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

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.

267 Cardiac biomarkers and mortality in COVID-19 infection

Aims The SARS-CoV-2 infection is mostly characterized by acute lung injury. Yet, some COVID-19 patients showed also neurological signs, acute myocardial injury, heart failure, myocarditis, and hypercoagulability, such as pulmonary embolism. Cardiac biomarkers can play an essential role in the diagnosis, management, and prognosis of COVID-19. In fact, during hospitalization, these patients develop biochemical abnormalities, with increasing of all Troponins (TnT), B-type natriuretic peptide (NT-pro-BNP) and creatine kinase-myocardial band (CK-MB) levels. This situation helps us to predict adverse outcomes, especially in patients with cardiovascular comorbidities or risk factors. Data emerged demonstrated a myocardial involvement which determines a high risk of adverse events and increasing of mortality. Methods and results Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such NT-pro-BNP, CK-MB, and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. Our purpose is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes. Results of aforementioned studies underline how cardiac biomarkers are associated with severe form of COVID-19 infection. Above all, higher levels of these biomarkers are significantly associated with an increased risk of the mortality in COVID-19 infected patients. Therefore, has been demonstrated COVID-19 infection is more severe in those patients with a previous history of arterial hypertension, cardiovascular diseases. In addition to classical laboratory parameters evaluated in COVID-19 infection, such as C Reactive Protein (CRP), d-dimer, and lactate dehydrogenase (LDH), which are currently used in clinical practice, others biomarkers could potentially be useful for screening, clinical management, and prevention of serious complications. Therefore, it is clinically significant that fluctuating levels of myocardial biomarkers are closely monitored and patients with high levels of myocardial biomarkers are treated promptly to improve prognosis. At the end, on basis of symptoms and cardiac biomarkers patients could be divided in mild, severe and critical. Conclusions Biomarkers of acute myocardial injury play an important role in predicting worsening prognosis for COVID-19 patients with and without myocardial injury. They are not only predictive of disease severity, but are also helpful for therapeutic management, based on drugs preventing the activation of coagulation processes. It’s important, above all, to identify a laboratory score, made by haematological, inflammatory, biochemical, and immunological parameters, may help to stratify COVID-19 positive patients into risk categories for deciding therapeutic management, thus avoiding cardiac compromise which, as we have previously analysed, is an indication of a poor prognosis.

251 Prognostic role of acute myocardial infarction diagnostic criteria in non-ST segment elevation myocardial infarction

Aims Although patients with ST segment elevation myocardial infarction (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI) share similar risk factors and similar pathophysiology, their outcomes differ considerably. The Fourth Universal Definition of Myocardial Infarction (UDMI) defined acute myocardial infarction (AMI) by an acute myocardial injury together with clinical evidence of acute myocardial ischaemia. However, the prognostic role of each single diagnostic criteria has never been explored. To evaluate the prognostic role of the different diagnostic criteria of AMI according to the Fourth UDMI in patients with STEMI vs. NSTEMI. Methods and results We enrolled all consecutive patients with AMI undergoing coronary angiogram at our Centre. We used a combination of criteria, according to the current ESC guidelines, to meet the diagnosis, namely the detection of an increase and/or decrease of high-sensitivity cardiac troponin I, with at least one value above the 99th percentile of the upper reference limit and at least one of the following: symptoms of ischaemia; ECG changes (new ST-T changes or new left bundle branch block); development of pathological Q waves in the ECG; echocardiographic evidence of new loss of viable myocardium, or new regional wall motion abnormality. According to the ECG presentation at admission, patients with AMI were divided into STEMI and NSTEMI subgroups. All-cause mortality and a composite endpoint of all-cause mortality, re-hospitalization for heart failure, and myocardial re-infarction were collected. The predictive value of diagnostic criteria alone and their association was evaluated using Kaplan–Meier survival curves and subsequent Cox-regression analysis to find independent predictors of adverse events. 2345 patients were evaluated (41.6% STEMI and 58.4% NSTEMI). The two groups had similar baseline characteristics. The total number of events was 689 (292 in STEMI group and 397 in NSTEMI group). We found that clinical criteria alone showed a positive predictive value in NSTEMI (P < 0.001). Moreover, electrocardiographic and echocardiographic criteria correlated with a worse prognosis in STEMI group (P < 0.01). No other significant prognostic correlation was found. Multivariable Cox-regression model demonstrated that clinical criteria were the only independent predictors of better prognosis in patients with NSTEMI (HR = 0.48; 95% CI: 0.31–0.74; P < 0.001). We did not find any predictor of outcome in patients with STEMI (HR = 0.6; 95% CI: 0.3–1.5, P = 0.3; HR = 1.1; 95% CI: 0.5–2.6, P = 0.7; HR = 0.6; 95% CI: 0.3–1.2, P = 0.2 for clinical and echocardiographic criteria alone and their combination, respectively). Conclusions Our data suggest that in NSTEMI the prognosis is considerably better if clinical criteria alone are present at admission. We hypothesize that the absence of electrocardiographic and echocardiographic alterations in NSTEMI could indirectly indicate smaller infarct sizes or other causes of acute myocardial injury.

Case Report: Stemi With Covid-19

BACKGROUND Severe acute respiratory syndrome coronavirus 2 (SARS-CoV‑2) causing coronavirus disease 2019 (COVID-19) has reached pandemic levels by March 2020. Patients with cardiovascular disease, particularly with cardiac injury represent a vulnerable population and increased risk of mortality and morbidity. There is still no guidelines for management of cardiovascular disease during the COVID-19 pandemic. CASE ILLUSTRATION An unconscious 52-year-old male brought to ER with complaints of abdominal discomfort and nausea. The patient had a cardiac arrest in ER and ROSC was obtained. The patient was intubated ECG showed anterior STEMI and primary PCI was performed. The endotracheal tube was changed due to blockage of excessive and thick slime. Tracheostomy was performed. Bronchoscopy was performed and found tracheal mucosal edema, hyperemic and easily bleed; mucous plug and blood clots in the tip of tracheostomy cannula. Thoracic CT-Scan showed ground-glass appearance and fibrosis of the 6th thoracic dextra segment. PCR SARS-CoV-2 showed reactive. The patient was discharged from our hospital after three weeks with clinically stable and referred to COVID-19 center hospital nearby his home for another two weeks. After PCR SARS CoV-2 was performed twice showed negative results, the patient was discharged. CONCLUSION SARS-CoV‑2 infection may lead to acute myocardial injury through viral systemic inflammation, although specific mechanism remained uncertain. A thick mucus plaque and stool cell may be a specific clinical features in COVID-19 patients. Tracheostomy has a continuing role in managing weaning from extended periods of mechanical ventilation during the COVID-19 pandemic.

Type IV myocardial infarction associated with acute stent thrombosis in the early period after revascularization in a patient with new coronavirus infection COVID-19

New facts suggest that COVID-19 coronavirus infection is partly mediated by hypercoagulability reactions characterized by micro- and macrovascular thrombotic angiopathy, which leads to acute myocardial injury, myocarditis, arrhythmias and numerous cases of pulmonary thromboembolic disease . The article presents a clinical observation of acute myocardial infarction development as a result of early thrombosis of an implanted coronary stent in a patient diagnosed with a new coronavirus infection COVID-19.

The Role of Endothelium in COVID-19

The 2019 novel coronavirus, known as severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) or coronavirus disease 2019 (COVID-19), is causing a global pandemic. The virus primarily affects the upper and lower respiratory tracts and raises the risk of a variety of non-pulmonary consequences, the most severe and possibly fatal of which are cardiovascular problems. Data show that almost one-third of the patients with a moderate or severe form of COVID-19 had preexisting cardiovascular comorbidities such as diabetes mellitus, obesity, hypertension, heart failure, or coronary artery disease. SARS-CoV2 causes hyper inflammation, hypoxia, apoptosis, and a renin–angiotensin system imbalance in a variety of cell types, primarily endothelial cells. Profound endothelial dysfunction associated with COVID-19 can be the cause of impaired organ perfusion that may generate acute myocardial injury, renal failure, and a procoagulant state resulting in thromboembolic events. We discuss the most recent results on the involvement of endothelial dysfunction in the pathogenesis of COVID-19 in patients with cardiometabolic diseases in this review. We also provide insights on treatments that may reduce the severity of this viral infection.