Abstract 16918: COVID-19 Associated Acute Myocardial Injury With Prolonged Troponin Elevation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ly Tran ◽  
Charlie Ervin ◽  
Mathew J Thomas ◽  
David Moore ◽  
Rahul Sampath ◽  
...  
Keyword(s):  
Chest Pain ◽  
Cardiac Catheterization ◽  
Myocardial Injury ◽  
Troponin I ◽  
Case Reports ◽  
Left Ventricular ◽  
Left Shoulder ◽  
Troponin Elevation ◽  
First Case ◽  
Acute Myocardial Injury

Introduction: Acute myocardial injury in the setting of COVID-19 has been well described and is associated with higher mortality. Hypothesis: Myocarditis has been reported as a rare cause of myocardial injury in at least seven recent case reports. Methods: A 70-year-old man with coronary artery disease status post bypass surgery with recent hospitalization for left shoulder septic arthritis with MSSA bacteremia was readmitted 10 days later with a positive PCR test for SARS-CoV-2 at a local nursing facility. His symptoms were dyspnea, chest pain, fever, nausea, and diarrhea. Previous hospitalization he underwent evaluation for chest pain with cardiac catheterization revealing ejection fraction (EF) of 45% and patency of all three grafts. Results: Laboratory investigation showed elevated markers of myocardial injury with high sensitivity troponin I (hs-TnI) of 17,643 ng/L and B-type natriuretic peptide of 2,627 pg/mL, elevated C-Reactive Protein, D-dimer, and sedimentation rate. Chest X-ray showed hazy opacity in the infrahilar right lung. ECG notable for a first degree AV block with no ST-segment elevation. Transthoracic echocardiogram (TTE) showed an EF of 20% with global left ventricular dysfunction with hypokinesis of the right ventricle. No evidence of pericardial effusion. Blood cultures were negative. Management of heart failure led to clinical improvement. Over the next three months, Hs-TnI level stayed elevated at 11,339 ng/L for four weeks and trended down to 6,791 ng/L. The patient was seropositive for COVID-19 IgG eight weeks after the diagnosis of COVID-19 was made. Conclusions: We report the first case of COVID-19 related myocardial injury with prolonged and extreme troponin elevation. Recent favorable cardiac catheterization further supports immune mediated myocarditis over ischemic cardiomyopathy. Unfortunately, no endomyocardial biopsy has been performed.

scholarly journals The role of neurohormonal blockers in the primary prevention of acute-, early-, and late-onset anthracycline-induced cardiotoxicity

2020 ◽  
Vol 72 (1) ◽  
Author(s):  
Ahmed Ayuna ◽  
Nik Abidin
Keyword(s):  
Primary Prevention ◽  
Myocardial Injury ◽  
Troponin I ◽  
Late Onset ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Main Body ◽  
Converting Enzyme Inhibitors ◽  
Ventricular Ejection Fraction

Abstract Background Anthracycline-induced cardiotoxicity has been classified based on its onset into acute, early, and late. It may have a significant burden on the quality and quantity of life of those exposed to this class of medication. Currently, there are several ongoing debates on the role of different measures in the primary prevention of cardiotoxicity in cancer survivors. Our article aims to focus on the role of neurohormonal blockers in the primary prevention of anthracycline-induced cardiotoxicity, whether it is acute, early, or late onset. Main body of the abstract PubMed and Google Scholar database were searched for the relevant articles; we reviewed and appraised 15 RCTs, and we found that angiotensin-converting enzyme inhibitors (ACEI) and B-blockers were the most commonly used agents. Angiotensin II receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRAs) were used in a few other trials. The follow-up period was on the range of 1–156 weeks (mode 26 weeks). Left ventricular ejection fraction (LVEF), left ventricular diameters, and diastolic function were assessed by either echocardiogram or occasionally by cardiac magnetic resonance imaging (MRI). The occurrence of myocardial injury was assessed by troponin I. It was obvious that neurohormonal blockers reduced the occurrence of LVEF and myocardial injury in 14/15 RCTs. Short conclusion Beta-blockers, especially carvedilol and ACEI, especially enalapril, should be considered for the primary prevention of acute- and early-onset cardiotoxicity. ARB and MRA are suitable alternatives when patients are intolerant to ACE-I and B-blockers. We recommend further studies to explore and establish the role of neurohormonal blockers in the primary prevention of the acute-, early-, and late-onset cardiotoxicity.

Elevations of Troponin I after interventional cardiac catheterization

2001 ◽  
Vol 11 (4) ◽  
pp. 375-378 ◽  
Author(s):  
Prince J. Kannankeril ◽  
David F. Wax ◽  
Elfriede Pahl
Keyword(s):  
Cardiac Catheterization ◽  
Cardiac Troponin ◽  
Baseline Level ◽  
Myocardial Injury ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Specific Marker ◽  
Before And After ◽  
Baseline Sample

Background: Elevation of cardiac troponin I in the serum is a specific marker for myocardial injury. We measured levels of troponin I in the serum in children before and after cardiac catheterization to determine if this procedure was associated with an increase in levels of troponin. Methods: We enrolled patients under 21 years of age undergoing cardiac catheterization at our institution. A baseline sample of serum was drawn at the start of the procedure. Repeat samples were obtained immediately after, and six hours subsequent to the procedure. All samples were analyzed for cardiac troponin I using the Abbott AxSYM microparticle immunoassay system. Levels were considered normal (0–0.4 ng/ml) or elevated (>0.4ng/ml). Patients were excluded if the baseline level was elevated. Results: Levels of cardiac troponin I were elevated in the serum from 11 of 14 (79%) cases immediately after the procedure (p < 0.0001), and in 12 of 14 (86%) six hours later (p < 0.0001). Only 2 patients had recognized complications potentially causing myocardial injury. Conclusion: Levels of cardiac troponin I increase in the serum in a high proportion of children after cardiac catheterization. These elevations can be observed immediately, and are maintained for at least six hours. Our study suggests that cardiac catheterization, predominantly intervention, is associated with myocardial injury, even in the absence of complications.

Abstract 14870: Clinical Significance of Troponin Elevation in a Contemporary Hospitalized Population: Endotypes, Morbidity and In-hospital Mortality

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Michael Briscoe ◽  
Robert A Sykes ◽  
Thomas Krysztofiak ◽  
Kenneth Mangion ◽  
Oliver H Peck ◽  
...  
Keyword(s):  
Clinical Significance ◽  
Myocardial Injury ◽  
Troponin I ◽  
Coronary Revascularization ◽  
High Sensitivity ◽  
Hospitalized Patients ◽  
Troponin Elevation ◽  
Reference Limit ◽  
Upper Reference Limit

Introduction: Unplanned hospitalizations are commonly associated with a circulating troponin concentration >99 th percentile upper reference limit (URL). In order to better understand the clinical significance of troponin elevation, we evaluated outcomes in hospitalized patients according to cardiac endotype. Methods: We prospectively screened consecutive hospitalized patients with elevated high-sensitivity troponin-I (hs-TnI) concentrations (Abbott ARCHITECT troponin-I assay; sex-specific URL, 99 th centile: male: >34ng/L; female: >16ng/L) within a regional cardiac care network (population 650,000). A cardiology clinical team adjudicated individual patient records and assigned endotypes by consensus agreement according to the Fourth Universal Definition of Myocardial Infarction (MI). Endotypes were sub-classified into etiological category by inciting event(s). Characteristics and comorbidity were compared and outcomes recorded on virtual follow-up until June 2 nd 2020. Results: A total of 390 consecutive patients with ≥1 hs-TnI value >URL between March 1-April 15, 2020, were evaluated; 44 patients were excluded ( Duplicates: 2; Missing data: 41; Research patient: 1 ). Of 346 who qualified for inclusion, an index diagnosis of Type 1 MI (T1MI), T2MI and myocardial injury were assigned in 115 (33.2%), 79 (22.8%) and 152 (43.9%) patients, respectively. Compared with T1MI, patients with T2MI and myocardial injury had lower peak hs-TnI values (median [IQR]: 86 [250-697] vs 5020 [853-7774]ng/L; p< 0.01), lower estimated 10-year survival (40.2% vs 53.4%; p=0.002), less frequently underwent coronary revascularization (1.4% vs 45.2%; p<0.0005) and had longer inpatient stay (13.0 vs 6.1 days). Inpatient and overall mortality rates from admission to follow-up (median [range]: 71 [0-151] days) were higher among patients with T2MI and myocardial injury (19.9% vs 7.8%; p=0.004; and 26.0% vs 11.3%; Log rank (Mantel-Cox) X 2 = 1.927; p=0.003) independent of similar cardiovascular risk profiles. Conclusions: Despite lower peak circulating troponin concentrations, patients with T2MI and myocardial injury had higher inpatient mortality, lower estimated 10-year survival and longer in-hospital stay compared to those with T1MI.

Abstract 15990: Incidence and Outcomes of Elevated Troponins in Patients With Rhabdomyolysis

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nitheesha Ganta ◽  
Hilda Gonzalez ◽  
Olubode Olufajo ◽  
Prafulla P Mehrotra
Keyword(s):  
Hospital Mortality ◽  
Hospital Cost ◽  
Myocardial Injury ◽  
Case Reports ◽  
Coronary Intervention ◽  
Troponin Elevation ◽  
Percutaneous Coronary ◽  
Artery Disease ◽  
The Relationship ◽  
Cost Differences

Introduction: The relationship between rhabdomyolysis and elevated troponins has not been clearly established. Literature has been limited to case reports and small single center studies. However, there are no studies that evaluated the incidence and outcomes of troponin elevation in patients with rhabdomyolysis. Methods: Patients of 18 years and older with rhabdomyolysis were selected from the Healthcare Cost and Utilization Project National Inpatient Sample, 2005 to 2014. Patients with elevated troponins were identified. Information on demographics, co-morbidities and interventions (percutaneous coronary intervention (PCI) vs. no PCI) were extracted. The two main outcomes were mortality and hospital cost. Differences in characteristics and outcomes of patients with elevated troponins and those without elevated troponins were evaluated using descriptive analyses and multivariate regression models. Results: A total of 404,369 rhabdomyolysis participants were identified with 24,986 (6.18%) having elevated troponins. Of these, only 133 (0.03%) patients underwent PCI. Compared to the patients without elevated troponins, patients with elevated troponins were older (69y vs. 61y; P <0.001), and the majority were white (73.9% vs. 66.0%; P <0.001). In-hospital mortality in patients with elevated troponins was 20.5% compared to 5.4% in patients without elevated troponins ( P <0.001) resulting in an adjusted odds ratio of 4.05 (95% CI: 3.90 - 4.20). Compared to the patients without elevated troponins, the median hospital cost in patients with elevated troponins was $17,308 vs. $8,434 ( P <0.001) resulting in an adjusted mean difference of $9,547 (95% CI: $9,189 - $9,904). Conclusions: Our analysis showed that 6.1% of rhabdomyolysis patients have elevated troponins. Of these, very few patients underwent PCI, suggesting myocardial injury in these patients. Patients with elevated troponins had higher in-hospital mortality and increased cost of hospitalization. Due to the bad prognosis associated with elevated troponins, there is need for further evaluation for underlying coronary artery disease in patients with myocardial injury.

Abstract 17250: Serum vs. Imaging Biomarkers of Myocardial Injury in Duchenne Muscular Dystrophy: Findings from the E-SCAR DMD Trial

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Subha V Raman ◽  
Kan N Hor ◽  
Wojciech Mazur ◽  
Nancy Halnon ◽  
Tam Tran ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Myocardial Injury ◽  
Troponin I ◽  
Left Ventricular ◽  
Serum Biomarkers ◽  
Left Ventricular Ejection ◽  
Imaging Biomarkers ◽  
Mineralocorticoid Receptor Antagonist ◽  
Lge Cmr

Introduction: Cardiomyopathy has become a leading cause of death in Duchenne muscular dystrophy (DMD). We previously showed that early mineralocorticoid receptor antagonist therapy reduces myocardial damage in a preclinical model of DMD. The Eplerenone for Subclinical Cardiomyopathy in DMD (E-SCAR DMD, NCT01521546) is a multicenter randomized placebo-controlled clinical trial evaluating eplerenone in boys with preserved left ventricular ejection fraction (LVEF) and evident myocardial injury by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR). Hypothesis: To better define biomarkers of early disease, we hypothesized that LGE has greater sensitivity vs. serum biomarkers for myocardial injury in DMD cardiomyopathy. Methods: Boys with DMD age ≥ 7 years were enrolled across 3 centers. LGE-CMR images were acquired using comparable techniques across 3T scanners, and core laboratory LGE quantification was performed blinded to laboratory findings as a percentage of LV mass using software based on the full-width half-maximum technique. Troponin-I, creatine kinase (CK) and CK isoenzymes were measured from blood samples obtained at the time of CMR examination using standardized clinical assays. Results: 42 boys age 16 ± 7 years had preserved LVEF (57 ± 6%), and LGE-positive regions averaged 5.0 ± 2.6% of LV myocardium. While 100% had evident myocardial injury by LGE, 43% had measurable CK-MB and only 18% had detectable troponin-I in serum (Figure). %LGE was higher (5.4 ± 2.7 vs. 3.3 ± 1.8%, p<0.05) and LVEF was lower (55.4 ± 4.9 vs. 59.0 ± 7.1%, p < 0.01) in boys with detectable vs. those with undetectable troponin-I, whereas detectable CK-MB did not predict higher %LGE or lower LVEF. Conclusion: DMD patients with abnormal myocardium by LGE-CMR may have no detectable abnormalities by serum biomarkers, underscoring the importance of myocardial injury imaging in identifying patients with subclinical cardiomyopathy who may benefit from early treatment.

scholarly journals Study of Cardiac Troponin I level in Acute Coronary Syndrome and its correlation with Left Ventricular Systolic Function

2019 ◽  
Vol 12 (1) ◽  
pp. 24-29
Author(s):  
Mohammad Jakir Hossain ◽  
Khondoker Asaduzzaman ◽  
Solaiman Hossain ◽  
Muhammad Badrul Alam ◽  
Nur Hossain
Keyword(s):  
Acute Coronary Syndrome ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiac Troponin I ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Coronary Syndrome

Background: In the diagnosis of acute coronary syndrome, cardiac troponin I is highly reliable and widely available biomarker. Serum level of cardiac troponin I is related to amount of myocardial damage and also closely relates to infarct size. Our aim of the study is to find out the relationship between cardiac troponin I and left ventricular systolic function after acute coronary syndrome. Methods: Total of 132 acute coronary syndrome patients were included in this study after admission in coronary care unit of Sir Salimullah Medical College, Mitford Hospital. Troponin I level was measured at admission and left ventricular ejection fraction (LVEF) was measured by echocardiography between 12-48 hours of onset of chest pain. Results: There was negative correlation between Troponin I at 12 to 48 hours of chest pain with LVEF in these study patients. With a cutoff value of troponin I e”6.8 ng/ml in STEMI patients there is a significant negative relation between 12 to 48 hrs troponin I and LVEF (p<0.001). Sensitivity of troponin I e” 6.8 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% in STEMI was 93.75% and specificity was 77.78%. In NSTEMI sensitivity of troponin I e” 4.5 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% was 65% and specificity was 54.05%. Conclusion: Serum troponin I level had a strong negative correlation with left ventricular ejection fraction after acute coronary syndrome and hence can be used to predict the LVEF in this setting. Cardiovasc. j. 2019; 12(1): 24-29

scholarly journals Noncompaction and Takotsubo Syndrome in a Neuromuscular Disorder

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Josef Finsterer ◽  
Claudia Stöllberger ◽  
Walter Benedikt Winkler
Keyword(s):  
Chest Pain ◽  
Beta Blockers ◽  
Liver Cyst ◽  
Neuromuscular Disorder ◽  
Sudden Onset ◽  
Left Ventricular ◽  
Takotsubo Syndrome ◽  
Troponin Elevation ◽  
History Of ◽  
St Elevation

Background. Takotsubo syndrome (TTS) in patients with left ventricular hypertrabeculation/noncompaction (LVHT) has been reported in four patients, and a TTS plus LVHT plus a neuromuscular disorder (NMD) was only reported once so far. Here, we present the fifth patient with LVHT and TTS and the second patient with LVHT, TTS, and a NMD. Methods and Results. The patient is a 68 yo female hobby choir singer with a history of skin dermatofibroma, skin fibrokeratoma, arterial hypertension, hyperlipidemia, hypothyroidism, anemia, hyponatremia, diverticulosis, LVHT detected at age 60 y, five syncopes, a liver cyst, and carotid endarterectomy 2 months prior to admission because of sudden-onset chest pain. Workup revealed ST elevation, troponin elevation, and mild coronary artery sclerosis. Ventriculography and transthoracic echocardiography (TTE) showed the apical type of a TTS. ECG normalised within 10 w and TTE within 6 w under beta-blockers and ATII-blockers. The TTS was triggered by being offended of being unable to sing anymore after endarterectomy. Neurological workup suggested the presence of a NMD. Conclusions. This case shows that LVHT occurs in NMD patients and that patients with LVHT and a NMD may develop a TTS. Whether patients with LVHT and a NMD are particularly prone to develop a TTS requires further confirmation. NMD patients with LVHT should avoid stress not to trigger a TTS.

scholarly journals Decitabine Induced Transient Cardiomyopathy: A Case Report

2012 ◽  
Vol 6 ◽  
pp. CMO.S8598 ◽  
Author(s):  
Chitradeep De ◽  
Jaya Phookan ◽  
Valay Parikh ◽  
Tarun Nagrani ◽  
Mayur Lakhani ◽  
...  
Keyword(s):  
Case Report ◽  
Chest Pain ◽  
Troponin I ◽  
Acute Myocarditis ◽  
Coronary Vessels ◽  
Left Ventricular ◽  
Ventricular Rate ◽  
Heart Catheterization ◽  
Exertional Dyspnea ◽  
Coronary Syndrome

Case Report A 75-yr-old gentleman, with a past medical history of diabetes mellitus and Acute Myeloid Leukemia presented to our emergency department with a chief complaint of exertional dyspnea and chest pain. A week prior to this visit, he had recieved a cycle of decitabine chemotherapy at 20 mg/metered square for ten days. This was his second cycle of decitabine. His out patient medications included megesterol, omeprazole, morphine sulfate and insulin glargine. The patient was admitted to the Coronary Care Unit for Acute Coronary Syndrome. His cardiac enzymes were elevated (peak troponin 30 ng/mL, CKMB 67.4 ng/mL). His 12 lead EKG revealed sinus tachycardia with a ventricular rate of 113, but without acute ST–T wave changes. The BNP was 259 pg/mL. A 2D echo revealed moderate diffuse hypokinesis with an EF of 35%. He subsequently underwent a left heart catheterization, which showed non-obstructive CAD. In our patient, the elevated troponins (peak troponin 30 ng/mL) and BNP were seen concomitant with the onset of cardiogenic shock. Two months ago, his 2 D echocardiogram revealed an ejection fraction of about 55%–65% with slightly increased left ventricular (LV) wall thickness. Discussion The most common adverse effects of decitabine include cytopenia, nausea, pain and erythema/nodules at the injection site. To date, there has been only one reported case of a hypomethylating agent inducing acute myocarditis. We a present a case of reversible, non-ischemic cardiomyopathy secondary to decitabine chemotherapy, which resolved after the drug was discontinued. Trials involving decitabine for the treatment of MDS reported no myocarditis. In our case, the diagnosis of transient cardiomyopathy was highly probable since the patient's troponins and echocardiogram returned to baseline after discontinuation of treatment. Also, the patient never had any further chest pain at his 6 month follow up. In this case, we believe that the elevated Troponin I levels, along with a cardiac catheterization revealing patent coronary vessels, favor our hypothesis that our patient suffered from acute myocarditis as a result of direct toxicity from decitabine chemotherapy. We doubt that there was an underlying infectious etiology, since the patient had three negative blood cultures, two negative urine cultures and a negative viral serology. Our case demonstrates that chest pains in a patient treated with hypomethylating agents should be further explored in order to rule out acute myocarditis.

Analytical Characteristics of Commercial Cardiac Troponin I and T Immunoassays in Serum from Rats, Dogs, and Monkeys with Induced Acute Myocardial Injury

2008 ◽  
Vol 54 (12) ◽  
pp. 1982-1989 ◽  
Author(s):  
Fred S Apple ◽  
MaryAnn M Murakami ◽  
Ranka Ler ◽  
Dana Walker ◽  
Malcolm York ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Myocardial Injury ◽  
First Generation ◽  
Animal Species ◽  
Troponin I ◽  
Background Information ◽  
Sprague Dawley ◽  
Acute Myocardial Injury ◽  
Species Specific ◽  
First And Second Generation

Abstract Background: Information is needed regarding analytical characteristics of cardiac troponin (cTn) assays used in preclinical studies. Methods: We measured cTnI and cTnT in serum from normal animals and animals with induced myocardial injury [Sprague–Dawley (SD) and Wistar rats, beagle dogs, and rhesus (Rh) and cynomolgus (Cy) monkeys]. We evaluated the following assays: for cTnI, Abbott Architect, Bayer Centaur (first and second generation), Beckman Access, DPC Immulite, Dade Dimension, Ortho Vitros ES, Tosoh AIA, and species-specific enzyme immunoassays; for cTnT, Roche Elecsys. Results: We found different species-specific responses for the troponin assays evaluated. Abbott, Bayer Ultra, Beckman, and Dade assays gave good responses across all species. In rats, weak responses were observed with DPC and Ortho, and no measurable response with Tosoh. In dogs, weak responses were observed with Tosoh cTnI, Roche cTnT, and species-specific cTnI. In cynomolgus monkeys, weak responses were observed with species-specific cTnI and Roche cTnT. Assay imprecision was ≤20% at 3 or more examined cTn concentrations for Beckman (rat, dog, monkey), Dade (rat, dog, monkey), Abbott (rat, dog, monkey), Bayer first generation (dog), Bayer Ultra (rat, dog, monkey), Roche (monkey), DPC (dog, monkey), Ortho (dog, monkey), and Tosoh (dog, monkey) assays, whereas imprecision was ≤20% at 2 or fewer concentrations for the Bayer first generation (rat, monkey), Roche cTnT (rat, dog), and DPC (rat) assays. Conclusions: Not all cTn assays are suitable for monitoring cTn in each animal species or strain. Individual assay characterization by animal species is needed to prevent misinterpretation of myocardial injury–based cardiac troponin findings.

scholarly journals Acute myocardial damage in new coronavirus infection (COVID-19)

2021 ◽  
Vol 20 (5) ◽  
pp. 98-104
Author(s):  
N. V. Izmozherova ◽  
A. A. Popov ◽  
A. I. Tsvetkov ◽  
M. A. Shambatov ◽  
I. P. Antropova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Medical Care ◽  
Myocardial Injury ◽  
Troponin I ◽  
Myocardial Damage ◽  
True Incidence ◽  
Wide Range ◽  
Acute Myocardial Injury ◽  
Coronavirus Infection

Introduction. Acute respiratory distress syndrome (ARDS) and cardiovascular events, acute myocardial injury being the most frequent of the latter, are among the leading causes of death in COVID-19 patients. The lack of consensus on acute myocardial injury pathogenesis mechanisms, the patients management, treatment an rehabilitation logistics, the anticoagulant treatment in identified SARS-CoV-2 or suspected COVID-19 patients setting indicates the need to assess, analyze and summarize the available data on the issue.Materials and methods. Scientific publications search was carried out in PubMed, Google Scholar databases for the period from December 2019 to September 2021.Results and Discussion. Cardiospecific troponin I increase beyond reference limits is reported to occur in at least every tenth patient with identified SARS-CoV-2, the elevated troponin detection rate increasing among persons with moderate to severe course of the infection. The mechanisms of acute myocardial injury in patients with COVID-19 are poorly understood. By September 2021, there are several pathogenesis theories. A high frequency viral myocarditis direct cardiomyocytes damage is explained by the high SARS-CoV-2 affinity to ACE2 expressed in the myocardium. The cytokine storm related myocardial damage is reported a multiple organ failure consequence. Coagulopathy may also trigger myocardial microvessels damage. Up to every third death of SARS-CoV-2 infected persons is related to the acute myocardial injury. At the same time, due to the high incidence of the acute myocardial injury, it is rather difficult to assess the true incidence of acute myocardial infarction in patients with COVID-19. In the pandemic setting, the waiting time for medical care increases, the population, trying to reduce social contacts, is less likely to seek medical help. In this regard, in order to provide effective medical care to patients with acute myocardial infarction, it is necessary to develop algorithms for providing care adapted to the current epidemiological situation.Conclusion. The treatment of patients with probable development of acute myocardial damage against the background of new coronavirus infection should be performed in accordance with the current clinical guidelines. Anticoagulant therapy should be administered in a prophylactic dose under control of hemostasis parameters and a wide range of biochemical parameters.

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