Clinical predictors of acute cardiac injury and normalization of troponin after hospital discharge from COVID-19.

BACKGROUND: Although acute cardiac injury (ACI) is a known COVID-19 complication, whether ACI acquired during COVID-19 recovers is unknown. This study investigated the incidence of persistent ACI and identified clinical predictors of ACI recovery in hospitalized patients with COVID-19 2.5 months post-discharge. METHODS: This retrospective study consisted of 10,696 hospitalized COVID-19 patients from March 11, 2020 to June 3, 2021. Demographics, comorbidities, and laboratory tests were collected at ACI onset, hospital discharge, and 2.5 months post-discharge. ACI was defined as serum troponin-T (TNT) level >99th-percentile upper reference limit (0.014ng/mL) during hospitalization, and recovery was defined as TNT below this threshold 2.5 months post-discharge. Four models were used to predict ACI recovery status. RESULTS: There were 4,248 (39.7%) COVID-19 patients with ACI, with most (93%) developed ACI on or within a day after admission. In-hospital mortality odds ratio of ACI patients was 4.45 [95%CI: 3.92, 5.05, p<0.001] compared to non-ACI patients. Of the 2,880 ACI survivors, 1,114 (38.7%) returned to our hospitals 2.5 months on average post-discharge, of which only 302 (44.9%) out of 673 patients recovered from ACI. There were no significant differences in demographics, race, ethnicity, major commodities, and length of hospital stay between groups. Prediction of ACI recovery post-discharge using the top predictors (troponin, creatinine, lymphocyte, sodium, lactate dehydrogenase, lymphocytes and hematocrit) at discharge yielded 63.73%-75.73% accuracy. INTERPRETATION: Persistent cardiac injury is common among COVID-19 survivors. Readily available patient data accurately predict ACI recovery post-discharge. Early identification of at-risk patients could help prevent long-term cardiovascular complications. FUNDING: None.

Exploring the Utility of Brain Natriuretic Peptide Measurement in Vascular Surgery.

BACKGROUND: The Canadian Cardiovascular Society 2016 guidelines recommend pre-operative measurement of brain natriuretic peptide (BNP) to risk-stratify patients for a 30-day composite outcome of death, myocardial infarction, or asymptomatic myocardial injury after noncardiac surgery (MINS). Whether this practice affects outcomes is unclear. The aim of this study was to examine the clinical utility of brain natriuretic peptide and myocardial injury after noncardiac surgery. METHODS: Analysis of a prospectively maintained database identified all elective open vascular surgery cases at an academic teaching hospital from January 2015 to December 2018. Pre-operative BNP values were available from June 2018 onward after becoming institutionally mandated. Co-morbidities were also collected to stratify patients using the Revised Cardiac Risk Index. The composite outcome of 30-day mortality, myocardial infarction, or MINS was determined. RESULTS: Prior to BNP becoming an institutionally required test, data was available from 1176 open cases. The 30-day mortality was 1.3% (15/1176) and post-operative myocardial infarction rate was 2.3% (27/1176). BNP measurements were collected in 91 consecutive patients. Ten patients (11%) experienced the composite outcome of mortality, myocardial infarction, or MINS. Elevated BNP was associated with increased odds of the composite outcome (P = 0.04), but not with mortality or myocardial infarction. Revised Cardiac Risk Index score was not predictive of outcomes. The majority of patients who qualified for the composite outcome experienced only an asymptomatic troponin rise (80%). Two patients met the universal definition of myocardial infarction, one of whom died. No other deaths occurred within 30 days. Detection of MINS did not result in any significant changes to patient management. CONCLUSIONS: Elevated BNP correlates with increased MINS. An asymptomatic troponin rise is the most commonly observed event, with unclear clinical implications. BNP may over-estimate surgical risk. Further studies on the long-term outcomes of patients with elevated BNP and MINS are required before widely adopting this strategy in vascular surgery patients.

COVID-19 and the Incidence of Acute Myocardial Injury.

Cardiovascular manifestations are frequent in COVID-19 infection and are predictive of adverse outcomes. Elevated cardiac biomarkers are common findings in patients with cardiovascular comorbidities and severe COVID-19 infection. Troponin, inflammatory and thrombotic markers may also improve risk prediction in COVID-19. In our comprehensive review, we provide an overview of the incidence, potential mechanisms and outcome of acute cardiac injury in COVID-19. Thereby, we discuss coagulation abnormalities in sepsis and altered immune response as contributing factors favoring myocardial injury. We further highlight the role of endothelial damage in the pathophysiological concepts. Finally, observational studies addressing the incidence of myocardial infarction during COVID-19 pandemic are discussed.

Effects of peak time of myocardial injury biomarkers on mid-term outcomes of patients undergoing OPCABG.

BACKGROUND: With the development of cardiac surgery techniques, myocardial injury is gradually reduced, but cannot be completely avoided. Myocardial injury biomarkers (MIBs) can quickly and specifically reflect the degree of myocardial injury. Due to various reasons, there is no consensus on the specific values of MIBs in evaluating postoperative prognosis. This retrospective study was aimed to investigate the impact of MIBs on the mid-term prognosis of patients undergoing off-pump coronary artery bypass grafting (OPCABG). METHODS: Totally 564 patients undergoing OPCABG with normal courses were included. Cardiac troponin T (cTnT) and creatine kinase myocardial band (CK-MB) were assessed within 48 h before operation and at 6, 12, 24, 48, 72, 96 and 120 h after operation. Patients were grouped by peak values and peak time courses of MIBs. The profile of MIBs and clinical variables as well as their correlations with mid-term prognosis were analyzed by univariable and multivariable Cox regression models. RESULT: Continuous assessment showed that MIBs increased first (12 h after surgery) and then decreased. The peak cTnT and peak CK-MB occurred within 24 h after operation in 76.8% and 67.7% of the patients respectively. No significant correlation was found between CK-MB and mid-term mortality. Delayed cTnT peak (peak cTnT elevated after 24 h after operation) was correlated with lower creatinine clearance rate (69.36 ± 21.67 vs. 82.18 ± 25.17 ml/min/1.73 m2), body mass index (24.35 ± 2.58 vs. 25.27 ± 3.26 kg/m2), less arterial grafts (1.24 ± 0.77 vs. 1.45 ± 0.86), higher EuroSCORE II (2.22 ± 1.12 vs.1.72 ± 0.91) and mid-term mortality (26.5 vs.7.9%). Age (HR: 1.067, CI: 1.006-1.133), left ventricular ejection fraction (HR: 0.950, CI: 0.910-0.993), New York Heart Association score (HR: 1.839, CI: 1.159-2.917), total venous grafting (HR: 2.833, CI: 1.054-7.614) and cTnT peak occurrence within 24 h (HR: 0.362, CI: 0.196-0.668) were independent predictors of mid-term mortality. CONCLUSION: cTnT is a better indicator than CK-MB. The peak value and peak occurrence of cTnT are related to mid-term mortality in patients undergoing OPCABG, and the peak phases have stronger predictive ability. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR2000033850. Registered 14 June 2020, http://www.chictr.org.cn/edit.aspx?pid=55162&htm=4 .

Impact of acute myocardial injury on prognosis in patients with COVID-19.

OBJECTIVE: The primary objective of this study was to evaluate the frequency and impact of acute myocardial injury on prognosis in hospitalized COVID-19 patients. PATIENTS AND METHODS: This was a retrospective study that included consecutive hospitalized patients with COVID-19. Clinic-demographic characteristics, laboratory values, and high-sensitivity troponin I were extracted from the electronic database. Mortality and other clinical complications, including respiratory failure requiring invasive mechanical ventilation and acute kidney injury were recorded. Myocardial injury was defined as having a serum troponin I value >19.8 ng/mL. We performed Kaplan-Meier survival analysis and Cox regression to determine survival times and independent predictors of mortality. RESULTS: A total of 324 patients were included. Seventy-seven patients (23.8%) had acute myocardial injury. The primary outcome measure, namely death, occurred in 54.5% and 3.2% of the patients with and without myocardial injury, respectively. Notably, 75.3% of the patients with myocardial injury and 6.5% of the patients without myocardial injury developed ARDS. Overall, 50 out of 324 patients (15.4%) died during the study period. The mortality rate was 54.5% in patients with myocardial injury and 3.2% in patients without myocardial injury. Mean survival times were significantly different between the groups (15.1±0.9 days in patients with myocardial injury and 24.4±0.7 days in patients without myocardial injury, log-rank test p-value <0.001). CONCLUSIONS: The presence of chronic kidney disease and application of invasive mechanical ventilation were found to be independent predictors of in-hospital mortality. The presence of acute myocardial injury was common but not independently associated with mortality among hospitalized COVID-19 patients.

The Challenges of Using ICD codes to Perform a Comparative Analysis between Patients with Penetrating Cardiac Injuries who Underwent Non-Resuscitative Thoracotomy versus Sternotomy.

Background: Comparative morbidity after either sternotomy or non-resuscitative thoracotomy in penetrating cardiac injuries (PCI) is unknown. Methods: Retrospective review of adults with PCI who underwent either sternotomy or non-resuscitative thoracotomy using the National Trauma Data Bank 2007-2015. Since there is no unique International Classification of Diseases Procedure Coding System (ICD-PCS) codes assigned for resuscitative vs. non-resuscitative thoracotomy, and both procedures were coded as "thoracotomy", propensity score (PS) methods were applied to avoid inclusion of resuscitative thoracotomy. Results: Despite well PS matching on injury severity score the non-thoracotomy group compared to the sternotomy group had a significantly increased risk of mortality (30 percent vs 8 percent, p<0.0001). The morbidity differed as well-25 percent vs. 12 percent, p=0.0007. Conclusions: The differences in mortality in PCI patients who underwent non-resuscitative thoracotomy vs. sternotomy may be biased by unintentional inclusion of resuscitative thoracotomy. To accurately capture thoracotomy type, separate unique resuscitative and non-resuscitative thoracotomy procedure codes should be created in future revisions of the ICD PCS.

Wide QRS Complex and Lateral ST-T Segment Abnormality Are Associated With Worse Clinical Outcomes in COVID-19 Patients.

BACKGROUND: The information on electrocardiographic features of patients with coronavirus disease 2019 (COVID-19) is limited. Our aim was to determine if baseline electrocardiographic features of hospitalized COVID-19 patients are associated with markers of myocardial injury and clinical outcomes. METHODS: In this retrospective, single center cohort study, we included 223 hospitalized patients with laboratory-confirmed COVID-19. Clinical, electrocardiographic and laboratory data were collected and analyzed. Primary composite endpoint of mortality, need for invasive mechanical ventilation, or admission to the intensive care unit was assessed. RESULTS: Forty patients (17.9%) reached the primary composite endpoint. Patients with the primary composite endpoint were more likely to have wide QRS complex (>120 ms) and lateral ST-T segment abnormality. The multivariable Cox regression showed increasing odds of the primary composite endpoint associated with acute respiratory distress syndrome (odds ratio 7.76, 95% CI 2.67-22.59; p < 0.001), acute cardiac injury (odds ratio 3.14, 95% CI 1.26-7.99; p = 0.016), high flow oxygen therapy (odds ratio 2.43, 95% CI 1.05-5.62; p = 0.037) and QRS duration longer than >120 ms (odds ratio 3.62, 95% CI 1.39-9.380; p = 0.008) Patients with a wide QRS complex (>120 ms) had significantly higher median level of troponin T and pro-BNP than those without it. Patients with abnormality of lateral ST-T segment had significantly higher median level of troponin T and pro-BNP than patients without. CONCLUSIONS: The presence of QRS duration longer than 120 ms and lateral ST-T segment abnormality were associated with worse clinical outcomes and higher levels of myocardial injury biomarkers.

Key factors leading to fatal outcomes in COVID-19 patients with cardiac injury.

Cardiac injury among patients with COVID-19 has been reported and is associated with a high risk of mortality, but cardiac injury may not be the leading factor related to death. The factors related to poor prognosis among COVID-19 patients with myocardial injury are still unclear. This study aimed to explore the potential key factors leading to in-hospital death among COVID-19 patients with cardiac injury. This retrospective single-center study was conducted at Renmin Hospital of Wuhan University, from January 20, 2020 to April 10, 2020, in Wuhan, China. All inpatients with confirmed COVID-19 (≥ 18 years old) and cardiac injury who had died or were discharged by April 10, 2020 were included. Demographic data and clinical and laboratory findings were collected and compared between survivors and nonsurvivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with mortality in COVID-19 patients with cardiac injury. A total of 173 COVID-19 patients with cardiac injury were included in this study, 86 were discharged and 87 died in the hospital. Multivariable regression showed increased odds of in-hospital death were associated with advanced age (odds ratio 1.12, 95% CI 1.05-1.18, per year increase; p < 0.001), coagulopathy (2.54, 1.26-5.12; p = 0·009), acute respiratory distress syndrome (16.56, 6.66-41.2; p < 0.001), and elevated hypersensitive troponin I (4.54, 1.79-11.48; p = 0.001). A high risk of in-hospital death was observed among COVID-19 patients with cardiac injury in this study. The factors related to death include advanced age, coagulopathy, acute respiratory distress syndrome and elevated levels of hypersensitive troponin I.

Cardiac injury and mortality in patients with Coronavirus disease 2019 (COVID-19): insights from a mediation analysis.

BACKGROUNDS: Patients at greatest risk of severe clinical conditions from coronavirus disease 2019 (COVID-19) and death are elderly and comorbid patients. Increased levels of cardiac troponins identify patients with poor outcome. The present study aimed to describe the clinical characteristics and outcomes of a cohort of Italian inpatients, admitted to a medical COVID-19 Unit, and to investigate the relative role of cardiac injury on in-hospital mortality. METHODS AND RESULTS: We analyzed all consecutive patients with laboratory-confirmed COVID-19 referred to our dedicated medical Unit between February 26th and March 31st 2020. Patients' clinical data including comorbidities, laboratory values, and outcomes were collected. Predictors of in-hospital mortality were investigated. A mediation analysis was performed to identify the potential mediators in the relationship between cardiac injury and mortality. A total of 109 COVID-19 inpatients (female 36%, median age 71 years) were included. During in-hospital stay, 20 patients (18%) died and, compared with survivors, these patients were older, had more comorbidities defined by Charlson comorbidity index ≥ 3(65% vs 24%, p = 0.001), and higher levels of high-sensitivity cardiac troponin I (Hs-cTnI), both at first evaluation and peak levels. A dose-response curve between Hs-cTnI and in-hospital mortality risk up to 200 ng/L was detected. Hs-cTnI, chronic kidney disease, and chronic coronary artery disease mediated most of the risk of in-hospital death, with Hs-cTnI mediating 25% of such effect. Smaller effects were observed for age, lactic dehydrogenase, and D-dimer. CONCLUSIONS: In this cohort of elderly and comorbid COVID-19 patients, elevated Hs-cTnI levels were the most important and independent mediators of in-hospital mortality.

Is it all in the heart? Myocardial injury as major predictor of mortality among hospitalized COVID-19 patients.

Coronavirus disease 2019 (COVID-19) is an infection caused by the virus SARS-CoV-2, and has caused the most widespread global pandemic in over 100 years. Given the novelty of the disease, risk factors of mortality and adverse outcomes in hospitalized patients remain to be elucidated. We present the results of a retrospective cohort study including patients admitted to a large tertiary-care, academic university hospital with COVID-19. Patients were admitted with confirmed diagnosis of COVID-19 between 1 March and 15 April 2020. Baseline clinical characteristics and admission laboratory variables were retrospectively collected. Patients were grouped based on mortality, need for ICU care, and mechanical ventilation. Prevalence of clinical co-morbidities and laboratory abnormalities were compared between groups using descriptive statistics. Univariate analysis was performed to identify predictors of mortality, ICU care and mechanical ventilation. Predictors significant at P ≤ .10 were included in multivariate analysis. Five hundred and sixty patients were included in the analysis. Age and myocardial injury were only independent predictors of mortality, in patients with/without baseline co-morbidities. Body mass index, elevated ferritin, elevated d-dimer, and elevated procalcitonin predicted need for ICU care, and these along with vascular disease at baseline predicted need for mechanical ventilation. Hence, inflammatory markers (ferritin and d-dimer) predicted severe disease, but not death.

Over time relationship between platelet reactivity, myocardial injury and mortality in patients with SARS-CoV-2-associated respiratory failure.

The aim of this study (NCT04343053) is to investigate the relationship between platelet activation, myocardial injury, and mortality in patients affected by Coronavirus disease 2019 (COVID-19). Fifty-four patients with respiratory failure due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection were enrolled as cases. Eleven patients with the same clinical presentation, but negative for SARS-CoV-2 infection, were included as controls. Blood samples were collected at three different time points (inclusion [T1], after 7 ± 2 days [T2] and 14 ± 2 days [T3]). Platelet aggregation by light transmittance aggregometry and the circulating levels of soluble CD40 ligand (sCD40L) and P-selectin were measured. Platelet biomarkers did not differ between cases and controls, except for sCD40L which was higher in COVID-19 patients (p = .003). In COVID-19 patients, P-selectin and sCD40L levels decreased from T1 to T3 and were higher in cases requiring admission to intensive care unit (p = .004 and p = .008, respectively). Patients with myocardial injury (37%), as well as those who died (30%), had higher values of all biomarkers of platelet activation (p < .05 for all). Myocardial injury was an independent predictor of mortality. In COVID-19 patients admitted to hospital for respiratory failure, heightened platelet activation is associated with severity of illness, myocardial injury, and mortality.ClinicalTrials.gov number: NCT04343053.

Myocardial Injury in Severe COVID-19 Compared With Non-COVID-19 Acute Respiratory Distress Syndrome.

BACKGROUND: Knowledge gaps remain in the epidemiology and clinical implications of myocardial injury in coronavirus disease 2019 (COVID-19). We aimed to determine the prevalence and outcomes of myocardial injury in severe COVID-19 compared with acute respiratory distress syndrome (ARDS) unrelated to COVID-19. METHODS: We included intubated patients with COVID-19 from 5 hospitals between March 15 and June 11, 2020, with troponin levels assessed. We compared them with patients from a cohort study of myocardial injury in ARDS and performed survival analysis with primary outcome of in-hospital death associated with myocardial injury. In addition, we performed linear regression to identify clinical factors associated with myocardial injury in COVID-19. RESULTS: Of 243 intubated patients with COVID-19, 51% had troponin levels above the upper limit of normal. Chronic kidney disease, lactate, ferritin, and fibrinogen were associated with myocardial injury. Mortality was 22.7% among patients with COVID-19 with troponin under the upper limit of normal and 61.5% for those with troponin levels >10 times the upper limit of normal (P<0.001). The association of myocardial injury with mortality was not statistically significant after adjusting for age, sex, and multisystem organ dysfunction. Compared with patients with ARDS without COVID-19, patients with COVID-19 were older and had higher creatinine levels and less favorable vital signs. After adjustment, COVID-19-related ARDS was associated with lower odds of myocardial injury compared with non-COVID-19-related ARDS (odds ratio, 0.55 [95% CI, 0.36-0.84]; P=0.005). CONCLUSIONS: Myocardial injury in severe COVID-19 is a function of baseline comorbidities, advanced age, and multisystem organ dysfunction, similar to traditional ARDS. The adverse prognosis of myocardial injury in COVID-19 relates largely to multisystem organ involvement and critical illness.

Comparison of pre- and postoperative myocardial injuries on mortality after non-cardiac surgery: a retrospective analysis using an inverse probability weighting adjustment.

Although both pre- and postoperative myocardial injuries are strongly associated with an increased postoperative mortality, no study has directly compared the effects of pre- and postoperative myocardial injuries on 30-day mortality after non-cardiac surgery. Therefore, we evaluated and compared the effects of pre- and postoperative myocardial injury on 30-day mortality after non-cardiac surgery. From January 2010 to December 2016, patients undergoing non-cardiac surgery were stratified into either the normal (n = 3182), preoperative myocardial injury (n = 694), or postoperative myocardial injury (n = 756) groups according to the peak cardiac troponin value. Myocardial injury was defined as a sole elevation of cardiac troponin value above the 99th percentile upper reference limit without ischemic symptom using the 4th universal definition of myocardial infarction. Patients in the preoperative myocardial injury group were further divided into the attenuated (n = 177) or persistent myocardial injury group (n = 517) according to the normalization of cardiac troponin level in postoperative period. As the primary outcome, postoperative 30-day mortalities were compared among the groups using the weighted Cox proportional-hazards regression models with the inverse probability weighting. Compared with the normal group, postoperative 30-day mortality was increased significantly both in the pre- and postoperative myocardial injury groups (1.4% vs. 10.7%; hazard ratio [HR] 3.12; 95% confidence interval [CI] 1.62-6.01; p = 0.001 and 1.4% vs. 7.4%; HR 4.49; 95% CI 2.34-8.60; p < 0.001, respectively), however, there was no difference between the pre- and postoperative myocardial injury groups (HR, 1.44; 95% CI 0.79-2.64; p = 0.45). In addition, the attenuated myocardial injury group showed a significantly lower postoperative 30-day mortality than the persistent myocardial injury group (5.6% vs. 12.4%; HR 2.23; 95% CI 1.17-4.44; p = 0.02). In patients undergoing non-cardiac surgery, preoperative myocardial injury also increased postoperative 30-day mortality to a similar degree of postoperative myocardial injury. Further studies on the importance of preoperative myocardial injury are needed.Clinical trial number and registry URL: KCT0004348 ( www.cris.nih.go.kr ).

Reduced cardiac function is associated with cardiac injury and mortality risk in hospitalized COVID-19 Patients.

BACKGROUND: Cardiac injury is common in COVID-19 patients and is associated with increased mortality. However, it remains unclear if reduced cardiac function is associated with cardiac injury, and additionally if mortality risk is increased among those with reduced cardiac function in COVID-19 patients. HYPOTHESIS: The aim of this study was to assess cardiac function among COVID-19 patients with and without biomarkers of cardiac injury and to determine the mortality risk associated with reduced cardiac function. METHODS/RESULTS: This retrospective cohort study analyzed 143 consecutive COVID-19 patients who had an echocardiogram during hospitalization between March 1, 2020 and May 5, 2020. The mean age was 67 ± 16 years. Cardiac troponin-I was available in 131 patients and an increased value (>0.03 ng/dL) was found in 59 patients (45%). Reduced cardiac function, which included reduced left or right ventricular systolic function, was found in 40 patients (28%). Reduced cardiac function was found in 18% of patients without troponin-I elevation, 42% with mild troponin increase (0.04-5.00 ng/dL) and 67% with significant troponin increase (>5 ng/dL). Reduced cardiac function was also present in more than half of the patients on mechanical ventilation or those deceased. The in-hospital mortality of this cohort was 28% (N = 40). Using logistic regression analysis, we found that reduced cardiac function was associated with increased mortality with adjusted odds ratio (95% confidence interval) of 2.65 (1.18 to 5.96). CONCLUSIONS: Reduced cardiac function is highly prevalent among hospitalized COVID-19 patients with biomarkers of myocardial injury and is independently associated with mortality.

Coagulopathy is a major extrapulmonary risk factor for mortality in hospitalized patients with COVID-19 with type 2 diabetes.

INTRODUCTION: To investigate the risk factors for the death in patients with COVID-19 with type 2 diabetes mellitus (T2DM). RESEARCH DESIGN AND METHODS: We retrospectively enrolled inpatients with COVID-19 from Wuhan Jinyintan Hospital (Wuhan, China) between December 25, 2019, and March 3, 2020. The epidemiological and clinical data were compared between non-T2DM and T2DM or between survivors and non-survivors. Univariable and multivariable Cox regression analyses were used to explore the effect of T2DM and complications on in-hospital death. RESULTS: A total of 1105 inpatients with COVID-19, 967 subjects with without T2DM (n=522 male, 54.0%) and 138 subjects with pre-existing T2DM (n=82 male, 59.4%) were included for baseline characteristics analyses. The complications were also markedly increased in patients with pre-existing T2DM, including acute respiratory distress syndrome (ARDS) (48.6% vs 32.3%, p<0.001), acute cardiac injury (ACI) (36.2% vs 16.7%, p<0.001), acute kidney injury (AKI) (24.8% vs 9.5%, p<0.001), coagulopathy (24.8% vs 11.1%, p<0.001), and hypoproteinemia (21.2% vs 9.4%, p<0.001). The in-hospital mortality was significantly higher in patients with pre-existing T2DM compared with those without T2DM (35.3% vs 17.4%, p<0.001). Moreover, in hospitalized patients with COVID-19 with T2DM, ARDS and coagulopathy were the main causes of mortality, with an HR of 7.96 (95% CI 2.25 to 28.24, p=0.001) for ARDS and an HR of 2.37 (95% CI 1.08 to 5.21, p=0.032) for coagulopathy. This was different from inpatients with COVID-19 without T2DM, in whom ARDS and cardiac injury were the main causes of mortality, with an HR of 12.18 (95% CI 5.74 to 25.89, p<0.001) for ARDS and an HR of 4.42 (95% CI 2.73 to 7.15, p<0.001) for cardiac injury. CONCLUSIONS: Coagulopathy was a major extrapulmonary risk factor for death in inpatients with COVID-19 with T2DM rather than ACI and AKI, which were well associated with mortality in inpatients with COVID-19 without T2DM.

Factors associated with acute cardiac injury and their effects on mortality in patients with COVID-19.

To determine the incidence of acute cardiac injury (ACI), the factors associated with ACI and the in-hospital mortality in patients with COVID-19, especially in severe patients. All consecutive in-patients with laboratory-confirmed COVID-19 from Tongji Hospital in Wuhan during February 1 and March 29, 2020 were included. The demographic, clinical characteristics, laboratory, radiological and treatment data were collected. Univariate and Firth logistic regression analyses were used to identify factors associated with ACI and in-hospital mortality, and Kaplan-Meier method was used to estimate cumulative in-hospital mortality. Among 1031 patients included, 215 (20.7%) had ACI and 501 (48.6%) were severe cases. Overall, 165 patients died; all were from the severe group, and 131 (79.39%) had ACI. ACI (OR = 2.34, P = 0.009), male gender (OR = 2.58, P = 0.001), oximeter oxygen saturation (OR = 0.90, P < 0.001), lactate dehydrogenase (OR = 3.26, P < 0.001), interleukin-6 (IL-6) (OR = 8.59, P < 0.001), high sensitivity C-reactive protein (hs-CRP) (OR = 3.29, P = 0.016), N-terminal pro brain natriuretic peptide (NT-proBNP) (OR = 2.94, P = 0.001) were independent risk factors for the in-hospital mortality in severe patients. The mortality was significantly increased among severe patients with elevated hs-CRP, IL-6, hs-cTnI, and/or NT-proBNP. Moreover, the mortality was significantly higher in patients with elevation of both hs-cTnI and NT proBNP than in those with elevation of either of them. ACI develops in a substantial proportion of patients with COVID-19, and is associated with the disease severity and in-hospital mortality. A combination of hs-cTnI and NT-proBNP is valuable in predicting the mortality.

Volatile versus total intravenous anesthesia for 30-day mortality following non-cardiac surgery in patients with preoperative myocardial injury.

We evaluated whether volatile anesthetics can improve the postoperative outcomes of non-cardiac surgery in patients with preoperative myocardial injury defined by the cardiac troponin elevation. From January 2010 to June 2018, 1254 adult patients with preoperative myocardial injury underwent non-cardiac surgery under general anesthesia and were enrolled in this study. Patients were stratified into following two groups according to anesthetic agents; 115 (9.2%) patients whose anesthesia was induced and maintained with continuous infusion of propofol and remifentanil (TIVA group) and 1139 (90.8%) patients whose anesthesia was maintainted with volatile anesthetics (VOLATILE group). The primary outcome was 30-day mortality. To diminish the remifentanil effect, a further analysis was conducted after excluding the patients who received only volatile anesthetics without remifentanil infusion. In a propensity-score matched analysis, 30-day mortality was higher in the TIVA group than the VOLATILE group (17.0% vs. 9.1%; hazard ratio [HR] 2.60; 95% confidence interval [CI], 1.14-5.93; p = 0.02). In addition, the TIVA group showed higher 30-day mortality than the VOLATILE group, even after eliminating the effect of remifentanil infusion (15.8% vs. 8.3%; HR 4.62; 95% CI, 1.82-11.74; p = 0.001). In our study, the use of volatile anesthetics showed the significant survival improvement after non-cardiac surgery in patients with preoperative myocardial injury, which appears to be irrelevant to the remifentanil use. Further studies are needed to confirm this beneficial effect of volatile anesthetics. Clinical trial number and registry URL: KCT0004349 (www.cris.nih.go.kr).

Penetrating cardiac trauma in stab wounds: A study of diagnostic accuracy of the cardiac area.

BACKGROUND: Stab wounds (SW) to the thorax raises suspicion for cardiac injuries; however, the topographic description is variable. The present study aims to evaluate different topographical descriptions within the thorax and establish their diagnostic value in penetrating cardiac trauma by SW. METHODS: Medical records of all patients admitted to our center with thoracic SW from January 2013 to June 2016 were included in this study. Diagnostic value potential was measured using different areas of the thorax described in the literature. RESULTS: In this study, we analyzed 306 cases. Thirty-eight (12.4%) patients had a cardiac injury managed surgically. Death by cardiac injury occurred in seven (18.4%) patients. The cardiac area defined between the right mid-clavicle line until the left anterior axillary line, and between 2nd and 6th intercostal spaces was the more accurate. It has sensitivity of 97.3%, specificity 72%, positive predictive value 33%, negative predictive value 99.4% and accuracy 75.1% for penetrating cardiac trauma. ROC was 0.894 IC 95% (0.760-0.901). CONCLUSION: Among the thoracic areas, topographical limits between the right mid-clavicle line and the left anterior axillary line, and between 2nd and 6th intercostal spaces are the more accurate and are highly indicative of cardiac injury in patients with SW to the thorax.

The association between cardiac injury and outcomes in hospitalized patients with COVID-19.

In this study, we aimed to assess the association between development of cardiac injury and short-term mortality as well as poor in-hospital outcomes in hospitalized patients with COVID-19. In this prospective, single-center study, we enrolled hospitalized patients with laboratory-confirmed COVID-19 and highly suspicious patients with compatible chest computed tomography features. Cardiac injury was defined as a rise of serum high sensitivity cardiac Troponin-I level above 99th percentile (men: > 26 ng/mL, women: > 11 ng/mL). A total of 386 hospitalized patients with COVID-19 were included. Cardiac injury was present among 115 (29.8%) of the study population. The development of cardiac injury was significantly associated with a higher in-hospital mortality rate compared to those with normal troponin levels (40.9% vs 11.1%, p value < 0.001). It was shown that patients with cardiac injury had a significantly lower survival rate after a median follow-up of 18 days from symptom onset (p log-rank < 0.001). It was further demonstrated in the multivariable analysis that cardiac injury could possibly increase the risk of short-term mortality in hospitalized patients with COVID-19 (HR = 1.811, p-value = 0.023). Additionally, preexisting cardiovascular disease, malignancy, blood oxygen saturation < 90%, leukocytosis, and lymphopenia at presentation were independently associated with a greater risk of developing cardiac injury. Development of cardiac injury in hospitalized patients with COVID-19 was significantly associated with higher rates of in-hospital mortality and poor in-hospital outcomes. Additionally, it was shown that development of cardiac injury was associated with a lower short-term survival rate compared to patients without myocardial damage and could independently increase the risk of short-term mortality by nearly two-fold.

Markers of Myocardial Stress, Myocardial Injury, and Subclinical Inflammation and the Risk of Sudden Death.

BACKGROUND: The majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first manifestation of cardiovascular disease (CVD). Biomarkers are screening tools that may identify subclinical cardiovascular disease and those at elevated risk for SCD. We aimed to determine whether the total to high-density lipoprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or high-sensitivity C-reactive protein individually or in combination could identify individuals at higher SCD risk in large, free-living populations with and without cardiovascular disease. METHODS: We performed a nested case-control study within 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, ethnicity, smoking status, and presence of cardiovascular disease. RESULTS: The median study follow-up time until SCD was 11.3 years. When examined as quartiles or continuous variables in conditional logistic regression models, each of the biomarkers was significantly and independently associated with SCD risk after mutually controlling for cardiac risk factors and other biomarkers. The mutually adjusted odds ratios for the top compared with the bottom quartile were 1.90 (95% CI, 1.30-2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76-3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12-2.44) for NT-proBNP, and 1.65 (95% CI, 1.13-2.41) for high-sensitivity C-reactive protein. A biomarker score that awarded 1 point when the concentration of any of those 4 biomarkers was in the top quartile (score range, 0-4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37-1.77) per 1-unit increase in the score. CONCLUSIONS: Widely available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show significant independent associations with SCD risk in apparently low-risk populations. In combination, these measures may have utility to identify individuals at risk for SCD.