Albuquerque, Felipe N.

Background Studies have shown that chronic total occlusion ( CTO ) in a noninfarct‐related artery in patients with ST‐segment–elevation myocardial infarction is linked to increased mortality. It remains unclear whether staged revascularization of a noninfarct‐related artery CTO in patients with ST‐segment–elevation myocardial infarction translates to improved outcomes. We performed a meta‐analysis to compare outcomes between patients presenting with ST‐segment–elevation myocardial infarction with concurrent CTO who underwent percutaneous coronary intervention of noninfarct‐related artery CTO versus those who did not. Method and Results We conducted an electronic database search of all published data. The primary end point was major adverse cardiovascular events. Secondary end points were all‐cause mortality, cardiovascular mortality, myocardial infarction, repeat revascularization with either percutaneous coronary intervention or coronary artery bypass grafting, stroke, and heart failure readmission. Odds ratios ( ORs ) and 95% confidence intervals ( CIs ) were computed. Random effects model was used and heterogeneity was considered if I 2 >25. Six studies (n=1253 patients) were included in the analysis. There was a significant difference in major adverse cardiovascular events ( OR , 0.54; 95% CI , 0.32–0.91), cardiovascular mortality ( OR , 0.43; 95% CI , 0.20–0.95), and heart failure readmissions ( OR , 0.57; 95% CI , 0.36–0.89), favoring the patients in the CTO percutaneous coronary intervention group. No significant differences were observed between the 2 groups for all‐cause mortality ( OR , 0.47; 95% CI , 0.22–1.00), myocardial infarction ( OR , 0.78; 95% CI , 0.41–1.46), repeat revascularization ( OR , 1.13; 95% CI , 0.56–2.27), and stroke ( OR , 0.51; 95% CI , 0.20–1.33). Conclusions In this meta‐analysis, CTO percutaneous coronary intervention of the noninfarct‐related artery in patients presenting with ST‐segment–elevation myocardial infarction was associated with a significant reduction in major adverse cardiovascular events, cardiovascular mortality, and heart failure readmissions.

Background Epidemiologic evidence suggests a link between short sleep duration and cardiovascular risk, although the nature of any relationship and mechanisms remain unclear. Short sleep duration has also been linked to an increase in cardiovascular events. Endothelial dysfunction has itself been implicated as a mediator of heightened cardiovascular risk. We sought to determine the effect of 8 days/8 nights of partial sleep restriction on endothelial function in healthy humans. Methods and Results Sixteen healthy volunteers underwent a randomized study of usual sleep versus sleep restriction of two‐thirds normal sleep time for 8 days/8 nights in a hospital‐based clinical research unit. The main outcome was endothelial function measured by flow‐mediated brachial artery vasodilatation ( FMD ). Those randomized to sleep restriction slept 5.1 hours/night during the experimental period compared with 6.9 hours/night in the control group. Sleep restriction was associated with significant impairment in FMD (8.6±4.6% during the initial pre‐randomization acclimation phase versus 5.2±3.4% during the randomized experimental phase, P =0.01) whereas no change was seen in the control group (5.0±3.0 during the acclimation phase versus 6.73±2.9% during the experimental phase, P =0.10) for a between‐groups difference of −4.40% (95% CI −7.00 to −1.81%, P =0.003). No change was seen in non‐flow mediated vasodilatation ( NFMD ) in either group. Conclusion In healthy individuals, moderate sleep restriction causes endothelial dysfunction. Clinical Trial Registration URL : ClinicalTrials.gov. Unique identifier: NCT 01334788.

OBJECTIVE The negative results of two randomized controlled trials (RCTs) have challenged current guideline recommendations for using aspirin for primary prevention of cardiovascular events among patients with diabetes. We therefore sought to determine if the effect of aspirin for primary prevention of cardiovascular events and mortality differs between patients with and without diabetes. RESEARCH DESIGN AND METHODS We conducted a systematic search of MEDLINE, EMBASE, Cochrane Library, Web of Science, and Scopus since their inceptions until November 2008 for RCTs of aspirin for primary prevention of cardiovascular events. Blinded pairs of reviewers evaluated studies and extracted data. Random-effects meta-analysis and Bayesian logistic regression were used to estimate the ratios of relative risks (RRs) of outcomes of interest among patients with and without diabetes. A 95% CI that crosses 1.00 indicates that the effect of aspirin does not differ between patients with and without diabetes. RESULTS Nine RCTs with moderate to high methodological quality contributed data to the analyses. The ratios of RRs comparing the benefit of aspirin among patients with diabetes compared with patients without diabetes for mortality, myocardial infarction, and ischemic stroke were 1.12 (95% CI 0.92–1.35), 1.19 (0.82–1.17), and 0.70 (0.25–1.97), respectively. CONCLUSIONS Whereas estimates of benefit among patients with diabetes remain imprecise, our analysis suggests that the relative benefit of aspirin is similar in patients with and without diabetes.

The combination of metabolic syndrome and obstructive sleep apnea (OSA) has been termed “syndrome Z.” The prevalence of both OSA and metabolic syndrome is increasing worldwide, in part linked to the epidemic of obesity. Beyond their epidemiologic relationship, growing evidence suggests that OSA may be causally related to metabolic syndrome. We are only beginning to understand the potential mechanisms underlying the OSA–metabolic syndrome interaction. Although there is no clear consensus, there is growing evidence that alterations in the hypothalamic–pituitary axis, generation of reactive oxygen species (ROS) due to repetitive hypoxia, inflammation, and generation of adipokines may be implicated in the changes associated with both OSA and metabolic syndrome. Whether some or all of these metabolic alterations mechanistically link OSA to metabolic syndrome remains to be proven, but it is an area of intense scientific interest.