Left ventricular summit arrhythmias with an abrupt V3 transition: Anatomy of the aortic interleaflet triangle vantage point.

BACKGROUND: While early precordial electrocardiographic (ECG) characteristics are useful to differentiate left-sided from the right-sided outflow tract ventricular arrhythmia (OTVA), few patterns predict an origin from the septal margin of the left ventricular (LV) summit. OBJECTIVE: The purpose of this study was to report mapping and ablation characteristics of a new ECG pattern with left bundle branch morphology and an abrupt R-wave transition in lead V3 (ATV3). METHODS: Over a 3-year period, 78 consecutive patients (mean age 57±15 years; 35% female) with OTVA were referred for mapping and ablation. Twenty patients (26%) exhibited an ATV3 pattern, of whom 65% failed prior ablation. RESULTS: Ninety-two percent of patients with ATV3 that underwent simultaneous epicardial and endocardial mapping demonstrated an intramural or epicardial site of origin. Eighty percent of OTVA with ATV3 was eliminated by ablation from the vantage point of the interleaflet triangle below the right-left coronary junction. The ATV3 pattern showed higher sensitivity, specificity, predictive value, and accuracy than validated ECG criteria (notch or "w" pattern in lead V1, qrS pattern in leads V1 through V3, and pattern break V2) for predicting successful ablation in the region of the anterior LV ostium. At 12±11 months, freedom from ventricular arrhythmia recurrence was 89% and 82% in the ATV3 and control groups, respectively. CONCLUSION: ATV3 is a simple and distinct ECG pattern indicative of a site of origin from the septal margin of the LV summit. The right-left aortic interleaflet triangle vantage point was effective to eliminate OTVA with ATV3 that overwhelmingly exhibited the earliest activation from the epicardium or mid-myocardium. Test characteristics for ATV3 were superior to ECG patterns validated for the anterior LV ostium.

Discharge Medical Complexity, Change in Medical Complexity and Pediatric 30-day Readmission.

BACKGROUND: While medical complexity is associated with pediatric readmission risk, less is known about how increases in medical complexity during hospitalization affect readmission risk. METHODS: We conducted a five-year retrospective, case-control study of pediatric hospitalizations at a tertiary care children's hospital. Cases with a 30-day unplanned readmission were matched to controls based on admission seasonality and distance from the hospital. Complexity variables included the number of medications prescribed at discharge, medical technology, and the need for home healthcare services. Change in medical complexity variables included new complex chronic conditions and new medical technology. We estimated odds of 30-day unplanned readmission using adjusted conditional logistic regression. RESULTS: Of 41,422 eligible index hospitalizations, we included 595 case and 595 control hospitalizations. Complexity: Polypharmacy after discharge was common. In adjusted analyses, being discharged with ≥2 medications was associated with higher odds of readmission compared with being discharged without medication; children with ≥5 discharge medications had a greater than four-fold higher odds of readmission. Children assisted by technology had higher odds of readmission compared with children without technology assistance. Change in complexity: New diagnosis of a complex chronic condition (Adjusted Odds Ratio (AOR) = 1.75; 1.11-2.75) and new technology (AOR = 1.84; 1.09-3.10) were associated with higher risk of readmission when adjusting for patient characteristics. However, these associations were not statistically significant when adjusting for length of stay. CONCLUSION: Polypharmacy and use of technology at discharge pose a substantial readmission risk for children. However, added technology and new complex chronic conditions do not increase risk when accounting for length of stay.

Mesenchymal Stem Cell-Induced DDR2 Mediates Stromal-Breast Cancer Interactions and Metastasis Growth.

Increased collagen deposition by breast cancer (BC)-associated mesenchymal stem/multipotent stromal cells (MSC) promotes metastasis, but the mechanisms are unknown. Here, we report that the collagen receptor discoidin domain receptor 2 (DDR2) is essential for stromal-BC communication. In human BC metastasis, DDR2 is concordantly upregulated in metastatic cancer and multipotent mesenchymal stromal cells. In MSCs isolated from human BC metastasis, DDR2 maintains a fibroblastic phenotype with collagen deposition and induces pathological activation of DDR2 signaling in BC cells. Loss of DDR2 in MSCs impairs their ability to promote DDR2 phosphorylation in BC cells, as well as BC cell alignment, migration, and metastasis. Female ddr2-deficient mice homozygous for the slie mutation show inefficient spontaneous BC metastasis. These results point to a role for mesenchymal stem cell DDR2 in metastasis and suggest a therapeutic approach for metastatic BC.