New Precordial T Wave Inversions in Hospitalized Patients.

BACKGROUND: The incidence of precordial T changes has been described in athletes and in specific populations, while the etiology in a large patient population admitted to the hospital has not previously been reported. METHODS: All electrocardiograms (ECGs) read by the same physician with new (compared to prior ECGs) or presumed new (no prior ECGs) precordial T wave inversions of >1 mm (0.1 mV) in multiple precordial leads were retrospectively reviewed and various ECG, patient-related, and imaging parameters assessed. A total of 226 patients and their ECGs were initially selected for analysis. Of these, 35 were eliminated leaving 191 for the final analysis. RESULTS: Patients and their ECGs were divided into 5 groups based on diagnosis and incidence including Wellens syndrome, takotsubo, type 2 myocardial infarction, other (including multiple diagnoses), and unknown. Although subtle differences including number of T inversion leads, depth of T waves, QTc intervals, and other variables were present between some groups, diagnosis in individual cases required appropriate clinical, laboratory, or imaging studies. For example, although Wellens syndrome was identified in <20% of cases, a presenting history of chest discomfort with precordial T changes either on the admission or next-day ECG was highly sensitive and specific for this diagnosis. In some cases, type 2 myocardial infarction can also have a Wellens-like ECG phenotype without significant left anterior descending disease. CONCLUSIONS: Precordial T wave changes in hospitalized patients have various etiologies, and in individual cases, the changes on the ECG alone cannot easily distinguish the presumptive diagnosis and additional data are required.

Recurrent ventricular tachycardia associated with lipomatous metaplasia of a myocardial scar.

Lipomatous metaplasia in chronic postmyocardial infarction scars is a common and underappreciated finding seen in histopathology and cardiac MRI. Evidence suggests that lipomatous metaplasia is capable of altering the electroconductivity of the myocardium leading to re-entry pathways that are implicated in the pathogenesis of postmyocardial infarction arrhythmogenesis. We report a case of a patient who presented with non-sustained ventricular tachycardia and was found to have lipomatous metaplasia of a prior myocardial infarct-related scar.

A Disease-Associated Microbial and Metabolomics State in Relatives of Pediatric Inflammatory Bowel Disease Patients.

BACKGROUND & AIMS: Microbes may increase susceptibility to inflammatory bowel disease (IBD) by producing bioactive metabolites that affect immune activity and epithelial function. We undertook a family based study to identify microbial and metabolic features of IBD that may represent a predisease risk state when found in healthy first-degree relatives. METHODS: Twenty-one families with pediatric IBD were recruited, comprising 26 Crohn's disease patients in clinical remission, 10 ulcerative colitis patients in clinical remission, and 54 healthy siblings/parents. Fecal samples were collected for 16S ribosomal RNA gene sequencing, untargeted liquid chromatography-mass spectrometry metabolomics, and calprotectin measurement. Individuals were grouped into microbial and metabolomics states using Dirichlet multinomial models. Multivariate models were used to identify microbes and metabolites associated with these states. RESULTS: Individuals were classified into 2 microbial community types. One was associated with IBD but irrespective of disease status, had lower microbial diversity, and characteristic shifts in microbial composition including increased Enterobacteriaceae, consistent with dysbiosis. This microbial community type was associated similarly with IBD and reduced microbial diversity in an independent pediatric cohort. Individuals also clustered bioinformatically into 2 subsets with shared fecal metabolomics signatures. One metabotype was associated with IBD and was characterized by increased bile acids, taurine, and tryptophan. The IBD-associated microbial and metabolomics states were highly correlated, suggesting that they represented an integrated ecosystem. Healthy relatives with the IBD-associated microbial community type had an increased incidence of elevated fecal calprotectin. CONCLUSIONS: Healthy first-degree relatives can have dysbiosis associated with an altered intestinal metabolome that may signify a predisease microbial susceptibility state or subclinical inflammation. Longitudinal prospective studies are required to determine whether these individuals have a clinically significant increased risk for developing IBD.