Elevated Cardiac Troponin Research Articles

Concomitant myocarditis and painless thyroiditis after AstraZeneca coronavirus disease 2019 vaccination: a case report

BackgroundIncidence of myocarditis following messenger RNA coronavirus disease 2019 vaccination has been widely described, but this clinical scenario after adenoviral vector coronavirus disease 2019 vaccination has only been rarely reported. In addition, a few case reports of thyroiditis after adenoviral vector coronavirus disease 2019 vaccination have been published.Case presentationA 55-year-old Thai woman presented with palpitation without neck pain 14 days after receiving AstraZeneca coronavirus disease 2019 vaccination. Electrocardiography revealed sinus tachycardia. Her blood tests showed elevation of cardiac troponin and free triiodothyronine with suppressed serum thyroid stimulating hormone, reflecting a hyperthyroid status. Evidence of myocardial inflammation and necrosis from cardiac magnetic resonance imaging supported the diagnosis of recent myocarditis. Laboratory results and imaging findings were consistent with thyroiditis. After 3 weeks of symptomatic treatment, her symptom and blood tests had returned to normal.ConclusionsThis case demonstrates that the adenoviral vector coronavirus disease 2019 vaccine could possibly cause myocarditis and painless thyroiditis. Clinicians should have a high index of suspicion and promptly evaluate these conditions, despite minimal symptoms.

Impact of Cardiac Troponin Elevation on Mortality of Patients with Acute Heart Failure: Insights from the Korea Acute Heart Failure (KorAHF) Registry.

We aimed to conduct the largest study evaluating the impact of cardiac troponin (TnI) status on mid- and long-term mortality in patients admitted for acute heart failure (AHF) as compared between patients with ischemic (IHF) vs. non-ischemic heart failure (non-IHF). Among 5625 patients from the Korea Acute Heart Failure (KorAHF) registry, 4396 eligible patients with TnI measurement were analyzed. The patients were included on admission with the diagnosis of AHF, and TnI level was measured on the day of admission. A TnI value of <0.05 ng/mL was considered normal. The patients were divided into four groups according to the etiology of heart failure and the status of TnI: non-IHF with normal TnI (n = 1009) vs. non-IHF with elevated TnI (n = 1665) vs. IHF with normal TnI (n = 258) vs. IHF with elevated TnI (n = 1464). The primary outcome was death from all causes according to the etiology (non-IHF vs. IHF) and TnI elevation during the entire follow-up period of 784 days (IQR 446–1116). Elevation of TnI was observed in 71.2% of all patients with AHF. Patients with IHF had higher all-cause mortality compared to those with non-IHF. Elevated TnI was associated with higher 90-day and post-90-day mortality in the non-IHF group. IHF as compared to non-IHF and elevation of TnI were independent predictors of mortality also in the adjustment analysis. In the IHF group, however, elevated TnI had a higher mortality with only 90-day follow-up (18.6% vs. 25.9%, log-rank p < 0.001), not in the post-90-day follow-up (31.1% vs. 32.5%, log-rank p = 0.799). In conclusion, elevated TnI in patients with heart failure is associated with increased all-cause mortality regardless of the etiology of HF. Elevation of TnI was associated to a higher post-90 day mortality in patients with non-IHF but not in patients with IHF.

Recurrent myocardial injury is a strong predictor of ICU mortality in COVID-19

Abstract Funding Acknowledgements Type of funding sources: None. Background Myocardial injury is common in COVID-19, and has been linked to disease severity and mortality.1 Its pathophysiology is not fully elucidated and suggested mechanisms include cytokine damage, endotheliitis, myocarditis, ferroptosis, acute coronary syndrome, oxygen supply-demand mismatch and pulmonary embolism.2-3 Elevated serum cardiac troponin (cTn) – as surrogate marker of myocardial injury – at admission and during hospitalisation is associated with poor outcome.4-5 Comparison of available trial data, however, is unfeasible, because of variable definition and sampling timing/intervals/assays.6 Peculiarly, prognostic cut-off cTn values are often – retrospectively – set much lower than recommended by the guidelines.6-8 Furthermore, robust intensive care unit (ICU) outcome data regarding cTn evolution over time is lacking. Purpose The aim of this study is to critically explore the correlation between myocardial injury and mortality in a tertiary ICU population, using both standard and high cTn cut-off values, and to scrutinise the impact of timing and recurrence. Methods All adult COVID-19 patients admitted to our tertiary ICU between 06/03/2020 and 27/09/2021 were enrolled in this large, retrospective, single centre, cohort study. Patients requiring extracorporeal membrane oxygenation (n=29) were excluded. Myocardial injury was defined – as per ESC guidelines - as high-sensitive cardiac troponin I (hs-cTnI) peak &amp;gt;45ng/L (99th percentile upper reference limit) and ‘major’ myocardial injury was defined as hs-cTnI &amp;gt;135ng/L (3x upper limit of normal).6-7 Recurrent myocardial injury was considered if a new hs-cTnI peak above cut-off point occurred after normalisation. Patients were categorised according to peak (‘standard’ &amp;gt;45ng/L vs ‘high’ &amp;gt;135ng/L), onset (‘on admission’ vs ‘during hospitalisation’) and recurrence (‘single’ vs ‘multiple’) of hs-cTnI rise. Statistical analysis was done by logistic regression, using IBM SPSS version 28. Results A total of 193 COVID-19 ICU patients were included. Patient characteristics, disease severity indices and treatment details are summarised in Table 1. The mean age was 62 years and ICU mortality was 22%. Myocardial injury overall occurred in 51% (n=99) and major myocardial injury occurred in 39% (n=75) of patients. Obtained results were consistent across standard (&amp;gt;45ng/L) and high (&amp;gt;135ng/L) hs-cTnI cut-off groups. Myocardial injury only present at ICU admission was not correlated with mortality in our cohort, contradicting prior (mostly non-ICU) trials. Single hs-cTnI peak during ICU hospitalisation, however, and, especially recurrent hs-cTnI peaks were strong predictors of ICU mortality. The respective incidence, odds ratio, 95% confidence intervals and p-values are displayed in Table 2. Conclusion Myocardial injury occurring during ICU hospitalisation and, especially, recurrent myocardial injury is strongly correlated with ICU mortality in COVID-19 patients.

Prognostic value of cardiac troponin in critically ill COVID-19 patients

Funding AcknowledgementsType of funding sources: None.Background/IntroductionAmong patients with COVID-19, there is a high prevalence of cardiovascular disease and myocardial injury from the infection, especially in critically ill patients.PurposeThis study sought to investigate the relationship between elevated admission high-sensitive troponin I in COVID-19 patients admitted to an intensive care unit (ICU) and prognosis.MethodsWe retrospectively analyzed patients consecutively admitted to an ICU with COVID-19, with a median follow-up of 10 months. Patients who were diagnosed with acute coronary syndrome, either died or were discharged within 48 hours of admission, and who did not have a cardiac troponin measurement in the first 48 hours, were excluded.Two groups were identified, with normal troponin and with elevated troponin. Groups were compared, with special interest regarding in-hospital mortality, duration of mechanical ventilation, in-hospital diagnosis of heart failure, and length of hospitalization. Global mortality (in-hospital and during follow up) and re-hospitalization were compared. To compare survival, a Kaplan-Meier curve with log rank test was performed.ResultsFrom a total of 219 patients, after applying the exclusion criteria, 100 patients were included in the analysis, mean age was 62.9 ±12.5 years, and 74% were male.Troponin was normal in 77% of patients and elevated in 23%. Median troponin was 11 (IQR=26) ng/L (reference range <34 ng/L).Patients with elevated troponin were older (66.5 ±12.0 vs 61.6 ±12.5 years, p=0.036). Gender, comorbidities, vasopressor use, and APACHE II score were similar among groups. Patients with elevated troponin presented a higher ICU mortality (16.9% vs 47.8%, p=0.002) and higher global mortality (22.1% vs 47.8%, p=0.016). Re-hospitalization rates, ICU length of stay and duration of mechanical ventilation were similar among groups.In multivariate analysis, after adjustment for age and APACHE II score, an elevated troponin remained an independent predictor of ICU mortality (OR=3.40, 95% CI 1.08-10.4, p=0.036), but not an independent predictor of global mortality (OR=2.75, 95% CI 0.86-8.80, p=0.087).Kaplan-Meier analysis (Figures 1 and 2) showed that patients with elevated troponin had higher ICU (p=0.008) and global mortality (p=0.008) when compared to patients with normal admission troponin.Conclusion(s)The present study shows that elevated high-sensitive cardiac troponin I at admission predicts ICU and global mortality in critically ill COVID-19 patients. Cardiac troponin is as easy-to-use tool that may help to identify patients who benefit from tighter monitoring both during hospitalization and after discharge.

Clinical Presentation of Acute Ruptured Sinus of Valsalva Aneurysm as a Mimic of Acute Coronary Syndrome

Acute ruptured sinus of Valsalva aneurysm may present with chest pain and rapidly worsening dyspnea. A 41-year-old male without known atherosclerotic risk factors presented with ST-segment elevation in leads aVR and V1 on electrocardiogram and elevated cardiac troponins and was diagnosed as acute coronary syndrome. After antiplatelet loading, statin, and heparin, he was referred due to worsening hypotension and tachycardia. Clinical examination and echocardiogram was challenging in the acutely dyspneic restless patient. Transesophageal echocardiography delineated the ruptured aneurysm and assisted in its management. Importance of physical examination and echocardiography in the emergency room is highlighted as manifestations may be varied.

D-19 | Elevated Troponin Predicts Death and In-Hospital Complications in COVID-19 patients: A Systematic Review and Meta-Analysis

COVID-19 infection is associated with multiple cardiac and noncardiac complications and adverse outcome. We performed a systematic review and meta-analysis to determine whether elevated cardiac troponin (cTn), a marker of myocardial injury, is a prognostic biomarker of outcomes in hospitalized COVID-19 patients (pts).

Natriuretic Peptides and Troponins to Predict Cardiovascular Events in Patients Undergoing Major Non-Cardiac Surgery.

Patients undergoing major surgery have a substantial risk of cardiovascular events during the perioperative period. Despite the introduction of several risk scores based on medical history, classical risk factors and non-invasive cardiac tests, the possibility of predicting cardiovascular events in patients undergoing non-cardiac surgery remains limited. The cardiac-specific biomarkers, natriuretic peptides (NPs) and cardiac troponins (cTn) have been proposed as additional tools for risk prediction in the perioperative period. This review paper aims to discuss the value of preoperative levels and perioperative changes in cardiac-specific biomarkers to predict adverse outcomes in patients undergoing major non-cardiac surgery. Based on several prospective observational studies and six meta-analyses, some guidelines recommended the measurement of NPs to refine perioperative cardiac risk estimation in patients undergoing non-cardiac surgery. More recently, several studies reported a higher mortality in surgical patients presenting an elevation in high-sensitivity cardiac troponin T and I, especially in elderly patients or those with comorbidities. This evidence should be considered in future international guidelines on the evaluation of perioperative risk in patients undergoing major non-cardiac surgery.

Neurogenic stunned myocardium resulting from surgical brainstem handling during resection of paediatric recurrent medulloblastoma—a possible brain heart interaction

Neurogenic stunned myocardium (NSM) is characterised by an acute onset cardiac dysfunction following an acute neurological insult which mimics acute coronary syndrome. A 12-year-old male child was admitted to the neuro-intensive care unit (NICU) following midline suboccipital craniotomy and resection of recurrent medulloblastoma. Postoperatively, in NICU, he developed tachycardia and hypotension, which was unresponsive to fluid challenge requiring norepinephrine infusion. Intraoperatively, during tumour resection from the dorsal medulla, episodes of hypertension and bradycardia were observed. Intraoperative blood loss was adequately managed with a stable hemodynamic profile without postoperative anaemia. An electrocardiogram showed sinus tachycardia with T wave inversion, and blood investigation revealed elevated cardiac troponin T levels. Point of care ultrasound (POCUS) of heart and lung showed features of NSM. Infusion dobutamine was added to achieve a target mean arterial pressure of 65mm Hg with concomitant furosemide infusion and fluid restriction. Daily POCUS assessment of cardiac contractility and volume status was done. The patient was weaned from vasoactive drugs and ventilator following improvement of cardiac function and was discharged from NICU after 17days. NSM results from the excessive release of catecholamines following stimulation of trigger zones in the brain. To date, a handful of cases of pediatric NSM following primary brain tumour are reported where hydrocephalus resulted in trigger zone activation. In this presented case, direct brain stem stimulation during tumour resection might have triggered NSM. Irrespective of the cause, timely diagnosis and execution of supportive management in our patient resulted in a positive outcome.

Development and preliminary validation of infrared spectroscopic device for transdermal assessment of elevated cardiac troponin

BackgroundThe levels of circulating troponin are principally required in addition to electrocardiograms for the effective diagnosis of acute coronary syndrome. Current standard-of-care troponin assays provide a snapshot or momentary view of the levels due to the requirement of a blood draw. This modality further restricts the number of measurements given the clinical context of the patient. In this communication, we present the development and early validation of non-invasive transdermal monitoring of cardiac troponin-I to detect its elevated state.MethodsOur device relies on infrared spectroscopic detection of troponin-I through the dermis and is tested in stepwise laboratory, benchtop, and clinical studies. Patients were recruited with suspected acute coronary syndrome.ResultsWe demonstrate a significant correlation (r = 0.7774, P < 0.001, n = 52 biologically independent samples) between optically-derived data and blood-based immunoassay measurements with and an area under receiver operator characteristics of 0.895, sensitivity of 96.3%, and specificity of 60% for predicting a clinically meaningful threshold for defining elevated Troponin I.ConclusionThis preliminary work introduces the potential of a bloodless transdermal measurement of troponin-I based on molecular spectroscopy. Further, potential pitfalls associated with infrared spectroscopic mode of inquiry are outlined including requisite steps needed for improving the precision and overall diagnostic value of the device in future studies.

Subclinical cardiovascular disease and frailty risk: the atherosclerosis risk in communities study

BackgroundCardiovascular disease (CVD) is associated with a greater frailty risk, but it remains unknown if pathways that contribute to CVD are associated with the frailty risk. Thus, we aimed to investigate whether elevations in high-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) for those without known CVD at baseline are associated with a higher frailty risk.MethodsThis study used data from the Atherosclerosis Risk in Communities study. Cardiac biomarkers were measured from stored plasma samples collected at Visit 2 (1991–1993). Frailty was recorded at Visit 5 (2011–2013). Cox regression models were used to determine the association of cardiac biomarkers with frailty risk.ResultsOverall, 360/5199 (6.9%) participants aged 55.1 ± 5.1 years developed frailty during a median follow-up of 21.7 years. The incidence of frailty was significantly higher in participants with hs-cTnT ≥14 ng/L (vs. < 14 ng/L: 17.9% vs. 6.7%) or NT-proBNP ≥300 pg/ml (vs. < 300 pg/ml: 19.7% vs. 6.8%) (all P < 0.001). Comparing higher vs. lower cut-off levels of either hs-cTnT (14 ng/l) or NT-proBNP (300 pg/ml) demonstrated a greater than two-fold higher frailty risk, with hazard ratios (HRs) of 2.13 (95% confidence interval (CI): 1.130–4.01, P = 0.020) and 2.61 (95% CI: 1.28–5.33, P = 0.008), respectively. Individuals with both elevated hs-cTnT and NT-proBNP had a higher frailty risk than those without it (HR: 4.15; 95% CI: 1.50–11.48, P = 0.006).ConclusionsHigh hs-cTnT and NT-proBNP levels are strongly associated with incident frailty in the community-dwelling population without known CVD. Subclinical cardiac damage (hs-cTnT) and/or wall strain (NT-proBNP) may be the key pathway of CVD patients developing frailty. Detection of hs-cTnT and NT-proBNP may help for early screening of high-risk frailty and providing individualised intervention.Trial registrationURL: https://www.clinicaltrials.gov; Unique identifier: NCT00005131.

Myocardial Infarction after ChAdOx1 nCoV-19 in a Young Male.

Sir, Myocardial infarction rarely happens in young age.[1] Hereby, we report the case of a 21-year-old patient who presented with myocardial infarction 14 days after receiving the ChAdOx1 nCoV-19 COVID-19 (AstraZeneca/Vaxzevria) vaccine. Sometimes thrombotic events associated with thrombocytopenia after immunisation occurs known as vaccine-induced immune thrombotic thrombocytopenia (VITT) which manifests 3–30 days post vaccination. Thrombocytopenia, raised Platelet factor-4 antibodies, increased d-dimer, thrombi are common findings in VITT.[23] Possible etiological factors such as hyperhomocystenemia, vegetation, autoimmune, nephrotic syndrome, obesity, metabolic syndrome, stress, hypercoagulability, comorbidities were evaluated and excluded.[4] The presentation here is chest pain radiating to arms and vomiting for 5 days. He received vaccination 14 days prior to symptoms. The patient has no history of smoking, alcohol, and substance abuse. Electrocardiogram showing ST elevation Anterior wall Myocardial infarction [Figure 1a]. Echocardiography showed akinetic anterior and lateral wall, left ventricular apical thrombus, severe left ventricular dysfunction, regional wall motion abnormality present, dilated left atrium, left ventricle, left ventricular ejection fraction-35%, grade 1 diastolic dysfunction. Biochemical parameters reveal elevated cardiac markers troponin I 96000 pg/ml, antinuclear antibody-0.11, homocysteine 14.5micromol/l, HbA1C-5%. Patient was treated with anticoagulants, dual antiplatelets, statins, beta blockers, ACE inhibitors, antianginals and diuretics. Coronary angiography revealed occluded mid left anterior descending artery and proximal diagonal artery [Figure 1b]. Later reperfusion was achieved through percutaneous transluminal coronary angioplasty by placing three stents.Figure 1: (a) ECG suggestive of ST elevation in lead 1, aVL, V1-V6, pathological q-waves in V1-V6, poor R-wave progression, QRS > 0.12 s in V1, V2, tall R-wave in V1, wide S-wave in L1, V5, V6, suggestive of acute anterior wall and (b) coronary angiographyIt is the onus of responsibility for dispelling erroneous or exaggerated reports of COVID-19 vaccination dangers. Further research study could be vital. It is commonly acknowledged that vaccination benefits outweigh the risks and must be mindful to link negative outcomes to vaccine, anticipate patient queries and findings should not be overstated. Declaration of patient consent We certify that we have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. Research quality and ethics statement We followed applicable EQUATOR Network (http://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Comparison of elevated cardiac troponin I with SAPS-II and APACHE-II score in predicting outcome of severe intoxications.

Background and Aims:To date, different methods have been invented to risk-stratify critically ill patients, however, there is a paucity of information regarding assessing the severity of poisonings. This study was designed to determine the comparative efficacy of Simplified Acute Physiology Score-II (SAPS-II) and Acute Physiology and Chronic Health Evaluation-II (APACHE-II)score with cardiac troponin I (cTnI) in predicting severe intoxication outcomes.Methods:This was a prospective study conducted on patients who fulfilled defined severe intoxication criteria necessitating intensive care unit (ICU) admission over a period of 6 months. SAPS-II and APACHE-II scores were calculated and cTnI concentrations were measured. These indicators were compared to determine which has the better ability to prognosticate mortality and complications.Results:A total of 55 cases (median age, 35 [24-49] years) were enroled. Eight patients (14.5%) died. Mean SAPS-II, median APACHE-II score and median cTnI concentrations were 32.05 ± 11.24, 13 [10-17] and 0.008 [0.002-0.300] ng/ml, respectively, which were significantly different between the survivors and non-survivors. Receiver operating characteristics curve results of SAPS-II, APACHE-II score and cTnI concentrations in predicting mortality were 0.945, 0.932 and 0.763 and in predicting complications were 0.779, 0.739 and 0.727, respectively. High cTnI concentration (>0.37 ng/ml) correlated with soft clinical outcomes, including length of ventilatory support, length of ICU stay and length of hospital stay (LOS) (r: 0.928, 0.881 and 0.735 respectively; all P < 0.001).Conclusion:SAPS-II scores were superior in predicting death and complications, while cTnI correlated more closely with soft clinical outcomes, such as the length of ventilator support, length of ICU stay or LOS.

Predictors of mortality related to Covid-19

Introduction: The new 2019 coronavirus has spread rapidly around the world, creating a pandemic. Since the beginning of the pandemic, 6.012.035 patients have died. The objective of this study is to identify clinical and biological parameters associated with high mortality in patients with COVID-19 pneumonia. Material and methods: We report a retrospective study carried out in a Covid department of the Mohamed VI University Hospital of Marrakech between 20 October and 20 December 2021. Patients were divided into 2 groups: a survivor group and a decedent group. Results: We collected 103 cases during this period. A male predominance was noted in 55.3% of cases. The group of deceased included 9 cases (8.7%) while the group of survivors contained 94 cases (91.2%). The average age of the patients in the survivor group was 44.6 years, while it was higher in the deceased group (60.6 years). We noted that the deceased patients had more arterial hypertension (55.6% vs. 10.6%) and heart disease (66.7% vs. 0%) than the survivors, and diabetes was more common in the deceased (77.8% vs. 12.8%). Clinical signs were more severe in the decedents. Biological tests showed lymphopenia in 88.9% of the deceased group. Cardiac troponins were also higher in the deceased group with a mean value of 172.7ng/l. Conclusion: Through our study, we identified four predictors of mortality: age ≥ 65 years, presence of comorbidities, lymphopenia and elevated cardiac troponins.

LCZ696 ameliorates doxorubicin-induced cardiomyocyte toxicity in rats

Doxorubicin (DOX)-based chemotherapy induces cardiotoxicity, which is considered the main bottleneck for its clinical application. In this study, we investigated the potential benefit of LCZ696, an angiotensin receptor–neprilysin inhibitor against DOX-induced cardiotoxicity in rats and H9c2 cells and determined whether the mechanism underlying any such effects involves its antioxidant activity. Male Sprague–Dawley rats were randomly separated into four groups, each consisting of 15 rats (DOX (1.5 mg/kg/day intraperitoneally for 10 days followed by non-treatment for 8 days); DOX + valsartan (31 mg/kg/day by gavage from day 1 to day 18); DOX + LCZ696 (68 mg/kg/day by gavage from day 1 to day 18); and control (saline intraperitoneally for 10 days). DOX-induced elevation of cardiac troponin T levels on day 18 was significantly reduced by LCZ696, but not valsartan. The DOX-induced increase in myocardial reactive oxygen species (ROS) levels determined using dihydroethidium was significantly ameliorated by LCZ696, but not valsartan, and was accompanied by the suppression of DOX-induced increase in p47phox. LCZ696 recovered the DOX-induced decrease in phosphorylation of adenosine monophosphate-activated protein kinase and increased the ratio of Bax and Bcl-2. In H9c2 cardiomyocytes, LCZ696 reduced DOX-induced mitochondrial ROS generation and improved cell viability more than valsartan. Our findings indicated that LCZ696 ameliorated DOX-induced cardiotoxicity in rat hearts in vivo and in vitro, possibly by mediating a decrease in oxidative stress.

Troponin Levels and the Severity of COVID-19 Pneumonia.

IntroductionIn late 2019, a novel coronavirus was identified as the pathogen responsible for a cluster of pneumonia cases in Wuhan, a city in the Hubei Province of China. Elevated cardiac troponin is a marker of myocardial injury, which is commonly seen in hospitalized patients with COVID-19 due to unclear reasons. The frequency of elevated troponin levels in patients with COVID-19 is variable and is reported in up to 7-36% of patients. The troponin level may be associated with the severity of COVID-19, and mild cases of COVID-19 tend to have a normal troponin level. This study aims to determine the frequency of patients with COVID-19 who had elevated troponin levels on presentation to the ED and determine the factors associated with elevated troponin levels. Additionally, the study aims to identify the association of elevated troponin and the outcome of COVID-19.MethodologyA retrospective study wherein the factors associated with elevated troponin levels in COVID-19 pneumonia were evaluated. The study was conducted in King Fahd Hospital of the Imam Abdulrahman Bin Faisal University. The Hospital Information System was used to identify all visits to the ED from March 2020 to November 2020 for patients who tested positive for SARS-CoV-2. In addition, a structured data collection form was used to collect data from the electronic health records. The data collection was conducted by emergency medicine physicians who were given a detailed explanation of the purpose of the study and had training and supervision by the principal investigator.ResultsThe study involved 214 patients who presented to the ED and had positive results on the SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) test and had troponin-I levels measured. Patients with elevated troponin levels were more likely to require supplementary oxygen compared with those with normal troponin levels (88.0 vs. 58.5%; P < 0.01). In total, 36 (76.6%) patients with elevated troponin levels required admission to the ICU compared with 58 (45.0%) patients with normal troponin levels (P < 0.01). Multivariable binary logistic regression analysis was used to identify the predictors of elevated troponin levels on presentation. The model revealed that being admitted in the ICU was the single independent predictor (P = 0.02).ConclusionThe study demonstrated that the troponin level on presentation to the ED was a viable independent prognostic factor in COVID-19 pneumonia. However, further studies are needed to investigate targeted therapeutic interventions among patients with elevated troponin levels, such as cardioprotective therapies like corticosteroids, immunosuppressants, antivirals, or immunoglobulins.

Novel oxygen desaturation parameters are associated with cardiac troponin I: Data from the Akershus Sleep Apnea Project.

Novel diagnostic markers for obstructive sleep apnea beyond the apnea-hypopnea index (AHI) have been introduced. There are no studies on their association with markers of subclinical myocardial injury. We assessed the association between novel desaturation parameters and elevated cardiac troponin I and T. Participants with polysomnography (498) from the Akershus Sleep Apnea study were divided into normal and elevated biomarker groups based on sex-specific concentration thresholds (cardiac troponin I: ≥4ng/L for women, ≥6ng/L for men; and cardiac troponin T: ≥7ng/L for women, ≥8ng/L for men). Severity of obstructive sleep apnea was evaluated with the AHI, oxygen desaturation index, total sleep time with oxygen saturation below 90% (T90), lowest oxygen saturation (Min SpO2 %), and novel oxygen desaturation parameters: desaturation duration and desaturation severity. How the AHI and novel desaturation parameters predicted elevated cardiac troponin I and cardiac troponin T levels was assessed by the area under the curve (AUC). Based on multivariable-adjusted linear regression, the AHI (β=0.004, p=0.012), desaturation duration (β=0.007, p=0.004), and desaturation severity (β=0.147, p=0.002) were associated with cardiac troponin I levels but not cardiac troponin T. T90 was associated with cardiac troponin I (β=0.006, p=0.009) and cardiac troponin T (β=0.005, p=0.007). The AUC for the AHI 0.592 (standard error 0.043) was not significantly different from the AUC of T90 (SD 0.640, p=0.08), desaturation duration 0.609 (SD0.044, p=0.42) or desaturation severity 0.616 (SD 0.043, p=0.26) in predicting myocardial injury as assessed by cardiac troponin I. Oxygen desaturation parameters and the AHI were associated with cardiac troponin I levels but not cardiac troponin Tlevels. Novel oxygen desaturation parameters did not improve the prediction of subclinical myocardial injury compared to the AHI.

Prognosis is worse with elevated cardiac troponin in nonacute coronary syndrome compared with acute coronary syndrome.

Cardiac troponin (cTn) can be elevated in many patients presenting to the emergency department (ED) with chest pain but without a diagnosis of acute coronary syndrome (ACS). We compared the prognostic significance of cTn in these different populations. We retrospectively analyzed the CHOPIN study, which enrolled patients who presented to the ED with chest pain. Patients were grouped as ACS, non-ACS cardiovascular disease, noncardiac chest pain and chest pain not otherwise specified (NOS). We examined the prognostic ability of cTnI for the clinical endpoints of mortality and major adverse cardiovascular event (MACE; a composite of acute myocardial infarction, unstable angina, revascularization, reinfarction, and congestive heart failure and stroke) at 180-day follow-up. Among 1982 patients analyzed, 14% had ACS, 21% had non-ACS cardiovascular disease, 31% had a noncardiac diagnosis and 34% had chest pain NOS. cTnI elevation above the 99th percentile was observed in 52, 18, 6 and 7% in these groups, respectively. cTnI elevation was associated with mortality and MACE, and their relationships were more prominent in noncardiac diagnosis and chest pain NOS than in ACS and non-ACS cardiovascular diagnoses for mortality, and in non-ACS patients than in ACS patients for MACE (hazard ratio for doubling of cTnI 1.85, 2.05, 8.26 and 4.14, respectively; P for interaction 0.011 for mortality; 1.04, 1.23, 1.54 and 1.42, respectively; P for interaction <0.001 for MACE). In patients presenting to the ED with chest pain, cTnI elevation was associated with a worse prognosis in non-ACS patients than in ACS patients.

High-Sensitivity Troponin I after Cardiac Surgery and 30-Day Mortality

BackgroundConsensus recommendations regarding the threshold levels of cardiac troponin elevations for the definition of perioperative myocardial infarction and clinically important periprocedural myocardial injury in patients undergoing cardiac surgery range widely (from >10 times to ≥70 times the upper reference limit for the assay). Limited evidence is available to support these recommendations.MethodsWe undertook an international prospective cohort study involving patients 18 years of age or older who underwent cardiac surgery. High-sensitivity cardiac troponin I measurements (upper reference limit, 26 ng per liter) were obtained 3 to 12 hours after surgery and on days 1, 2, and 3 after surgery. We performed Cox analyses using a regression spline that explored the relationship between peak troponin measurements and 30-day mortality, adjusting for scores on the European System for Cardiac Operative Risk Evaluation II (which estimates the risk of death after cardiac surgery on the basis of 18 variables, including age and sex).ResultsOf 13,862 patients included in the study, 296 (2.1%) died within 30 days after surgery. Among patients who underwent isolated coronary-artery bypass grafting or aortic-valve replacement or repair, the threshold troponin level, measured within 1 day after surgery, that was associated with an adjusted hazard ratio of more than 1.00 for death within 30 days was 5670 ng per liter (95% confidence interval [CI], 1045 to 8260), a level 218 times the upper reference limit. Among patients who underwent other cardiac surgery, the corresponding threshold troponin level was 12,981 ng per liter (95% CI, 2673 to 16,591), a level 499 times the upper reference limit.ConclusionsThe levels of high-sensitivity troponin I after cardiac surgery that were associated with an increased risk of death within 30 days were substantially higher than levels currently recommended to define clinically important periprocedural myocardial injury. (Funded by the Canadian Institutes of Health Research and others; VISION Cardiac Surgery ClinicalTrials.gov number, NCT01842568.)

Abstract MP76: Association Of Elevated High-sensitive Cardiac Troponin T And Low Ankle-brachial Index With Incident Cardiovascular Events. The Multi-ethnic Study Of Atherosclerosis And The Cardiovascular Health Study

Introduction: Elevated high-sensitive cardiac troponin T (hs-cTnT&gt;14 ng/L) and low ankle-brachial index (ABI &lt; 0.9) are known to be associated with cardiovascular diseases (CVD) but their joint effect on the risk of CVD events is unknown. Methods: We used data from the MESA and CHS among 10,900 participants free of CVD events at baseline (mean age 66.3 years, 44.7% males). Incident coronary heart disease (CHD) was defined as fatal or non-fatal myocardial infarction or revascularization and incident CVD was defined as CHD, transient ischemic attack, stroke, or atrial fibrillation. Hazard ratio (HR) and 95% CI was calculated from a Cox regression model. Interaction on the additive scale was assessed using relative excess risk due to interaction (RERI) and interaction on the multiplicative scale was assessed by Likelihood ratio (LR) test. Results: At baseline (2000-2002 for MESA and 1989-1990 for CHS), 10.2% of participants had elevated hs-cTnT and 7.5% had low ABI. During 26.1 years of total follow-up (median follow-up 18.4 years), there were 3,911 incident CVD events. The risk of CHD and CVD was higher in participants with both elevated hs-cTnT and low ABI [CHD HR: 2.1 (1.5, 2.9), CVD HR: 2.1 (1.7, 2.5)], only elevated hs-cTnT [CHD HR: 1.7 (1.4, 2.0), CVD HR: 1.6 (1.5, 1.8)], and only low ABI [CHD HR: 1.8 (1.5, 2.2), CVD HR: 1.5 (1.3, 1.7)] than those with unelevated hs-cTnT and normal ABI. Interaction on the multiplicative scale was observe in both adjusted and unadjusted models for CHD (unadjusted LR test p-value=0.002, adjusted LR test p-value=0.042) and only in unadjusted model for CVD (LR test p-value=0.001). No significant additive interaction was detected for both CHD and CVD (RERI p-value≥0.25 for unadjusted and adjusted models). Conclusion: Having both elevated cTnT and low ABI was associated more strongly with CVD events than only elevated cTnT or low ABI. Antagonistic multiplicative interaction was found indicating the observed joint effect of elevated cTnT and low ABI was smaller than the expected combined individual effects.

Short-term exposure to traffic-related air pollution and STEMI events: Insights into STEMI onset and related cardiac impairment

AimsEvidence on the impacts of traffic-related air pollution (TRAP) on ST-segment elevation myocardial infarction (STEMI) events is limited. We aimed to assess the acute effects of TRAP exposure on the clinical onset of STEMI and related cardiac impairments. Methods and resultsWe recruited patients who were admitted for STEMI and underwent primary percutaneous coronary intervention at Peking University Third Hospital between 2014 and 2020. Indicators relevant to cardiac impairments were measured. Concomitantly, hourly concentrations of traffic pollutants were monitored throughout the study period, including fine particulate matter, black carbon (BC), particles in size ranges of 5–560 nm, oxides of nitrogen (NOX), nitrogen dioxide, and carbon monoxide. The mean (SD) age of participants was 62.4 (12.5) years. Daily average (range) concentrations of ambient BC and NOX were 3.9 (0.1–25.0) μg/m3 and 90.8 (16.6–371.7) μg/m3. Significant increases in STEMI risks of 5.9% (95% CI: 0.1, 12.0) to 21.9% (95% CI: 6.0, 40.2) were associated with interquartile range increases in exposure to TRAP within a few hours. These changes were accompanied by significant elevations in cardiac troponin T levels of 6.9% (95% CI: 0.2, 14.1) to 41.7% (95% CI: 21.2, 65.6), as well as reductions in left ventricular ejection fraction of 1.5% (95% CI: 0.1, 2.9) to 3.7% (95% CI: 0.8, 6.4). Furthermore, the associations were attenuated in participants living in areas with higher residential greenness levels. ConclusionsOur findings extend current understanding that short-term exposure to higher levels of traffic pollution was associated with increased STEMI risks and exacerbated cardiac impairments, and provide evidence on traffic pollution control priority for protecting vulnerable populations who are at greater risks of cardiovascular events.