Impact of Emergency Medical Services Activation of the Cardiac Catheterization Laboratory and a 24-Hour/Day In-Hospital Interventional Cardiology Team on Treatment Times (Door to Balloon and Medical Contact to Balloon) for ST-Elevation Myocardial Infarction.

The incremental benefit of emergency medical services (EMS) activation of the cardiac catheterization laboratory (CCL) for ST-elevation myocardial infarction (STEMI) in the setting of an established in-house interventional team (IHIT) is uncertain. We evaluated the impact of EMS activation on door-to-balloon (D2B) time and first medical contact-to-balloon (FMC2B) time for STEMI when coupled with a 24-hour/day IHIT. All patients presenting with STEMI to Loyola University Medical Center had demographic, procedural, and outcome data consecutively entered in a STEMI Data Registry. From 223 consecutive patients presenting between April 2009 and December 2015, a retrospective analysis was performed on 190 patients. Patients were divided into 2 groups depending on CCL activation mode (EMS activation or emergency department activation) and STEMI treatment process times were compared. The primary end point was D2B process times. The secondary end point was FMC2B process times in a subgroup analysis of EMS-transported patients. D2B times were shorter (37 ± 14 minutes vs 57 ± 27 minutes, p < 0.001) with EMS activation. Subgroup analysis of EMS-transported patients demonstrated shorter FMC2B times with EMS activation (52 ± 17 minutes vs 67 ± 32 minutes, p = 0.002). EMS activation was the only predictor of D2B ≤60 minutes in multivariable analysis of EMS-transported patients (odds ratio 9.4; 95% confidence interval 2.1 to 43.0; p = 0.04). In conclusion, EMS activation of the CCL in STEMI was associated with significant improvements in already excellent D2B and FMC2B times even in the setting of a 24-hour/day IHIT.

Angiogenic endothelial cell invasion into fibrin is stimulated by proliferating smooth muscle cells.

These studies aimed to determine the effect of smooth muscle cells (SMCs) on angiogenic behavior of endothelial cells (ECs) within fibrin hydrogels, an extracellular matrix (ECM) commonly used in tissue engineering. We developed a 3-D, fibrin-based co-culture assay of angiogenesis consisting of aggregates of SMCs with ECs seeded onto the aggregates' surface. Using digital fluorescence micrography, EC matrix invasion was quantified by average length of sprouts (ALS) and density of sprout formation (DSF). We demonstrated that ECs and SMCs co-invade into the ECM in close proximity to one another. ECs that were co-cultured with SMCs demonstrated increased invasion compared to ECs that were cultured alone at all time points. At Day 19, the ALS of ECs in co-culture was 327+/-58µm versus 70+/-11µm of ECs cultured alone (p=.01). The DSF of co-cultured ECs was also significantly greater than that of ECs cultured alone (p=.007 on Day 19). This appeared to be a function of both increased EC invasion as well as improved persistence of EC sprout networks. At 7days, ECs in co-culture with proliferation-inhibited SMCs previously treated with Mitomycin-C (MMC) demonstrated significantly attenuated sprouting compared to ECs co-cultured with SMCs that were untreated with MMC (82+/-14µm versus 205+/-32µm; p<.05). In assays in which multiple co-culture aggregates were cultured within a single hydrogel, we observed directional invasion of sprouts preferentially towards the other aggregates within the hydrogel. In co-culture assays without early EC/SMC contact, the ALS of ECs cultured in the presence of SMCs was significantly greater than those cultured in the absence of SMCs by Day 3 (320+/-21µm versus 187+/-16µm; p<.005). We conclude that SMCs augment EC matrix invasion into 3-D fibrin hydrogels, at least in part resulting from SMC proliferative and invasive activities. Directed invasion between co-culture aggregates and augmented angiogenesis in the absence of early contact suggests a paracrine mechanism for the observed results.

Inflammatory bowel disease and endothelin-1: a review.

Inflammatory bowel disease (IBD) appears to be an inappropriate response to an antigen that leads to chronic inflammation rather than repair. This review looks at the role of endothelin-1 (ET-1) as a proinflammatory agent in IBD. ET-1 antagonists in animal models reduce the incidence and severity of IBD. These antagonists may be useful for treatment of IBD in humans.