Abstract 1711: Effect of Obesity on Activation of the Renin Angiotensin-Aldosterone system in Patients with Moderate to Advanced Heart Failure
Epidemiologic studies have shown that obesity is a risk factor for the development of heart failure (HF); however, the mechanism(s) that link obesity to the development of HF are not known. Given that components of the renin angiotensin aldosterone system (RAAS) are synthesized within adipose tissue, we tested the hypothesis that RAAS is progressively activated in HF patients in direct relation to their body mass index (BMI). Accordingly, we prospectively studied plasma renin activity (PRA) and aldosterone (ALDO) in patients (n =25 group) with NYHA class II–III heart failure (HF) and an ejection fraction (EF) < 40% who were normal weight (NW; BMI < 25), overweight (OW;BMI 25 – 29.9) and obese (OB; BMI > 30). Measurements of PRA and ALDO were obtained after 12 hours of fasting in the sitting and standing position. All HF medications were withheld on the day of study.
Results: There was no difference in age in the NW (64.4 ± 11 y), OW (62.8 ± 13.6 y), and OB patients (59.5 ± 8 y), nor was there a difference in NYHA class and EF between groups: NW (21.6 ± 8 %), OW (26.9 ± 7%), and OB patients (21.7 ± 7%). The prevalence of co-morbidities were similar among groups, with the exception of diabetes, which was higher in the OW and OB patients compared to NW patients. Although there was no significant difference in the sitting and standing levels of PRA in NW and OW patients, there was a trend (p < 0.58) towards a significant increase in PRA in the OB patients. There was also no significant difference in the sitting and standing levels of ALDO in the NW patients; however there was a significant difference in sitting and standing ALDO levels in the OW (p < 0.002) and OB patients (p < 0.005). Moreover, the standing levels of ALDO were significantly higher (p <0.002) in the OB than in the OW patients.
Conclusion: Taken together these data show for the first time that there is a increase in RAAS activation in HF patients in direct relation to their BMI, and thus provide a plausible biological mechanism that links obesity to the increased incidence of HF observed in epidemiological studies.