Predictive Value of Myocardial injury in Patients with COVID-19 Admitted to a Quaternary Hospital in the City of Rio de Janeiro

Abstract Background In Brazil the factors involved in the risk of death in patients with COVID-19 have not been well established. Objective To analyze whether elevations of high-sensitivity troponin I (hTnI) levels influence the mortality of patients with COVID-19. Methods Clinical and laboratory characteristics of hospitalized patients with COVID-19 were collected upon hospital admission. Univariate and binary logistic regression analyzes were performed to assess the factors that influence mortality. P-value<0.05 was considered significant. Results This study analyzed192 patients who received hospital admission between March 16 and June 2, 2020 and who were discharged or died by July 2, 2020. The mean age was 70±15 years, 80 (41.7%) of whom were women. In comparison to those who were discharged, the 54 (28.1%) who died were older (79±12 vs 66±15years; P=0.004), and with a higher Charlson´s index (5±2 vs 3±2; P=0.027). More patients, aged≥60years (P <0.0001), Charlson´s index>1 (P=0.004), lung injury>50% in chest computed tomography (P=0.011), with previous coronary artery disease (P=0.037), hypertension (P=0.033), stroke (P=0.008), heart failure (P=0.002), lymphocytopenia (P=0.024), high D-dimer (P=0.024), high INR (P=0.003), hTnI (P<0.0001), high creatinine (P<0.0001), invasive mechanical ventilation (P<0.0001), renal replacement therapy (P<0.0001), vasoactive amine (P<0.0001), and transfer to the ICU (P=0.001), died when compared to those who were discharged. In logistic regression analysis, elevated hTnI levels (OR=9.504; 95% CI=1.281-70.528; P=0.028) upon admission, and the need for mechanical ventilation during hospitalization (OR=46.691; 95% CI=2.360-923.706; P=0.012) increased the chance of in-hospital mortality. Conclusion This study suggests that in COVID-19 disease, myocardial injury upon hospital admission is a harbinger of poor prognosis.

Biomarker evaluation for prognostic stratification of patients with COVID-19: the added value of quantitative chest CT.

Aim: Pulmonary disease burden and biomarkers are possible predictors of outcomes in patients with COVID-19 and provide complementary information. In this study, the prognostic value of adding quantitative chest computed tomography (CT) to a multiple biomarker approach was evaluated among 148 hospitalized patients with confirmed COVID-19. Materials & methods: Patients admitted between March and July 2020 who were submitted to chest CT and biomarker measurement (troponin I, D-dimer and C-reactive protein) were retrospectively analyzed. Biomarker and tomographic data were compared and associated with death and intensive care unit admission. Results: The number of elevated biomarkers was significantly associated with greater opacification percentages, lower lung volumes and higher death and intensive care unit admission rates. Total lung volume <3.0 l provided further stratification for mortality when combined with biomarker evaluation. Conclusion: Adding automated CT data to a multiple biomarker approach may provide a simple strategy for enhancing risk stratification of patients with COVID-19.

Role of a lower cutoff of high sensitivity troponin I in identification of early cardiac damage in non-severe patients with COVID-19.

Cardiac damage in non-severe patients with coronavirus disease 2019 (COVID-19) is poorly explored. This study aimed to explore the manifestations of cardiac damage at presentation in non-severe patients with COVID-19. In this study, 113 non-severe patients with COVID-19 were grouped according to the duration from symptoms onset to hospital admission: group 1 (≤ 1 week, n = 27), group 2 (> 1 to 2 weeks, n = 28), group 3 (> 2 to 3 weeks, n = 27), group 4 (> 3 weeks, n = 31). Clinical, cardiovascular, and radiological data on hospital admission were compared across the four groups. The level of high sensitivity troponin I (hs-cTnI) in group 2 [10.25 (IQR 6.75-15.63) ng/L] was significantly higher than those in group 1 [1.90 (IQR 1.90-8.80) ng/L] and group 4 [1.90 (IQR 1.90-5.80) ng/L] (all Pbonferroni < 0.05). The proportion of patients who had a level of hs-cTnI ≥ 5 ng/L in group 2 (85.71%) was significantly higher than those in the other three groups (37.04%, 51.85%, and 25.81%, respectively) (all Pbonferroni < 0.05). Compared with patients with hs-cTnI under 5 ng/L, those with hs-cTnI ≥ 5 ng/L had lower lymphocyte count (P = 0.000) and SpO2 (P = 0.002) and higher CRP (P = 0.000). Patients with hs-cTnI ≥ 5 ng/L had a higher incidence of bilateral pneumonia (P = 0.000) and longer hospital length of stay (P = 0.000). In conclusion, non-severe patients with COVID-19 in the second week after symptoms onset were most likely to suffer cardiac damage. A detectable level of hs-cTnI ≥ 5 ng/L might be a manifestation of early cardiac damage in the patients.

Myocardial injury in hospitalized COVID-19 patients: a retrospective study, systematic review, and meta-analysis.

INTRODUCTION: The majority of studies evaluating the effect of myocardial injury on the survival of COVID-19 patients have been performed outside of the United States (U.S.). These studies have often utilized definitions of myocardial injury that are not guideline-based and thus, not applicable to the U.S. METHODS: The current study is a two-part investigation of the effect of myocardial injury on the clinical outcome of patients hospitalized with COVID-19. The first part is a retrospective analysis of 268 patients admitted to our healthcare system in Toledo, Ohio, U.S.; the second part is a systematic review and meta-analysis of all similar studies performed within the U.S. RESULTS: In our retrospective analysis, patients with myocardial injury were older (mean age 73 vs. 59 years, P 0.001), more likely to have hypertension (86% vs. 67%, P 0.005), underlying cardiovascular disease (57% vs. 24%, P 0.001), and chronic kidney disease (26% vs. 10%, P 0.004). Myocardial injury was also associated with a lower likelihood of discharge to home (35% vs. 69%, P 0.001), and a higher likelihood of death (33% vs. 10%, P 0.001), acute kidney injury (74% vs. 30%, P 0.001), and circulatory shock (33% vs. 12%, P 0.001). Our meta-analysis included 12,577 patients from 8 U.S. states and 55 hospitals who were hospitalized with COVID-19, with the finding that myocardial injury was significantly associated with increased mortality (HR 2.43, CI 2.28-3.6, P 0.0005). The prevalence of myocardial injury ranged from 9.2 to 51%, with a mean prevalence of 27.2%. CONCLUSION: Hospitalized COVID-19 patients in the U.S. have a high prevalence of myocardial injury, which was associated with poorer survival and outcomes.

ECG pathology and its association with death in critically ill COVID-19 patients, a cohort study.

BACKGROUND: We investigated the prevalence of ECG abnormalities and their association with mortality, organ dysfunction and cardiac biomarkers in a cohort of COVID-19 patients admitted to the intensive care unit (ICU). METHODS: This cohort study included patients with COVID-19 admitted to the ICU of a tertiary hospital in Sweden. ECG, clinical data and laboratory findings during ICU stay were extracted from medical records and ECGs obtained near ICU admission were reviewed by two independent physicians. RESULTS: Eighty patients had an acceptable ECG near ICU-admission. In the entire cohort 30-day mortality was 28%. Compared to patients with normal ECG, among whom 30-day mortality was 16%, patients with ECG fulfilling criteria for prior myocardial infarction had higher mortality, 63%, odds ratio (OR) 9.61 (95% confidence interval (CI) 2.02-55.6) adjusted for Simplified Acute Physiology Score 3 and patients with ST-T abnormalities had 50% mortality and OR 6.05 (95% CI 1.82-21.3) in univariable analysis. Both prior myocardial infarction pattern and ST-T pathology were associated with need for vasoactive treatment and higher peak plasma levels of troponin-I, NT-pro-BNP (N-terminal pro-Brain Natriuretic Peptide), and lactate during ICU stay compared to patients with normal ECG. CONCLUSION: ECG with prior myocardial infarction pattern or acute ST-T pathology at ICU admission is associated with death, need for vasoactive treatment and higher levels of biomarkers of cardiac damage and strain in severely ill COVID-19 patients, and should alert clinicians to a poor prognosis.

A close-up view of dynamic biomarkers in the setting of COVID-19: Striking focus on cardiovascular system.

Based on the recent reports, cardiovascular events encompass a large portion of the mortality caused by the COVID-19 pandemic, which drawn cardiologists into the management of the admitted ill patients. Given that common laboratory values may provide key insights into the illness caused by the life-threatening SARS-CoV-2 virus, it would be more helpful for screening, clinical management and on-time therapeutic strategies. Commensurate with these issues, this review article aimed to discuss the dynamic changes of the common laboratory parameters during COVID-19 and their association with cardiovascular diseases. Besides, the values that changed in the early stage of the disease were considered and monitored during the recovery process. The time required for returning biomarkers to basal levels was also discussed. Finally, of particular interest, we tended to abridge the latest updates regarding the cardiovascular biomarkers as prognostic and diagnostic criteria to determine the severity of COVID-19.

Improvement of outcome prediction of hospitalized patients with COVID-19 by a dual marker strategy using high-sensitive cardiac troponin I and copeptin.

BACKGROUND: COVID-19 has been associated with a high prevalence of myocardial injury and increased cardiovascular morbidity. Copeptin, a marker of vasopressin release, has been previously established as a risk marker in both infectious and cardiovascular disease. METHODS: This prospective, observational study of patients with laboratory-confirmed COVID-19 infection was conducted from June 6th to November 26th, 2020 in a tertiary care hospital. Copeptin and high-sensitive cardiac troponin I (hs-cTnI) levels on admission were collected and tested for their association with the primary composite endpoint of ICU admission or 28-day mortality. RESULTS: A total of 213 eligible patients with COVID-19 were included of whom 55 (25.8%) reached the primary endpoint. Median levels of copeptin and hs-cTnI at admission were significantly higher in patients with an adverse outcome (Copeptin 29.6 pmol/L, [IQR, 16.2-77.8] vs 17.2 pmol/L [IQR, 7.4-41.0] and hs-cTnI 22.8 ng/L [IQR, 11.5-97.5] vs 10.2 ng/L [5.5-23.1], P < 0.001 respectively). ROC analysis demonstrated an optimal cut-off of 19.3 pmol/L for copeptin and 16.8 ng/L for hs-cTnI and an increase of either biomarker was significantly associated with the primary endpoint. The combination of raised hs-cTnI and copeptin yielded a superior prognostic value to individual measurement of biomarkers and was a strong prognostic marker upon multivariable logistic regression analysis (OR 4.274 [95% CI, 1.995-9.154], P < 0.001). Addition of copeptin and hs-cTnI to established risk models improved C-statistics and net reclassification indices. CONCLUSION: The combination of raised copeptin and hs-cTnI upon admission is an independent predictor of ICU admission or 28-day mortality in hospitalized patients with COVID-19.

Relationship of magnesemia with myocardial damage and mortality in patients with COVID-19.

Magnesium (Mg) is the second most abundant intracellular cation and plays a significant role in immune system and cardiac protection. Mg deficiency contributes to chronic low-grade inflammation leading to cardiovascular diseases, and low Mg level exacerbates virus-induced inflammation. The aim of the study was to investigate whether serum magnesium level is associated with myocardial damage and prognosis of COVID-19. This was a single-center, observational retrospective study of patients with COVID-19. The study population was divided into two groups according to in-hospital mortality: a survivor group (SG) and a non-survivor group (NSG). Myocardial damage was defined as blood levels of cardiac troponin I (cTnI) above the 99th percentile upper reference limit. Magnesium, variables regarding inflammation, and myocardial damage were compared between the groups. A total of 629 patients with COVID-19 were included. Mortality rate was 11.85% (n = 82). There were 61 (74.4%) and 294 male patients (53.7%) in NSG and SG, respectively (p = 0.001). The median age of NSG was 64.5 years (min-max: 37-93) and the median age of SG was 56.0 years (min-max: 22-92) (p < 0.001). Median serum magnesium levels of NSG and SG were 1.94 mg/dL (min-max: 1.04-2.87) and 2.03 mg/dL (min-max: 1.18-2.88), respectively (p = 0.027). Median cTnI levels of NSG and SG were 25.20 pg/mL (min-max: 2.10-2240.80) and 4.50 pg/mL (min-max: 0.50-984.3), respectively (p < 0.001). The cTnI levels were lower in those patients whose serum Mg levels were higher than 1.94. Although serum magnesium level was not a predictor for in-hospital mortality, there was a significant negative correlation between magnesemia and myocardial damage.

Association of Myocardial Enzyme Abnormality with Clinical Outcomes of Patients with COVID-19: A Retrospective Study.

BACKGROUND: It has been observed that COVID-19 may cause myocardial damage, but there are few detailed reports on myocardial enzyme abnormalities. METHODS: In this retrospective study, we analyzed data from 157 consecutive laboratory-confirmed and hospitalized COVID-19 patients from Wuhan. We collected information on demographic and clinical characteristics, laboratory findings, and clinical outcomes. Logistic regression analysis was used to explore the risk factors associated with the severity of COVID-19. The association between myocardial enzyme abnormalities and the mortality was also investigated. RESULTS: The mortality in abnormal myocardial enzyme group was obviously higher than the normal group (P < 0.001). The majority of patients (n = 72, 97.3%) with normal cardiac enzyme group were of the common novel coronavirus pneumonia (NCP) type, whereas half of the patients with cardiac enzyme abnormalities (n = 40, 48.2%) developed critical and severe NCP type. The multivariable logistic regression analysis indicated that COVID-19 patients with increasing age (P = 0.035), higher levels of CRP (P = 0.038), and TNI (P = 0.036) were associated with increased death than other patients. CONCLUSIONS: Myocardial enzyme abnormality and myocardial injury were associated with the severity and fatal outcomes of COVID-19. Clinicians should pay attention to the markers of myocardial injury in COVID-19 patients, especially those with older age, comorbidities, and inflammation.

Cardiac biomarkers alterations in patients with SARS-CoV-2 infection.

Reliable biomarkers are necessary for the risk stratification of patients infected with SARS-CoV-2. This novel coronavirus is now established to affect several organs in addition to the lungs, most prominently the heart. This is achieved through direct damage to the myocardium and indirect immune-associated effects during the cytokine storm. We performed a literature review aiming to identify the prognostic value of alterations of cardiac biomarkers in SARS-CoV-2 infection. Cardiac biomarkers are significantly elevated in patients with severe COVID-19 and are independent predictors of mortality. High-sensitivity troponin I and T are correlated with multiple inflammatory indexes and poor outcomes. Although cut-off values have been established for most of cardiac biomarkers, lower limits for troponins may have better prognostic values and longitudinal monitoring of cardiac biomarkers can help the clinician assess the patient's course. Additional measurements of NT-proBNP, can detect the subgroup of patients with poor prognosis.

ST-elevation in an adolescent with COVID-19: Myopericarditis or myocardial infarction?

Myocardial infarctions (MI) have been reported in adults with COVID-19. Although MIs are rare in children with COVID-19, cardiac involvement is still possible. In this case report, we present an adolescent with recent COVID-19 infection who presented with an ECG initially suggestive of myocardial infarction (MI). We describe how to differentiate between myocardial infarctions and myopericarditis. A 15-year-old boy, with a history of COVID-19 infection a month prior, presented to the emergency department with fever, abdominal pain, diarrhea, and chest pain. On ECG, he was found to have focal ST-segment elevations in V3 through V6. Given the immediate concern for MI, an emergent echocardiogram was done and showed normal left ventricular systolic function with no regional dyskinesia and normal coronary artery diameters. A repeat ECG showed diffuse ST elevations in the inferior leads and T-wave inversions on V5 and V6, confirming the diagnosis of myopericarditis. In conclusion, multisystem-inflammatory syndrome in children associated with COVID-19 (MIS-C) is a new entity describing a post-infectious inflammatory response in children with prior COVID-19 exposure. Cardiac involvement can include myopericarditis. Initial ECGs may show ST-changes suggestive of MI. However, serial ECGs and echocardiograms can differentiate between MI and myocarditis/myopericarditis. Even with COVID-19, MIs are extremely rare in children, and it is important to be aware of MIS-C and its cardiac complications.

Evolution of Management and Outcomes of Patients with Myocardial Injury During the COVID-19 Pandemic.

Cardiac involvement in coronavirus disease 2019 (COVID-19) has been established. This is manifested by troponin elevation and associated with worse patient prognosis. We evaluated whether patient outcomes improved as experience accumulated during the pandemic. We analyzed COVID-19-positive patients with myocardial injury (defined as troponin elevation) who presented to the MedStar Health system (11 hospitals in Washington, DC, and Maryland) 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 "Later Phase" of the pandemic (October 1, 2020 - January 31, 2021). The cohort included 788 COVID-19-positive admitted patients for whom troponin was elevated, 167 during the "Early Phase" and 621 during the "Later Phase." Maximum troponin-I in the "Early Phase" was 13.46±34.72 ng/mL versus 11.21±20.57 ng/mL in the "Later Phase" (p = 0.553). In-hospital mortality was significantly higher in the "Later Phase" (50.3% vs. 24.6%; p<0.001), as were incidence of intensive-care-unit admission (77.8% vs. 46.1%; p<0.001) and need for mechanical ventilation (61.7% versus 28%; p<0.001). In addition, more "Early Phase" patients underwent coronary angiography (6% vs. 2.3%; p=0.013). Finally, 3% of "Early Phase" and 0.8% of "Later Phase" patients underwent percutaneous coronary intervention (p=0.025). In conclusion, 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.

The role of antibody-based troponin detection in cardiovascular disease: A critical assessment.

Cardiovascular disease has remained the world's biggest killer for 30 years. To aid in the diagnosis and prognosis of patients suffering cardiovascular-related disease accurate detection methods are essential. For over 20 years, the cardiac-specific troponins, I (cTnI) and T (cTnT), have acted as sensitive and specific biomarkers to assist in the diagnosis of various types of heart diseases. Various cardiovascular complications were commonly detected in patients with COVID-19, where cTn elevation is detectable, which suggested potential prognostic value of cTn in COVID-19-infected patients. Detection of these biomarkers circulating in the bloodstream is generally facilitated by immunoassays employing cTnI- and/or cTnT-specific antibodies. While several anti-troponin assays are commercially available, there are still obstacles to overcome to achieve optimal troponin detection. Such obstacles include the proteolytic degradation of N and C terminals on cTnI, epitope occlusion of troponin binding-sites by the cTnI/cTnT complex, cross reactivity of antibodies with skeletal troponins or assay interference caused by human anti-species antibodies. Therefore, further research into multi-antibody based platforms, multi-epitope targeting and rigorous validation of immunoassays is required to ensure accurate measurements. Moreover, in combination with various technical advances (e.g. microfluidics), antibody-based troponin detection systems can be more sensitive and rapid for incorporation into portable biosensor systems to be used at point-of care.

Longitudinal monitoring of laboratory markers characterizes hospitalized and ambulatory COVID-19 patients.

Early detection of severe forms of COVID-19 is absolutely essential for timely triage of patients. We longitudinally followed-up two well-characterized patient groups, hospitalized moderate to severe (n = 26), and ambulatory mild COVID-19 patients (n = 16) at home quarantine. Human D-dimer, C-reactive protein (CRP), ferritin, cardiac troponin I, interleukin-6 (IL-6) levels were measured on day 1, day 7, day 14 and day 28. All hospitalized patients were SARS-CoV-2 positive on admission, while all ambulatory patients were SARS-CoV-2 positive at recruitment. Hospitalized patients had higher D-dimer, CRP and ferritin, cardiac troponin I and IL-6 levels than ambulatory patients (p < 0.001, p < 0.001, p = 0.016, p = 0.035, p = 0.002 respectively). Hospitalized patients experienced significant decreases in CRP, ferritin and IL-6 levels from admission to recovery (p < 0.001, p = 0.025, and p = 0.001 respectively). Cardiac troponin I levels were high during the acute phase in both hospitalized and ambulatory patients, indicating a potential myocardial injury. In summary, D-dimer, CRP, ferritin, cardiac troponin I, IL-6 are predictive laboratory markers and can largely determine the clinical course of COVID-19, in particular the prognosis of critically ill COVID-19 patients.

Predictive value of cardiac markers in the prognosis of COVID-19 in children.

BACKGROUND AND AIM: Occasionally, children with COVID-19 may develop arrhythmia, myocarditis, and cardiogenic shock involving multisystemic inflammatory syndrome in children (MIS-C). This study aimed to identify the laboratory parameters that may predict early cardiovascular involvement in these patients. MATERIALS AND METHODS: Data of 320 pediatric patients, aged 0-18 years (average age, 10.46 ± 5.77 years; 156 female), with positive COVID-19 reverse transcription-polymerase chain reaction test and with cardiac biomarkers at the time of admission to the pediatric emergency department were retrospectively scanned. The age, sex, COVID-19-associated symptoms, pro-brain natriuretic peptide (proBNP), CK-MB, and troponin I levels of the patients were recorded. RESULTS: Fever was noted in 58.1% of the patients, cough in 29.7%, diarrhea in 7.8%, headache in 14.7%, sore throat in 17.8%, weakness in 17.8%, abdominal pain in 5%, loss of taste in 4.1%, loss of smell in 5.3%, nausea in 3.4%, vomiting in 3.8%, nasal discharge in 4.4%, muscle pain in 5%, and loss of appetite in 3.1%. The proBNP value ≥282 ng/L predicted the development of MIS-C with 100% sensitivity and 93% specificity [AUC: 0.985 (0.959-1), P < 0.001]; CK-MB value ≥2.95 with 80% sensitivity and 77.6% specificity [AUC: 0.792 (0.581-1), P = 0.026]; and troponin I value ≥0.03 with 60% sensitivity and 99.2% specificity [AUC: 0.794 (0.524-1)]. CONCLUSIONS: Cardiac markers (proBNP and troponin I), especially proBNP, could be used to detect early diagnosis of cardiac involvement and/or MIS-C in pediatric patients with COVID-19 and to predict related morbidity and mortality.

Troponin and Other Biomarker Levels and Outcomes Among Patients Hospitalized With COVID-19: Derivation and Validation of the HA2T2 COVID-19 Mortality Risk Score.

Background The independent prognostic value of troponin and other biomarker elevation among patients with coronavirus disease 2019 (COVID-19) are unclear. We sought to characterize biomarker levels in patients hospitalized with COVID-19 and develop and validate a mortality risk score. Methods and Results An observational cohort study of 1053 patients with COVID-19 was conducted. Patients with all of the following biomarkers measured-troponin-I, B-type natriuretic peptide, C-reactive protein, ferritin, and d-dimer (n=446) -were identified. Maximum levels for each biomarker were recorded. The primary end point was 30-day in-hospital mortality. Multivariable logistic regression was used to construct a mortality risk score. Validation of the risk score was performed using an independent patient cohort (n=440). Mean age of patients was 65.0±15.2 years and 65.3% were men. Overall, 444 (99.6%) had elevation of any biomarker. Among tested biomarkers, troponin-I ≥0.34 ng/mL was the only independent predictor of 30-day mortality (adjusted odds ratio, 4.38; P<0.001). Patients with a mortality score using hypoxia on presentation, age, and troponin-I elevation, age (HA2T2) ≥3 had a 30-day mortality of 43.7% while those with a score <3 had mortality of 5.9%. Area under the receiver operating characteristic curve of the HA2T2 score was 0.834 for the derivation cohort and 0.784 for the validation cohort. Conclusions Elevated troponin and other biomarker levels are commonly seen in patients hospitalized with COVID-19. High troponin levels are a potent predictor of 30-day in-hospital mortality. A simple risk score can stratify patients at risk for COVID-19-associated mortality.

Myocarditis After SARS-CoV-2 Vaccination: A Vaccine-Induced Reaction?

Vaccination plays an important role in the fight against SARS-CoV-2 to minimie the spread of coronavirus disease 2019 (COVID-19) and its life-threatening complications. Myocarditis has been reported as a possible and rare adverse consequence of different vaccines, and its clinical presentation can range from influenza-like symptoms to acute heart failure. We report a case of a 30-year-old man who presented progressive dyspnea and constrictive retrosternal pain after receiving SARS-CoV-2 vaccine. Cardiac magnetic resonance and laboratory data revealed typical findings of acute myopericarditis.

Type 2 myocardial infarction and myocardial injury: eligibility for novel medical therapy to derisk clinical trials.

BACKGROUND: Patients with type 2 myocardial infarction (T2MI) and other mechanisms of nonthrombotic myocardial injury have an unmet therapeutic need. Eligibility for novel medical therapy is generally uncertain. METHODS: We predefined colchicine, eplerenone and ticagrelor as candidates for repurposing towards novel therapy for T2MI or myocardial injury. Considering eligibility for randomisation in a clinical trial, each drug was classified according to indications and contraindications for therapy and survival for at least 24 hours following admission. Eligibility criteria for prescription were evaluated against the Summary of Medical Product Characteristics. Consecutive hospital admissions were screened to identify patients with ≥1 high-sensitivity troponin-I value >99th percentile. Endotypes of myocardial injury were adjudicated according to the Fourth Universal Definition of MI. Patients' characteristics and medication were prospectively evaluated. RESULTS: During 1 March to 15 April 2020, 390 patients had a troponin I>URL. Reasons for exclusion: type 1 MI n=115, indeterminate diagnosis n=42, lack of capacity n=14, death <24 hours n=7, duplicates n=2. Therefore, 210 patients with T2MI/myocardial injury and 174 (82.8%) who survived to discharge were adjudicated for treatment eligibility. Patients who fulfilled eligibility criteria initially on admission and then at discharge were colchicine 25/210 (11.9%) and 23/174 (13.2%); eplerenone 57/210 (27.1%) and 45/174 (25.9%); ticagrelor 122/210 (58.1%) and 98/174 (56.3%). Forty-six (21.9%) and 38 (21.8%) patients were potentially eligible for all three drugs on admission and discharge, respectively. CONCLUSION: A reasonably high proportion of patients may be considered eligible for repurposing novel medical therapy in secondary prevention trials of type 2 MI/myocardial injury.

A simple and readily available inflammation-based risk scoring system on admission predicts the need for mechanical ventilation in patients with COVID-19.

OBJECTIVE: To investigate whether a simplified inflammation-based risk scoring system comprising three readily available biomarkers (albumin, C-reactive protein, and leukocytes) may predict major adverse outcomes in patients with COVID-19. METHODS: Upon admission to the emergency room, the inflammation-based risk scoring system was applied and patients were classified as having mild, moderate, or severe inflammation. In-hospital occurrence of thrombosis, need for mechanical ventilation, and death were recorded. RESULTS: One-hundred patients (55 ± 13 years; 71% men) were included and classified as having mild (29%), moderate (12%), or severe (59%) inflammation. The need for mechanical ventilation differed among patients in each group (16%, 50%, and 71%, respectively; P < 0.0001), yielding a 4.1-fold increased risk of requiring mechanical ventilation in patients with moderate inflammation and 5.4 for those with severe inflammation. On the contrary, there were no differences for the occurrence of thrombosis (10%, 8%, and 22%, respectively; P = 0.142) or death (21%, 42%, and 39%, respectively; P = 0.106). In the multivariate analysis, only severe inflammation (hazard ratio [HR] = 4.1), D-dimer > 574 ng/mL (HR = 3.0), and troponin I ≥ 6.7 ng/mL (HR = 2.4) at hospital admission were independent predictors of the need for mechanical ventilation. CONCLUSION: The inflammation-based risk scoring system predicts the need for mechanical ventilation in patients with severe COVID-19.