Ten case reports of disseminated Mycobacterium chimaera infections associated with cardiovascular surgery were published from Europe. We report 3 cases of disseminated M chimaera infections with histories of aortic graft and/or valvular surgery within the United States. Two of 3 patients demonstrated ocular involvement, a potentially important clinical finding.

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Catheter-based ablation for patients with CA appears to provide important symptomatic relief. However, mortality from the underlying disease remains a significant issue for the amyloid light-chain subtype.

Background The genetic mechanisms of atrial fibrillation (AF) remain incompletely understood. Previous differential expression studies in AF were limited by small sample size and provided limited understanding of global gene networks, prompting the need for larger-scale, network-based analyses. Methods and Results Left atrial tissues from Cleveland Clinic cardiac surgery patients were assayed using Illumina Human HT-12 mRNA microarrays. The dataset included three groups based on cardiovascular co-morbidities: mitral valve (MV) disease without coronary artery disease (CAD) (n=64); CAD without MV disease (n=57); and lone AF (LAF) (n=35). Weighted gene co-expression network analysis was conducted in the MV group to detect modules of correlated genes. Module preservation was assessed in the other two groups. Module eigengenes were regressed on AF severity or atrial rhythm at surgery. Modules whose eigengenes correlated with either AF phenotype were analyzed for gene content. 14 modules were detected in the MV group; all were preserved in the other two groups. One module (124 genes) was associated with AF severity and atrial rhythm across all groups. Its top hub gene, RCAN1, is implicated in calcineurin-dependent signaling and cardiac hypertrophy. Another module (679 genes) was associated with atrial rhythm in the MV and CAD groups. It was enriched with cell signaling genes and contained cardiovascular developmental genes including TBX5. Conclusions Our network-based approach found two modules strongly associated with AF. Further analysis of these modules may yield insight into AF pathogenesis by providing novel targets for functional studies.

Left bundle branch block may be due to conduction system degeneration or a reflection of myocardial pathology. Left bundle branch block may also develop following aortic valve disease or cardiac procedures. Patients with heart failure with reduced ejection fraction and left bundle branch block may respond positively to cardiac resynchronization therapy. Lead placement via the coronary sinus is the mainstay approach of cardiac resynchronization therapy. However, other options, including physiological pacing, are being explored. In this review, we summarize the salient pathophysiologic and clinical aspects of left bundle branch block, as well as current and future strategies for management.