Although the frequency of myocarditis in the general population is very difficult to accurately determine due to the large number of asymptomatic cases, the incidence of this disease is increasing significantly due to better defined criteria for diagnosis and the development of modern diagnostic methods. The multitude of different etiological factors, the diversity of the clinical picture, and the variability of the diagnostic findings make this disease often demanding both for the selection of the diagnostic modality and for the proper therapeutic approach. The previously known most common viral etiology of this disease is today overshadowed by new findings based on immune-mediated processes, associated with diseases that in their natural course can lead to myocardial involvement, as well as the iatrogenic cause of myocarditis, which is due to use of immune checkpoint inhibitors in the treatment of cancer patients. Suspecting that a patient with polymorphic and non-specific clinical signs and symptoms, such as changes in ECG and echocardiography readings, has myocarditis is the starting point in the diagnostic algorithm. Cardio magnetic resonance imaging is non-invasive and is the gold standard for diagnosis and clinical follow-up of these patients. Endomyocardial biopsy as an invasive method is the diagnostic choice in life-threatening cases with suspicion of fulminant myocarditis where the diagnosis has not yet established or there is no adequate response to the applied therapeutic regimen. The treatment of myocarditis is increasingly demanding and includes conservative methods of treating heart failure, immunomodulatory and immunospressive therapy, methods of mechanical circulatory support, and heart transplantation. The goal of developing new diagnostic and therapeutic methods is to reduce mortality from this complex disease, which is still high.

The COVID-19 pandemic has led to numerous negative implications for all aspects of society. Although COVID-19 is a predominant lung disease, in 10–30% of cases, it is associated with cardiovascular disease (CVD). The presence of myocardial injury in COVID-19 patients occurs with a frequency between 7–36%. There is growing evidence of the incidence of acute coronary syndrome (ACS) in COVID-19, both due to coronary artery thrombosis and insufficient oxygen supply to the myocardium in conditions of an increased need. The diagnosis and treatment of patients with COVID-19 and acute myocardial infarction (AMI) is a major challenge for physicians. Often the presence of mixed symptoms, due to the combined presence of COVID-19 and ACS, as well as possible other diseases, nonspecific changes in the electrocardiogram (ECG), and often elevated serum troponin (cTn), create dilemmas in diagnosing ACS in COVID-19. Given the often-high ischemic risk, as well as the risk of bleeding, in these patients and analyzing the benefit/risk ratio, the treatment of patients with AMI and COVID-19 is often associated with dilemmas and difficult decisions. Due to delays in the application of the therapeutic regimen, complications of AMI are more common, and the mortality rate is higher.

Objective. The objective of this study is to analyze the impact of declining kidney function on the occurrence of the slow-flow/no-reflow phenomenon in patients with ST-elevation myocardial infarction (STEMI) treated with primary PCI (pPCI), as well as the analysis of the prognostic impact of the slow-flow/no-reflow phenomenon on short- and long-term mortality in these patients. Methods. We analyzed 3,115 consecutive patients. A value of the glomerular filtration rate (eGFR) at the time of admission of eGFR <90 ml/min/m² was considered a low baseline eGFR. The follow-up period was 8 years. Results. The slow-flow/no-reflow phenomenon through the IRA was registered in 146 (4.7%) patients. Estimated GFR of <90 ml/min/m² was an independent predictor for the occurrence of the slow-flow/no-reflow phenomenon (OR 2.91, 95% CI 1.25–3.95, < 0.001), and the risk for the occurrence of the slow-flow/no-reflow phenomenon increased with the decline of the kidney function: eGFR 60–89 ml/min/m²: OR 1.94 (95% CI 1.22–3.07, = 0.005), eGFR 45–59 ml/min/m²: OR 2.55 (95% CI 1.55–4.94, < 0.001), eGFR 30–44 ml/min/m²: OR 2.77 (95% CI 1.43–5.25, < 0.001), eGFR 15–29 ml/min/m²: OR 5.84 (95% CI 2.84–8.01, < 0.001). The slow-flow/no-reflow phenomenon was a strong independent predictor of short- and long-term all-cause mortality: 30-day mortality (HR 2.62, 95% CI 1.78–3.57, < 0.001) and 8-year mortality (HR 2.09, 95% CI 1.49–2.09, < 0.001). Conclusion. Reduced baseline kidney function was an independent predictor for the occurrence of the slow-flow/no-reflow phenomenon, and its prognostic impact started with the mildest decrease in eGFR (below 90 ml/min/m²) and increased with its further decline. The slow-flow/no-reflow phenomenon was a strong independent predictor of mortality in the short- and long-term follow-up of the analyzed patients.

Background/Aim. The RISK-PCI is a simple score for the prediction of 30-day major adverse cardiovascular events (MACE) and mortality in patients treated with primary PCI (pPCI). The aim of the present study is to evaluate the prognostic performance of the RISK-PCI score in predicting MACE and mortality in the long-term follow-up of STEMI patients treated with pPCI. Method. The present study enrolled 2,096 STEMI patients treated with pPCI included in the RISK-PCI trial. Patients presenting with cardiogenic shock were excluded. The composite end-point MACE comprising cardiovascular mortality, nonfatal reinfarction and stroke. Patients were followed up at 6 years after enrollment. Results. One-year and 6-year MACE occurred in 229 (10.9%) and 285 (13.6%) patients, respectively; and 1-year and 6-year mortality occurred in 128 (6.2%) and 151 (7.2%) patients, respectively. The RISK-PCI score was an independent predictor for 1-year MACE (HR 1.24, 95% CI 1, 18–1.31, p<0.001), 6-year MACE (HR 1.22, 95% CI 1.16–1.28, p<0.001), 1-year mortality (HR 1.21, 95% CI 1.13–1.29, p<0.001), and 6-year mortality (HR 1.23, 95% CI 1.15–1.31, p<0.001). The discrimination of the RISK-PCI score to predict 1-year and 6-year MACE and mortality was good: for 1-year MACE c-statistic 0.78, for 6-year MACE c-statistic 0.75, for 1-year mortality c-statistic 0.87, and for 6-year mortality c-statistic 0.83. The nonsignificant Hosmer–Lemeshow goodness-of-fit estimates for 1-year MACE (p=0.619), 6-year MACE (p=0.319), 1-year mortality (p=0.258), and 6-year mortality (p=0.540) indicated a good calibration of the model. Conclusion. The RISK-PCI score demonstrates good characteristics in the assessment of the risk for the occurrence of MACE and mortality during long-term follow-up after pPCI.

The incidence of atrial fibrillation (AF) in acute coronary syndrome (ACS) ranges from 2.3–23%. This difference in the incidence of AF is explained by the different ages of the patients in different studies and the different times of application of both reperfusion and drug therapies in acute myocardial infarction (AMI). About 6–8% of patients who underwent percutaneous intervention within AMI have an indication for oral anticoagulant therapy with vitamin K antagonists or new oral anticoagulants (NOAC).The use of oral anticoagulant therapy should be consistent with individual risk of bleeding as well as ischemic risk. Both HAS-BLED and CHA2DS2VASc scores are most commonly used for risk assessment. Except in patients with mechanical valves and antiphospholipid syndrome, NOACs have an advantage over vitamin K antagonists (VKAs). One of the advantages of NOACs is the use of fixed doses, where there is no need for successive INR controls, which increases the patient’s compliance in taking these drugs. The use of triple therapy in ACS is indicated in the case of patients with AF, mechanical valves as well as venous thromboembolism. The results of the studies showed that when choosing a P2Y12 receptor blocker, less potent P2Y12 blockers such as Clopidogrel should be chosen, due to the lower risk of bleeding. It has been proven that the presence of AF within AMI is associated with a higher degree of reinfarction, more frequent stroke, high incidence of heart failure, and there is a correlation with an increased risk of sudden cardiac death. With the appearance of AF in ACS, its rapid conversion into sinus rhythm is necessary, and in the last resort, good control of heart rate in order to avoid the occurrence of adverse clinical events.

Cardiac troponins (cTn) T and I are biochemical markers of myocardial injury. In this review article, we aim to summarize the mechanisms and significance of cardiac troponin (cTn) elevation unrelated to acute myocardial infarction (AMI) in the most frequently occurring non-cardiac conditions, where the accurate interpretation of elevated cTn levels is often challenging. Different mechanisms in non-cardiac conditions can cause non-ischemic myocardial injury. Understanding the pathophysiology of cTn release is an essential precondition for minimizing unnecessary, costly, and potentially risky (cardiac) interventions and for providing timely and appropriate medical care. Elevated cTn in critically ill patients and in patients with chronic disease/conditions is an independent predictor (risk factor) of cardiovascular and overall mortality. Treatment of underlying conditions is of primary importance, and close monitoring for the occurrence of cardiovascular complications during hospitalizations should be considered in these patients. Also, when the patient recovers from the underlying disease, clinical judgement should be employed to decide whether and to what extent further cardiological evaluation is indicated.