Sharing and Teaching Electrocardiograms to Minimize Infarction (STEMI): reducing diagnostic time for acute coronary occlusion in the emergency department.

BACKGROUND: Limits to ST-Elevation Myocardial Infarction (STEMI) criteria may lead to prolonged diagnostic time for acute coronary occlusion. We aimed to reduce ECG-to-Activation (ETA) time through audit and feedback on STEMI-equivalents and subtle occlusions, without increasing Code STEMIs without culprit lesions. METHODS: This multi-centre, quality improvement initiative reviewed all Code STEMI patients from the emergency department (ED) over a one-year baseline and one-year intervention period. We measured ETA time, from the first ED ECG to the time a Code STEMI was activated. Our intervention strategy involved a grand rounds presentation and an internal website presenting weekly local challenging cases, along with literature on STEMI-equivalents and subtle occlusions. Our outcome measure was ETA time for culprit lesions, our process measure was website views/visits, and our balancing measure was the percentage of Code STEMIs without culprit lesions. RESULTS: There were 51 culprit lesions in the baseline period, and 64 in the intervention period. Median ETA declined from 28.0 min (95% confidence interval [CI] 15.0-45.0) to 8.0 min (95%CI 6.0-15.0). The website garnered 70.4 views/week and 27.7 visitors/week in a group of 80 physicians. There was no change in percentage of Code STEMIs without culprit lesions: 28.2% (95%CI 17.8-38.6) to 20.0% (95%CI 11.2-28.8%). Conclusions Our novel weekly web-based feedback to all emergency physicians was associated with a reduction in ETA time by 20 min, without increasing Code STEMIs without culprit lesions. Local ECG audit and feedback, guided by ETA as a quality metric for acute coronary occlusion, could be replicated in other settings to improve care.

Using ECG-To-Activation Time to Assess Emergency Physicians' Diagnostic Time for Acute Coronary Occlusion.

BACKGROUND: There is no quality metric for emergency physicians' diagnostic time for acute coronary occlusion. OBJECTIVE: We sought to quantify diagnostic time associated with automated interpretation, classic ST-elevation myocardial infarction (STEMI) criteria, STEMI-equivalents, and subtle occlusions, using electrocardiogram (ECG)-to-activation of catheterization laboratory time. METHODS: This multicenter retrospective study reviewed all code STEMI patients from the emergency department (ED) with confirmed culprit lesions from January 2016 to December 2018. We measured door-to-ECG (DTE) time and ECG-to-activation (ETA) time. We examined the first ED ECGs to determine whether automated interpretation labeled "STEMI," and they met classic STEMI criteria, STEMI-equivalents, or rules for subtle occlusion. ECG analysis was performed by two emergency physicians blinded to clinical scenario, automated interpretation, and angiographic outcome. RESULTS: There were 177 code STEMIs with culprit lesions, with a median DTE time of 9.0 min and a median ETA time of 16.0 min. Automated interpretation labeled 55.4% of first ECGs "STEMI" (ETA 6.5 min) and 44.6% not "STEMI" (ETA 66 min, p < 0.0001). Of first ECGs, 63.8% met classic STEMI criteria (ETA 8.0 min), 8.5% had STEMI-equivalents (ETA 32.0 min, p = 0.0026), 16.4% had subtle occlusions (ETA 89.0 min, p = 0.045), and 11.3% had no diagnostic sign of occlusion (ETA 68.0 min, p = 0.20). CONCLUSIONS: STEMI criteria missed more than one-third of occlusions on first ECG, but most had STEMI-equivalents or rules for subtle occlusion. ETA time can serve as a quality metric for emergency physicians to promote new ECG insights and assess quality improvement initiatives.

8-Isoprostane-induced endothelin-1 production by infant rat pulmonary artery smooth muscle cells is mediated by Rho-kinase.

We have reported that 8-isoprostane stimulated the production of endothelin (ET)-1, a potent vasoconstrictor and critical mediator of chronic pulmonary hypertension, by infant rat pulmonary artery smooth muscle cells (PASMCs), through stimulation of the thromboxane A2 receptor. The aim of this study was to examine the contribution of putative downstream intracellular mediators of thromboxane A2 receptor stimulation to this effect. PASMCs from infant rats were treated with calcium ionophore (A23187), 8-isoprostane, or 8-isoprostane together with inhibitors of tyrosine kinase, protein kinase C, phosphatidylinositol 3-kinase, mitogen-activated protein kinases, or Rho-kinases (ROCK). A23187 had no effect on ET-1 production, excluding raised intracellular Ca2+ as a major contributor. Increased ET-1 production induced by 8-isoprostane was significantly attenuated by the ROCK inhibitors Y-27632 and hydroxyfasudil, but not by inhibitors of the other pathways. 8-Isoprostane also increased membrane binding of RhoA, a major determinant of ROCK activity, and ROCK-II expression through the protein kinase C pathway. These data indicate that the RhoA/ROCK pathway mediates increased ET-1 production by PASMCs, which we speculate may at least partly explain the beneficial effects of both antioxidants and ROCK inhibitors in animal models of chronic pulmonary hypertension.