Mechanical chest compressions improve rate of return of spontaneous circulation and allow for initiation of percutaneous circulatory support during cardiac arrest in the cardiac catheterization laboratory.

BACKGROUND: Performing advanced cardiac life support (ACLS) in the cardiac catheterization laboratory (CCL) is challenging. Mechanical chest compression (MCC) devices deliver compressions in a small space, allowing for simultaneous percutaneous coronary intervention and reduced radiation exposure to rescuers. In refractory cases, MCC devices allow rescuers to initiate percutaneous mechanical circulatory support (MCS) and extracorporeal life support (ECLS) during resuscitation. This study sought to assess the efficacy and safety of MCC when compared to manual compressions in the CCL. METHODS: We performed a retrospective analysis of patients who received ACLS in the CCL at our institution between May 2011 and February 2016. Baseline characteristics, resuscitation details, and outcomes were compared between patients who received manual and mechanical compressions. RESULTS: Forty-three patients (67% male, mean age 58 years) required chest compressions for cardiac arrest while in the CCL (12 manual and 31 MCC). Patients receiving MCC were more likely to achieve return of spontaneous circulation (ROSC) (74% vs. 42%, p=0.05). Of those receiving MCC, twenty-two patients (71%) were treated with MCS. Patients receiving percutaneous ECLS were more likely to achieve ROSC (100% vs. 53%, p=0.003) and suffered no episodes of limb loss or TIMI major bleeding. There were no significant differences in 30-day survival or survival to hospital discharge between groups. CONCLUSIONS: Use of MCC during resuscitation of cardiac arrest in the CCL increases the rate of ROSC. Simultaneous implantation of MCS, including percutaneous ECLS, is feasible and safe during MCC-assisted resuscitation in the CCL

Factors Associated with the Use of Drug-Eluting Stents in Patients Presenting with Acute ST-Segment Elevation Myocardial Infarction

Background. Drug-eluting stents (DES) have proven clinical superiority to bare-metal stents (BMS) for the treatment of patients with ST-segment elevation myocardial infarction (STEMI). Decision to implant BMS or DES is dependent on the patient’s ability to take dual antiplatelet therapy. This study investigated factors associated with DES placement in STEMI patients. Methods. Retrospective analysis was performed on 193 patients who presented with STEMI and were treated with percutaneous coronary intervention at an urban, tertiary care hospital. Independent factors associated with choice of stent type were determined using stepwise multivariate logistic regression. Odds ratio (OR) was used to evaluate factors significantly associated with DES and BMS. Results. 128 received at least one DES, while 65 received BMS. BMS use was more likely in the setting of illicit drug or alcohol abuse ([OR] 0.15, 95% CI 0.05–0.48, p≤0.01), cardiogenic shock (OR 0.26, 95% CI 0.10–0.73, p=0.01), and larger stent diameter (OR 0.28, 95% CI 0.11–0.68, p≤0.01). Conclusions. In this analysis, BMS implantation was associated with illicit drug or alcohol abuse and presence of cardiogenic shock. This study did not confirm previous observations that non-White race, insurance, or income predicts BMS use

Distinct Roles for TGN/Endosome Epsin-like Adaptors Ent3p and Ent5p

Clathrin adaptors are key factors in clathrin-coated vesicle formation, coupling clathrin to cargo and/or the lipid bilayer. A physically interacting network of three classes of adaptors participate in clathrin-mediated traffic between the trans-Golgi network (TGN) and endosomes: AP-1, Gga proteins, and epsin-like proteins. Here we investigate functional relationships within this network through transport assays and protein localization analysis in living yeast cells. We observed that epsin-like protein Ent3p preferentially localized with Gga2p, whereas Ent5p distributed equally between AP-1 and Gga2p. Ent3p was mislocalized in Gga-deficient but not in AP-1–deficient cells. In contrast, Ent5p retained localization in cells lacking either or both AP-1 and Gga proteins. The Ent proteins were dispensable for AP-1 or Gga localization. Synthetic genetic growth and α-factor maturation defects were observed when ent5Δ but not ent3Δ was introduced together with deletions of the GGA genes. In AP-1–deficient cells, ent3Δ and to a lesser extent ent5Δ caused minor α-factor maturation defects, but together resulted in a near-lethal phenotype. Deletions of ENT3 and ENT5 also displayed synthetic defects similar to, but less severe than, synthetic effects of AP-1 and Gga inactivation. These results differentiate Ent3p and Ent5p function in vivo, suggesting that Ent3p acts primarily with Gga proteins, whereas Ent5p acts with both AP-1 and Gga proteins but is more critical for AP-1–mediated transport. The data also support a model in which the Ent adaptors provide important accessory functions to AP-1 and Gga proteins in TGN/endosome traffic