Pathophysiology of Cardiac Injury in COVID-19 Patients with Acute Ischaemic Stroke: What Do We Know So Far?—A Review of the Current Literature

With the onset of the COVID-19 pandemic, it became apparent that, in addition to pulmonary infection, extrapulmonary manifestations such as cardiac injury and acute cerebrovascular events are frequent in patients infected with SARS-CoV-2, worsening clinical outcome. We reviewed the current literature on the pathophysiology of cardiac injury and its association with acute ischaemic stroke. Several hypotheses on heart and brain axis pathology in the context of stroke related to COVID-19 were identified. Taken together, a combination of disease-related coagulopathy and systemic inflammation might cause endothelial damage and microvascular thrombosis, which in turn leads to structural myocardial damage. Cardiac complications of this damage such as tachyarrhythmia, myocardial infarction or cardiomyopathy, together with changes in hemodynamics and the coagulation system, may play a causal role in the increased stroke risk observed in COVID-19 patients. These hypotheses are supported by a growing body of evidence, but further research is necessary to fully understand the underlying pathophysiology and allow for the design of cardioprotective and neuroprotective strategies in this at risk population.

Aortic Root Dissection In A Patient With Previous Aortic Valve Replacement Due To External Automated Chest Compression Device For Cardiac Arrest

Myocardial damage from external cardiac massage can occur with either manual massage or with an automatic external device. We report the case of a patient with an aortic valve bioprosthesis undergoing advanced resuscitation with an automated external device for out-of-hospital-cardiac arrest, in whom the prolonged compressions caused an aortic root dissection.

Survival of patients with cardiomyopathies

Cardiomyopathies are a heterogeneous group of diseases. The main pathogenetic mechanism is myocardial damage due to genetic mutations. Cardiomyopathies are one of the leading causes of heart failure, sudden cardiac death, and life-threatening arrhythmias. Certain factors associated with poor prognosis determined the prognosis in this group of patients. Survival in different types of cardiomyopathies depends on the time of diagnosis and initial treatment. The types of cardiomyopathies discussed in this review are hypertrophic cardiomyopathy, dilative cardiomyopathy, restrictive cardiomyopathy, left ventricle non-compaction, and arrhythmogenic right ventricular cardiomyopathy.

Сardiac troponin I for assessment of myocardial damage and prediction of complications in cardiac surgery patients

The study analysed the level of troponin I (Tn) in the blood in patients with coronary artery disease after coronary artery bypass grafting in comparison with patients after aortic valve replacement surgery. The dynamics of troponin in the early postoperative period was studied, a parallelism was established between the occurrence of complications after surgery and the degree of myocardial damage. A new method has been developed for assessing the degree of intraoperative myocardial damage and the risk of complications using the «index of myocardial damage», the Tn level is determined twice after the operation, in the period up to 6 hours – Tn early and 12–24 hours later – Tn late, the index is calculated as the ratio of Tn late one to Tn early one. A correlation analysis of the «index» with other laboratory parameters was carried out, as a result of which no significant correlations were found, which indicates the absence of duplication and the significance of the developed indicator for assessing myocardial damage after cardiac surgery.

Influence of Low Concentrations of Carbon Monoxide on Metabolism of Isolated Heart under Conditions of Ischemia-Reperfusion

The purpose of the study was to determine the effect of different concentrations of carbon monoxide on the metabolism of isolated mice hearts. Materials and methods. To elucidate the effect of low concentrations of carbon monoxide on the myocardium, we performed retrograde perfusion of isolated hearts of laboratory mice with Krebs-Henseleit solution, which was saturated with carbon monoxide for 5, 10, and 30 minutes. We then determined how different concentrations of carbon monoxide affected coronary volumetric flow rate, myocardial glucose and calcium uptake, creatinine release, and aspartate aminotransferase release. During perfusion, R-wave amplitude and R-R interval were measured using an electrocardiograph. To determine the effect of ischemia on the heart muscle during perfusion with solutions of different concentrations, we measured the area of the affected myocardium after staining with 2,3,5-triphenyltetrazolium chloride. Results and discussion. After these studies, it was found that different concentrations of carbon monoxide had a dose-dependent effect on the isolated mouse heart. However, the dependence of the effects does not follow the pattern «lowest concentration – lowest effect». At the same time, an increase in concentration did not mean an increase in adverse effects on the myocardium. Even on the contrary, the smallest concentration led to increased signs of ischemic myocardial damage. In particular, the use of the solution, through which carbon monoxide was passed for 5 minutes, caused vasoconstrictor effect during perfusion. At the end of reperfusion, vasoconstrictor effect was observed after using a solution through which carbon monoxide was passed for 10 minutes. Increased glucose uptake was observed in the group with 30-minute carbon monoxide permeation against the background of the minimal myocardial creatinine release. In this group there was also a decrease in Ca2+ loss at the beginning of reperfusion (immediately after ischemia). The above phenomenon explains the least degree of ischemic myocardial damage in the isolated mouse heart. The obtained data should be expanded. Since it is difficult to accurately determine the dose of carbon monoxide, then the use of donor compounds is promising. Such compounds include CORM-2 and CORM-3. Under physiological conditions, they decompose in a controlled manner, releasing a specific amount of carbon monoxide. Conclusion. The obtained results indicate that at different concentrations of carbon monoxide can differently influence different structures of cardiomyocyte: at one concentration it binds to calcium channels, other concentrations influence ion channels of plasma membrane, which can explain all these dependencies

Is COVID-19 multisystem inflammatory syndrome a new variant of Kawasaki Disease?

Objectives: In this systematic review, we aimed to evaluate the clinical features, therapeutic options, and outcomes of children with multisystem inflammatory syndrome in children (MIS-C) and to investigate whether MIS-C is a new variant of Kawasaki disease. Materials and methods: Adhering to PRISMA principles, we searched for eligible studies between December 2019 and June 2020 through the following databases: PubMed, ISI Web of Science, SCOPUS, and Science Direct. Studies including original data of patients aged <21 years with MIS-C and descriptions of clinical signs, laboratory or radiological investigations were selected. Results: A total of 84 studies were identified, for which 48 were eligible for full screening and only 13 studies (n=657) met our inclusion criteria. More than 70% of patients with MIS-C tested positive for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). The most common symptoms were gastrointestinal (80 to 100%) and most patients presented with fever for >4 days. Mucocutaneous manifestations are similar to Kawasaki disease presented in up to 64% in some studies. Almost all patients had significant elevations in inflammatory markers, and up to 50 to 100% had elevated troponin suggesting myocardial damage. Intravenous immunoglobulin (IVIG) was administered to 60% of patients in 12 studies and 80 to 100% in five studies. Steroids were administered to 10 to 95% of patients. The overall mortality rate was 0.9%. Conclusion: The temporal association between novel coronavirus disease 2019 (COVID-19) onset and Kawasaki-like disease and MIS-C suggests a causal link. Both syndromes have similar cascades of symptoms and hyperinflammation, which likely explain their response to the same immunomodulatory agents. However, it is unclear yet why some children appear more susceptible to develop MIS-C.

Sleep Apnoea and Heart Failure

Heart Failure (HF) and Sleep-Disordered-Breathing (SDB) are two common conditions that frequently overlap and have been studied extensively in the past three decades. Obstructive Sleep Apnea (OSA) may result in myocardial damage, due to intermittent hypoxia increased sympathetic activity and transmural pressures, low-grade vascular inflammation and oxidative stress. On the other hand, central sleep apnoea and Cheyne-Stokes respiration (CSA-CSR) occurs in HF, irrespective of ejection fraction either reduced (HFrEF), preserved (HFpEF) or mildly reduced (HFmrEF). The pathophysiology of CSA-CSR relies on several mechanisms leading to hyperventilation, breathing cessation and periodic breathing. Pharyngeal collapse may result at least in part from fluid accumulation in the neck, owing to daytime fluid retention and overnight rostral fluid shift from the legs. Although both OSA and CSA-CSR occur in HF, the symptoms are less suggestive than in typical (non-HF related) OSA. Overnight monitoring is mandatory for a proper diagnosis, with accurate measurement and scoring of central and obstructive events, since the management will be different depending on whether the sleep apnea in HF is predominantly OSA or CSA-CSR. SDB in HF are associated with worse prognosis, including higher mortality than in patients with HF but without SDB. However, there is currently no evidence that treating SDB improves clinically important outcomes in patients with HF, such as cardiovascular morbidity and mortality.

Myocardial damage in new coronavirus infection (review)

Introduction. Myocardial damage characteristic of novel coronavirus infection is a confirmed risk factor for its severe course and high mortality. There are biomarkers of this condition correlating with an unfavorable prognosis for the patient. However, the information on the problem of myocardial damage in the available literature is not fully systematic. It concerns pathogenesis, differential diagnosis of its causes, routing of patients with acute coronary syndrome. All the above is very important for choosing the right tactics of examination and treatment of patients, who are often limited in time. Aim. To summarize the data available at the time of writing from domestic and foreign researchers on the problem of myocardial damage and its main causes (acute coronary syndrome, myocarditis, stress cardiomyopathy) in COVID-19. Materials and methods. This review summarizes the data from articles published over the past two years found in PubMed, Google Scholar and eLIBRARY. Results. The authors tried to form a generalized modern understanding of the causes and structure of cardiovascular pathology and risk factors of its destabilization in patients infected with SARS-CoV-2, the markers of increased risk of COVID-infected heart and vascular diseases, the tactics of examination and treatment of this category of patients, routing individuals with acute coronary syndrome and its differential diagnosis with non-coronary heart diseases. The questions of organization and availability of the medical care in the conditions of the pandemic and social aspects of the world cardiology problems in the current situation have been studied. Conclusion. Patients with cardiovascular disease have a more severe prognosis of the severity and outcome of COVID-19, which is explained by its pathogenesis. The group at highest risk of lethal events is composed of individuals with signs of myocardial damage, the causes of which are the above mentioned conditions. Their differential diagnosis is a difficult clinical task, which requires a systematic analysis of the dynamics of clinical syndromes and data of additional diagnostic methods from routine to the most modern (high-tech) and, of course, deep knowledge of the present problem. The correct determination of the cause of myocardial damage and the choice of the right patient’s route through the treatment network determines the effectiveness of treatment and, therefore, the prognosis of the patient’s life.

Acute Pediatric Chagas Disease in Antioquia, Colombia: A Geographic Location of Suspected Oral Transmission

Chagas disease, Trypanosoma cruzi infection, is an insidious cause of heart failure in Latin America. Early diagnosis and treatment are critical to prevent irreversible myocardial damage that progressively accumulates over decades. Several structural barriers account for the less than 1% of cases in Colombia being treated, including poor physician knowledge, especially considering that some regions are considered non-endemic. The two cases reported here represent an emerging epidemiologic scenario associated with pediatric Chagas disease. Both cases are suspected oral transmitted parasitic infection in a geographic region of Colombia (Andean region of Antioquia) where no previous oral transmission of Chagas disease had been reported. Their clinical histories and course of disease are presented here to increase physician awareness of the epidemiologic risk factors and clinical manifestations associated with pediatric oral Chagas disease in Antioquia department, Colombia.