Obesity and metabolic phenotypes (metabolically healthy and unhealthy variants) are significantly associated with prevalence of elevated C-reactive protein and hepatic steatosis in a large healthy Brazilian population.

BACKGROUND: Among the obese, the so-called metabolically healthy obese (MHO) phenotype is thought to confer a lower CVD risk as compared to obesity with typical associated metabolic changes. The present study aims to determine the relationship of different subtypes of obesity with inflammatory-cardiometabolic abnormalities. METHODS: We evaluated 5,519 healthy, Brazilian subjects (43 ± 10 years, 78% males), free of known cardiovascular disease. Those with <2 metabolic risk factors (MRF) were considered metabolically healthy, and those with BMI ≥ 25 kg/m(2) and/or waist circumference meeting NCEP criteria for metabolic syndrome as overweight/obese (OW). High sensitivity C reactive protein (hsCRP) was measured to assess underlying inflammation and hepatic steatosis (HS) was determined via abdominal ultrasound. RESULTS: Overall, 40% of OW individuals were metabolically healthy, and 12% normal-weight had ≥2 MRF. The prevalence of elevated CRP (≥3 mg/dL) and HS in MHO versus normal weight metabolically healthy group was 22% versus 12%, and 40% versus 8% respectively (P < 0.001). Both MHO individuals and metabolically unhealthy normal weight (MUNW) phenotypes were associated with elevated hsCRP and HS. CONCLUSION: Our study suggests that MHO and MUNW phenotypes may not be benign and physicians should strive to treat individuals in these subgroups to reverse these conditions.

Delayed heart rate recovery is strongly associated with early and late-stage prehypertension during exercise stress testing.

BACKGROUND: Heart rate recovery (HRR) has been shown to predict cardiovascular disease mortality. HRR is delayed in hypertension, but its association with prehypertension (PHT) has not been well studied. METHODS: The study population consisted of 683 asymptomatic individuals (90% men, aged 47±7.9 years). HRR was defined as peak heart rate minus heart rate after a 2-minute rest. PHT was categorized into stage I (systolic blood pressure (SBP) 120-129mm Hg or diastolic BP (DBP) 80-84mm Hg) or stage II (SBP 130-139mm Hg or DBP 85-89mm Hg). Logistic regression was used to generate odds ratios (ORs) for the relationship between HRR and PHT. RESULTS: The mean HRR was lower in the PHT groups than in those who were normotensive (60 bpm and 58 bpm in stages I and II PHT vs. 65 bpm in normal BP; P <0.01). Persons with PHT were more likely to be in the lowest quartile of HRR compared with those with normal BP (adjusted OR, 3.80 and 95% confidence interval [CI], 1.06, 13.56 for stage II PHT and adjusted OR, 3.01 and 95% CI 1.05, 8.66 for stage I PHT). In a fully adjusted model, HRR was still significantly associated with both stages of PHT. CONCLUSION: Among asymptomatic patients undergoing stress testing, delayed HRR was independently associated with early and late stages of PHT. Further studies are needed to determine the usefulness of measuring HRR in the prevention and management of hypertension.