Citations

Background— Despite complete interruption of antegrade coronary artery flow in the setting of a chronic total occlusion (CTO), clinical recognition of myocardial infarction is often challenging. Using cardiac MRI, we investigated the frequency and extent of myocardial infarction in patients with CTO, and assessed their relationship with regional systolic function and the extent of angiographic collateral flow. Methods and Results— We included 170 consecutive patients (median age, 62 years) with angiographically documented CTO. Regional late gadolinium enhancement and wall motion score index were assessed by cardiac MRI with the use of a 17-segment model. Angiographic collateral flow was assessed by the collateral connection grade and the Rentrop score. Evidence of previous myocardial infarction was found in 25% of patients by ECG Q waves, in 69% by regional wall motion abnormality, and in 86% of patients by late gadolinium enhancement. Increased angiographic collateral flow was associated with a lower frequency of Q waves on ECG, and a lower regional wall motion score index, late gadolinium enhancement volume (%), and degree of late gadolinium enhancement transmurality (all P <0.001), as well. Conclusions— The frequency of myocardial infarction in territories subtended by CTO is significantly higher than previously recognized. The degree of myocardial injury downstream epicardial CTO is inversely correlated with the degree of angiographic collaterals.

BACKGROUND:The American Academy of Pediatrics (AAP) introduced revised return-to-care recommendations for mildly ill children in 2009 that were added to national standards in 2011. Child care directors' practices in a state without clear emphasis on return-to-care guidelines are unknown. We investigated director return-to-care practices just before the release of recently revised AAP guidelines.METHODS:A telephone survey with 5 vignettes of mild illness (cold symptoms, conjunctivitis, vomiting/diarrhea, fever, and ringworm) was administered to randomly sampled directors in metropolitan Milwaukee, Wisconsin. Directors were asked about return-to-care criteria for each illness. Questions for return-to-care criteria were open-ended; multiple responses were allowed. Answers were compared with AAP return-to-care recommendations.RESULTS:A total of 305 directors participated. Based on director responses to vignettes, the percentage of correct responses regarding return-to-child care management compared with AAP return-to-care recommendations was low: fever (0%); conjunctivitis (0%); diarrhea (1.6%); cold symptoms (12%); ringworm (21%); and vomiting (80%). Two illnesses (conjunctivitis and cold symptoms) would require the child to have an urgent medical evaluation or treatment not recommended by the AAP, as follows: Conjunctivitis—antibiotics for 24 hours (62%), physician visit (49%), any antibiotic treatment (6%), and symptom resolution (4%); and Cold Symptoms—physician visit (45.6%), antibiotics (10%), and symptom resolution (25%).CONCLUSIONS:Directors’ self-reported return-to-child care practices differed substantially before the release of revised AAP return-to-care recommendations. Active adoption of AAP return-to-child care guidelines would decrease the need for unnecessary urgent medical evaluation and treatment as well as unnecessary exclusion of a child from child care.

Background— Mutations in genes including SCN5A encoding the α-subunit of the cardiac sodium channel (hNav1.5) cause Brugada syndrome via altered function of cardiac ion channels, but more than two-thirds of Brugada syndrome remains pathogenetically elusive. T-tubules and sarcoplasmic reticulum are essential in excitation of cardiomyocytes, and sarcolemmal membrane-associated protein (SLMAP) is a protein of unknown function localizing at T-tubules and sarcoplasmic reticulum. Methods and Results— We analyzed 190 unrelated Brugada syndrome patients for mutations in SLMAP . Two missense mutations, Val269Ile and Glu710Ala, were found in heterozygous state in 2 patients but were not found in healthy individuals. Membrane surface expression of hNav1.5 in the transfected cells was affected by the mutations, and silencing of mutant SLMAP by small interfering RNA rescued the surface expression of hNav1.5. Whole-cell patch-clamp recordings of hNav1.5-expressing cells transfected with mutant SLMAP confirmed the reduced hNav1.5 current. Conclusions— The mutations in SLMAP may cause Brugada syndrome via modulating the intracellular trafficking of hNav1.5 channel.