), with such changes associated with increased mortality and poor cardiovascular health. Obesity was associated with increased TPR which may result inworsening hypertension and endothelial dysfunction.eGFR and BPwerewell-controlled and comparable across all groups.The promotion of exercise and proper nutritionshould be a keyfactor in the prevention of obesity and its related cardiac dysfunctionin CKD patients.