Elevated Cardiac Troponin Levels Research Articles

Cardiac troponin as a prognosticator of mortality in patients with sepsis: A systematic review and meta-analysis.

The impact of cardiac troponin on the short-term and long-term prognosis of patients with sepsis remains uncertain. Therefore, we conducted a meta-analysis to investigate the role of cardiac troponin as a potential indicator for sepsis mortality. We performed a comprehensive search for articles published before November 2022 using Google Scholar, PubMed, and Web of Science. Inclusion criteria for the studies were: (1) investigation of cardiac troponin, and (2) investigation of sepsis. Exclusion criteria included: (1) inability to obtain or calculate hazard ratio (HR) and 95% confidence interval (CI) for the relationship between cardiac troponin level and sepsis mortality, and (2) reviews, meta-analyses, and case reports. Analysis of HRs and 95% CIs for the association between cardiac troponin level and sepsis mortality was conducted using STATA 12.0 software. Our study included 24 prospective studies (comprising 20,457 sepsis patients) and 4 retrospective studies (comprising 1416 sepsis patients). Meta-analysis demonstrated that elevated cardiac troponin levels were significantly associated with increased sepsis mortality using a random effects model (HR = 1.57, 95% CI 1.41-1.75). Moreover, elevated cardiac troponin levels were also significantly associated with increased hospital mortality of sepsis (HR = 1.35, 95% CI 1.19-1.53) and long-term mortality of sepsis (HR = 1.96, 95% CI 1.51-2.55) using the random effects model. Overall, our finding revealed that elevated cardiac troponin for sepsis patients was a predictor of hospital and long-term mortality. Clinicians may treat septic patients with elevated cardiac troponin more cautious to avoid extra death. Moreover, large clinical studies are warranted to validate this association.

Elevated level of high-sensitivity cardiac troponin I as a predictor of adverse cardiovascular events in patients with heart failure with preserved ejection fraction.

The relationship between the elevation of cardiac troponin and the increase of mortality and hospitalization rate in patients with heart failure with reduced ejection fraction is clear. This study investigated the association between the extent of elevated levels of high-sensitivity cardiac troponin I (hs-cTnI) and the prognosis in heart failure with preserved ejection fraction patients. A retrospective cohort study consecutively enrolled 470 patients with heart failure with preserved ejection fraction from September 2014 to August 2017. According to the level of hs-cTnI, the patients were divided into the elevated level group (hs-cTnI >0.034 ng/mL in male and hs-cTnI >0.016 ng/mL in female) and the normal level group. All of the patients were followed up once every 6 months. Adverse cardiovascular events were cardiogenic death and heart failure hospitalization. The mean follow-up period was 36.2 ± 7.9 months. Cardiogenic mortality (18.6% [26/140] vs. 1.5% [5/330], P <0.001) and heart failure (HF) hospitalization rate (74.3% [104/140] vs. 43.6% [144/330], P <0.001) were significantly higher in the elevated level group. The Cox regression analysis showed that the elevated level of hs-cTnI was a predictor of cardiogenic death (hazard ratio [HR]: 5.578, 95% confidence interval [CI]: 2.995-10.386, P <0.001) and HF hospitalization (HR: 3.254, 95% CI: 2.698-3.923, P <0.001). The receiver operating characteristic curve demonstrated that a sensitivity of 72.6% and specificity of 88.8% for correct prediction of adverse cardiovascular events when a level of hs-cTnI of 0.1305 ng/mL in male and a sensitivity of 70.6% and specificity of 90.2% when a level of hs-cTnI of 0.0755 ng/mL in female were used as the cut-off value. Significant elevation of hs-cTnI (≥0.1305 ng/mL in male and ≥0.0755 ng/mL in female) is an effective indicator of the increased risk of cardiogenic death and HF hospitalization in heart failure with preserved ejection fraction patients.

Cell-Specific Mechanisms in the Heart of COVID-19 Patients.

From the onset of the pandemic, evidence of cardiac involvement in acute COVID-19 abounded. Cardiac presentations ranged from arrhythmias to ischemia, myopericarditis/myocarditis, ventricular dysfunction to acute heart failure, and even cardiogenic shock. Elevated serum cardiac troponin levels were prevalent among hospitalized patients with COVID-19; the higher the magnitude of troponin elevation, the greater the COVID-19 illness severity and in-hospital death risk. Whether these consequences were due to direct SARS-CoV-2 infection of cardiac cells or secondary to inflammatory responses steered early cardiac autopsy studies. SARS-CoV-2 was reportedly detected in endothelial cells, cardiac myocytes, and within the extracellular space. However, findings were inconsistent and different methodologies had their limitations. Initial autopsy reports suggested that SARS-CoV-2 myocarditis was common, setting off studies to find and phenotype inflammatory infiltrates in the heart. Nonetheless, subsequent studies rarely detected myocarditis. Microthrombi, cardiomyocyte necrosis, and inflammatory infiltrates without cardiomyocyte damage were much more common. In vitro and ex vivo experimental platforms have assessed the cellular tropism of SARS-CoV-2 and elucidated mechanisms of viral entry into and replication within cardiac cells. Data point to pericytes as the primary target of SARS-CoV-2 in the heart. Infection of pericytes can account for the observed pericyte and endothelial cell death, innate immune response, and immunothrombosis commonly observed in COVID-19 hearts. These processes are bidirectional and synergistic, rendering a definitive order of events elusive. Single-cell/nucleus analyses of COVID-19 myocardial tissue and isolated cardiac cells have provided granular data about the cellular composition and cell type-specific transcriptomic signatures of COVID-19 and microthrombi-positive COVID-19 hearts. Still, much remains unknown and more in vivo studies are needed. This review seeks to provide an overview of the current understanding of COVID-19 cardiac pathophysiology. Cell type-specific mechanisms and the studies that provided such insights will be highlighted. Given the unprecedented pace of COVID-19 research, more mechanistic details are sure to emerge since the writing of this review. Importantly, our current knowledge offers significant clues about the cardiac pathophysiology of long COVID-19, the increased postrecovery risk of cardiac events, and thus, the future landscape of cardiovascular disease.

High-Sensitivity Troponins and Subclinical Coronary Atherosclerosis Evaluated by Coronary Calcium Score Among Older Asians Living With Well-Controlled Human Immunodeficiency Virus.

Elevated levels of high-sensitivity cardiac troponin (hs-cTn) are suggestive of myocardial cell injury and coronary artery disease. We explored the association between hs-cTn and subclinical arteriosclerosis using coronary artery calcification (CAC) scoring among 337 virally suppressed patients with human immunodeficiency virus (HIV) who were ≥50 years old and without evidence of known coronary artery disease. Noncontrast cardiac computed tomography and blood sampling for hs-cTn, both subunit I (hs-cTnI) and subunit T (hs-cTnT), were performed. The relationship between CAC (Agatston score) and serum hs-cTn levels was analyzed using Spearman correlation and logistic regression models. The patients, of whom 62% were male, had a median age of 54 years and had been on antiretroviral therapy for a median of 16 years; the CAC score was >0 in 50% of patients and ≥100 in 16%. Both hs-cTn concentrations were positively correlated with the Agatston score, with correlation coefficients of 0.28 and 0.27 (P < .001) for hs-cTnI and hs-cTnT, respectively. hs-cTnI and hs-cTnT concentrations of ≥4 and ≥5.3 pg/mL, respectively, provided the best performance for discriminating patients with Agatston scores ≥100, with a sensitivity and specificity of 76% and 60%, respectively, for hs-cTnI and 70% and 50% for hs-cTnT. In multivariable logistic regression analysis, each log unit increase in hs-cTnI level was independently associated with increased odds of having an Agatston score ≥100 (odds ratio, 2.83 [95% confidence interval, 1.69-4.75]; P <.001). Although not an independent predictor, hs-cTnT was also associated with an increased odds of having an Agatston score ≥100 (odds ratio, 1.58 [95% confidence interval, .92-2.73]; P = .10). Among Asians aged ≥50 years with well-controlled HIV infection and without established cardiovascular disease, 50% had subclinical arteriosclerosis. Increasing hs-cTnI and hs-cTnT concentrations were associated with an increased risk of severe subclinical arteriosclerosis, and hs-cTn may be a potential biomarker to detect severe subclinical arteriosclerosis.

Cardio-Pulmonary Histopathology with Clinical Correlations of Deceased Patients with COVID-19: A Case Series in Tehran, Iran.

SARS-CoV-2 may affect vital organs. The present study investigated the histopathology of pulmonary and cardiac tissues with clinical correlation in deceased patients with COVID-19. We obtained pulmonary and cardiac tissues from 30 deceased patients with COVID-19 in Tehran, Iran, from January to May 2021. Sampling was performed through a percutaneous needle biopsy. After slide preparation, two expert pathologists studied them. We assessed the correlation between clinical and pathological data by Fisher's exact test. The mean age of the patients was 73.8±13.4 years, and the male-to-female ratio was 23/7. The most common underlying disease was hypertension (HTN) in 25 patients (83%). Fifty-five tissue samples were achieved, including 28 pulmonary and 27 cardiac samples. Our results showed that all patients (100%) developed diffuse alveolar damage (DAD), and 26 (93%) developed hyaline membrane formation. The most common phase of DAD was the exudative-proliferative phase in 16 (57.1%). Three cardiac samples (11%) revealed myocarditis, and seven (26%) showed cardiomyocyte hypertrophy. In univariate analysis using Fischer's exact test, myocarditis had significant relationships with C-reactive protein (CRP) levels higher than 80 mg/dL (P=0.008) and elevated cardiac troponin levels higher than two-fold (P=0.01). COVID-19 can affect the major vital organs. However, only myocarditis had a significant relationship with the circulating levels of inflammatory factors.

Androgen-deprivation therapy with leuprolide increases abdominal adiposity without causing cardiac dysfunction in middle-aged male mice: effect of sildenafil.

Androgen-deprivation therapy (ADT) is the primary systemic therapy for treating advanced or metastatic prostate cancer (PCa), which has improved survival outcomes in patients with PCa. However, ADT may develop metabolic and cardiovascular adverse events that impact the quality of life and lifespan in PCa survivors. The present study was designed to establish a murine model of ADT with a gonadotropin-releasing hormone (GnRH) agonist leuprolide and to investigate its effects on metabolism and cardiac function. We also examined the potential cardioprotective role of sildenafil (inhibitor of phosphodiesterase 5) under chronic ADT. Middle-aged male C57BL/6J mice received a 12-wk subcutaneous infusion via osmotic minipumps containing either saline or 18 mg/4 wk leuprolide with or without 1.3 mg/4 wk sildenafil cotreatment. Compared with saline controls, leuprolide treatment significantly reduced prostate weight and serum testosterone levels, confirming chemical castration in these mice. The ADT-induced chemical castration was not affected by sildenafil. Leuprolide significantly increased the weight of abdominal fat after 12-wk treatment without a change in total body weight, and sildenafil did not block the proadipogenic effect of leuprolide. No signs of left ventricular systolic and diastolic dysfunction were observed throughout the leuprolide treatment period. Interestingly, leuprolide treatment significantly elevated serum levels of cardiac troponin I (cTn-I), a biomarker of cardiac injury, and sildenafil did not abolish this effect. We conclude that long-term ADT with leuprolide increases abdominal adiposity and cardiac injury biomarker without cardiac contractile dysfunction. Sildenafil did not prevent ADT-associated adverse changes.

A Scoping Review on COVID-19-Induced Cardiovascular Complications

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a type of human coronavirus that resulted in the 2019 coronavirus disease (COVID-19). Although it was generally categorized as a respiratory disease, its involvement in cardiovascular complications was identified from the onset. Elevated cardiac troponin levels (a myocardial injury marker) and echocardiograms, which showed the anomalous performance of the patients’ hearts, were noted in the early case reports obtained from Wuhan, China. A couple of mechanisms have been proposed to explain COVID-19-induced cardiovascular complications, with systemic inflammation being the major focus recently. Chest pain and palpitations are among the prevalent symptoms in moderate to severe COVID-19-recovering patients. Cardiac damage potentially occurs due to multifactorial factors, which include cytokine-induced inflammation, direct cardiotoxicity, and disseminated intravascular coagulation (DIC), among others. The cardiovascular manifestations include cardiac arrhythmia, cardiogenic shock, venous thromboembolism, and elevated cardiac biomarkers. Both the long- and short-term effects of these cardiovascular complications remain puzzling to researchers, as substantial evidence is yet to be gathered to reach a consensus on the severity of COVID-19 in the heart. The treatment considerations currently include antiarrhythmic management, ACEI or ARB use, anticoagulation, hemodynamic support, and immunosuppression. This review aimed to outline the pathogenesis of the various cardiac complications due to COVID-19 as well as the available treatment modalities of COVID-19 infection. Both the mechanisms and the treatments have been succinctly explained in a proper manner to ensure understanding.

Ventricular fibrillation and arrhythmia associated with cardiac fibromas involving both ventricles in a1.5-year-old girl.

This article reports the autopsy findings of a1.5-year-old girl with no history of previous hospital admission who suddenly collapsed at home. After 45 minutes of resuscitation efforts, the cardiac activity was restored. During hospitalization, she had ventricular arrhythmia and extremely elevated cardiac troponin levels. Internal examination and immunohistochemistry revealed cardiac fibromas of the right and left ventricles and extensive hypoxic myocardial damage. The right ventricular fibroma demonstrated interdigitating and entrapped myocardium visible at the edges and within the central portion of the tumor. The left ventricular fibroma originated in the subepicardial region and propagated towards the endocardium.

Acute pulmonary embolism with coexisting right heart thrombi in transit-surgical treatment of 20 consecutive patients.

The presence of right heart thrombi in transit (RHTiT) in the setting of acute pulmonary embolism (PE) is associated with high mortality. The optimal management in such cases is inconclusive. We present the results of surgical treatment of 20 consecutive patients diagnosed with high- or intermediate-high-risk PE with coexisting RHTiT. A retrospective analysis was performed of all consecutive patients undergoing surgical treatment in the Medicover Hospital between 2013 and 2021 for acute PE with coexisting thrombi in-transit in right heart cavities. The diagnosis was based on echocardiography, computed tomography pulmonary angiography and laboratory tests. Eligibility criteria for surgical treatment were acute PE with RHTiT, right ventricular overload on imaging studies and significantly elevated levels of cardiac troponin and NTproBNP. All patients were operated on with extracorporeal circulation using deep hypothermia and total circulatory arrest. The primary end point was hospital all-cause mortality; secondary end points were perioperative complications and long-term mortality. The analysis included 20 patients. There was no in-hospital death. Nearly one-third of patients required temporal hemofiltration for postoperative renal failure, but this did not involve the need for dialysis at discharge. No neurological complications occurred in any patient. The mean follow-up was 46 months (range 13-98). There was 1 death in the long-term follow-up, not related to PE. Surgical treatment of patients with acute PE and coexisting RHTiT can provide favourable results.

Prognostic value of echocardiographic indices in risk stratification of intermediate-risk pulmonary embolism

BackgroundRegarding risk stratification of intermediate-risk pulmonary embolism, data are still not sufficient. Transthoracic echocardiography parameters may be useful in risk evaluation in those patients. Some novel echocardiographic indices mainly tricuspid regurgitation peak gradient (TRPG), pulmonary artery acceleration time, and tricuspid annulus plane systolic excursion (TAPSE) were evaluated showing that they may be used for risk stratification of normotensive cases with acute pulmonary embolism (APE).ResultsThe studied cases were subdivided into two classes:Class I with intermediate-low-risk pulmonary embolism included 32 patients (53.3%) and class II with intermediate high-risk pulmonary embolism involved 28 cases (46.7%). Dyspnea, tachypnea, troponin level, RVD, RVD/LVD, TR velocity, and TRPG/TAPSE were statistically higher in cases of class II than that of class I (p < 0.001). On the other hand, TAPSE and PA acceleration time were markedly lower in the case of class II than that of class I (p < 0.001). Ten cases (35.7%) of group II required thrombolytic agents with a significant difference (p<0.001).ConclusionsRVD/LVD ratio, TAPSE, TRPG/TAPSE ratio, and PA acceleration time are echocardiographic parameters that might be helpful for risk stratification of cases with moderate-risk pulmonary embolism. The addition of elevated levels of cardiac troponins to imaging and clinical findings can improve PE-related risk identification.Trial registrationNCT04020250. Registered on 16 July 2019.

Gender Specificities of Cardiac Troponin Serum Levels: From Formation Mechanisms to the Diagnostic Role in Case of Acute Coronary Syndrome.

Cardiac troponins T and I are the main (most sensitive and specific) laboratory indicators of myocardial cell damage. A combination of laboratory signs of myocardial cell damage (elevated levels of cardiac troponins T and I) with clinical (severe chest pain spreading to the left side of the human body) and functional (rise or depression of the ST segment, negative T wave or emergence of the Q wave according to electrocardiography and/or decrease in the contractility of myocardial areas exposed to ischemia according to echocardiography) signs of myocardial ischemia is indicative of the ischemic damage to cardiomyocytes, which is characteristic of the development of acute coronary syndrome (ACS). Today, with early diagnostic algorithms for ACS, doctors rely on the threshold levels of cardiac troponins (99th percentile) and on the dynamic changes in the serum levels over several hours (one, two, or three) from the moment of admission to the emergency department. That said, some recently approved highly sensitive methods for determining troponins T and I show variations in 99th percentile reference levels, depending on gender. To date, there are conflicting data on the role of gender specificities in the serum levels of cardiac troponins T and I in the diagnostics of ACS, and the specific mechanisms for the formation of gender differences in the serum levels of cardiac troponins T and I are unknown. The purpose of this article is to analyze the role of gender specificities in cardiac troponins T and I in the diagnostics of ACS, and to suggest the most likely mechanisms for the formation of differences in the serum levels of cardiac troponins in men and women.

Thyroid Dysfunction among the Patients with Critical COVID-19.

Since the angiotensin-converting enzyme (ACE) is the functional receptor for SARS-CoV-2, predominantly expressed by the alveoli, SARS-CoV-2 primarily involves the lungs. Aside from the lungs, ACE is expressed in other organs, including the thyroid gland. This study aimed to evaluate the incidence of thyroid dysfunction (TD) in patients admitted to the intensive care unit (ICU) with critical COVID-19, with inflammatory markers and disease severity, compared to patients with normal thyroid function. This retrospective study included 52 patients admitted to the ICU with PCR-confirmed critical COVID-19 between April 2020 and September 2021.Thyroid function tests were obtained within the first three days after ICU admission. TD was defined as the detection of any abnormal level in thyroid-stimulating hormone (TSH), free thyroxine hormone (FT4), and free triiodothyronine hormone (FT3).None of the patients had a prior history of thyroid disease or received medications related to thyroid diseases. TD was detected in 34 patients (65.4%). The majority of patients (67%) required extracorporeal membrane oxygenation (ECMO), with a higher frequency in patients with TD (74%). Patients with and without TD were similar concerning age, gender, and the need for ECMO. Patients with TD had significantly decreased levels of TSH, FT3, and FT4 (p=0.002, <0.001, =0.005, respectively); a significantly greater acute physiology and chronic health evaluation II (APACHE-II) score (p=0.048); a significantly higher white blood cell count (p=0.031) and elevated levels of procalcitonin (p=0.003), C-reactive protein (p=0.049) and cardiac troponin T (p=0.025). Other parameters, such as ICU stay, sequential organ failure assessment [SOFA] score, and mortality, did not differ significantly (p=0.449, p=0.315, p=0.142, respectively). Our findings suggest that patients admitted to the ICU with critical COVID-19 are at an increased risk for the development of TD, which should also be taken into account in relation to inflammatory markers, cardiac troponin T levels, and APACHE-II scores.

Implementing screening for myocardial injury in non-cardiac surgery: perspectives of an ad-hoc interdisciplinary expert group

Objectives. Perioperative myocardial injury (PMI) is increasingly recognised as an important complication of non-cardiac surgery, with often clinically silent presentation, but detrimental prognosis. Active screening for PMI, involving the detection of dynamic and elevated levels of cardiac troponin, has recently been advocated by an increasing number of guidelines; however, active PMI screening has not been reflected in clinical practice. Design. As consensus on a common screening and management pathway is lacking, we synthesise the current evidence to provide suggestions on the selection of patients for screening, organisation of a screening program, and a potential management pathway, building upon a recently published perioperative screening algorithm. Results. Screening should be performed using high-sensitivity assays both preoperatively and postoperatively (postoperative Days 1 and 2) in patients at high-risk of experiencing perioperative complications. Conclusion. This expert opinion piece by an interdisciplinary group of predominantly Norwegian clinicians aims to assist healthcare professionals planning to implement guideline-recommended PMI screening at a local level in order to improve patient outcomes following non-cardiac surgery.

Hip Fracture With Elevated Troponin: Harbinger of Mortality or Need for Accelerated Surgery?

To determine the association of elevated troponin levels with time to surgery and the risk of mortality and other key clinical outcomes among elderly patients with hip fracture who had measured troponin levels at hospital admission. Retrospective cohort study. Single academic trauma center. We included 299 consecutive patients 60 years of age or older with a hip fracture and cardiac troponin levels measured at the time of hospital admission. Patients with elevated cardiac troponin levels at hospital admission (n = 43) compared with patients with normal troponin levels at admission (n = 256). Time to surgery, 90-day mortality, and major complications within 90 days of injury. The median age of the cohort was 80 years (interquartile range, 70-87 years), 59% were female, and 86% were living independently before their injury. Elevated troponin levels were associated with a 21-hour [95% confidence interval (CI), 12 to 32, P < 0.001] increase in the median time from admission to surgery (43 vs. 22 hours). Elevated troponin levels were also associated with a 14% (95% CI, 0% to 29%, P = 0.01) absolute increase in 90-day mortality (28% vs. 14%). Patients with elevated troponins were 15% (95% CI, -1% to 30%, P = 0.06) more likely to have a major complication (37% vs. 23%); however, the difference did not reach statistical significance. Among patients with a hip fracture and measured troponin levels, elevated troponin levels were associated with significant delays in surgery and increased 90-day mortality. Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

Cardiac myosin-specific autoimmune Tcells contribute to immune-checkpoint-inhibitor-associated myocarditis.

Immune checkpoint inhibitors (ICIs) are an effective therapy for various cancers; however, they can induce immune-related adverse events (irAEs) as a side effect. Myocarditis is an uncommon, but fatal, irAE caused after ICI treatments. Currently, the mechanism of ICI-associated myocarditis is unclear. Here, we show the development of myocarditis in A/J mice induced by anti-PD-1 monoclonal antibody (mAb) administration alone without tumor cell inoculation, immunization, or viral infection. Mice with myocarditis have increased cardiac infiltration, elevated cardiac troponin levels, and arrhythmia. Anti-PD-1 mAb treatment also causes irAEs in other organs. Autoimmune Tcells recognizing cardiac myosin are activated and increased in mice with myocarditis. Notably, cardiac myosin-specific Tcells are present in naive mice, showing a phenotype of antigen-experienced Tcells. Collectively, we establish a clinically relevant mouse model for ICI-associated myocarditis and find a contribution of cardiac myosin-specific Tcells to ICI-associated myocarditis development and pathogenesis.

Clinical Profile, Immediate- and Short-term Outcome of Patients with Intermediate-risk Acute Pulmonary Thromboembolism.

Long-term outcomes of acute pulmonary thromboembolism (PTE) have been reported. However, the immediate- and short-term outcomes have not been reported adequately. Primary objective was to determine the patient characteristics, and immediate- and short-term outcomes of intermediate-risk PTE, and the secondary objective was to evaluate the benefit of thrombolysis in normotensive PTE patients. This study included patients diagnosed with acute intermediate PTE. Patient's electrocardiography (ECG) parameters along with echocardiography (echo), etc., conducted at the time of admission, during their stay in hospital, at the time of discharge, and during follow-up were recorded. The patients were treated using thrombolysis or anticoagulants depending on hemodynamic decompensation. During follow-up, they were reassessed for echo parameters-right ventricular (RV) function and pulmonary arterial hypertension (PAH). Among 55 patients, 29 (52.73%) were diagnosed with intermediate high-risk PTE and 26 (47.27%) with intermediate low-risk PTE. They were normotensive and most of them had a simplified pulmonary embolism severity index (sPESI) score <2. Typical ECG pattern S1Q3T3 along with echo patterns and elevated cardiac troponin levels were observed in most of the patients. Patients treated with thrombolytic agents showed a reduction in hemodynamic decompensation as opposed to patients treated with anticoagulants who had clinical signs of right heart failure (RHF) on follow-up after 3 months. This study contributes to the existing literature on outcomes of intermediate-risk PTE and the effect of thrombolysis on patients with hemodynamic stability. Thrombolysis reduced the incidence and progression of RHF in patients with hemodynamic instability. Mathiyalagan P, Rajangam T, Bhargavi K, Gnanaraj R, Sundaram S. Clinical Profile, Immediate- and Short-term Outcome of Patients with Intermediate-risk Acute Pulmonary Thromboembolism. Indian J Crit Care Med 2022;26(11):1192-1197.

Serum biomarkers, including nitric oxide metabolites (NOx), for prognosis of cardiovascular death and acute myocardial infarction in an ESSE-RF case–control cohort with 6.5-year follow up

The present case–control study aimed to assess associations of routine and experimental biomarkers with risk for cardiovascular death and acute myocardial infarction (AMI) in a cohort recruited from the multicenter study “Cardiovascular Epidemiology in Russian Federation” (ESSE-RF) to identify experimental biomarkers potentially suitable for expanded evaluation. A total of 222 subjects included cardiovascular death (N = 48) and AMI cases (N = 63) during 6.5-year follow up and matched healthy controls. Seven routine and eight experimental biomarkers were assayed to analyze associations with outcomes using logistic and Cox proportional hazard regressions. Elevated levels of cardiac troponin I (cTnI), C-reactive protein (CRP), and nitric oxide metabolites (NOx) were independently associated (P < 0.001) with higher risk of cardiovascular death (estimated hazard ratio (eHR) = 1.83–3.74). Elevated levels of NOx and cTnI were independently (P < 0.001) associated with higher risk of nonfatal AMI (eHRs = 1.78–2.67). Elevated levels of angiopoietin-like protein 3 (ANGPTL3) were independently associated (P < 0.001) with lower risk of cardiovascular death (eHRs 0.09–0.16) and higher risk of nonfatal AMI (eHR = 2.07; P = 0.01). These results indicated that subsequent expanded validation should focus on predictive impact of cTnI, NOx, CRP, and ANGPTL3 to develop nationwide recommendations for individual stratification of patients with cardiovascular risks.

Impact of myocardial injury on mortality and adverse events in hospitalized patients with influenza: a prospective cohort study

Abstract Background and aim Myocardial injury (MINJ) defined as elevated high-sensitivity cardiac troponin level (hs-cTnT) above normal values is a well-recognized prognostic marker in different clinical conditions, nonetheless, its relevance in Influenza remains poorly defined. We aimed to analyse incidence, predictors, short and mid-term prognostic role of MINJ in hospitalized patients (pts) with Influenza. Material and methods During 2018–2019 Influenza epidemic, a prospective multicentre observational cohort study was conducted enrolling all hospitalized adult patients with laboratory confirmed Influenza infection. MINJ was prospectively assessed at admission and defined as hs-cTnT &amp;gt;14 ng/L. Primary endpoint was all-cause death at 28-days. Secondary endpoints were all-cause death at 28-days or intensive care unit (ICU) admission/mechanical ventilation and all-cause death at follow up. Results 145 consecutive pts were enrolled. MINJ was evident in 94 (65.5%) pts. At a 28-days follow up, 7 deaths (4.8%) occurred, all in patients with MINJ at admission (log rank p=0.048). MINJ showed a strong association with the occurrence of death, ICU admission or mechanical ventilation (OR 5.74, 95% CI 1.28–53.29; p=0.015). At a median follow-up of 32.7 months, 15 (10.3%) deaths occurred, all among patients with MINJ at index hospitalization leading to a significantly high mortality rate at follow-up among patients with MINJ (log-rank p=0.003). Conclusions Influenza related MINJ is common and identifies patients at higher likelihood of short-term adverse events and midterm mortality. Funding Acknowledgement Type of funding sources: None.

COVID-19 and the autonomic nervous system

Abstract Background COVID-19 infection has been shown to have an adverse impact on the cardiovascular system. Cardiac injury, as indicated by elevated cardiac troponin and NT-proBNP levels have been confirmed in COVID-19 cases. There is still ambivalent data on the effect of left ventricular function. Cases of left ventricular impairment, persistent hypotension, acute myopericarditis, myocarditis, arrhythmia and heart failure have been reported in the short term, but there is a significant lacuna when it comes to medium and long-term follow-up of subjects previously infected with COVID-19. Purpose To assess any residual myocardial and autonomic injury in subjects previously infected with COVID-19 at a median follow-up of 5 months. Methods A case-control study was performed. Cases were randomly selected subjects who were previously diagnosed with COVID-19 infection following nasopharyngeal swabbing. Controls were subjects who had not been found to be infected with COVID-19 following swabbing and were negative for COVID-19 IgG antibodies. All participants were submitted a standardised questionnaire regarding past medical history. Blood investigations were taken including NT-proBNP and troponin I levels. In addition, all participants underwent 24-hour ambulatory blood pressure monitoring (ABPM) and 24-hour ECG monitoring. The latter was used to assess both for underlying arrhythmias as well as heart rate variability (HRV), a measure of autonomic regulation of the heart. All data was analysed using SPSS version 23.0. Results The study comprised 259 subjects, whereby cases included 174 participants while 75 subjects were age- and gender-matched controls. The study cohort was relatively young with a mean age of 46.1±13.8 years. The median follow-up was of approximately 5 months (median 173.5 days, IQR 129–193.25 days). There was no statistically significant difference between cases and controls with regards cardiovascular risk factors and underlying medical conditions. Likewise, there was no difference in blood investigations, including troponin I and NT-proBNP levels at 5-months follow-up. No difference was noted between the two groups in both awake and asleep blood pressure (BP) readings, as well as dipping BP status. No significant arrhythmias were noted in both groups on 24-hour ECG monitoring. However, when assessing for heart rate variability, it was shown that subjects who had been previously infected with COVID-19 exhibited lower root-mean square differences of successive R-R intervals (RMSSD), p=0.028. This indicates poor vagus nerve-mediated autonomic control of the heart. Conclusion Subjects previously infected with COVID-19 exhibited lower HRV as exhibited by low RMSSD as compared to controls. Reduced HRV is a known biomarker for mortality and sudden death in cardiac disease. The possible long-term implications of reduced HRV in subjects previously infected with COVID-19 merits further investigation. Funding Acknowledgement Type of funding sources: None.

Increased troponin levels can ­detect transient global amnesia mimics

Transient global amnesia (TGA) is a well-defined syndrome with temporarily impaired memory formation lasting several hours. Retrospective case series with diffusion-weighted magnetic resonance imaging (DWI) demonstrated that on average 5.4% of putative TGA cases are actually mimicked by strokes. To avoid a delay in stroke diagnosis – because DWI in TGA is usually deferred by a day or two – results from one large retrospective case series indicate that acutely elevated cardiac troponin levels will preselect those at highest risk of stroke as a TGA mimic and so are in need of urgent imaging and also cardiological work-up. Prospective studies will have to ascertain whether measuring troponin in suspected TGA will be helpful and improve outcome.