Citations

Background— Heart failure (HF) and atrial fibrillation (AF) share common risk factors and often coexist. The combination of HF and AF may carry a worse prognosis than either condition alone; however, the magnitude of this risk remains controversial and it is not known whether the timing of AF influences the risk of death. Methods and Results— We determined the risk of all-cause mortality in relation to the presence of AF prior to or after HF diagnosis in a community-based cohort of persons diagnosed as having HF between 1983 and 2006. Of 1664 individuals with HF, 553 had a history of AF and 384 developed AF after HF. During a median follow-up of 4.0 years, 450 deaths occurred among persons with prior AF, 314 among those with AF after HF, and 572 among patients without AF. In fully adjusted models, compared with patients without AF, those with AF prior to HF had a 29% increased risk of death, whereas those who developed AF after HF exhibited >2-fold increased risk of death. Conclusions— In the community, AF is frequent in the setting of HF and is associated with a large excess risk of death. The magnitude of this excess risk differs markedly according to the timing of AF, with AF developing after HF conferring the largest increased risk of death compared with HF patients without AF.

Background— Although older patients frequently undergo percutaneous coronary interventions (PCI), frailty, comorbidity, and quality of life are seldom part of risk prediction approaches. We assessed their incremental prognostic value over and above the risk factors in the Mayo Clinic risk score. Methods and Results— Patients ≥65 years who underwent PCI were assessed for frailty (Fried criteria), comorbidity (Charlson index), and quality of life [SF-36]. Of the 628 discharged [median follow-up of 35.0 months (interquartile range, 22.7 to 42.9)], 78 died and 72 had a myocardial infarction (MI). Three-year mortality was 28% for frail patients, 6% for nonfrail patients. The respective 3-year rates of death or MI were 41% and 17%. After adjustment, frailty [hazard ratio (HR), 4.19 [95% confidence interval (CI), 1.85, 9.51], physical component score of the SF-36 (HR, 1.59; 95% CI, 1.24 to 2.02), and comorbidity, (HR, 1.10; 95% CI, 1.05, 1.16) were associated with mortality. Frailty was associated with mortality/MI (HR, 2.61, 1.52, 4.50). Models with conventional Mayo Clinic risk score had C-statistics of 0.628, 0.573 for mortality and mortality/MI, respectively. Adding frailty, quality of life, and comorbidity, the C-statistic was (0.675, 0.694, 0.671) for mortality and (0.607, 0.587, 0.576) for mortality/MI, respectively. Including frailty, comorbidities and SF-36, conferred a discernible improvement to predict death and death/MI (integrated discrimination improvement, 0.027 and 0.016, and net reclassification improvement of 43% and 18%, respectively). Conclusions— After PCI, frailty, comorbidity and poor quality of life are prevalent and are associated with adverse long-term outcomes. Their inclusion improves the discriminatory ability of the Mayo Clinic risk score derived from the routine cardiovascular risk factors.

Abstract We tested whether the association between bone mineral density (BMD) and coronary artery calcification (CAC) varies according to dyslipidemia in community-living individuals. Between 2002 and 2005, 305 women and 631 men (mean age of 64 years), who were not taking lipid-lowering medications or estrogen were assessed for spine BMD, CAC, and total (TC), HDL- and LDL-cholesterol and triglycerides. Participants were a random sample from the Multi-Ethnic Study of Atherosclerosis (MESA) without clinical cardiovascular disease. Spine BMD at the L3 vertebrate was performed by computer tomography (CT). CAC prevalence was measured by CT. The total cholesterol to HDL ratio (TC:HDL) ≥ 5.0 was used as the primary marker of hyperlipidemia. The association of BMD with CAC differed in women with TC:HDL < 5.0 versus higher (p-interaction = 0.01). In age- and race-adjusted models, among women with TC:HDL < 5.0, each SD (43.4 mg/cc) greater BMD was associated with a 25% lower prevalence of CAC (prevalence ratio [PR] 0.75, 95% confidence interval [CI] 0.63–0.89), whereas among women with higher TC:HDL, higher BMD was not significantly associated with CAC (PR 1.22, 95% CI 0.82–1.82). Results were similar using other definitions of hyperlipidemia. In contrast, no consistent association was observed between BMD and CAC in men, irrespective of the TC:HDL ratio (p interaction 0.54). The inverse association of BMD with CAC is stronger in women without dyslipidemia. These data argue against the hypothesis that dyslipidemia is the key factor responsible for the inverse association of BMD with atherosclerosis. © 2011 American Society for Bone and Mineral Research

Background— Data on the association between myocardial infarction (MI) and fractures are scarce. Recent changes in the epidemiology of MI justify exploring this relationship. We evaluated whether MI constitutes a risk factor for osteoporotic fracture and examined secular trends in this association. Methods and Results— Consecutive Olmsted County, Minnesota, residents with incident MI diagnosed in 1979 to 2006 and community control subjects individually matched (1:1) to cases on age, sex, and year of onset (n=6642) were followed up through 2009. Outcome measures were time to osteoporotic fracture, overall and by anatomic site, and death. Fracture incidence rates were stable in controls but increased markedly over time among MI cases. Accordingly, although an overall excess of fracture risk after MI was observed (adjusted hazard ratio, 1.32; 95% confidence interval, 1.12 to 1.56), substantial temporal variations were noted (1979 to 1989: hazard ratio, 0.81; 95% confidence interval, 0.58 to 1.12; 1990 to 1999: hazard ratio, 1.47; 95% confidence interval, 1.10 to 1.96; 2000 to 2006: hazard ratio, 1.73; 95% confidence interval, 1.32 to 2.27; P for trend <0.001). Trends were similar regardless of age, sex or fracture site. Conversely, the overall hazard ratio for death in MI cases versus controls did not change materially despite a continuous decline in 30-day case fatality rate (12.5% in 1979 to 1989; 6.7% in 2000 to 2006). Observed changes in the baseline prevalence of cardiovascular risk factors, MI characteristics, and comorbidities did not fully account for the trends in fracture risk. Conclusions— Over the past decades, the association between MI and osteoporotic fractures increased steadily. The trend is consistent with the displacement of post-MI outcomes toward noncardiovascular events, highlighting the need for comprehensive prevention strategies to accommodate the changing epidemiology of MI.

This study, in biologically bred hyperglycemic diabetic rats, examined the effect of a intravenous insulin infusion (1.5 units.hr-1) on blood, plasma, and brain glucose concentrations to determine their relationship during decreasing blood and plasma glucose levels. The data were compared to saline-treated diabetic rats and saline-treated nondiabetic littermates. The volume and duration of the treatment infusion were similar in all groups. Insulin infusion in diabetic rats produced the expected reduction in blood and plasma glucose, and normoglycemia was produced within 78 +/- 37 minutes (mean +/- SD). However, once normoglycemia was achieved, brain glucose was still significantly greater by 44% than in nondiabetic rats (p = 0.015). Moreover, the ratio of brain to plasma glucose was more than 50% greater in diabetic than nondiabetic rats, irrespective of whether or not they received insulin (p less than 0.01). We conclude that measurement of blood or plasma glucose in diabetic subjects will tend to underestimate the amount of glucose in the brain and that this relationship is not influenced by acute insulin therapy.