Chest pain can be a challenging complaint to manage in the emergency department. A missed diagnosis can result in significant morbidity or mortality, whereas avoidable testing and hospitalizations can lead to increased health care costs, contribute to hospital crowding, and increase risks to patients. The HEART score is a validated decision aid to identify patients at low risk for acute coronary syndrome who can be safely discharged without admission or objective cardiac testing. In the largest and one of the longest studies to date (N = 31,060; 30 months), we included the HEART score into a larger, newly developed low-risk chest pain decision pathway, using a retrospective observational pre/post study design with the objective of safely lowering admissions. The modified HEART score calculation tool was incorporated in our electronic medical record. A significant increase in discharges of low-risk chest pain patients (relative increase of 21%; p < 0.0001) in the postimplementation period was observed with no significant difference in the rates of major adverse cardiac events between the pre and post periods. There was a decrease in the amount of return admissions for 30 days (4.65% fewer; p = 0.009) and 60 days (3.78% fewer; p = 0.020). No significant difference in length of stay was observed for patients who were ultimately discharged. A 64% decrease in monthly coronary computed tomography angiograms was observed in the post period (p < 0.0001). These findings support the growing consensus in the literature that the adoption of the HEART pathway or similar protocols in emergency departments, including at large and high-volume medical institutions, can substantially benefit patient care and reduce associated health care costs.
Thrombin appears to underlie myometrial contractions in response to intrauterine bleeding. In a similar fashion, thrombin generated within the uterus in the absence of active bleeding could also produce contractions. These studies sought to determine whether functionally active prothrombin is expressed in the pregnant and nonpregnant rat uterus. Uteri were obtained from proestrus/estrus and timed-pregnant Sprague-Dawley rats. Western blots were performed using antithrombin antibodies. Immunohistochemical studies were performed using the same antibodies along with the Vector Elite ABC kit. Qualitative reverse transcriptase-polymerase chain reaction studies were performed using rat prothrombin-specific oligonucleotide primers. In vitro uterine contraction studies were performed using Taipan snake venom (an exogenous prothrombinase) and components of the plasma prothrombinase complex (Factors Xa and V) with and without pretreatment with thrombin inhibitors (heparin or hirudin). The Western blots demonstrated prothrombin peptides in myometrial tissue from estrus and pregnant rats. The immunohistochemical studies confirmed prothrombin peptides in both the circular and longitudinal myometrium, along with the endometrium. The reverse transcriptase-polymerase chain reaction studies demonstrated prothrombin mRNA in the endometrium and placenta, but not in the myometrial smooth muscle. The Taipan snake venom stimulated a significant increase in contractions, which were suppressed by pretreatment with heparin and hirudin. The Factor Xa and V complex also significantly stimulated uterine contractions, which were likewise inhibited by hirudin. These studies provide evidence supporting the expression of functionally active prothrombin in the pregnant and nonpregnant rat uterus. Based on the presence of its mRNA, prothrombin appears to be synthesized in the endometrium and placenta; in contrast, the myometrial smooth-muscle cells appear to sequester preformed prothrombin. These results support the hypothesis that intrauterine thrombin could play an autocrine/paracrine role in the regulation of contractile activity.
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