Evidence Of Myocardial Injury Research Articles

Emergency Department Referral of Patients With Chest Pain for Noninvasive Cardiac Testing and 2-Year Clinical Outcomes.

Noninvasive cardiac testing (NICT) has been associated with decreased long-term risks of major adverse cardiac events (MACEs) among emergency department patients at high coronary risk. It is unclear whether this association extends to patients without evidence of myocardial injury on initial ECG and cardiac troponin testing. A retrospective cohort study was conducted of patients presenting with chest pain between 2013 and 2019 to 21 emergency departments within an integrated health care system in Northern California, excluding patients with ST-segment-elevation myocardial infarction or myocardial injury by serum troponin testing. To account for confounding by indication, we grouped patient encounters by the NICT referral rate of the initially assigned emergency physician relative to local peers within discrete time periods. The primary outcome was MACE within 2 years. Secondary outcomes were coronary revascularization and MACE, inclusive of all-cause mortality. Associations between the NICT referral group (low, intermediate, or high) and outcomes were assessed using risk-adjusted proportional hazards methods with censoring for competing events. Among 144 577 eligible patient encounters, the median age was 58 years (interquartile range, 48-68) and 57% were female. Thirty-day NICT referral was 13.0%, 19.9%, and 27.8% in low, intermediate, and high NICT referral groups, respectively, with a good balance of baseline covariates between groups. Compared with the low NICT referral group, there was no significant decrease in the adjusted hazard ratio of MACE within the intermediate (adjusted hazard ratio, 1.08 [95% CI, 1.02-1.14]) or high (adjusted hazard ratio, 1.05 [95% CI, 0.99-1.11]) NICT referral groups. Results were similar for MACE, inclusive of all-cause mortality, and coronary revascularization, as well as subgroup analyses stratified by estimated risk (history, electrocardiogram, age, risk factors, troponin [HEART] score: percent classified as low risk, 48.2%; moderate risk, 49.2%; and high risk, 2.7%). Increases in NICT referrals were not associated with changes in the hazard of MACE within 2 years following emergency department visits for chest pain without evidence of acute myocardial injury. These findings further highlight the need for evidence-based guidance regarding the appropriate use of NICT in this population.

Cardiovascular Follow-up of Patients Treated for MIS-C.

To assess the prevalence of residual cardiovascular pathology by cardiac MRI (CMR), ambulatory rhythm monitoring, and cardiopulmonary exercise testing (CPET) in patients ∼6 months after multisystem inflammatory disease in children (MIS-C). Patients seen for MIS-C follow-up were referred for CMR, ambulatory rhythm monitoring, and CPET ∼6 months after illness. Patients were included if they had ≥1 follow-up study performed by the time of data collection. MIS-C was diagnosed on the basis of the Centers for Disease Control and Prevention criteria. Myocardial injury during acute illness was defined as serum Troponin-I level >0.05 ng/mL or diminished left ventricular systolic function on echocardiogram. Sixty-nine of 153 patients seen for MIS-C follow-up had ≥1 follow-up cardiac study between October 2020-June 2022. Thirty-seven (54%) had evidence of myocardial injury during acute illness. Of these, 12 of 26 (46%) had ≥1 abnormality on CMR, 4 of 33 (12%) had abnormal ambulatory rhythm monitor results, and 18 of 22 (82%) had reduced functional capacity on CPET. Of the 37 patients without apparent myocardial injury, 11 of 21 (52%) had ≥1 abnormality on CMR, 1 of 24 (4%) had an abnormal ambulatory rhythm monitor result, and 11 of 15 (73%) had reduced functional capacity on CPET. The prevalence of abnormal findings was not statistically significantly different between groups. The high prevalence of abnormal findings on follow-up cardiac studies and lack of significant difference between patients with and without apparent myocardial injury during hospitalization suggests that all patients treated for MIS-C warrant cardiology follow-up.

Transient myocardial thickening: a retrospective analysis on etiological, clinical, laboratory, therapeutic, and outcome findings in 27 cats

Introduction/objectiveTransient myocardial thickening (TMT) in cats is a poorly characterized clinical entity. Therefore, this study aimed to provide descriptions of additional cats diagnosed with this clinical phenomenon. Animals, materials, and methodsFor this multicenter observational retrospective study, cats diagnosed with TMT were searched in three medical databases. TMT was defined for cats with at least two echocardiograms showing an increased end-diastolic left ventricular wall thickness (LVWTd; i.e. ≥6 mm) at presentation and subsequent echocardiographic normalization (i.e. LVWTd <5.5 mm). Signalment, history, clinical, laboratory, therapeutic, and outcome data were retrieved. ResultsTwenty seven cats were included. The median age was 3 years. In 9/27 cats, an antecedent event was documented. At admission, 27/27 cats had evidence of myocardial injury (median value of cardiac troponin I 5.5 ng/mL), 25/27 cats had congestive heart failure, 13/27 cats had hypothermia, 8/27 cats had systemic hypotension, 7/27 cats had bradycardia, and 7/27 cats had electrocardiographic evidence of an arrhythmia. The median LVWTd was 6.4 mm. A potential cause of myocardial injury was identified in 14/27 cats. The median time from diagnosis to a significant reduction in LVWTd was 43 days. DiscussionTMT can be diagnosed in a wide range of cats, including young subjects. An antecedent predisposing event and/or a possible causative trigger can be identified in some. The reduction in LVWTd that defines this phenomenon usually occurs over a variable time frame. ConclusionsThis study represents the largest investigation of TMT in cats and provides additional information on this uncommon clinical entity.

The value of speckle tracking echocardiography in diagnosing minoxidil-induced cardiotoxicity: a case report.

Minoxidil is a drug designed for the treatment of arterial hypotension. Due to its secondary effect of hypertrichosis, it is also used for alopecia treatment. We present a case of a 50-year-old female patient who was orally consuming Minoxidil for medical reasons. She presented with severe hypotension, requiring vasoactive drugs, and evidence of myocardial injury was detected using speckle tracking echocardiography. It is worth noting that the patient did not have any coronary heart disease, and the myocardial injury was found to be associated with Minoxidil consumption. Remarkably, the patient showed signs of reversal 72h after stopping the drug. To our knowledge, this is the first reported case of subendocardial injury associated with Minoxidil, using speckle tracking echocardiography. In the resolution of the case, it was essential to rule out differential diagnoses, administer vasopressors, and use the speckle tracking echocardiography, which allowed for the objective assessment of myocardial injury and the monitoring of the patient during their hospitalization.

Do Chest Pain Characteristics in Patients with Acute Myocardial Infarction Differ between Those with and without Obstructive Coronary Artery Disease?

The universal definition of acute myocardial infarction (MI) requires both evidence of myocardial injury and myocardial ischaemia. In MINOCA (MI with non-obstructive coronary arteries), patients must fulfil this MI criteria, but is their chest pain similar to those who have MI with obstructive CAD (MICAD)? This study compares prospectively collected chest pain features between patients with MINOCA and MICAD. Utilising the Coronary Angiogram Database of South Australia (CADOSA), consecutive MI patients were categorized as MINOCA or MICAD based on angiographic findings. Chest pain data were collected via direct patient interviews by trained staff members. Of 6811 consecutive patients fulfilling a clinical MI diagnosis, 411 (6.0%) were MINOCA, and 5948 MICAD. The MINOCA patients were younger, more often female and had less cardiovascular risk factors than those with MICAD. There were no significant differences in chest pain characteristics between the MINOCA and MICAD cohorts in relation to pain location, quality, associated symptoms, or duration. In conclusion, MINOCA patients have chest pain characteristics that are indistinguishable from MICAD patients, suggesting that their pain is ischaemic in nature. Thus, in the presence of positive myocardial injury markers, ischaemic chest pain fulfils the universal criteria for MI, despite the absence of obstructive coronary artery disease.

Significance of myocardial injury on in-hospital clinical outcomes of in-hospital and COVID-19 patients.

Acute Myocardial injury defined by increased troponin I level is associated with poor in-hospital outcomes and cardiovascular complications in patients with COVID-19. The current study was designed to determine the implications and clinical outcome of myocardial injury in COVID-19. This retrospective study included hospitalized COVID-19 patients. Myocardial injury was defined by high sensitivity Troponin I (hs-TNI)≥26ng/l. Cardiac biomarkers, inflammatory markers and clinical data were systemically collected and analyzed. Hazard ratio for in-hospital mortality and logistic regression for predictors of acute myocardial injury were analyzed. Of the 1821 total patients with COVID-19, 293(16.09%) patients died and 1528 (83.91%) patients survived. Patients who died had significantly higher association with presence of cardiovascular risk factors, severe CTSS ( CT severity score ) and myocardial injury as compared to survived group. 628 (34.5%) patients had evidence of myocardial injury and they had statistically significant association with cardiovascular risk factors, in-hospital mortality, procalcitonin; higher hospital, and ICCU stay. We found significant hazard ratio of diabetes (HR=2.66, (CI:1.65-4.29)), Severe CT score (HR=2.81, (CI:1.74-4.52)), hs-TNI≥26 ng/l (HR=4.68, (CI:3.81-5.76)) for mortality. Severe CTSS score (OR=1.95, CI: 1.18-3.23, P=0.01) and prior CVD history (OR=1.65, CI:1.00-2.73, P=0.05) were found significant predictors of myocardial injury in regression analysis. Almost one third of hospitalized patients had evidence of acute myocardial injury during hospitalization. Acute myocardial injury is associated with higher hospital and ICCU stay, mortality, higher in-hospital infection which indicates more severe disease and the poor in-hospital outcomes.

COVID-19 and the Cardiovascular System: Requiem for a Medical Minotaur.

COVID-19 and the Cardiovascular System: Requiem for a Medical Minotaur.

The Evolving Impact of Myocardial Injury in Patients With COVID-19 Amid the Omicron Wave of the Pandemic

COVID-19 with myocardial injury, defined as troponin elevation, is associated with worse outcomes. The temporal changes in outcomes during various phases of the pandemic remain unclear. We evaluated outcomes during the Omicron phase compared with previous phases of the pandemic. We analyzed patients who were COVID-19-positive with evidence of myocardial injury who presented to the MedStar Health system (11 hospitals in Washington, District of Columbia, and Maryland) during phase 1 of the pandemic (March to June 2020), phase 2 (October 2020 to January 2021), and phase 3 (Omicron; December 2021 to March 2022), comparing their characteristics and outcomes. The primary end point was in-hospital mortality. The cohort included 2,079 patients admitted who were COVID-19 positive and for whom troponin was elevated (phase 1: n=150, phase 2: n=854, phase 3: n=1,075). Baseline characteristics were similar overall. Inflammatory markers were significantly elevated in phase 1 compared with phases 2 and 3. The use of remdesivir and dexamethasone was highest in phase 2. In phase 3, 52.6% of patients were fully vaccinated. In-hospital mortality, though high, was lower in phase 3 than in phases 1 and 2 (59.3% vs 28.1% vs 23.3%; p <0.001). Patients who were vaccinated showed more favorable in-hospital outcomes than did those who were unvaccinated (18.3% vs 24.2%, p=0.042). In conclusion, patients with COVID-19 with elevated troponin during phase 3 tended to have improved outcomes when compared with patients in earlier waves of the pandemic. This improvement could be attributed to the implementation of the COVID-19 vaccines, advances in COVID-19 treatment options, provider experience, and less virulent variants.

Abstract 10255: The Evolving Impact of Myocardial Injury in COVID-19 Patient Amid the Omicron Wave of the Pandemic

Introduction: Coronavirus disease 2019 (COVID-19) with evidence of myocardial injury, defined as troponin elevation, has been demonstrated to be associated with worse outcomes. The temporal changes in outcomes in these patients during various phases of the pandemic remain unclear. Hypothesis: We sought to evaluate outcomes during the Omicron phase compared to previous phases of the pandemic. Methods: We analyzed COVID-19-positive patients with myocardial injury who presented to the MedStar Health system (11 hospitals in Washington, DC and Maryland) during Phase 1 of the pandemic (March 1 - June 30, 2020), Phase 2 (October 1, 2020 - January 31, 2021) and Phase 3 (Omicron) (December 1, 2021 - March 31, 2022) comparing their characteristics and outcomes. The primary end point was in-hospital mortality. Results: The cohort included 2079 COVID-19-positive admitted patients for whom troponin-I or high-sensitive troponin was elevated (Phase 1: n=150, Phase 2: n=854, Phase 3 [Omicron]: n=1075). Baseline characteristics were overall similar. Inflammatory markers were significantly elevated in Phase 1 as compared to Phase 2 and the Omicron Phase. The use of remdesivir and dexamethasone was most seen in Phase 2. In the Omicron Phase, 52.6% of patients were fully vaccinated. In-hospital mortality although high was lower in the Omicron Phase as compared to Phase 1 and Phase 2 (23.3% vs. 59.3% vs. 28.1%; p&lt;0.001). Those vaccinated demonstrated even more favorable outcomes as compared to those patients unvaccinated (18.3% vs 24.2%, p = 0.042). Conclusions: COVID-19 patients with elevated troponin during the Omicron Phase still have significant mortality rates despite overall improved outcomes when compared to the first and second waves of the pandemic. This improvement in outcomes could be attributed to the implementation of the COVID-19 vaccine, advances in available COVID-19 treatment options, provider experience with the novel disease and less virulent variants.

Apports diagnostique et pronostique de l'imagerie par résonance magnétique cardiaque dans la myocardite

Cardiac magnetic resonance imaging (CMR) became over the last 30 years an essential tool in the management of patients with myocarditis. Noninvasive diagnosis of acute myocarditis relies on a clinical picture compatible with myocarditis and fulfilling of the updated 2018 Lake Louise criteria. These criteria include highlights of myocardial edema by conventional T2-weighted sequences or by T2 mapping in one hand and evidence of myocardial injury using late gadolinium enhancement sequences, T1 mapping or extra-cellular volume measurement in the other hand. It is recommended to perform basal examination in the 2 or 3 weeks following acute episode and to repeat CMR during follow-up. The literature reports excellent diagnostic accuracy, between 80% and 90%, making CMR a robust and reliable noninvasive alternative to endomyocardial biopsy. Besides, beyond its diagnostic performance, CMR can also help to identify patients with unfavourable long-term outcome. For instance, medio-ventricular and septal location of late gadolinium enhancement, degree of late gadolinium enhancement extent or high T2 mapping values are independent predictive factors of major cardio-vascular events.

Increased incidence of immune-mediated myocarditis in advanced skin malignancies treated with immune checkpoint inhibitors in the COVID-19 era.

2664 Background: Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of advanced stage skin malignancies. Immunotherapy related adverse events (irAE) are toxicities associated with ICI therapy. Myocarditis is a rare life-threatening irAE. We attempt to characterize cases of myocarditis related to ICI therapy that have occurred since the start of the COVID-19 pandemic. Methods: We performed a single-center, retrospective cohort analysis of patients with advanced stage skin cancers who were treated with ICIs and identified cases of ICI-mediated myocarditis. ICI-mediated myocarditis was defined as evidence of myocardial injury in the setting of irAEs and exclusion of cardiovascular causes. Clinicopathologic variables and clinical outcomes were assessed in these patients. Results:A review of 361 patients that received ICI from 9/2014 – 10/2019 found 0 cases of ICI-mediated myocarditis. From 11/2019 – 12/2021, an additional 425 patients were identified of whom 11 (2.6%) developed ICI-mediated myocarditis. 10 patients had melanoma and 1 patient had Merkel cell carcinoma. 10/11 patients were male. 9/11 were treated with anti-PD-1 monotherapy and 2/11 were treated with ipilimumab with nivolumab. All patients had elevated high sensitivity troponin (median 361 pg/mL on presentation, reference range 0-19 pg/mL). 11/11 patients presented with elevated CPK (median 1734 IU/L, reference range 38-240 IU/L) and 8/11 presented with elevated AST:ALT ratio (median 1.58:1) on routine screening which prompted further investigation. 1 patient tested positive for COVID-19 13 days after initial biochemical concern for myocarditis, and 5 patients had received COVID-19 vaccines between 2.5-11 months prior to myocarditis onset. All patients were treated with high dose steroids, and 4 were treated with abatacept. 2 patients died within 30 days after diagnosis of myocarditis and 2 patients later died from malignancy progression. 2 patients developed progressive disease and 1 was successfully rechallenged with ICI with no myocarditis recurrence. 2 patients remain on active surveillance, 2 continue on a steroid taper, and 1 was lost to follow up. All patients with at least 5 months of follow up from myocarditis onset (n = 5) had persistently elevated HS-troponin despite normalization of CPK levels. Conclusions: In this single center study, we noted an increase in the frequency of ICI-mediated myocarditis in patients with advanced skin cancers during the pandemic era (2.6% vs 0% pre-pandemic) which is higher than reported in the literature (0.04-1.14%). The impact of COVID-19 during this time is suspicious and warrants further investigation. Therefore, we suggest heightened awareness in the COVID-19 era that elevated CPK levels and AST:ALT ratios merits further diagnostic investigation of ICI-mediated myocarditis.

Myocarditis following administration of COVID-19 Vaccine: Should we be worried?

The COVID-19 vaccines have raised scepticism surrounding their accelerated approval due to their suspected adverse side effects.(1) Recently emerging clinical cases such as flu, fever, tachycardia, Bell’s palsy, and swelling of the lymph nodes have further heightened public distrust. Interestingly, the United States Food and Drug Administration has recently announced an inflammatory heart disease, Myocarditis, as a potential risk of the Pfizer-BioNTech COVID-19 vaccine. In efforts to find an association between the Pfizer vaccine and Myocarditis, researchers recently carried out extensive clinical trials; two new studies tracked cases having biomarker evidence of myocardial injury and Cardiac Magnetic Resonance Imaging.(2,3) Moreover, the United States Centers for Disease Control and Prevention (CDC) has recorded 323 confirmed cases of myocarditis, most documented within a week after each patient had received the Pfizer-BioNTech COVID-19 vaccine.(4) A recent emergent theory suggests a cytokine response as the leading cause of myocarditis; the immune system identifies the mRNA in the vaccine as an antigen, leading to the activation of proinflammatory cascades and immunological pathways. The expression of cytokines and activation markers is due to the exposure of the dendritic cells to mRNA, which eventually causes inflammation of the heart muscle.(4) Furthermore, according to the CDC, the myocarditis is mainly observed in male adolescents and young adults, more often after getting the second dose of the COVID-19 vaccine. A week after administrating the vaccine, symptoms such as chest pain, shortness of breath, and tachycardia may appear, which tend to resolve following conservative treatment with nonsteroidal anti-inflammatory drugs.(3) Despite the previously mentioned occurrences of myocarditis after administration of the Pfizer-BioNtech vaccine, we would like to highlight the results of a large-scale cohort study in Israel with 2.5 million participants, where the estimated incidence of myocarditis after the administration of the Pfizer vaccine was only 2.13 cases per 100,000 persons.(5) These statistics allow us to draw the readers’ attention towards the benefits of the COVID-19 vaccination, which outweigh potential adverse risks such as Myocarditis. The Pfizer-BioNtech vaccine has proven to be 95% effective and to keep track of other possible complications, patients are advised to report to the Vaccine Adverse Event Reporting System (VAERS) to document any unusual side effects.(4) Despite the few reported complications, we would further like to emphasize the importance of population- wide vaccination to overcome the COVID-19 pandemic with a minimum mortality rate.

Characteristics and Outcomes of Critically Ill Patients with Raised Cardiac Troponins Admitted in the Intensive Care Unit: A single centre experience from Oman.

ObjectivesCritically ill patients have raised troponins. This study aimed to assess the incidence of myocardial injury in the intensive care unit (ICU) at a tertiary care hospital and assess the management and prognosis.MethodsThis retrospective study included adult patients who were admitted to the ICU of Sultan Qaboos University Hospital, Muscat, Oman, between January and December 2019 and had undergone a high-sensitive cardiac troponin (hs-cTn) assay. Patients admitted with a primary diagnosis of myocardial infarction were excluded.ResultsA total of 264 patients had their hs-cTn measured during the study period. Of these, 128 (64.3 ± 17.1 years; 58.6% male) had elevated levels, giving an incidence rate of approximately 48.5%. Those with raised troponin were older and had more co-morbidities. These patients were also more critically ill with lower blood pressure, higher heart rates and increased hypotensive episodes. Of these, 47 were treated for acute coronary syndrome, 32 underwent coronary angiography and only three required stenting. Patients with raised troponin had a poor outcome with only 45 (35.2%) surviving to discharge compared to 101 (74.3%) with normal troponin. Patients with raised troponin had shorter hospital stays than those with normal troponin (16 versus 19 days; P = 0.017).ConclusionA high proportion of critically ill patients showed evidence of myocardial injury without significant coronary artery disease, which is associated with a poor prognosis. Further prospective studies are required to ascertain the best course of treatment for these patients.

Unstable Angina Pectoris With Myocardial Injury Versus Myocardial Infarction in the Era of High-Sensitivity Cardiac Troponin

It is unknown whether outcomes in patients with unstable angina pectoris (UAP) and myocardial injury are different from outcomes in patients with non-ST-segment myocardial infarction (NSTEMI) with low peak concentrations of high-sensitivity cardiac troponin T (hs-cTnT). This study aimed to compare the prognosis in patients with UAP and evidence of myocardial injury, with prognosis in patients with NSTEMI and different peak hs-cTnT concentrations. All visits to 7 different emergency departments in Sweden from December 9, 2009 to December 31, 2016 were identified (n=5,225,075). We included all hospitalized patients with hs-cTnT >14ng/L and a diagnosis of UAP or NSTEMI, with ≥2hours-cTnT measurements. Hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated for all-cause mortality and cardiovascular events, in patients with NSTEMI categorized according to peak hs-cTnT concentrations, compared with patients with UAP. Altogether, 11,944 patients were included, of whom 1,253 (10%) received a diagnosis of UAP. During a median follow-up of 3.0 years (interquartile [IQR] 1.6 to 4.7), 3,297 patients died. There was no difference comparing patients with NSTEMI with peak hs-cTnT of 15 to 49ng/L to patients with UAP, with regards to long-term cardiovascular mortality (HR 1.15; 95% CI, 0.85 to 1.56), but the risk of recurrent myocardial infarction was higher in patients with NSTEMI (HR, 1.61; 95% CI, 1.29 to 2.00), and the risk of heart failure hospitalization slightly lower (HR 0.80, 95% CI, 0.64 to 0.99). In conclusion, patients with UAP and myocardial injury have a similar risk of death after discharge, but a lower risk of recurrent myocardial infarction and a marginally higher risk of heart failure, compared with patients with NSTEMI with moderately elevated hs-cTnT levels.

Evidence of myocardial injury in horses with colic

Development of endotoxemia associated with gastrointestinal injury is often observed in horses with colic. Such patients are likely to develop cardiovascular complications associated with endotoxemia, including myocardial injury. Few studies have investigated the prevalence of myocardial injury in horses with colic. Cardiac biomarkers such as cardiac troponin I (cTnI) have been extensively used in human and veterinary medicine for diagnosis of myocardial injury. The aim of the present study was to investigate the occurrence of myocardial injury in horses with colic by measuring serum cTnI concentrations. Myocardial tissue samples from non-surviving horses were also subjected to histopathological evaluation. Serum cTnI concentration was measured in 10 healthy horses and 39 horses with colic. Associations were determined of cTnI concentration, and variables such as health status (healthy and horses with colic), type of colic (inflammatory, impaction, and unknown), the severity of abdominal pain (mild, moderate and severe), and clinical outcome (survivor to discharge and non-survivor). As compared with healthy horses, cTnI concentrations were significantly elevated in horses with colic (P = 0.004). In horses with colic, an abnormal cTnI concentration was significantly associated with inflammatory colic (P&lt;0.05), severe abdominal pain (P&lt;0.01), and negative clinical outcome (P&lt;0.0001). Further, histopathological evaluation of the myocardial muscles revealed a varying degree of myocardial degeneration and necrosis. The present study suggested that horses with severe colic and increased cTnI levels are more likely to develop myocardial injury. Elevated levels of cTnI may also be indicative of poor prognosis in horses with severe colic.

Abstract 11859: Elevated Troponins and Ischemic Cardiomyopathy Are Predictive of Percutaneous Coronary Intervention in Patients With Pulmonary Embolism

Introduction: Pulmonary embolism is a common cause of myocardial strain. As such, patients with pulmonary embolism will have evidence of myocardial injury on laboratory assessment. This can be measured using a troponin assay. Of the patients who present with elevated troponins and pulmonary embolism, there is minimal evidence to guide the decision on whether a patient will benefit from left heart catheterization and coronary angiography. We sought to analyze troponin levels and risk factors for percutaneous coronary intervention (PCI) in a large dataset of patients hospitalized with pulmonary embolism. Methods: This was a retrospective study of 3929 patients who were admitted with pulmonary embolism in 2018 and 2019 at HCA Healthcare hospitals across the United States. Patients with other factors that could cause troponin elevation, such as a ST elevation myocardial infarction, chronic kidney disease, and sepsis, were excluded. Binary logistic regression model was utilized to examine risk factors for PCI. Results: Troponin I level was elevated in 68.9% (2707) of patients, 7.68% (208) of those patients with an elevated troponin had a left heart catheterization, and, of the patients that underwent a left heart catheterization, 26.92% (56) had PCI. The mean age of all subjects was 65.1 years and 52.4% of subjects were female. A total of 73.07% (2871) of subjects had coronary artery disease. Multivariable logistic regression showed maximum troponin value was associated with increased chance of PCI. For every ng/mL increase in troponin level, the odds of PCI increased by 2.5% (p=0.017). Patients with ischemic cardiomyopathy were 4.4-times more likely to have PCI than those without (p=0.010). Race, gender, and age were not significantly associated with risk of PCI. Conclusions: Elevated troponin is common in patients admitted with pulmonary embolism. In our dataset 7.7% of patients with elevated troponin received left heart catheterization and 26.9% of left heart catheterizations resulted in PCI. Higher troponin and known ischemic cardiomyopathy were independently associated with increased likelihood of PCI. Further analysis may help find additional factors to suggest which patients with elevated troponin should have left heart catheterization.

Myeloid/Lymphoid Neoplasm with Eosinophilia and a Novel RUFY1-Pdgfrb Rearrangement

▪Myeloid/lymphoid neoplasms associated with eosinophilia (MLN-Eo) and tyrosine kinase fusion genes include rearrangements of PDGFRB with over 30 different partner genes, most commonly ETV6-PDGFRB. Rearrangements are evident by cytogenetic analysis and fluorescence in situ hybridization (FISH) break-apart probes. Herein, we describe a novel rearrangement partner for PDGFRB.A 25-year-old man with a medical history significant for gout and hypertension presented to medical care after several days of progressive dyspnea, chest pain, fatigue, epistaxis, and rash. Physical exam revealed palpable cervical, axillary, and inguinal lymphadenopathy and massive splenomegaly. By CT scan the spleen measured 25 cm and diffuse lymphadenopathy was identified in the chest, abdomen and pelvis with the largest lymph node mass measuring 8.9 x 2.5 cm. Transthoracic echocardiogram showed normal heart function and no evidence of myocardial injury. The patient subsequently developed respiratory failure requiring intubation and mechanical ventilation, shock requiring vasopressors, and renal failure requiring renal replacement therapy. Initial laboratory evaluation demonstrated a leukocytosis to 83.3 x 10 9/L with neutrophilic predominance with left shift and eosinophilia (10% of WBCs, absolute eosinophil count of 8.2 x 10 9/L); hemoglobin of 8.3 g/dL and hematocrit of 25%; and thrombocytopenia to 50 x 10 9/L. Ferritin was 660 ng/mL, lactate dehydrogenase 384 U/L, and uric acid 10.4 mg/dL. Secondary causes of eosinophilia including infection, immunodeficiency, atopy, medications, and rheumatologic disease were ruled out. The patient was positive for strongyloides IgG antibodies and received ivermectin.Core biopsy of a lymph node was non-diagnostic and could not repeated safely due to progressive severe thrombocytopenia. Skin biopsy demonstrated a perivascular leukocytoclasis, but no abnormal B or T cell population. Bone marrow aspirate and biopsy revealed a hypercellular marrow (90%) with mild trilineage dysplasia, granulocytic hyperplasia, moderate reticulin fibrosis, and slightly increased mast cells. Blasts were not increased and no hemophagocytic histiocytes were identified. Eosinophils accounted for 6.9% of myeloid cells. Flow cytometry did not reveal an abnormal B or T lymphoid, blast or myeloid population.Peripheral blood flow cytometry did not reveal an abnormal B or T-cell population and T-cell rearrangement studies showed an oligoclonal population. No clonal B cell population was identified.FISH, which identified a rearrangement of PDGFRB in 28% of cells, confirmed the diagnosis. Karyotype analysis revealed an abnormal male karyotype with a paracentric inversion of 5q with breakpoints at 5q32 and 5q35. FusionPlex® Solid Tumor Panel (Clinical Genomics Laboratory, University of Washington SOM) identified a novel fusion between RUFY1 and PDGFRB. RUFY1 is expressed in most tissues and encodes a protein that contains a RUN domain and a FYVE-type zinc finger domain and plays a role in early endosomal trafficking (Figure). We are currently demonstrating the fusion is oncogenic and sensitive to tyrosine kinase inhibition in Ba/F3 cells. The patient's remarkable clinical response, however, supports imatinib sensitivity and is in keeping with other published reports of MLN-Eo with PDGFRB rearrangements. Initial treatment included high dose steroids for 7 days and hydroxyurea briefly. Imatinib 400 mg daily was started, then decreased to 200 mg daily due to gastrointestinal toxicity. Follow-up is limited (8 weeks). However, the patient has recovered clinically. Six weeks after starting imatinib he had renal recovery and has achieved a complete hematologic response except for mild anemia due to resolving acute kidney injury. Splenomegaly and peripheral lymphadenopathy have resolved. PDGFRB FISH has declined to 9%.Inversions of chromosome 5 have very rarely been described in association with eosinophilia, but only one report has specifically identified a rearrangement of PDGFRB. This report described a novel rearrangement involving exons 12 to 23 of PDGFRB at 5q32 and the 5′ (UTR) of G3BP1 at 5q33.1. Notably, this specific rearrangement was undetectable by PDGFRB break-apart FISH. These reports and ours highlight the clinical relevance of NGS in identifying novel rearrangement partners. Furthermore, patient-specific ddPCR assays can be designed for sensitive monitoring. [Display omitted] DisclosuresOehler: BMS: Consultancy; OncLive: Honoraria; Pfizer: Research Funding; Takeda: Consultancy; Blueprint Medicines: Consultancy.

Implications of left ventricular function on short-term outcomes in COVID-19 patients with myocardial injury

Abstract Background/Introduction Myocardial injury is a complication of coronavirus disease 2019 (COVID-19). Purpose We sought to describe a large multi-centre experience of COVID-19 patients with myocardial injury, examining the prognostic role left ventricular function plays on short-term outcomes. Methods We included adult COVID-19 patients admitted to our health system with evidence of myocardial injury and who underwent a transthoracic echocardiogram (TTE) during index admission. Patients were dichotomized into those with reduced ejection fraction (EF; &amp;lt;50%) and preserved EF (&amp;gt;50%). Results Across our 11-hospital system, 5032 adult patients were admitted with COVID-19 from March-September 2020. Of these, 235 had evidence of myocardial injury (troponin &amp;gt;1 ng/mL). Included were 134 patients who underwent TTE, of whom 43.3% (n=58) had reduced EF and 56.7% (n=76) preserved EF (Figure 1). A subset of 6 patients had newly reduced EF, with 5 demonstrating evidence of stress cardiomyopathy and subsequently dying. Overall, mortality was high in those with reduced EF and preserved EF (in-hospital: 34.5% vs. 28.9%; p=0.494; 6 months: 63.6% vs. 50.0%; p=0.167; Kaplan-Meier estimates: p=0.2886). Readmissions were frequent in both groups (30 days: 22.2% vs. 26.0%; p=0.162; 6 months: 52.0% vs. 54.5%; p=0.839) (Figure 2). Conclusions Many COVID-19 patients admitted with evidence of myocardial injury did not undergo TTE. For those who did, short-term mortality was high. Patients who survived hospitalisation had frequent readmissions. In patients with newly reduced EF, most had evidence of stress cardiomyopathy and expired. Larger studies are needed to fully evaluate the prognosis of COVID-19 patients with evidence of myocardial injury and left ventricular dysfunction. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2

The evolution of management and outcomes of patients with myocardial injury during the COVID-19 pandemic

Abstract Background Cardiac involvement in coronavirus disease 2019 (COVID-19) has been established. This is manifested by troponin elevation, and associated with worse prognosis as compared with patients without myocardial injury. Purpose We sought to evaluate if the outcomes of these patients has improved as experience accumulated during the pandemic. Methods We analyzed COVID-19-positive patients with the evidence of myocardial injury (defined as troponin elevation) who presented to our large US healthcare system in the northeast region during the “Early Phase” of the pandemic (March 1–June 30, 2020) and compared their characteristics and outcomes to the COVID-19-positive patients with the presence of troponin elevation in the “Current Phase” of the pandemic (October 1, 2020–January 31, 2021). Results The cohort included 788 COVID-19-positive admitted patients for whom troponin was elevated, 167 during the “Early Phase” and 621 during the “Current Phase”. The cohort's mean age was 70.2±14.9 years; 54.3% were men (Figure 1). Maximum troponin-I in the “Early Phase” was 13.46±34.72 versus 11.21±20.57 in the “Current Phase” (p=0.553) In-hospital mortality was significantly higher (50.3%) in the “Early Phase” group compared to the “Current Phase” group (24.6%; p&amp;lt;0.001). Similarly, the incidence of intensive care unit admission (77.8% versus 46.1%; p&amp;lt;0.044) and requirement for mechanical ventilation (61.7% versus 28%; p&amp;lt;0.001) were higher in the “Early Phase” (Figure 2). In addition, 6% of those in the “Early Phase” underwent coronary angiography compared to 2.3% in the “Current Phase” (p=0.013). Finally, 3% of “Early Phase” and 0.8% of “Current Phase” patients underwent percutaneous coronary intervention (p=0.025). Conclusions Treatment outcomes have significantly improved since the beginning of the pandemic in COVID-19-positive patients with troponin elevation. This may be attributed to awareness, severity of the disease, improvements in therapies and provider experience. Funding Acknowledgement Type of funding sources: None.

AN INTERESTING CASE OF DELAYED ONSET MYOCARDITIS FOLLOWING COVID-19 INFECTION

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The first case of SARS-CoV-2 (COVID-19) virus was reported in December, 2019 and is well known to cause febrile illness, gastrointestinal symptoms, respiratory disease, and coagulopathy. One of the less common sequelae of this illness is myocarditis. Here we present an interesting case of delayed onset myocarditis which occurred following COVID-19 infection. CASE PRESENTATION: A 32-year-old female with a past medical history significant for obesity presented with complaints of dull, left sided chest pain. She had associated symptoms of diaphoresis, lightheadedness, and nausea. Patient denied prior history of angina. Patient had a strong family history of coronary artery disease.Chest pain was reproducible with palpation to the chest. EKG showed T wave inversions in anterolateral and inferior leads. Troponin was elevated to 1.12 ng/mL (<0.05 ng/mL) and trended up to 9.57 ng/mL. NT proBNP was mildly elevated to 253 pg/mL (<126 pg/mL). Chest x-ray revealed no acute abnormalities. Patient tested positive for COVID-19 six months prior to admission. During the current admission patient's COVID-19 PCR was negative. Patient was given aspirin 324mg and started on heparin and nitroglycerin infusions.Echocardiography showed hypokinesis of apical myocardium and left ventricular (LV) ejection fraction of 60%. Patient was taken for coronary angiogram which revealed normal coronary arteries without evidence of stenosis or spasm. Cardiac magnetic resonance imaging (MRI) revealed increased signal in the mid-apical septum on short tau inversion recovery image (STIR) suggestive of edema or inflammation. LV systolic function was normal;however, hypokinesis of the apical septal wall was noted. These findings on MRI are highly suggestive of acute myocarditis. Endomyocardial biopsy was not performed as the patient was hemodynamically stable and showed no signs of heart failure or arrhythmia. DISCUSSION: A meta-analysis of 8971 hospitalized COVID-19 infected patients demonstrated that 20.0% of patient's had myocardial injury manifested by elevated troponin I levels [1]. Guo et al showed 28% of patients with COVID-19 had evidence of myocardial injury (elevated troponin T greater than 99th percentile upper limit) and Chen et al showed elevated BNP in 27.5% of patients. There have been reports of patients with myocarditis during active episodes of COVID-19 infection but limited published literature provides insight into patients who may develop myocardial injury in the time following the primary COVID-19 infection. CONCLUSIONS: This case represents an interesting presentation of delayed onset myocarditis following COVID-19 infection which must be considered in the differential for patients who present with NSTEMI. Delayed onset could be suggestive of prolonged systemic inflammatory response in the setting of COVID-19. It also displays a less frequently identified sequela of COVID-19 infection. REFERENCE #1: Prasitlumkum, N., Chokesuwattanaskul, R., Thongprayoon, C., Bathini, T., Vallabhajosyula, S., & Cheungpasitporn, W. (2020). Incidence of Myocardial Injury in COVID-19-Infected Patients: A Systematic Review and Meta-Analysis. Diseases, 8(4), 40. REFERENCE #2: Guo, T., Fan, Y., Chen, M., Wu, X., Zhang, L., He, T., … & Lu, Z. (2020). Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA cardiology, 5(7), 811-818. REFERENCE #3: Chen, C., Zhou, Y., & Wang, D. W. (2020). SARS-CoV-2: a potential novel etiology of fulminant myocarditis. Herz, 45(3), 230-232. DISCLOSURES: No relevant relationships by Joseph Adams, source=Web Response No relevant relationships by Sheraz Hussain, source=Web Response No relevant relationships by Ibrahim Kassas, source=Web Response No relevant relationships by Shermeen Memon, source=Web Response No relevant relationships by Mohammed Siddiqui, source=Web Response