Elevated Cardiac Troponin Levels Research Articles

Association between coronary artery stenosis and myocardial injury in patients with acute pulmonary embolism: A case-control study.

The potential impact of pre-existing coronary artery stenosis (CAS) on acute pulmonary embolism (PE) episodes remains underexplored. This study aimed to investigate the association between pre-existing CAS and the elevation of high-sensitivity cardiac troponin I (hs-cTnI) levels in patients with PE. In this multicenter, prospective case-control study, 88 cases and 163 controls matched for age, sex, and study center were enrolled. Cases were patients with PE with elevated hs-cTnI. Controls were patients with PE with normal hs-cTnI. Coronary artery assessment utilized coronary computed tomographic angiography or invasive coronary angiography. CAS was defined as ≥50% stenosis of the lumen diameter in any coronary vessel >2.0mm in diameter. Conditional logistic regression was used to evaluate the association between CAS and hs-cTnI elevation. The percentage of CAS was higher in the case group compared to the control group (44.3% [39/88] vs. 30.1% [49/163]; P=0.024). In multivariable conditional logistic regression model 1, CAS (adjusted odds ratio [OR], 2.680; 95% confidence interval [CI], 1.243-5.779), heart rate >75 beats/min (OR, 2.306; 95% CI, 1.056-5.036) and N-terminal pro-B type natriuretic peptide (NT-proBNP) >420 pg/mL (OR, 12.169; 95% CI, 4.792-30.900) were independently associated with elevated hs-cTnI. In model 2, right CAS (OR, 3.615; 95% CI, 1.467-8.909) and NT-proBNP >420 pg/mL (OR, 13.890; 95% CI, 5.288-36.484) were independently associated with elevated hs-cTnI. CAS was independently associated with myocardial injury in patients with PE. Vigilance towards CAS is warranted in patients with PE with elevated cardiac troponin levels.

Acute ischemic stroke and troponin elevation: update of the Mannheim clinical algorithm

Elevated high-sensitivity cardiac troponin (hs-cTn) levels should be expected in about half of all patients with acute ischemic stroke (AIS). Since those patients are at risk of increased morbidity and mortality, often attributable to cardiac causes, an adequate work-up of the underlying etiology is required. This can only be achieved by ateam of cardiologists and neurologists. Since underlying causes of hs-cTn elevation in AIS patients are diverse, often atypical or silent in their clinical presentation and some, such as an accompanying myocardial infarction, can be acutely life-threatening, the work-up should follow astandardized clinical algorithm. The vast majority of hs-cTn elevations are caused by non-ischemic myocardial injury associated with AIS. This work presents apractice-oriented approach to differential diagnosis with the update of the Mannheim clinical algorithm for acute ischemic stroke and troponin elevation.

Incidence and associated in-hospital mortality of myocardial injury characterised by elevated cardiac troponin in adult patients with traumatic brain injury: protocol for a systematic review and meta-analysis

IntroductionMyocardial injury is a relatively common complication of traumatic brain injury (TBI). However, the incidence and clinical impact of myocardial injury characterised by elevated cardiac troponin (cTn) levels after TBI...

The central role of natural killer cells in mediating acute myocarditis after mRNA COVID-19 vaccination

Vaccine-related acute myocarditis is recognized as a rare and specific vaccine complication following mRNA-based COVID-19 vaccinations. The precise mechanisms remain unclear. We hypothesized that natural killer (NK) cells play a central role in its pathogenesis. Samples from 60 adolescents with vaccine-related myocarditis were analyzed, including pro-inflammatory cytokines, cardiac troponin T, genotyping, and immunophenotyping of the corresponding activation subsets of NK cells, monocytes, and Tcells. Results were compared with samples from 10 vaccinated individuals without myocarditis and 10 healthy controls. Phenotypically, high levels of serum cytokines pivotal for NK cells, including interleukin-1β (IL-1β), interferon α2 (IFN-α2), IL-12, and IFN-γ, were observed in post-vaccination patients with myocarditis, who also had high percentage of CD57+ NK cells in blood, which in turn correlated positively with elevated levels of cardiac troponin T. Abundance of the CD57+ NK subset was particularly prominent in malesand in those after the second dose of vaccination. Genotypically, killer cell immunoglobulin-like receptor (KIR) KIR2DL5B(-)/KIR2DS3(+)/KIR2DS5(-)/KIR2DS4del(+) was a risk haplotype, in addition to single-nucleotide polymorphisms related to the NK cell-specific expression quantitative trait loci DNAM-1 and FuT11, which also correlated with cardiac troponin T levels in post-vaccination patients with myocarditis. Collectively, these data suggest that NK cell activation by mRNA COVID-19 vaccine contributed to the pathogenesis of acute myocarditis in genetically and epidemiologically vulnerable subjects. This work was funded by the Hong Kong Collaborative Research Fund (CRF) 2020/21 and the CRF Coronavirus and Novel Infectious Diseases Research Exercises (reference no. C7149-20G).

Troponin efficacy in the diagnosis of acute coronary syndrome in patients with chronic renal failure.

There is no consensus on whether cardiac troponins with high reliability values should be different diagnostic criteria for acute myocardial infarction in patients with and without renal dysfunction. Although it is often emphasized that the etiology of elevated troponin levels in chronic kidney disease (CKD) remains unclear, elevated cardiac troponin (cTnT) levels have been associated with increased subclinical cardiac damage in these patient groups. In this study, we investigated the value of cTnT value in diagnosing acute coronary syndrome in CKD patients with high clinical suspicion of acute coronary syndrome and without acute ST segment elevation on electrocardiogram. The aim was to prevent cardiac ischemia from being overlooked in CKD patients. Coronary angiography revealed vessel occlusion in 192 patients, and the mortality rate after treatment decisions was 6.7%. The first measured troponin results showed a significant difference in patients who did not survive, indicating the prognostic value of troponin levels. Troponin values were compared with cardiovascular pathologies obtained by angiography, and elevated troponin levels strongly correlated with pathologic angiography results. The conclusion highlighted that despite prognostic uncertainties, biomarkers used for acute myocardial infarction diagnosis in patients with renal insufficiency are reliable in those with renal dysfunction. Elevated cTnT levels in CKD patients are considered a clear marker of cardiac ischemia, emphasizing the need for careful consideration of troponin values in this population.

Perioperative myocardial injury and infarction after noncardiac surgery: a review of pathophysiology, diagnosis, and management.

Perioperative myocardial injury is a relatively common complication after noncardiac surgery associated with significant morbidity and mortality. It is frequently driven by physiologic factors such as hypotension, tachycardia, and anemia. Diagnosis of perioperative myocardial injury after noncardiac surgery is based on elevated cardiac troponin levels, greater than the 99th percentile of the assay's upper reference limit within 30 days of surgery. Perioperative myocardial injury is further classified into non-ischemic and ischemic based on the underlying pathophysiology. Ischemic injury, also called myocardial injury after non-cardiac surgery (MINS), is further classified into perioperative myocardial infarction or myocardial injury without infarction. Classifying perioperative myocardial injury further is particularly important for clinical management and prognosis. MINS-with or without infarction-is independently and strongly associated with short- and long-term mortality. Compared to nonoperative myocardial infarction, perioperative myocardial infarction carries an increased risk of adverse outcomes including all-cause mortality. Preventative measures include a thorough preoperative risk assessment, risk factor optimization, and avoidance of intraoperative mismatch of myocardial oxygen supply and demand. Surveillance of patients at higher risk of cardiovascular complications is warranted and can lead to early recognition, closer monitoring, and appropriate management. This review will provide a framework for understanding perioperative myocardial injury and highlight the contemporary literature addressing its diagnosis and management.

Quantification of hs-Troponin Levels and Global Longitudinal Strain among Critical COVID-19 Patients with Myocardial Involvement.

Background. Myocardial involvement among critically ill patients with coronavirus disease 2019 (COVID-19) often has worse outcomes. An imbalance in the oxygen supply causes the excessive release of pro-inflammatory cytokines, which results in increased ventilation requirements and the risk of death in COVID-19 patients. Purpose. We evaluated the association between the hs-troponin I levels and global longitudinal strain (GLS) as evidence of myocardial involvement among critical COVID-19 patients. Methods. We conducted a prospective cohort study from 1 February to 31 July 2021 at RSUD Dr. Soetomo, Surabaya, as a COVID-19 referral center. Of the 65 critical COVID-19 patients included, 41 (63.1%) were men, with a median age (interquartile range) of 51.0 years (20.0-75.0). Subjects were recruited based on WHO criteria for severe COVID-19, and myocardial involvement in the form of myocarditis was assessed using CDC criteria. Subjects were examined using echocardiography to measure the GLS, and blood samples were taken to measure the hs-troponin. Subjects were then followed for their need for mechanical ventilation and in-hospital mortality. Results. Severe COVID-19 patients with cardiac injury were associated with an increased need for intubation (78.5%) and an increased incidence of myocarditis (50.8%). There was a relationship between the use of intubation and the risk of death in patients (66.7% vs. 33.3%, p-value < 0.001). Decreased GLS and increased hs-troponin were associated with increased myocarditis (p values < 0.001 and 0.004, respectively). Decreased GLS was associated with a higher need for mechanical ventilation (12.17 + 4.79 vs. 15.65 + 4.90, p-value = 0.02) and higher mortality (11.36 + 4.64 vs. 14.74 + 4.82; p-value = 0.005). Elevated hs-troponin was associated with a higher need for mechanical ventilation (25.33% vs. 3.56%, p-value = 0.002) and higher mortality (34.57% vs. 5.76%, p-value = 0.002). Conclusions. Critically ill COVID-19 patients with myocardial involvement and elevated cardiac troponin levels are associated with a higher need for mechanical ventilation and higher mortality.

Myocardial Infiltration in Primary Mediastinal B-Cell Lymphoma Detected by Cardiac Magnetic Resonance Imaging

Introduction: Cardiac involvement, particularly myocardial infiltration in primary mediastinal lymphoma, is a rare occurrence with an incidence of only 9% in known cases of primary malignancy. Neoplasm infiltration into the myocardium manifests through direct invasion, hematogenous spread, transvenous invasion through the great veins, or lymphangitic spreading in the mediastinal. Myocardial infiltration in lymphoma presents a grim prognosis and its treatment may be associated with specific risks, such as myocardial rupture. Various imaging modalities may detect cardiac involvement, with cardiac magnetic resonance (CMR) imaging considered the gold standard. CMR enables clear delineation of myocardial infiltration, making it valuable for local staging, pretreatment planning, and evaluating treatment response. Case Presentation: : A 37-year-old woman patient was diagnosed with primary mediastinal large B-cell lymphoma. Mild chest discomfort and shortness of breath were observed 3 months before hospital admission. A thorax CT scan showed a heterogeneous contrast-enhancing mass with a central necrotic area in the anterior mediastinum. Following thoracotomy and tumor debulking, the patient complained of severe crushing chest pain radiating to her back, accompanied by new T wave inversion on ECG and elevated cardiac troponin levels a week after surgery. Coronary angiogram results showed a normal coronary artery. Subsequent cardiac MRI showed tumor infiltration into the anterior pericardial space, as well as the myocardium of the left and right ventricles. Chemotherapy was promptly initiated, resulting in a gradual improvement of symptoms. Conclusions: In this study, we discuss the use of 3D-CRT in the re-irradiation of NPC with its limitation on obtaining optimum dose sculpture compared to more sophisticated and widely spread modalities like IMRT. However, with careful planning, we can still obtain optimum tumor dose, minimize OAR dose, and subsequently late toxicities that come after. We hope that this study can bring hope to centers with limited facilities, and we suggest further studies on reirradiation, especially in OAR dose tolerance guidelines.

Malva parviflora seed oil; Isolation, gas chromatographic profiling and its cardioprotective activity against myocardial infraction in animal model

Myocardial infarction (MI), one of the most perilous types of cardiac illness, carries a significant burden of mortality and morbidity. This study aims to shed light on the impact of Malva parviflora seed oil (MPSO) on plasma cardiac function tests, levels of cardiac inflammatory mediators, and the expression of cardiac miRNA140-5p and miRNA208b genes in a rat model of MI induced by isoproterenol (ISO). The methods involved the extraction of MPSO using hexane, with the determination of fatty acid contents accomplished through GC spectrometry. Adult albino rats, weighing 185 ± 7 g, were divided into five groups (n = 6): normal control rats, ISO-treated rats, ISO-treated rats with MPSO (157 and/or 314 mg/kg, respectively), and ISO-treated rats with omega (100 mg/kg, respectively) for a duration of four weeks. The results revealed that Malva parviflora seeds yielded 3.3 gm/100 dry seeds. Among the nine fatty acid components identified, coriolic acid was the most abundant (31.60 %), followed by pentadecanoic acid (30.05 %). The cardioprotective potential of MPSO was assessed in rats subjected to ISO-induced cardiac injury. Following 24 h of ISO treatment, rats displayed elevated levels of plasma cardiac troponin I (cTnI), troponin T (cTnT), lactate dehydrogenase (LDH), and B-Type Natriuretic Peptide (BNP), as well as cardiac BcL-2, P53, toll-like receptor 4 (TLR4), NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells), thiobarbituric acid reactive substances (TBARs), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), miRNA-140-5p, and miRNA-208b gene expression. Histopathological examination confirmed cardiac injury in ISO-treated rats. Furthermore, MPSO mitigated the elevation of cardiac enzymes and TBARS, as well as cardiac inflammatory mediators, while concurrently downregulating the expression levels of miRNA-140-5p and miRNA-208b genes. Conversely, the enhancement of cardiac GSH, SOD, and CAT activity demonstrated the antioxidant capabilities of MPSO against ISO-induced cardiac injury. Histopathological findings underscored MPSO's protective effect on cardiac tissue against oxidative damage in ISO-treated rats. In nutshel, the findings of this study unveil the cardioprotective and free radical scavenging attributes of MPSO in rats with ISO-induced cardiac damage. MPSO appears to provide cardiac protection against free radicals and inflammation induced by xenobiotics, potentially owing to its rich content of polyphenols, flavonoids, polyunsaturated fatty acids (PUFAs), and cyclopropenoid fatty acids.

Prevalence and prognostic impact of myocardial injury following hypertensive crisis

Abstract Background In patients with acute chest pain, hypertensive crisis is a common possible diagnosis. Severe hypertension may even cause elevated levels of cardiac troponin indicating myocardial injury. Whether this biomarker response is linked to poorer outcome is unknown. Methods We included patients presenting to the emergency department with suspected myocardial infarction. In accordance with the 4th definition of myocardial infarction the final diagnosis and main cause of symptoms was adjudicated by two trained cardiologists based on all available clinical, imaging and laboratory data, including high-sensitive troponin T (hs-TnT). Hypertensive crisis was confirmed by the adjudicators if an elevation of systolic blood pressure (&amp;gt;160 mmHg) was detected and after careful review of all available data other differential diagnoses were less likely. Patients were stratified in those with myocardial injury (acute or chronic) based on sex-specific hs-TnT cutoffs or those without. Kaplan-Meier survival analysis were calculated for all-cause mortality and a composite of death, myocardial infarction, revascularization or cardiac rehospitalization. The event-rates during two-year follow-up were compared using the log-rank test. Cox-proportional hazard ratios were calculated for each patient group with adjustment for age and sex for 2-year all-cause mortality. Results Out of 2,565 patients 446 (17.4%) had a final diagnosis of hypertensive crisis. Of these, 213 (47.8%) developed myocardial injury with a baseline hs-TnT of 15.0 (IQR 10.0-22.0) ng/L. Among the remaining 2,119 patients with other diagnoses than hypertensive crisis, 910 (42.9%) showed myocardial injury with a baseline hs-TnT of 28.5 (IQR 17.0-67.2) ng/L. Patients with hypertensive crisis accompanied by myocardial injury were older (76 (IQR 68-82) vs 60 (IQR 52-71) years, p=0.001) and more often female (61.0% vs 39.5%, p=0.001). Among patients with hypertensive crisis, 2-year mortality rates were higher in patients with myocardial injury compared to non-injury. However, compared to patients with myocardial injury due to other causes, hypertensive patients showed significantly better outcome (p=0.027; Figure 1A). This was consistent for the combined clinical endpoint (Figure 1B). Compared to non-injury/non-hypertensive patients, hazard ratio (HR) for all-cause death after 2 years was not significant for non-injury/hypertensive patients (HR 0.52 (95% CI 0.19-1.48), p=0.22), while patients with myocardial injury and hypertensive crises had significantly increased risk of death after 2 years (HR 1.81 (95% CI 1.02-3.22), p=0.044). In patients with myocardial injury caused by other reasons risk of death was even higher (HR 3.58 (95% CI 2.38-5.39), p=0.001). Conclusion Patients with myocardial injury due to hypertensive crisis are at high risk for adverse outcome within 2 years after presentation. However, compared to other reasons for myocardial injury hypertensive crisis seems less hazardous.Figure 1

Relationship of troponins with in-hospital mortality in adults with covid-19 in a colombian caribbean city: a nested case-control study

Background: myocardial injury, characterized by elevated cardiac troponin levels, is a common finding in severe COVID-19 cases, occurring in up to 38% of patients. It has been identified as an independent predictor of mortality. Objective: our aim is to assess the predictive value of cardiac troponin levels for in-hospital mortality among adults hospitalized with COVID-19 in Barranquilla, Colombia, during the period from January to June 2021. Methods: this study is a nested case-control analysis within a retrospective cohort. It encompasses individuals aged 18 and older with a confirmed diagnosis of COVID-19 who were hospitalized between January and June 2021 (n = 358). We describe the demographic and paraclinical characteristics of the patients and their association with outcomes at the time of discharge. We also estimate the diagnostic accuracy, including sensitivity, specificity, and predictive values, of elevated troponin levels in predicting in-hospital mortality. Results: patients with elevated troponin levels demonstrated a significantly increased risk of in-hospital mortality (OR: 9.4; 95% CI: 5.5-16.0; p &lt; 0.05) and had a notably higher in-hospital mortality rate (55.6%) compared to those with non-elevated troponin levels (11.7%). The troponin biomarker exhibited a sensitivity of 77.9% and specificity of 72.7%, with positive and negative predictive values of 55.6% and 88.3%, respectively, for in-hospital mortality. Conclusion: troponin elevation in subjects with COVID-19 is positively related to in-hospital mortality, independently of other conditions such as age group, comorbidities, or oxygen therapy requirement.

Serial echocardiographic evaluation of COVID-19 patients without prior history of structural heart disease: a 1-year follow-up CRACoV-HHS study.

It is a well-known fact that COVID-19 affects the cardiovascular system by exacerbating heart failure in patients with preexisting conditions. However, there is a poor insight into the cardiovascular involvement and sequelae in patients without preexisting conditions. The aim of the study is to analyse the influence of COVID-19 on cardiac performance in patients without prior history of structural heart disease. The study is part of the CRACoV project, which includes a prospective design and a 12-month follow-up period. The study included 229 patients hospitalised with a diagnosis of COVID-19 (median age of 59 years, 81 were women). A standard clinical assessment and laboratory tests were performed in all participants. An extended echocardiographic image acquisition was performed at baseline and at a 3-, 6-, and 12-month follow-up. All analyses were performed off-line. A series of echocardiographic parameters was compared using repeated measures or Friedman analysis of variance. In all subjects, the left ventricular (LV) ejection fraction at baseline was preserved [63.0%; Q1:Q3 (60.0-66.0)]. Elevated levels of high-sensitivity cardiac troponin T were detected in 21.3% of the patients, and elevated NT-proBNP levels were detected in 55.8%. At the 1-year follow-up, no significant changes were observed in the LV diameter and volume (LV 48.0 ± 5.2 vs. 47.8 ± 4.8 mm, p = 0.08), while a significant improvement of the parameters in the biventricular strain was observed (LV -19.1 ± 3.3% vs. -19.7 ± 2.5%, p = 0.01, and right ventricular -19.9 ± 4.5% vs. -23.2 ± 4.9%, p = 0.002). In addition, a decrease in the LV wall thickness was also observed (interventricular septum 10.4 ± 1.6 vs. 9.7 ± 2.0 mm, p < 0.001; LV posterior wall 9.8 ± 1.4 vs. 9.1 ± 1.5 mm, p < 0.001). In an acute phase of COVID-19, the elevation of cardiac biomarkers in patients with normal left ventricular ejection fraction is a frequent occurrence; however, it does not translate into clinically significant cardiac dysfunction after 1 year. The serial echocardiographic evaluations conducted in patients without preexisting structural heart disease demonstrate an overall trend towards an improved cardiac function and a reduced myocardial thickening at 1-year follow-up. This suggests that the acute cardiac consequences of COVID-19 are associated with systemic inflammation and haemodynamic stress in patients without preexisting conditions.

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.