SARS-CoV-2 infection and myocarditis / Infección por SARS-CoV-2 y miocarditis

COVID-19 es una enfermedad infecciosa respiratoria aguda, causada por el SARS-CoV-2, un nuevo coronavirus, que se extendió rápidamente por todo el mundo, dando como resultado una pandemia. Los pacientes presentan un amplio espectro de manifestaciones clínicas, entre ellas, la miocarditis, y de manera alterna, algunos pacientes sin síntomas de enfermedad cardíaca, tienen anomalías en las pruebas, como elevación de la troponina y arritmias cardíacas en el electrocardiograma, o anomalías en las imágenes cardíacas. La patogenia del compromiso miocárdico no es clara, pero las dos principales teorías prevén un papel directo de la enzima convertidora de angiotensina 2, que funciona como el receptor viral, y una respuesta hiperinmune, que también puede conducir a una presentación aislada. El estándar de oro del diagnóstico es la biopsia endomiocárdica, la cual no está disponible en la mayoría de los escenarios. En esta revisión, se pretende brindar al lector pautas para identificar las manifestaciones clínicas, ayudas diagnósticas y manejo de los pacientes con sospecha de miocarditis por COVID-19

COVID-19 is an acute respiratory infectious disease caused by a new coronavirus, SARS-CoV-2 virus, that spread rapidly around the world, resulting in a pandemic. Patients present with a wide spectrum of clinical manifestations, including myocarditis, and alternately, some patients without symptoms of heart disease have abnormalities in tests, such as elevated troponin, arrhythmias in the ECG orabnormalities in cardiac imaging testing. The pathogenesis of myocardial involvement is not completely clear, but the two main theories suggest a direct role of the angiotensin-converting enzyme, which functions as the virus receptor, and a hyperimmune response, which can also lead to an isolated presentation. The gold standard for the diagnosis is the endomyocardial biopsy, which is not available in most settings. In this review, we intend to provide the reader with guidelines to identify the clinical manifestations, diagnostic tools, and management of patients with suspected COVID-19 myocarditis

Neurological implications of cardiac compromise in COVID-19.

OBJECTIVES: There is increasing evidence that particularly in patients with severe SARS-CoV-2 infection (COVID-19) the heart can be primarily or secondarily compromised. Neurological disease as a complication of SARS-CoV-2 associated cardiac disease is conceivable. This review aims at summarising and discussing previous and recent advances in the clinical presentation, pathophysiology, diagnosis, treatment, and outcome of cardiac complications and its implications on the brain of SARS-CoV-2 infected patients. METHOD: Literature review using appropriate search terms and applying inclusion and exclusion criteria. RESULTS: Cardiac complications in SARS-CoV-2 infected patients not only include myocardial injury, myocarditis, Takotsubo cardiomyopathy (TTS), coagulation abnormalities, heart failure, cardiac arrest, arrhythmias, acute myocardial infarction, or cardiogenic shock, but a number of other more rarely occurring cardiac abnormalities. Additionally considered should be endocarditis due to superinfection, viral or bacterial pericarditis, aortic dissection, pulmonary embolism from the right atrium, ventricle or outflow tract, and cardiac autonomic denervation. Cardiac damage due to side effects from the anti-COVID medication should not be neglected. Several of these conditions may be complicated by ischemic stroke, intracerebral bleeding, or dissection of cerebral arteries. CONCLUSION: The heart can be definitively affected in severe SARS-CoV-2 infection. Heart disease in COVID-19 may be complicated by stroke, intracerebral bleeding, or dissection of cerebral arteries. Treatment of SARS-CoV-2 associated cardiac disease is not at variance from that of cardiac disease without this infection.

Systematic Investigation Of Cardiovascular Problems In Children And Adult With Covid-19 And Multiple Trauma In Icu Based On Radiology And Analgesia View

This study deals with the systematic investigation of cardiovascular problems in Covid-19 and multiple trauma patients hospitalized in special units, relying on radiology and analgesia stereotypes. Abnormal heart rhythm, which includes high heart rate, irregular heart rate and slow heart rate, can be one of the complications of Corona disease. Also, some of the drugs used for Corona may have side effects such as lowering the heart rate. For example, in one of the recent studies, after starting treatment with Remdesivir, some patients experienced a drop in heart rate. In this study, doctors used dopamine injections to stabilize the patient's heart rate during the 5-day period of Redemsivir treatment, and the patients' heart problems resolved spontaneously at the end of the treatment. Corona virus damages the heart in different ways. The formation of a blood clot is one of the serious complications of Corona, which in some cases leads to death. Its symptoms include severe pain in the chest (heart and lungs), as well as shortness of breath. If the infection caused by Corona disease is severe enough to damage the lungs, less oxygen reaches the heart, which can also reduce the delivery of nutrients to the heart. Therefore, the heart needs more oxygen. The lack of this oxygen and nutrients causes damage to the heart muscles, which is accompanied by pain. Among the other causes of heart pain during the Corona disease, we can mention the inflammation of the heart muscle (myocarditis) and the inner wall of the heart (pericarditis), which can be caused by viral infections. At first, scientists thought that this inflammation was caused by the direct attack of the Corona virus on the heart muscle, but with further research, it became clear that this condition is a result of the overreaction of the body's immune system to the infection caused by the virus and can Another reason for pain in the chest and heart and arrhythmia (irregular heartbeat). [ FROM AUTHOR] Copyright of Journal of Pharmaceutical Negative Results is the property of ResearchTrentz and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

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.

Cardiac troponins: Mechanisms of release and role in healthy and diseased subjects.

The cardiac troponins (cTns), cardiac troponin C (cTnC), cTnT, and cTnI are key elements of myocardial apparatus, fixed as protein complex on the thin filament of sarcomere and are involved in the regulation of excitation-contraction coupling of cardiomyocytes in the presence of Ca2+ . Circulating cTnT and cTnI (cTns) increase following cardiac tissue necrosis, and they are consolidated biomarkers of acute myocardial infarction (AMI). However, the use of high sensitivity (hs)-immunoassay tests for cTnT and cTnI has made it possible to identify a multitude of other clinical conditions associated with increased circulating levels of cTns. cTns can be measured also in the peripheral circulation of healthy subjects or athletes, suggesting that different mechanisms are involved in the release of cTns in the blood independently of cardiac cell necrosis. In this review, the molecular/cellular mechanisms involved in cTns release in blood and the exploitation of cTnI and cTnT as biomarkers of cardiac adverse events, in addition to cardiac necrosis, are discussed.

The Impact of COVID-19 upon Intracardiac Hemodynamics and Heart Rate Variability in Stable Coronary Artery Disease Patients

The aim. To study the impact of COVID-19 upon intracardiac hemodynamics and heart rate variability (HRV) in stable coronary artery disease (SCAD) patients. Materials and methods. In this cross-sectional study we analyzed clinical and instrumental data obtained from a sample of 80 patients. The patients were divided into three groups: group 1 included patients with SCAD without COVID-19 (n=30), group 2 included patients with SCAD and COVID-19 (n=25), and group 3 included patients with COVID-19 without SCAD (n=25). The control group included 30 relatively healthy volunteers. Results. The changes in intracardiac hemodynamics and HRV in group 2 were characterized by the impaired left ventricular systolic and diastolic function, dilation of both ventricles and elevated systolic pulmonary artery pressure. Left ventricular end-diastolic volume was higher in group 2 (205±21 ml) than that in group 1 (176±33 ml;р<0.001) and group 3 (130±21 ml;р<0.001). Patients in the groups 1–3, compared to controls, presented with the decrease in the overall HRV (by standard deviation [SD] of all NN intervals [SDNN];SD of the averages of NN intervals in all 5 min segments of the entire recording;and mean of the SDs of all NN intervals for all 5 min segments of the entire recording) and parasympathetic activity (root-mean-square difference of successive NN intervals;the proportion derived by dividing the number of interval differences of successive NN intervals greater than 50 ms [NN50] by the total number of NN intervals [pNN50], and high frequency spectral component), along with QT interval prolongation and increase in its variability. Group 2 demonstrated the most advanced changes in HRV (by SDNN and pNN50) and both QT interval characteristics. Conclusions. The patients with SCAD and concomitant COVID-19, along with both ventricles dilation and intracardiac hemodynamics impairment, presented with the sings of autonomic dysfunction, QT interval prolongation and increase in its variability. The heart rate variability and QT interval characteristics should be additionally considered in the management of such patients. © 2023 The Authors.

Cardiovascular complications in patients after coronavirus disease-2019

The data of the modern literature describing the long-term consequences of infection of the body with SARS-CoV-2 on the cardiovascular system in the framework of postcovid syndrome are analyzed. To date, postcovid syndrome refers to a condition in which symptoms continue to persist for more than 12 weeks from the moment of diagnosis of COVID-19. Various complaints of patients after undergoing a new coronavirus infection are described, the distinguishing feature of which is their versatility, where cardiovascular manifestations are assigned one of the leading roles. Postural orthostatic tachycardia syndrome, cardiac arrhythmia and conduction disorders are considered. The role of SARS-CoV-2 in the formation of de novo and decompensation of pre-existing cardiovascular diseases has been demonstrated. The possibility of developing heart failure in patients with COVID-19 as an outcome of inflammation of the heart muscle is shown. Particular attention is paid to the analysis of the incidence of myocarditis after 3 months or more from the diagnosis of COVID-19, as well as thrombotic complications, in the genesis of which the main role belongs to the formation of endothelial dysfunction resulting from the interaction of SARS-CoV-2 with vascular endothelial cells. The autoimmune component of the pathogenesis of damage to the cardiovascular system as a result of the formation of endothelial dysfunction in COVID-19 is also considered. The authors present a laboratory-instrumental algorithm for determining cardiovascular complications in people who have undergone COVID-19, including the determination of the N-terminal fragment of the brain natriuretic peptide B-type prohormone, the level of anticardial antibodies, electrocardiography, echocardiography, as well as magnetic resonance imaging of the heart with contrast.

Myocardial extracellular volume assessment at CT in hospitalized COVID-19 patients with regards to pulmonary embolism.

PURPOSE: To evaluate myocardial status through the assessment of extracellular volume (ECV) calculated at computed tomography (CT) in patients hospitalized for novel coronavirus disease (COVID-19), with regards to the presence of pulmonary embolism (PE) as a risk factor for cardiac dysfunction. METHOD: Hospitalized patients with COVID-19 who underwent contrast-enhanced CT at our institution were retrospectively included in this study and grouped with regards to the presence of PE. Unenhanced and portal venous phase scans were used to calculate ECV by placing regions of interest in the myocardial septum and left ventricular blood pool. ECV values were compared between patients with and without PE, and correlations between ECV values and clinical or technical variables were subsequently appraised. RESULTS: Ninety-four patients were included, 63/94 of whom males (67%), with a median age of 70 (IQR 56-76 years); 28/94 (30%) patients presented with PE. Patients with PE had a higher myocardial ECV than those without (33.5%, IQR 29.4-37.5% versus 29.8%, IQR 25.1-34.0%; p = 0.010). There were no correlations between ECV and patients' age (p = 0.870) or sex (p = 0.122), unenhanced scan voltage (p = 0.822), portal phase scan voltage (p = 0.631), overall radiation dose (p = 0.569), portal phase scan timing (p = 0.460), and contrast agent dose (p = 0.563). CONCLUSIONS: CT-derived ECV could help identify COVID-19 patients at higher risk of cardiac dysfunction, especially when related to PE, to potentially plan a dedicated, patient-tailored clinical approach.

Post COVID cardiopulmonary symptoms: self-limiting or life threatening? (An unexplored and mysterious status): needs evaluation

A good proportion of patients complain of cardiopulmonary symptoms even after COVID recovery. Post-COVID symptoms were reported most often as mild and self-limiting. On the other hand, severe post COVID cardiopulmonary complications had also been reported. Therefore, the status of extent and severity of underlying cardiopulmonary disease in this group of patients is very mysterious. Evaluation of underlying disease in such patients is extremely essential. Whereas evaluation is a tough challenge during this COVID pandemic due to the high epidemiological burden of symptomatic post COVID patients. Therefore a systemic review was conducted, collecting and compiling all the literature related to post COVID cardiopulmonary symptoms to understand their pathophysiology and severity of underlying disease. At the same time, an attempt was initiated to derive an approach and strategy for evaluation. During analysis, we obtained useful information as described below. Post COVID cardiopulmonary symptoms can arise due to causes like cardiac, pulmonary, psychogenic, neurogenic, and endocrine, etc. COVID manifests a spectrum of post COVID cardiopulmonary sequelae like myocarditis (2/3rd cases), pericarditis (3% cases), pericardial effusion (5% cases), LV dysfunction (12% cases), pulmonary fibrosis (20% cases), pulmonary function abnormalities (40% cases) etc., which can manifest cardiopulmonary symptoms in post COVID patients. However, the extent and severity of cardiopulmonary involvement is very limited. Reported abnormalities during cardiopulmonary evaluation were found to be mild and self-limiting. However, there is higher chance of developing life threatening complications like pulmonary embolism, acute coronary syndrome, left ventricular failure and arrhythmia in a few rare post COVID cases due to the persistence of hyper inflammatory and hypercoagulable states. Stratification of cases based on past history, records during acute COVID period, clinical findings and biomarkers, can guide in identifying high risk cases. A selective, systemic, and step wise clinical and laboratory approach can help in proper evaluation of patients. However, exclusion of other non COVID related causes is extremely essential, before designating symptoms as post COVID symptoms.

Development of post-COVID-19 cardiovascular events: an Indian perspective

Background: Most common cardio vascular disease events after COVID-19 were hypertension, pulmonary embolism, acute coronary syndrome, myocarditis, stress-Cardiomyopathy, arrhythmias, carcinogenic shock, and cardiac arrest. Aim: To evaluate cardio vascular disease events in patients recovered from COVID-19 in central Indian population Methods: This retrospective observational study was carried out in the department of medicine in a tertiary care hospital, central India. Asses all the participants for post covid cardio vascular events, detailed history, clinical examination and all necessary investigation was done Results: in our study Post COVID 19 cardio vascular events was occur in 17.6%. Majority of the patient was male (69.3%), most common age group were 51-60 years. Higher incidence of cardio vascular disease was reported in obese person. Common cardio vascular diseases found after COVID 19 infection were, hypertension (35.3%), pulmonary embolism (23.5%), Myocarditis (20.6%), myocardial infection (11.8%) and Arrhythmias were in 8.8% cases. Conclusion: Overall observations indicate an increased incidence of hypertension and CVDs post recovery from COVID-19. A dual therapy of ARBs was the preferred choice for management of hypertension. Regular follow-up and close monitoring of symptoms to prevent further CV complications in COVID-19 recovered patients is recommended.

Decreased Heart Rate Variability in COVID-19.

Purpose: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which primarily infects the lower airways and binds to angiotensin-converting enzyme 2 (ACE2) on alveolar epithelial cells. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system. Therefore, SARS-CoV-2 can also damage the myocardium. This report aimed to highlight decreased heart rate variability (HRV) and cardiac injury caused by SARS-CoV-2. Materials and Methods: We evaluated three COVID-19 patients who died. Patients' data were collected from electronic medical records. We collected patient's information, including baseline information, lab results, body temperature, heart rate (HR), clinical outcome and other related data. We calculated the HRV and the difference between the expected and actual heart rate changes as the body temperature increased. Results: As of March 14, 2020, 3 (2.2%) of 136 patients with COVID-19 in Tianjin died in the early stage of the COVID-19 epidemic. The immediate cause of death for Case 1, Case 2, and Case 3 was cardiogenic shock, cardiac arrest and cardiac arrest, respectively. The HRV were substantially decreased in the whole course of all three cases. The actual increases in heart rate were 5 beats/min, 13 beats/min, and 4 beats/min, respectively, less than expected as their temperature increased. Troponin I and Creatine Kinase MB isoenzyme (CK-MB) were substantially increased only in Case 3, for whom the diagnosis of virus-related cardiac injury could not be made until day 7. In all three cases, decreased in HRV and HR changes occurred earlier than increases in cardiac biomarkers (e.g., troponin I and CK-MB). Conclusions: In conclusion, COVID-19 could affect HRV and counteract tachycardia in response to increases in body temperature. The decreases of HRV and HR changes happened earlier than the increases of myocardial markers (troponin I and CK-MB). It suggested the decreases of HRV and HR changes might help predict cardiac injury earlier than myocardial markers in COVID-19, thus its early identification might help improve patient prognosis. Supplementary Information: The online version contains supplementary material available at 10.1007/s44231-022-00024-1.

Successful Correction of Postinfarction Interventricular Septum Rupture Diagnosed Online During the COVID-19 Pandemic (Clinical Case).

Postinfarction interventricular septum defect is a rare, but very serious and sometimes fatal, complication of acute myocardial infarction. This article describes a clinical case of online diagnosis of a late-stage myocardial infarction and the subsequent successful endovascular repair of a postinfarction ventricular septum defect with a Myval™ occluder.

Autopsies Revealed Pathological Features of COVID-19 in Unvaccinated vs. Vaccinated Patients.

Background: In Italy, by the end of 2021, a new pandemic wave led to increased hospitalizations and death, even in some vaccinated people. We aimed to investigate the death of COVID-19-vaccinated patients who acquired infection and developed severe disease, and to assess differences with fatal COVID-19 in unvaccinated subjects by studying the pathological events triggered by SARS-CoV-2. Methods: Detailed autoptic examination was performed on five fully vaccinated compared to five unvaccinated patients. Histopathological analysis focused on the lung and heart, the two major affected organs. Results: COVID-19 caused, or contributed to death, in all the unvaccinated cases. By contrast, in vaccinated group, pre-existing pathologies played a major role, and death was not COVID-19-related in four out of five patients. These patients did not show the histological features of SARS-CoV-2 lung damage. Diffuse inflammatory macrophages infiltration recently emerged as the main feature of COVID-19 cardiac injury. Interestingly, the most striking difference between the two groups was the absence of increased macrophage infiltration in the heart of vaccinated patients. Conclusions: Results of this study confirm the efficacy of anti-SARS-CoV-2 vaccination in protecting organs from injury and support the need to maintain an adequate immune response by booster dose administration.

Measures for the Prevention and Treatment of Covid-19 Infection

This article discusses measures to prevent and treat Covid-19 infection. Collaboration at the local, regional, national and international levels, with a focus on high-quality research, evidence-based practice, the sharing of data and resources, and upholding all ethical standards in the face of unprecedented challenges, will be key to the success of these efforts. In addition, the demand for unproven therapies can lead to shortages of drugs that are approved and indicated for other conditions, leaving patients who rely on these drugs for chronic conditions without effective therapy. Copyright © 2022 Wolters Kluwer Medknow Publications. All rights reserved.

Risk Factors and Mechanisms of Cardiovascular Diseases in Posttraumatic Stress Disorder Model in Wistar Rats as Dependent on Stress Resistance and Age.

The article focuses on the pathogenetic mechanisms of posttraumatic stress disorder (PTSD), which is associated with psychological stress because of the coronavirus pandemic. The molecular mechanisms responsible for disease susceptibility in some individuals and stress resistance in others are amongst crucial research interests of experimental and clinical medicine. Priority data were obtained to indicate that distortions of synthesis and metabolism and, most significantly, a switch between two energy transport forms, glucose and lipids, underlie myocardial dysfunction in young and old stress-sensitive Wistar rats in a PTSD model. Histochemistry and polarization microscopy showed energy deficit in cardiomyocytes and signs of ischemic and hypoxic areas emerging in the myocardium as a result of an accumulation of NADH and NADPH, which initiate excessive production of reactive oxygen species.

SARS-CoV-2 infection and heart disease in dogs and cats

Since the appearance of COVID-19 in humans, there have been numerous reports of dogs and cats being infected with SARSCoV- 2, with cats appearing to be particularly susceptible. The portal of entry of the virus into the body's cells is a membrane receptor called ACE2 (angiotensin converting enzyme 2) belonging to the renin-angiotensin-aldosterone system. The ACE2 receptor is expressed in airway epithelial cells, myocardium, venous and arterial endothelial cells, kidney, liver, oral cavity, intestine and also adipose tissue, explaining the diversity of clinical expression of the disease, with respiratory manifestations predominating. SARS-CoV-2 causes an imbalance in the renin-angiotensin- aldosterone system. In addition, the virus has a direct action combined with an immune reaction, that is sometimes intense, causing a cascade of lesions, mainly in the lungs but also in the heart. The clinical expression of SARS-CoV-2 infection remains rare in dogs and cats and mainly includes fever, depression, anorexia, digestive, respiratory or ocular disorders. As in humans, various cardiovascular clinical signs are less frequently seen. Several cases of myocarditis, correlated with a positive SARS-CoV-2 test (PCR or serology), have been identified in England and at least one in France. In the latter case, further investigation led to a strong suspicion of hypertrophic cardiomyopathy complicated by myocarditis. It is highly likely that obesity (with significant fat deposition in the pleural and pericardial spaces, tissues with high expression of the ACE2 receptor) may have favoured these complications. SARS-CoV-2 infection should therefore now be included in the differential diagnosis of agents causing myocarditis and pneumonia in both cats and dogs.

The first report of myocarditis followed by AstraZeneca vaccination in Iran

BACKGROUND: Coronavirus disease 2019 (COVID-19) is an emerging disease caused by the coronavirus. The initiation of vaccination significantly reduced the incidence and mortality of these patients. Some studies reported myocarditis as a rare complication after messenger ribonucleic acid (mRNA)-based vaccines (such as Pfizer). CASE REPORT: The patient was a 26-year-old man without any history of the underlying disease with typical chest pain which spread to the back and left arm;he was diagnosed with myocarditis after the second dose of the AstraZeneca vaccine. The mechanism of myocarditis after AstraZeneca is not known precisely. It seems to be due to the AstraZeneca vaccine using adenovirus as a vector of the spike (S) protein of the virus, and it causes the production of antibodies in the body, while adenovirus can be one of the causes of myocarditis. On the other hand, it may be due to spike protein-mediated toxicity, which causes an inflammatory reaction such as myocarditis after the virus protein enters the bloodstream and eventually accumulates in various tissues, including the heart. CONCLUSION: Myocarditis is a rare complication of the AstraZeneca vaccine, and this study could not recommend neglecting this vaccine.

Comparative characteristics of hospitalized patients with myocardial infarction in the era of the COVID-19 pandemic - single-centre retrospective analysis

COVID-19 has become a global pandemic affecting more than 260 million people and taking more than 5 million lives (WHO data from December 2021). The infection has a unique interaction with the cardiovascular system and is associated with an increased risk of arterial and venous thromboembolic complications. Aim: To evaluate the impact of the COVID-19 pandemic and the concomitant COVID-19 infection on the characteristics of patients with acute myocardial infarction (AMI) and its course. Material and methods: We analyzed all patients admitted for AMI with and without ST-segment elevation for the period November 1, 2020 - February 1, 2021, at National Heart Hospital, and they were further compared according to the presence of COVID-19 infection. The control group included patients with AMI treated between March 13 and May 13, 2019 when no case of COVID-19 had been reported worldwide. The comparative characteristics include risk profile, index event, examinations and treatment performed, and the scores GRACE, CRUSADE, SAPS II, APACHE II and mSOFA.

Cardiac complications in COVID-19 infected patients admitted in a tertiary care hospital in Karachi

The objective of the current cross-sectional study was to determine the frequency, types, associations, and outcome of cardiac complications in hospitalized COVID-19 infected patients. This study was conducted at Dr. Ziauddin University Hospital, Clifton campus, Karachi, from 1st April 2020 to 31st March 2021. A total number of 1,050 patients were included in the study through consecutive sampling with the diagnosis of COVID-19 infection. Patients were labeled as having complications secondary to COVID pneumonia only after comparing their hospital's clinical course with their baseline status. The independent variables were age, gender, cardiovascular risk factors (smoking status, diabetes mellitus, and hypertension), while the dependent variables were cardiac complications including acute coronary syndrome, myocarditis, pericarditis, and arrhythmias. The Association of complications with independent variables was analyzed by applying the Chi-Square test and statistical significance was set at a P-value of 0.05. There were 599 (57.0%) males and 451 (43.0%) females with the mean age of the participants being 55.1 years (+or- 13.08) years. Diabetes and hypertension were present in 451 (43.0%) and 490 (46.6%) patients respectively. Out of 1050 patients, the primary endpoint occurred in 55.6% of patients, including 23.1% acute coronary syndrome, 19.3% arrhythmias, 10.8% myocarditis, and 2.2% pericarditis. Analysis of secondary endpoint showed that 31.1% of patients had severe disease out of which the mortality was 39.4%. Acute coronary syndrome and atrial fibrillation are frequent complications, especially in those with severe disease and multi-organ dysfunction. Furthermore, the incidence of these complications is higher in patients with multiple co-morbidities. Considering the devastating impact this pandemic has had globally, it is important to know the cardiac involvement this condition can have along with the debilitating outcome so that healthcare facilities can be upgraded to provide better care to save lives.