Prehospital use of a modified HEART Pathway and point-of-care troponin to predict cardiovascular events.

CLINICAL TRIAL REGISTRATION: clinicaltrials.gov (NCT02709135).

Point-of-Care Troponin Testing during Ambulance Transport to Detect Acute Myocardial Infarction.

Objective: Use of point-of-care (POC) troponin (cTn) testing in the Emergency Department (ED) is well established. However, data examining POC cTn measurement in the prehospital setting, during ambulance transport, are limited. The objective of this study was to prospectively test the performance of POC cTn measurement by paramedics to detect myocardial infarction (MI) among patients transported to the ED for acute chest pain. Methods: A prospective cohort study of adults with non-traumatic chest pain was conducted in three Emergency Medical Services agencies (December 2016 to January 2018). Patients with ST-elevation MI on ECG were excluded. During ambulance transport paramedics initiated intravenous access, collected blood, and used a POC device (i-STAT; Abbott Laboratories) to measure cTn. Following ED arrival, participants received standard evaluations including clinical blood draws for cTn measurement in the hospital central lab (AccuTnI +3 assay; Beckman Coulter, or cTnI-Ultra assay; Siemens). Blood collected during ambulance transport was also analyzed for cTn in the central lab. Index visit MI was adjudicated by 3 experts using central lab cTn measures from the patient's clinical blood draws. Test characteristics (sensitivity, specificity, and predictive values) for detection of MI were calculated for POC and central lab cTn measurement of prehospital blood and compared with McNemar's test. Results: During the study period prehospital POC cTn results were obtained on 421 patients, of which 5.0% (21/421) had results >99th percentile upper reference limit. MI was adjudicated in 16.2% (68/421) during the index visit. The specificity and positive predictive value of the POC cTn measurement were 99.2% (95% CI 97.5-99.8%) and 85.7% (95% CI 63.7-97.0%) for MI. However, the sensitivity and NPV of prehospital POC cTn were 26.5% (95% CI 16.5-38.6%) and 87.5% (95% CI 83.9-90.6%). Compared to POC cTn, the central lab cTn measurement of prehospital blood resulted in a higher sensitivity of 67.9% (95% CI 53.7-80.1%, p < 0.0001), but lower specificity of 92.4% (95% CI 88.4-95.4%, p = 0.0001). Conclusions: Prehospital POC i-STAT cTn measurement in patients transported with acute chest pain was highly specific for MI but had low sensitivity. This suggests that prehospital i-STAT POC cTn could be useful to rule-in MI, but should not be used to exclude MI.

Prehospital Modified HEART Score Predictive of 30-Day Adverse Cardiac Events.

Introduction The History, Electrocardiogram (ECG), Age, Risk Factors, and Troponin (HEART) score is a decision aid designed to risk stratify emergency department (ED) patients with acute chest pain. It has been validated for ED use, but it has yet to be evaluated in a prehospital setting. Hypothesis A prehospital modified HEART score can predict major adverse cardiac events (MACE) among undifferentiated chest pain patients transported to the ED. METHODS: A retrospective cohort study of patients with chest pain transported by two county-based Emergency Medical Service (EMS) agencies to a tertiary care center was conducted. Adults without ST-elevation myocardial infarction (STEMI) were included. Inter-facility transfers and those without a prehospital 12-lead ECG or an ED troponin measurement were excluded. Modified HEART scores were calculated by study investigators using a standardized data collection tool for each patient. All MACE (death, myocardial infarction [MI], or coronary revascularization) were determined by record review at 30 days. The sensitivity and negative predictive values (NPVs) for MACE at 30 days were calculated. RESULTS: Over the study period, 794 patients met inclusion criteria. A MACE at 30 days was present in 10.7% (85/794) of patients with 12 deaths (1.5%), 66 MIs (8.3%), and 12 coronary revascularizations without MI (1.5%). The modified HEART score identified 33.2% (264/794) of patients as low risk. Among low-risk patients, 1.9% (5/264) had MACE (two MIs and three revascularizations without MI). The sensitivity and NPV for 30-day MACE was 94.1% (95% CI, 86.8-98.1) and 98.1% (95% CI, 95.6-99.4), respectively. CONCLUSIONS: Prehospital modified HEART scores have a high NPV for MACE at 30 days. A study in which prehospital providers prospectively apply this decision aid is warranted. Stopyra JP , Harper WS , Higgins TJ , Prokesova JV , Winslow JE , Nelson RD , Alson RL , Davis CA , Russell GB , Miller CD , Mahler SA . Prehospital modified HEART score predictive of 30-day adverse cardiac events. Prehosp Disaster Med. 2018;33(1):58-62.

Impact of a "Team-focused CPR" Protocol on Out-of-hospital Cardiac Arrest Survival in a Rural EMS System.

BACKGROUND: More than 300,000 persons in the United States experience an out-of-hospital cardiac arrest every year. The American Heart Association emphasizes on the rapid, effective delivery of cardiac arrest interventions by bystanders and emergency medical services (EMS) on scene. In July 2013, the EMS of Randolph County, a rural county in central North Carolina, implemented a team-focused cardiopulmonary resuscitation(CPR) protocol. The protocol emphasized early chest compressions and resuscitation on scene until the return of spontaneous circulation (ROSC) or until efforts were deemed futile. METHODS: Data were collected on all cardiac out-of-hospital cardiac arrest cases from June 30, 2012 to June 30, 2014. Outcomes for the year before the institution of the team-focused CPR protocol were compared with rates for the year following implementation. RESULTS: A significantly higher proportion of patients achieved ROSC after protocol implementation: 25/38 [66%, 95% confidence interval (CI), 49%-80%] versus 19/67 (28%; 95% CI, 18-41%, P < 0.001). More patients survived to hospital admission in the team-focused CPR group (16/38, 42.1%, 95% CI, 26%-59%) versus the preprotocol period (10/67, 14.9%, 95% CI, 7.4%-26%, P = 0.004). Although survival to discharge was higher in the team-focused protocol period (6/38, 15.8%, 95% CI, 6.0%-31%) than the preprotocol period (4/67, 6.0%, 95% CI, 1.7%-14.6%), this did not meet statistical significance (P = 0.16). CONCLUSION: The introduction of a team-focused CPR protocol in a single rural county-based EMS system dramatically improved ROSC and hospital admission rates, but not survival to discharge. Continued surveillance, as well as evaluation and optimization of inpatient care, is warranted.

Infection of endothelial cells with Anaplasma marginale and A. phagocytophilum.

Anaplasma marginale and A. phagocytophilum are obligate intracellular, tick-borne pathogens that target erythrocytes and neutrophil granulocytes, respectively. Because ticks do not directly tap blood vessels, an intermediate tissue may mediate infection of blood cells. We considered that vascular endothelium interacts with circulating blood cells in vivo, and could be involved in pathogenesis and dissemination of the organisms. We used light and electron microscopy and immune labeling to show that A. phagocytophilum invaded rhesus (RF/6A), human (HMEC-1, MVEC), as well as bovine (BCE C/D-1b) endothelial cell lines, whereas A. marginale infected rhesus and bovine endothelial cells. A. marginale formed large intracellular inclusions that appeared smooth and solid at first, and subsequently coalesced into discrete granules. A. phagocytophilum formed numerous smaller inclusions in each cell. Within 1-3 weeks, the monolayers were destroyed, and lysed cultures were diluted onto fresh monolayers. Electron microscopy demonstrated uneven distribution of A. marginale inside large inclusions, with reticulated forms grouped more tightly than denser cells, whereas in A. phagocytophilum individual organisms appeared more evenly spaced. Specific polyclonal and monoclonal antibodies both labeled A. marginale and A. phagocytophilum in endothelial cells, and oligonucleotide primers complimentary to either A. marginale or A. phagocytophilum amplified their expected target from these cultures. In conclusion, we demonstrate that relevant microvascular endothelium is susceptible to anaplasmas in vitro and may present a link that could explain development of the immune response and persistent infection.

Mactinin: a modulator of the monocyte response to inflammation.

During inflammatory processes, monocytes leave the blood stream at increased rates and enter inflammation tissue, where they undergo phenotypic transformation to mature macrophages with enhanced phagocytic activity. alpha-Actinin, a cytoskeletal protein, is present in focal adhesion complexes and left in the microenvironment as a result of cell movement. Mactinin, a 31 kDa amino-terminal fragment of alpha-actinin, is generated by the degradation of extracellular alpha-actinin by monocyte-secreted urokinase. We have previously demonstrated that mactinin promotes monocyte/macrophage maturation. We now report that 0.5-10 nM mactinin has significant chemotactic activity for monocytes. Mactinin seems to be present in inflammatory arthritis synovial fluid, because affinity-purified antisera reacted with a protein of the expected molecular mass in various types of arthritis fluids that were immunoaffinity-purified and subjected to Western analysis. Thus, six of seven samples from patients with psoriatic arthritis, reactive arthritis, gout, or ankylosing spondylitis contained mactinin at levels that are active in vitro. Initially, mactinin was not found in affinity-purified rheumatoid arthritis samples. However, it was detectable after the dissociation of immune complexes, suggesting that it was complexed to anti-microfilament auto-antibodies. In addition, mactinin was found in the lavage fluid from the arthritic knee joints of rabbits with antigen-induced arthritis and was absent from the contralateral control knee fluids. We conclude that mactinin is present in several types of inflammatory arthritis and might modulate mononuclear phagocyte response to inflammation.