Arterial stiffness is related to insulin resistance in nondiabetic hypertensive older adults.

Hypertension, diabetes, obesity, and aging are associated with increased arterial stiffness. Both insulin resistance and hyperglycemia may contribute to the development of arterial stiffness. Older nondiabetic hypertensive adults were recruited to test the following hypotheses: (1) insulin resistance is associated with arterial stiffness, and (2) this relationship is independent of glucose tolerance status. Aortic pulse wave velocity (PWV), pulse pressure (PP), insulin sensitivity index (S(I), measured by insulin-assisted frequently sampled iv glucose test), glucose tolerance status, and abdominal fat mass were assessed in 37 older (23 male, 14 female, mean age 69.4 +/- 5.9 yr), nondiabetic, hypertensive adults after a 4-wk antihypertensive medication withdrawal. Both PWV and PP were negatively correlated with S(I) (r = -0.49, P = 0.002, and r = -0.38, P = 0.02, respectively). The mean PWV and PP in those with normal glucose tolerance were not significantly different from those with impaired glucose tolerance (9.8 +/- 2.4 vs. 10.0 +/- 3.1 m/sec, P = 0.79 and 71 +/- 17 vs. 72 +/- 18 mm Hg, P = 0.80, respectively). In multiple regression analysis, PWV and PP remained independently correlated with S(I) (P < 0.05) after adjusting for age, gender, fasting glucose, glucose tolerance status, body mass index, or abdominal fat mass. These results suggest that in hypertensive, nondiabetic, older adults, insulin resistance is associated with arterial stiffness independent of glucose tolerance status.

Asthma, beta-agonists, and development of congestive heart failure: results of the ABCHF study.

BACKGROUND: Previous studies demonstrated an association between asthma and idiopathic dilated cardiomyopathy (IDCM), raising concerns regarding chronic beta-agonist inhaler use. The purpose of this investigation was to replicate that association. METHODS AND RESULTS: We identified 67 patients with IDCM and 130 controls with predominately ischemic cardiomyopathy. Patients were administered a structured, detailed phone survey by blinded interviewers, and had chart abstractions performed. We had 80% power to detect an odds ratio (OR) > or = 2.6 for the relation of asthma and IDCM. A history of asthma was present in 19.4% v 12.3% for cases and controls respectively, OR, 1.72, (95% confidence interval [CI], 0.72, 4.09), P = .18. The duration of asthma was higher in cases: 32.3 (19.7) years v 13.8 (15.0) years (P = 0.007). With adjustment for confounders, multivariate analyses revealed no significant relations between asthma or beta-agonist use and the later development of IDCM. CONCLUSIONS: It is unlikely that previously occurring asthma or beta-agonist use has a strong relationship to the development of IDCM; however, IDCM and atopic diseases may cluster in families, warranting further work into the genetic relations between atopy and IDCM.