Association between smoking and outcomes in older adults with atrial fibrillation.

Tobacco smoking is a risk factor for atrial fibrillation (AF), but little is known about the impact of smoking in patients with AF. Of the 4060 patients with recurrent AF in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, 496 (12%) reported having smoked during the past two years. Propensity scores for smoking were estimated for each of the 4060 patients using a multivariable logistic regression model and were used to assemble a matched cohort of 487 pairs of smokers and nonsmokers, who were balanced on 46 baseline characteristics. Cox and logistic regression models were used to estimate the associations of smoking with all-cause mortality and all-cause hospitalization, respectively, during over 5 years of follow-up. Matched participants had a mean age of 70 ± 9 years (± S.D.), 39% were women, and 11% were non-white. All-cause mortality occurred in 21% and 16% of matched smokers and nonsmokers, respectively (when smokers were compared with nonsmokers, hazard ratio=HR=1.35; 95% confidence interval=95%CI=1.01-1.81; p=0.046). Unadjusted, multivariable-adjusted and propensity-adjusted HR (95% CI) for all-cause mortality associated with smoking in the pre-match cohort were: 1.40 (1.13-1.72; p=0.002), 1.45 (1.16-1.81; p=0.001), and 1.39 (1.12-1.74; p=0.003), respectively. Smoking had no association with all-cause hospitalization (when smokers were compared with nonsmokers, odds ratio=OR=1.21; 95%CI=0.94-1.57, p=0.146). Among patients with AF, a recent history of smoking was associated with an increased risk of all-cause mortality, but had no association with all-cause hospitalization.

A propensity-matched study of the association of diabetes mellitus with incident heart failure and mortality among community-dwelling older adults.

Diabetes mellitus (DM) is a risk factor for incident heart failure (HF) in older adults. However, the extent to which this association is independent of other risk factors remains unclear. Of 5,464 community-dwelling adults ≥65 years old in the Cardiovascular Health Study without baseline HF, 862 had DM (fasting plasma glucose levels ≥126 mg/dl or treatment with insulin or oral hypoglycemic agents). Propensity scores for DM were estimated for each of the 5,464 participants and were used to assemble a cohort of 717 pairs of participants with and without DM who were balanced in 65 baseline characteristics. Incident HF occurred in 31% and 26% of matched participants with and without DM, respectively, during >13 years of follow-up (hazard ratio 1.45 for DM vs no DM, 95% confidence interval [CI] 1.14 to 1.86, p = 0.003). Of the 5,464 participants before matching unadjusted and multivariable-adjusted hazard ratios for incident HF associated with DM were 2.22 (95% CI 1.94 to 2.55, p <0.001) and 1.52 (95% CI 1.30 to 1.78, p <0.001), respectively. All-cause mortality occurred in 57% and 47% of matched participants with and without DM, respectively (hazard ratio 1.35, 95% CI 1.13 to 1.61, p = 0.001). Of matched participants DM-associated hazard ratios for incident peripheral arterial disease, incident acute myocardial infarction, and incident stroke were 2.50 (95% CI 1.45 to 4.32, p = 0.001), 1.37 (95% CI 0.97 to 1.93, p = 0.072), and 1.11 (95% CI 0.81 to 1.51, p = 0.527), respectively. In conclusion, the association of DM with incident HF and all-cause mortality in community-dwelling older adults without HF is independent of major baseline cardiovascular risk factors.

Relationship between stage of kidney disease and incident heart failure in older adults.

BACKGROUND: The relationship between stage of chronic kidney disease (CKD) and incident heart failure (HF) remains unclear. METHODS: Of the 5,795 community-dwelling adults ≥65 years in the Cardiovascular Health Study, 5,450 were free of prevalent HF and had baseline estimated glomerular filtration rate (eGFR: ml/min/1.73 m(2)) data. Of these, 898 (16%) had CKD 3A (eGFR 45-59 ml/min/1.73 m(2)) and 242 (4%) had CKD stage ≥3B (eGFR <45 ml/min/1.73 m(2)). Data on baseline proteinuria were not available and 4,310 (79%) individuals with eGFR ≥60 ml/min/1.73 m(2) were considered to have no CKD. Propensity scores estimated separately for CKD 3A and ≥3B were used to assemble two cohorts of 1,714 (857 pairs with CKD 3A and no CKD) and 557 participants (148 CKD ≥3B and 409 no CKD), respectively, balanced on 50 baseline characteristics. RESULTS: During 13 years of follow-up, centrally-adjudicated incident HF occurred in 19, 24 and 38% of pre-match participants without CKD (reference), with CKD 3A [unadjusted hazard ratio (HR) 1.40; 95% confidence interval (CI) 1.20-1.63; p < 0.001] and with CKD ≥3B (HR 3.37; 95% CI 2.71-4.18; p < 0.001), respectively. In contrast, among matched participants, incident HF occurred in 23 and 23% of those with CKD 3A and no CKD, respectively (HR 1.03; 95% CI 0.85-1.26; p = 0.746), and 36 and 28% of those with CKD ≥3B and no CKD, respectively (HR 1.44; 95% CI 1.04-2.00; p = 0.027). CONCLUSIONS: Among community-dwelling older adults, CKD is a marker of incident HF regardless of stage; however, CKD ≥3B, not CKD 3A, has a modest independent association with incident HF.

Urine biomarkers predict acute kidney injury and mortality in very low birth weight infants.

OBJECTIVES: To test the hypothesis that noninvasive urinary biomarkers may improve early identification, differentiate causes, and predict outcomes of acute kidney injury (AKI) in very low birth weight subjects. STUDY DESIGN: We performed 2 nested case-control studies to compare the ability of 6 urine biomarkers to predict AKI (rise in serum creatinine of at least 0.3 mg/dL) and mortality (death before 36 weeks postmenstrual age). RESULTS: Compared to subjects without AKI (n = 21), those with AKI (n = 9) had higher maximum neutrophil gelatinase-associated lipocalin (OR = 1.2 [1.0, 1.6]; P < .01; receiver operator characteristics [ROC] area under the curve [AUC] = .80) and higher maximum osteopontin (OR = 3.2 [1.5, 9.9]; P < .01; ROC AUC = 0.83). Compared with survivors (n = 100), nonsurvivors (n = 23) had higher maximum kidney injury molecule 1 (OR = 1.1 [1.0, 1.2]; P < .02; ROC AUC = 0.64) and higher maximum osteopontin (OR = 1.8 (1.2, 2.7); P < .001; AUC of ROC = 0.78). The combination of biomarkers improved predictability for both AKI and mortality. Controlling for gestational age and birth weight did not affect results considerably. CONCLUSIONS: Urinary biomarkers can predict AKI and mortality in very low birth weight infants independent of gestational age and birth weight.