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STUDY OBJECTIVE: The real-world effectiveness and safety of a 0/1-hour accelerated protocol using high-sensitivity cardiac troponin (hs-cTn) to exclude myocardial infarction (MI) compared to routine care in the United States is uncertain. The objective was to compare a 0/1-hour accelerated protocol for evaluation of MI to a 0/3-hour standard care protocol. METHODS: The RACE-IT trial was a stepped-wedge, randomized trial across 9 emergency departments (EDs) that enrolled 32,609 patients evaluated for possible MI from July 2020 through April 2021. Patients undergoing high-sensitivity cardiac troponin I testing with concentrations less than or equal to 99th percentile were included. Patients who had MI excluded by the 0/1-hour protocol could be discharged from the ED. Patients in the standard care protocol had 0- and 3-hour troponin testing and application of a modified HEART score to be eligible for discharge. The primary endpoint was the proportion of patients discharged from the ED without 30-day death or MI. RESULTS: There were 13,505 and 19,104 patients evaluated in the standard care and accelerated protocol groups, respectively, of whom 19,152 (58.7%) were discharged directly from the ED. There was no significant difference in safe discharges between standard care and the accelerated protocol (59.5% vs 57.8%; adjusted odds ratio (aOR)=1.05, 95% confidence interval [CI] 0.95 to 1.16). At 30 days, there were 90 deaths or MIs with 38 (0.4%) in the standard care group and 52 (0.4%) in the accelerated protocol group (aOR=0.84, 95% CI 0.43 to 1.68). CONCLUSION: A 0/1-hour accelerated protocol using high-sensitivity cardiac troponin I did not lead to more safe ED discharges compared with standard care.
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Objective: Protocols to evaluate for myocardial infarction (MI) using high-sensitivity cardiac troponin (hs-cTn) have the potential to drive costs upward due to the added sensitivity. We performed an economic evaluation of an accelerated protocol (AP) to evaluate for MI using hs-cTn to identify changes in costs of treatment and length of stay compared with conventional testing. Methods: We performed a planned secondary economic analysis of a large, cluster randomized trial across nine emergency departments (EDs) from July 2020 to April 2021. Patients were included if they were 18 years or older with clinical suspicion for MI. In the AP, patients could be discharged without further testing at 0 h if they had a hs-cTnI < 4 ng/L and at 1 h if the initial value were 4 ng/L and the 1-h value ≤7 ng/L. Patients in the standard of care (SC) protocol used conventional cTn testing at 0 and 3 h. The primary outcome was the total cost of treatment, and the secondary outcome was ED length of stay. Results: Among 32,450 included patients, an AP had no significant differences in cost (+$89, CI: -$714, $893 hospital cost, +$362, CI: -$414, $1138 health system cost) or ED length of stay (+46, CI: -28, 120 min) compared with the SC protocol. In lower acuity, free-standing EDs, patients under the AP experienced shorter length of stay (-37 min, CI: -62, 12 min) and reduced health system cost (-$112, CI: -$250, $25). Conclusion: Overall, the implementation of AP using hs-cTn does not result in higher costs.
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INTRODUCTION: Ventricular premature contractions (VPCs) are a common finding during cardiac stress tests. The independent prognostic value of these findings in patients in asymptomatic patients is unclear. METHODS: We conducted a systematic review and meta-analysis of observational studies exploring the independent prognostic value of VPCs to predict all-cause mortality. The secondary outcome was cardiovascular (CV) mortality. We excluded studies that did not report outcomes after adjusting for ≥1 confounder. Random effect meta-analyses were used to predict cumulative hazard ratios. We stratified results based on VPC during exercise or recovery. RESULTS: We found 7 studies with 24,518 patients that met our inclusion criteria. Two studies reported all-cause mortality only, 1 study reported CV mortality only, rest 4 reported both. There was significant heterogeneity in the baseline population, definition of high-risk VPCs, and variables used in adjusted models. Using multivariable summary estimates from individual studies, only VPCs during exercise were associated with a higher risk of all-cause mortality (HR 1.27, 95 % CI 1.07, 1.48). Both VPCs during exercise and recovery were associated with a higher risk CV mortality (HR 1.69, 95 % CI 1.19, 2.20, I2 = 17.6 % and 1.62, 95 % CI 1.25, 2.00, p < 0.001 for both). CONCLUSION: High-risk VPCs during exercise is associated with increased risk of all-cause and CV mortality, while those during recovery are associated with an increased risk of CV mortality only.
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Complejos Prematuros Ventriculares , Humanos , Electrocardiografía , Prueba de Esfuerzo , Pronóstico , Complejos Prematuros Ventriculares/complicaciones , Estudios Observacionales como AsuntoRESUMEN
BACKGROUND: SARS-CoV-2 is a novel viral illness originating out of Wuhan China in late 2019. This global pandemic has infected nearly 3 million people and accounted for 200 000 deaths worldwide, with those numbers still climbing. CASE SUMMARY: We present a 54-year-old patient who developed respiratory failure requiring endotracheal intubation from her infection with SARS-CoV-2. This patient was subsequently found to have a right ventricular thrombus and bilateral pulmonary emboli, likely contributing to her respiratory status. On the 14th day of hospitalization, the patient was successfully extubated, and 5 days later was discharged to the rehabilitation unit. DISCUSSION: SARS-CoV-2 presents primarily with pulmonary symptoms; however, many patients, particularly those who are severely ill, exhibit adverse events related to hypercoagulability. The exact mechanism explaining this hypercoagulable state has yet to be elucidated, but these thrombotic events have been linked to the increased inflammation caused by SARS-CoV-2. This novel viral illness is still largely misunderstood, but the hypercoagulable state, seen in severely ill patients, appears to play a major role in disease progression and prognosis.
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Magnesium is the second most common intracellular cation and serves as an important metabolic cofactor to over 300 enzymatic reactions throughout the human body. Among its various roles, magnesium modulates calcium entry and release from sarcoplasmic reticulum and regulates ATP pumps in myocytes and neurons, thereby regulating cardiac and neuronal excitability. Therefore, deficiency of this essential mineral may result in serious cardiovascular and neurologic derangements. In this case, we present the clinical course of a 76-year-old woman who presented with marked cardiac and neurological signs and symptoms which developed as a result of severe hypomagnesemia. The patient promptly responded to magnesium replacement once the diagnosis was established. We herein discuss the clinical presentation, pathophysiology, diagnosis, and management of severe hypomagnesemia and emphasize the implications of magnesium deficiency in the cardiovascular and central nervous systems. Furthermore, this case highlights the importance of having high vigilance for hypomagnesemia in the appropriate clinical setting.
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This study sought to determine the association of abdominal aortic calcium (AAC) with coronary artery calcium (CAC) and obstructive coronary artery disease (CAD). We included 58 patients (mean age 54.4 years, 40% males) without known CAD who underwent a non-contrast abdominal computed tomography (CT) scan and 64-slice coronary computed tomography angiography (CCTA) within 2 years. A total AAC score using Agatston method was calculated in the abdominal aorta from the takeoff of the celiac artery to the aortic bifurcation. A total of 43/58 patients had AAC. Patients with AAC were older with no differences in other baseline characteristics. None of the patients with a zero AAC score had obstructive CAD. Thus, an AAC score of zero had a 100% negative predictive value (NPV) and 23% positive predictive value (PPV) for the detection of obstructive CAD and an 80% NPV and 79% PPV for detection of any coronary plaque. Using multivariate linear regression, AAC score was an independent predictor of CAC score after adjusting for age (P < 0.001). In our analysis, AAC score correlates with CAC score and has a high NPV to rule out CAD. The absence of AAC may help exclude obstructive coronary disease and improve the selection of patients that may benefit from further risk stratification.
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Aneurisma de la Aorta Abdominal/metabolismo , Calcio/análisis , Estenosis Coronaria/metabolismo , Calcificación Vascular/metabolismo , Adulto , Anciano , Aneurisma de la Aorta Abdominal/diagnóstico por imagen , Aneurisma de la Aorta Abdominal/epidemiología , Aortografía/métodos , Angiografía Coronaria/métodos , Estenosis Coronaria/diagnóstico por imagen , Estenosis Coronaria/epidemiología , Femenino , Humanos , Modelos Lineales , Masculino , Michigan/epidemiología , Persona de Mediana Edad , Análisis Multivariante , Proyectos Piloto , Valor Predictivo de las Pruebas , Estudios Retrospectivos , Medición de Riesgo , Factores de Riesgo , Tomografía Computarizada por Rayos X , Calcificación Vascular/diagnóstico por imagen , Calcificación Vascular/epidemiologíaRESUMEN
In the human epidermis, the cells most at risk for the development of cancer due to sunlight exposure are the keratinocytes. In animal models, ultraviolet-B is a complete carcinogen, capable of inducing and promoting the development of malignant cells. A key element of ultraviolet-B-induced carcinogenesis is the ability of ultraviolet-B to induce the expression of a number of cellular proteins and activate growth factor receptor tyrosine kinases, including the erbB receptor family. Keratinocytes express the erbB1 (also called EGF-R, HER1), the erbB2 (also known as neu or HER2), and the erbB3 (HER3) subtypes. In general, activation of the erbB receptor family leads to a cellular proliferative response. In certain instances, however, activation of an erbB receptor can induce differentiation, cell cycle arrest, and even apoptosis. The inhibition of tyrosine kinase activity in rodent models and human skin has been shown to inhibit some ultraviolet-B response pathways. We have shown that the inhibition of erbB receptors, by both pharmaceutical and immunologic means, will inhibit ultraviolet-B-induced apoptosis in the HaCaT human keratinocyte cell line. This inhibition was specific for the erbB receptor family and specific for ultraviolet-B-induced apoptosis. These results suggest that, in certain instances, ultraviolet-B-induced apoptotic signaling requires erbB family receptor activity.