This review provides a contemporary, evidence-based update on the pathophysiological mechanisms and rapidly evolving therapeutic options for recurrent pericarditis.

Recent studies have elucidated the pathogenesis of recurrent pericarditis, identifying autoinflammation as a key mechanism and interleukin-1 (IL-1) as a central modulator of the inflammatory cascade. Multiple clinical trials have investigated novel therapeutic approaches, particularly focusing on IL-1 inhibition. The recent FDA approval of IL-1 pathway blockade for recurrent pericarditis has revolutionized treatment, offering patients significantly improved quality of life and symptom management.

The enhanced understanding of the autoinflammatory nature of recurrent pericarditis, coupled with groundbreaking advances in targeted therapies, has transformed the treatment landscape for affected patients. The emergence of IL-1 inhibitors as an effective therapeutic option promises substantial improvements in clinical outcomes and patient well being. Clinicians must familiarize themselves with these new treatments, their efficacy, and potential limitations to optimize patient care and guide therapeutic decision-making in this challenging condition.

Pericardial effusion is a relatively common complication associated with inflammatory and non-inflammatory diseases. The primary etiology of this condition could be considered when choosing therapeutic options and factors such as effusion size and its hemodynamic consequence. In most cases, small to moderate pericardial effusions can be managed with observation and anti-inflammatory medications unless the effusion develops rapidly. However, in a small proportion of patients, large effusions lead to impaired cardiac filling with hemodynamic compromise and cardiovascular collapse due to cardiac tamponade. The rate at which fluid accumulates is the primary determinant of hemodynamic impact and thus guides the choice of treatment, irrespective of the effusion's size. Severe cases are typically treated with pericardiocentesis with echocardiographic guidance. More aggressive treatments may be necessary for cases due to purulent or malignant etiologies. These cases may require a pericardial window to allow for long-term drainage of the pericardial fluid. This comprehensive review focuses on the epidemiology of pericardial effusion and discusses pathophysiology, diagnostic approaches, and therapeutic options for different causes of secondary pericardial effusions.

Post-Cardiac Injury Syndrome (PCIS) refers to a collective term encompassing post-myocardial infarction syndrome, post-pericardiotomy syndrome, and post-traumatic pericarditis. With an aging population, the incidence of PCIS is on the rise annually. This condition is considered to be an autoimmune-mediated inflammatory response leading to pericarditis as the primary manifestation of the cardiac disease. Early diagnosis and effective treatment can improve the quality of life and prognosis for PCIS patients. This review aims to provide a comprehensive explicit of the epidemiological characteristics, relevant pathophysiological mechanisms, diagnostic methods, and treatment strategies associated with PCIS, further fostering a deeper understanding and promoting advancements in the prevention and treatment of PCIS.

Uniportal video-assisted thoracoscopic surgery (Uni-VATS) is an effective minimally invasive technique for pericardial drainage, biopsy and window creation in cases of pericardial effusion (PE).

This retrospective study evaluated 73 patients with PE who underwent pericardial window procedures between 2012 and 2024. Intraoperative and post-operative data related to Uni-VATS were assessed.

The mean age of the patients was 53.79 ± 17.79 years (10-82 years), with 34 (46.6%) females and 39 (53.4%) males. The mean volume of pericardial fluid drained after window creation was 446.23 ± 199.81 cc (75-1100 cc). The mean operation time was 42.87 ± 12.79 min, and chest drain removal occurred after an average of 1.8 ± 1.2 days. The mean duration until discharge or referral to the follow-up clinic was 5.98 ± 2.14 days. In addition to the pericardial window procedure, pleural biopsy was performed in 12 patients, mediastinal mass biopsy in eight patients and wedge resection for parenchymal nodules in six patients. Microbiologic and virologic cultures of the fluids were negative in all cases. Among the 41 patients with benign cytology, pericardial biopsy results indicated tuberculosis in four patients (5.4%), amyloidosis in one patient (1.3%) and chronic or subacute nonspecific pericarditis in the remaining patients.

Uni-VATS is a novel and safe technique that may be the preferred choice for pericardial window due to its diagnostic and therapeutic efficacy, ability to perform simultaneous procedures, favourable impact on operation duration/hospital stay, low complication rates and superiority compared to traditional methods.

Pericardial effusions, though relatively rare, can lead to life-threatening complications such as cardiac tamponade. While viral etiologies are common culprits, rapid and accurate diagnosis remains challenging. We present the case of a 74-year-old male with a history of upper respiratory infection who developed sudden onset dyspnea and chest discomfort. Bedside point-of-care ultrasound (POCUS) revealed a large pericardial effusion, prompting urgent intervention. Despite initially stable vital signs, the patient rapidly deteriorated, necessitating emergent pericardiocentesis. Laboratory findings and pathology results eventually ruled out common viral causes, guiding diagnosis toward coxsackieviruses A and B, echovirus, adenoviruses, or influenza. This case highlights the critical role of POCUS in resident-led community hospitals, in expediting the diagnosis of pericardial effusions and underscores the need for prompt intervention in cases of cardiac tamponade to prevent adverse outcomes.

Acute pericarditis is caused by inflammation of the pericardial sac. Among the vast number of potential causes, viruses tend to trigger pericarditis most frequently. Some of the more common viral causes are Coxsackie A/B, echovirus, adenovirus, cytomegalovirus, herpes simplex virus, and human immunodeficiency virus. Pericardial effusion is a common complication and can be visualized on echocardiogram. In some cases, the pericardial effusion can be hemorrhagic in nature, which is extremely rare in the setting of viral pericarditis. The most common causes of hemorrhagic effusion are myocardial infarction, trauma, aortic dissection, or coronary artery bypass graft surgery. Pericardial effusion can sometimes result in serious complications such as cardiac tamponade. In cases of significant pericardial effusion, pericardiocentesis may be required. We present an interesting case of pericarditis caused by the Coxsackie B virus, causing significant hemorrhagic pericardial effusion requiring pericardiocentesis in a young patient. A 37-year-old female with no relevant past medical history presented with substernal chest pain radiating to the left arm and shoulder that improved with leaning forward and dyspnea for two weeks. She had a two-week history of a cough, dysphagia, fever, and chills that started two days prior to the presentation. EKG showed widespread ST elevations and PR interval depressions, which is consistent with a diagnosis of pericarditis. A large pericardial effusion was present on echocardiogram, further suggesting possible pericarditis. Around 350 mL of fluid was removed by pericardiocentesis. Cell count showed 201,000 red blood cells (RBCs)/mcL and 9,350 nucleated cells/mcL. Cytology was negative for malignancy. Cultures were negative for bacteria and fungi. Serum serology showed elevated inflammatory markers (C-reactive protein of 140 mg/L and erythrocyte sedimentation rate of 112 mm/hr) and increased Coxsackie B antibody titers (1:160 for type 2 and 1:320 for type 3). She was started on non-steroidal anti-inflammatory drugs and colchicine. This is a unique case showing that while small exudative pericardial effusions may occur with viral pericarditis, viral infections can also cause a significant hemorrhagic pericardial effusion. Most Coxsackie virus infections are benign. However, there are a few documented case reports of hemorrhagic pericardial effusion from Coxsackie B causing tamponade and death. The importance of this case is that it highlights the consideration of viral infections such as Coxsackie B as a potential cause of hemorrhagic tamponade, especially during autumn and winter months, seasons with the highest risk.

Background. Pericarditis has a heterogeneous clinical spectrum and rate of relapse. Data on aetiology, real-life treatment strategies, and long-term course from contemporary pericarditis cohorts are lacking. Methods. Pericarditis patients referred to the Cardioimmunology Outpatient Clinic at Padua University Hospital in 2001-2020 were retrospectively included. Kaplan-Meier method was used for recurrence-free survival probability estimation. The appropriateness of treatment was assessed based on the European Society of Cardiology guidelines. Results. One-hundred forty-four patients (57% males, mean age 50 years) followed up for 18 months (IQR 7-45) were included; of those, 52% had acute, 35% recurrent, 8% incessant, and 5% chronic pericarditis; 9% had cardiac tamponade at diagnosis. Time to pericardial effusion resolution was 53 days (IQR 16-124); median medical treatment duration was 87 days (IQR 48-148). Treatment was readjusted following the ESC guidelines for nonsteroidal anti-inflammatory drugs in 29% of the cases, steroids in 12%, and colchicine in 25%. Eleven (8%) patients were treated with anti-IL1 agents. Recurrence-free survival probability was 86% at 1st-year follow-up, and 23 patients (16%) had at least one recurrence, with a mean of two relapses per patient. Compared to patients without recurrences, they had a higher frequency of cardiac tamponade (27% vs. 6%, p = 0.006) and left bundle branch block (14% vs. 1%, p = 0.034). Out of the 144 patients, 5 (3%) were diagnosed as having constrictive pericarditis at first evaluation at our clinic, underwent successful pericardiectomy, and are currently alive and asymptomatic. Conclusions. When treated following a guideline-based approach, pericarditis has a favourable evolution. A relevant quote of cases benefits from the treatment readjustment of previously prescribed medical therapy when not in line with ESC recommendations. Cases relapsing despite treatment readjustment should receive anti-IL1 therapies.

Nocardial infections are rare but serious, often leading to systemic and cardiopulmonary complications. This is the first reported case of Nocardia beijingensis causing constrictive pericarditis in an immunocompetent individual. We present a 37-year-old Caucasian female patient with no significant medical history who developed pericarditis symptoms after handling crates from China. Despite initial treatment for presumed viral pericarditis, her condition worsened. Further investigation identified Nocardia beijingensis as the cause of effusive constrictive pericarditis. The patient underwent a pericardiectomy, which resolved her symptoms. This case demonstrates the need to consider rare pathogens in cases of refractory pericarditis, regardless of the patient's immune status. Clinicians should maintain a high level of suspicion for uncommon infections in progressively worsening cases and adopt a multidisciplinary diagnostic approach for timely intervention.

Pericardial disease is increasingly recognized in cancer patients, including acute pericarditis, pericardial effusion, and constrictive pericarditis, often indicating a poor prognosis. Acute pericarditis arises from direct tumor involvement, cancer therapies, and radiotherapy. Immune checkpoint inhibitor (ICI)-related pericarditis, though rare, entails significant mortality risk. Treatment includes NSAIDs, colchicine, and corticosteroids or anti-IL1 drugs in refractory cases. Pericardial effusion is the most frequent manifestation, primarily caused by lung cancer, followed by breast cancer, lymphoma, leukemia, gastrointestinal tumors, and melanoma. Chemotherapy, immunotherapy, and radiotherapy may also cause fluid accumulation in the pericardial space. Symptomatic relief for pericardial effusion may require pericardiocentesis, prolonged catheter drainage, or a pericardial window. Instillation of intrapericardial cytostatic agents may reduce recurrence. Constrictive pericarditis, though less common, often develops from radiotherapy and requires multimodality imaging for diagnosis, with pericardiectomy as the definitive treatment. Primary pericardial tumors are rare, with metastases being more frequent. Patients with cancer and pericardial disease generally have poor survival, emphasizing the need for early detection. A multidisciplinary approach involving hematologists, oncologists, and cardiologists is crucial to tailoring pericardial disease treatment to a patient's clinical status, thereby improving the quality of life and prognosis.

Nearly 35 years after its initial publication in 1989, the Italian Society of Sports Cardiology and the Italian Federation of Sports Medicine (FMSI), in collaboration with other leading Italian Cardiological Scientific Associations (ANCE - National Association of Outpatient Cardiology, ANMCO - National Association of Inpatient Cardiology, SIC - Italian Society of Cardiology), proudly present the 2023 version of the Cardiological Guidelines for Competitive Sports Eligibility. This publication is an update of the previous guidelines, offering a comprehensive and detailed guide for the participation of athletes with heart disease in sports. This edition incorporates the latest advances in cardiology and sports medicine, providing current information and recommendations. It addresses various topics, including the details of the pre-participation screening in Italy and recommendations for sports eligibility and disqualification in competitive athletes with various heart conditions. This revised version of the Cardiological Guidelines for Competitive Sports Eligibility, recorded in the Italian Guidelines Registry of the Italian Minister of Health, stands as a crucial resource for sports medicine professionals, cardiologists, and healthcare providers, marked by its completeness, reliability, and scientific thoroughness. It is an indispensable tool for those involved in the care, management and eligibility process of competitive athletes with heart conditions.

Dressler's syndrome, a rare complication of myocardial infarction, is a form of secondary pericarditis that typically develops within one to six weeks following the infarction. In this report, we present a case of a 68-year-old woman who was diagnosed with Dressler's syndrome after nine weeks from acute coronary syndrome. The patient first presented with an ill-tolerated episode of atrial fibrillation. Based on clinical, laboratory, and imaging findings, accompanied by a history of respiratory tract infections, an infection of an unknown origin was initially suspected. Lack of response to the applied treatment prompted the suspicion of Dressler's syndrome. This was followed by a cardiac MRI, which showed features of pericarditis. The patient responded well to a seven-day treatment with ibuprofen and was discharged home in good general condition.

Recurrent pericarditis poses a significant challenge to patients and clinicians given its high morbidity and health care burden. Since the last iteration of European Society of Cardiology Guidelines in 2015, further insights have been gained into the pathophysiology, multimodality imaging assessment, and treatment of this condition. The purpose of this review is to discuss each of these aspects and highlight the role of imaging-guided therapy and interleukin-1 inhibitors in autoinflammatory phenotypes that together have transformed the care of these patients. Although future investigations are needed to optimize diagnostic surveillance and timing of therapy, recent evidence points at an encouraging paradigm shift in the treatment of recurrent pericarditis.

Acute perimyocarditis is commonly preceded by viral illness and presents with non-specific complaints that can be a manifestation of serious cardiac complications such as arrhythmias and heart failure. While pericarditis is a known complication of thyrotoxicosis, termed "thyrotoxic pericarditis," concomitant new-onset perimyocarditis and Graves' disease, termed "thyro-pericarditis," has been reported. We present a case of thyro-pericarditis as the initial presentation of undiagnosed and untreated Graves' disease co-occurring with recent Coxsackievirus A and B infection. A 27-year-old male with a family history of undifferentiated hyperthyroidism presented with acute pleuritic chest pain and shortness of breath. Laboratory testing showed elevated cardiac troponin I with ST elevations and PR depressions on initial ECG. Left heart catheterization was normal, but transthoracic echocardiogram showed right ventricular systolic dysfunction and enlargement. Cardiac MRI demonstrated diffuse pericardial enhancement suggesting pericarditis. Thyroid function testing and thyroid ultrasound suggested auto-immune thyrotoxicosis. Serology noted abnormal Coxsackievirus A and B IgG antibody titers, suggesting prior infection. The patient was treated with colchicine, ibuprofen, methimazole, and metoprolol, with resolution of symptoms. Thyro-pericarditis is a rare concomitant presentation of both Graves' disease and myopericarditis, and it remains unknown whether there is an increased risk of adverse cardiac outcomes.

Medical therapy of pericarditis should be targeted at its aetiology. Unfortunately, many cases of pericarditis remain idiopathic after a complete diagnostic workup. In such cases, empiric anti-inflammatory therapy for pericarditis is aimed at controlling symptoms and preventing recurrences. The aim of the present clinical review is to summarize published evidence, guidelines, and to provide tips and tricks for clinical management of acute and recurrent pericarditis.

Pericardial effusion (PE) presentation varies from an incidental finding to a life-threatening situation; thus, its etiology and clinical course remain unknown. The aim of the present study was to retrospectively investigate these factors.We analyzed 171 patients (0.4%) who presented with PE among 34,873 patients who underwent echocardiography between 2011 and 2021 at our hospital. Clinical and prognostic information was retrieved from electronic medical records. The primary endpoints were all-cause death, hospitalization due to heart failure (HF), and other cardiovascular events such as cardiovascular death, acute coronary syndrome, elective percutaneous coronary intervention, and stroke.The etiologies of PE were as follows: idiopathic (32%), HF-related (18%), iatrogenic (11%), cardiac surgery-related (10%), radiation therapy-related (9%), malignancy (8%), pericarditis/myocarditis (8%), myocardial infarction-related (2%), and acute aortic dissection (2%). Patients with idiopathic/HF etiology were more likely to be older than the others.During a mean follow-up period of 2.5 years, all-cause death occurred in 21 patients (12.3%), cardiovascular events in 10 patients (5.8%), and hospitalization for HF in 24 patients (14.0%). All-cause death was frequently observed in patients with malignancy (44% per person-year). Cardiovascular events were mostly observed in patients with radiation therapy-related and malignancy (8.6% and 7.3% per person-year, respectively).The annual incidence of hospitalization for HF was the highest in patients with HF-related (25.1% per person-year), followed by radiation therapy-related (10.4% per person-year).This retrospective study is the first, to the best of our knowledge, to reveal the contemporary prevalence of PE, its cause, and outcome in patients who visited a cardiovascular hospital in an urban area of Japan.

Colchicine-an anti-inflammatory alkaloid-has assumed an important role in the management of cardiovascular inflammation ≈3500 years after its first medicinal use in ancient Egypt. Primarily used in high doses for the treatment of acute gout flares during the 20th century, research in the early 21st century demonstrated that low-dose colchicine effectively treats acute gout attacks, lowers the risk of recurrent pericarditis, and can add to secondary prevention of major adverse cardiovascular events. As the first Food and Drug Administration-approved targeted anti-inflammatory cardiovascular therapy, colchicine currently has a unique role in the management of atherosclerotic cardiovascular disease. The safe use of colchicine requires careful monitoring for drug-drug interactions, changes in kidney and liver function, and counseling regarding gastrointestinal upset. Future research should elucidate the mechanisms of anti-inflammatory effects of colchicine relevant to atherosclerosis, the potential role of colchicine in primary prevention, in other cardiometabolic conditions, colchicine's safety in cardiovascular patients, and opportunities for individualizing colchicine therapy using clinical and molecular diagnostics.

Acute purulent pericarditis is a rare infection in developed countries. We herein report a case with diabetic nephropathy under maintenance hemodialysis who suffered from acute purulent pericarditis caused by methicillin-resistant Staphylococcus aureus (MRSA). The treatment of purulent pericarditis mainly involves rapid administration of appropriate antibiotics and drainage. However, in this case, the patient was unresponsive to vancomycin and performing early surgical intervention was challenging due to highly pathogenic MRSA. Therefore, we performed pericardial fenestration in the chronic phase to suppress the risk of fatal secondary infections after daily irrigation for one month to reduce bacterial load mechanically.

In a case of purulent pericarditis caused by highly pathogenic methicillin-resistant Staphylococcus aureus resistant to antibiotics and resulting in constrictive pericarditis, it was possible to perform pericardial fenestration in the chronic phase, while mitigating the risk of fatal secondary infections, by controlling the inflammation through daily irrigation for a long time to reduce the bacterial load mechanically.

Chest pain is a common chief complaint in pediatric emergency departments (EDs). Coronavirus disease-2019 (COVID-19) has been shown to increase the risk of cardiac disease. It remains unclear how COVID-19 changed how pediatric emergency clinicians approach patients presenting with chest pain. The goal of this study was to characterize the diagnostic testing for chest pain in a pediatric ED before and during the COVID-19 pandemic.

This was a retrospective study of children between the ages of 2-17 years presenting to a pediatric ED from 1/1/2018-2/29/2020 (Pre-COVID-19) and 3/1/2020-4/30/2022 (COVID-19) with chest pain. We excluded patients with a previous history of cardiac disease.

Of the 10,721 encounters during the study period, 5,692 occurred before and 5,029 during COVID-19. Patient demographics showed minor differences by age, weight, race and ethnicity. ED encounters for chest pain consisted of an average of 18% more imaging studies during COVID-19, including 14% more EKGs and 11% more chest x-rays, with no difference in the number of echocardiograms. Compared to Pre-COVID-19, 100% more diagnostic tests were ordered during COVID-19, including cardiac markers Troponin I (p < 0.001) and BNP (p < 0.001). During COVID-19, 1.1% of patients had a cardiac etiology of chest pain compared with 0.7% before COVID-19 (p = 0.03).

During COVID-19, pediatric patients with chest pain underwent more diagnostic testing compared to Pre-COVID-19. This may be due to higher patient acuity, emergence of multisystem inflammatory syndrome in children (MIS-C) that necessitated more extensive testing and possible changes in ED clinician behavior during COVID-19.

Pericarditis is an inflammatory process that affects the pericardium, the fibrous sac surrounding the heart. Acute pericarditis accounts for approximately 0.1% of inpatient admissions and 5% of non-ischemic chest pain visits to the emergency departments (EDs). Most patients who present with acute pericarditis have a benign course and good prognosis. However, a rare percent of the patients develop complicated pericarditis. Examples of complications include pericardiac effusion, cardiac tamponade, constrictive pericarditis, effusive and constrictive pericarditis and, even more rarely, large pleural effusion The occurrence of complicated pericarditis can lead to high morbidity and mortality if not urgently managed in most patients. Our case presents a 60-year-old male that presented to the emergency room with flu-like symptoms. However, the viral panel test was negative. He initially got discharged with supportive care but was brought back to the ED by his wife in a critical, life-threatening state due to pericarditis symptoms complicated by tamponade and shock. His condition required urgent intervention and critical level of care. The patient's course was also complicated by myopericarditis and recurrent bilateral pleural effusions, which required therapeutic interventions. This unique case presents the patient group that develop multiple life-threatening complications of acute pericarditis, including cardiac tamponade and shock, affecting several end organs. This case also highlights clues to the predisposing factors to complications of acute pericarditis. Patients who present with high-risk signs and symptoms indicating poorer prognosis warrant further observation and admission. This will also add to the literature reviews regarding the risk factors associated with development of complicated acute pericarditis. This will also serve as a review of pathophysiology, etiology, current diagnosis and available novel treatment for such patients.

Background Pericardial diseases manifest in various clinical forms, including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade, with acute pericarditis being the most prevalent. These conditions significantly contribute to mortality rates. Therefore, this article aimed to analyze mortality trends in the Brazilian population based on age and sex, shedding light on the impact of pericardial diseases on public health outcomes. Methods  This is a retrospective time-series analysis of pericardial disease mortality rates in Brazil (2000-2022). Data was obtained from the Department of Informatics of the Unified Health System (DATASUS), and the 10th edition of the International Classification of Diseases (ICD-10) codes: I30, I31, and I32 were included for analysis. We gathered population and demographic data categorized by age range and sex from the Brazilian Institute of Geography and Statistics (IBGE). Subsequently, we computed the age-standardized mortality rate per 100,000 individuals and assessed the annual percentage changes (APCs) and average annual percentage changes (AAPCs) using joinpoint regression, along with their corresponding 95% confidence intervals (CIs). Results  In terms of mortality trends based on sex, overall mortality rates remained stable for males and combined sexes over the study period. However, there was a notable increase in mortality rates among females (AAPC=1.18), particularly between 2020 and 2022, with a significant APC of 27.55. Analyzing pericardial diseases across different age groups (20 to 80 years and above), it wasobserved that mortality rates significantly increased in the 70-79 and 80 years and above age groups throughout the study period (AAPC=1.0339 and AAPC=3.4587, respectively). These two age groups experienced the highest significant rise in mortality between 2020 and 2022. Other age groups did not exhibit a significant change in AAPC. Conclusions  This comprehensive analysis spanning two decades (2000-2022), examined the mortality trends of pericardial diseases in Brazil and revealed relative stability overall. Males exhibited an overall higher mortality number due to pericardial diseases; however, females showed the most significant increase in mortality trend throughout the whole period. In the first segment (2000-2015), mortality rose across all cohorts, which was attributed to substandard healthcare facilities and infectious diseases like tuberculosis. The second segment (2016-2020) saw a decline in mortality, likely due to improved healthcare, particularly the increased availability of echocardiograms. However, the third segment (2020-2022) witnessed a sharp rise in mortality, coinciding with the COVID-19 pandemic, with post-COVID-19 symptoms, particularly pericarditis. Pericarditis-related death rates declined compared to pericardial effusion, and mortality rates correlated directly with age, with older cohorts experiencing higher mortality due to increased comorbidities, and decline in health and immunocompetency.

Acute pericarditis is an inflammatory condition involving the pericardium, the double-layered sac that surrounds the heart. It is characterized by chest pain, typically pleuritic and sharp, along with other clinical and laboratory findings indicative of pericardial inflammation. While acute pericarditis following influenza vaccination is rare, it has been reported in medical literature. The relationship between vaccinations, including the influenza vaccine, and pericarditis is particularly interesting, as it has implications for public health and vaccination programs. Understanding the pathophysiological mechanisms behind vaccine-induced pericarditis and recognizing the clinical presentation are essential for healthcare professionals to diagnose, manage, and educate patients appropriately.

Increasing evidence indicating that coronavirus disease 2019 (COVID-19) increased the incidence and related risks of pericarditis and whether COVID-19 vaccine is related to pericarditis has triggered research and discussion. However, mechanisms behind the link between COVID-19 and pericarditis are still unknown. The objective of this study was to further elucidate the molecular mechanisms of COVID-19 with pericarditis at the gene level using bioinformatics analysis.

Genes associated with COVID-19 and pericarditis were collected from databases using limited screening criteria and intersected to identify the common genes of COVID-19 and pericarditis. Subsequently, gene ontology, pathway enrichment, protein-protein interaction, and immune infiltration analyses were conducted. Finally, TF-gene, gene-miRNA, gene-disease, protein-chemical, and protein-drug interaction networks were constructed based on hub gene identification.

A total of 313 common genes were selected, and enrichment analyses were performed to determine their biological functions and signaling pathways. Eight hub genes (IL-1β, CD8A, IL-10, CD4, IL-6, TLR4, CCL2, and PTPRC) were identified using the protein-protein interaction network, and immune infiltration analysis was then carried out to examine the functional relationship between the eight hub genes and immune cells as well as changes in immune cells in disease. Transcription factors, miRNAs, diseases, chemicals, and drugs with high correlation with hub genes were predicted using bioinformatics analysis.

This study revealed a common gene interaction network between COVID-19 and pericarditis. The screened functional pathways, hub genes, potential compounds, and drugs provided new insights for further research on COVID-19 associated with pericarditis.

We describe the manifestations and course of patients with pleuropericarditis (PP). Serum parameters were analyzed to evaluate the contribution of autoimmune and autoinflammatory mechanisms to PP pathogenesis. Finally, we outline risk factors for recurrent PP attacks.

Electronic medical records of the University Hospital Heidelberg were screened for PP diagnosis between the years 2009 and 2021. A total of 164 patients were detected and compared to patients suffering from systemic lupus erythematosus (SLE)-associated PP. Follow-up data were collected until January 2023.

In 57.3% of a total of 164 PP cases, no trigger was identified (idiopathic PP). The clinical manifestations were similar in subgroups with different triggers (idiopathic, post-cardiac injury and post-infectious). None of the patients in the idiopathic-PP (i-PP) group fulfilled the diagnostic criteria of an autoimmune disease and the i-PP group could be clearly discriminated by clinical, epidemiological and serological means from the control cohort of SLE-associated PP. After a median follow-up of 1048 days, the majority of PP patients (72.7%) had at least one PP relapse. Univariate analyses showed that CRP, SAA (serum amyloid A), troponin T, NT-BNP and post-cardiac injury were negatively correlated, while the presence of fever and an idiopathic trigger were positively correlated with recurrence of PP. Multivariate analyses showed that fever, an idiopathic trigger and low SAA values were risk factors for PP recurrence.

This study highlights that most cases of PP are idiopathic and PP cases with various triggers have an identical clinical phenotype. Our data suggest that the clinical, epidemiological and serological characteristics of idiopathic PP considerably differ from patients with PP caused by autoimmune disease like SLE. We further demonstrate that PP has a high risk of recurrence and identify factors associated with this risk, allowing for a targeted secondary prophylaxis.

Recurrent pericarditis is a treatment challenge and often a debilitating condition. Drugs inhibiting interleukin 1 cytokines are a promising new treatment option, but their use is based on scarce biological evidence and clinical trials of modest sizes, and the contributions of innate and adaptive immune processes to the pathophysiology are incompletely understood.

To use human genomics, transcriptomics, and proteomics to shed light on the pathogenesis of pericarditis.

This was a meta-analysis of genome-wide association studies of pericarditis from 5 countries. Associations were examined between the pericarditis-associated variants and pericarditis subtypes (including recurrent pericarditis) and secondary phenotypes. To explore mechanisms, associations with messenger RNA expression (cis-eQTL), plasma protein levels (pQTL), and CpG methylation of DNA (ASM-QTL) were assessed. Data from Iceland (deCODE genetics, 1983-2020), Denmark (Copenhagen Hospital Biobank/Danish Blood Donor Study, 1977-2022), the UK (UK Biobank, 1953-2021), the US (Intermountain, 1996-2022), and Finland (FinnGen, 1970-2022) were included. Data were analyzed from September 2022 to August 2023.

Genotype.

Pericarditis.

In this genome-wide association study of 4894 individuals with pericarditis (mean [SD] age at diagnosis, 51.4 [17.9] years, 2734 [67.6%] male, excluding the FinnGen cohort), associations were identified with 2 independent common intergenic variants at the interleukin 1 locus on chromosome 2q14. The lead variant was rs12992780 (T) (effect allele frequency [EAF], 31%-40%; odds ratio [OR], 0.83; 95% CI, 0.79-0.87; P = 6.67 × 10-16), downstream of IL1B and the secondary variant rs7575402 (A or T) (EAF, 45%-55%; adjusted OR, 0.89; 95% CI, 0.85-0.93; adjusted P = 9.6 × 10-8). The lead variant rs12992780 had a smaller odds ratio for recurrent pericarditis (0.76) than the acute form (0.86) (P for heterogeneity = .03) and rs7575402 was associated with CpG methylation overlapping binding sites of 4 transcription factors known to regulate interleukin 1 production: PU.1 (encoded by SPI1), STAT1, STAT3, and CCAAT/enhancer-binding protein β (encoded by CEBPB).

This study found an association between pericarditis and 2 independent sequence variants at the interleukin 1 gene locus. This finding has the potential to contribute to development of more targeted and personalized therapy of pericarditis with interleukin 1-blocking drugs.

Infectious diseases have consistently served as pivotal influences on numerous civilizations, inducing morbidity, mortality, and consequently redirecting the course of history. Their impact extends far beyond the acute phase, characterized by the majority of symptom presentations, to a multitude of adverse events and sequelae that follow viral, parasitic, fungal, or bacterial infections. In this context, myriad sequelae related to various infectious diseases have been identified, spanning short to long-term durations. Although these sequelae are known to affect thousands of individuals individually, a comprehensive evaluation of all potential long-term effects of infectious diseases has yet to be undertaken. We present a comprehensive literature review delineating the primary sequelae attributable to major infectious diseases, categorized by systems, symptoms, and duration. This compilation serves as a crucial resource, illuminating the long-term ramifications of infectious diseases for healthcare professionals worldwide. Moreover, this review highlights the substantial burden that these sequelae impose on global health and economies, a facet often overshadowed by the predominant focus on the acute phase. Patients are frequently discharged following the resolution of the acute phase, with minimal long-term follow-up to comprehend and address potential sequelae. This emphasizes the pressing need for sustained vigilance, thorough patient monitoring, strategic health management, and rigorous research to understand and mitigate the lasting economic and health impacts of infectious diseases more fully.

Objective: This study aimed to investigate the potential association between biological disease-modifying antirheumatic drugs (bDMARDs) and pericarditis and uncover relevant clinical characteristics in ankylosing spondylitis (AS). Methods: Reports of pericarditis recorded in the FDA Adverse Event Reporting System (FAERS) (January 2004-December 2022) were identified through the preferred term "pericarditis." Demographic and clinical characteristics were described, and disproportionality signals were assessed through the reporting odds ratio (ROR) and information component (IC). A significant signal was detected if the lower bound of IC (IC025) was more than zero. Results: We found 1,874 reports of pericarditis with bDMARDs (11.3% of cases with fatal outcomes). Adalimumab (IC025 3.24), infliximab (IC025 4.90), golimumab (IC025 5.40), certolizumab (IC025 5.43), etanercept (IC025 3.24), secukinumab (IC025 3.97), and ustekinumab (IC025 7.61) exhibit significant disproportionality signals compared to other medications in the FAERS database. After excluding pre-existing diseases and co-treated drugs that may increase the susceptibility of pericarditis, the disproportionality signal associated with infliximab, certolizumab, etanercept, secukinumab, and ustekinumab remained strong. Pericarditis cases associated with all bDMARDs were predominantly recorded in women aged 25-65 years. Conclusion: More reports of pericarditis were detected with AS patients on bDMARDs than with other drugs in the overall database. Further studies are warranted to investigate the underlying mechanisms and identify patient-related susceptibility factors, thus supporting timely diagnosis and safe(r) prescribing of bDMARDs.

Cardiac magnetic resonance (CMR) studies reported CMR abnormalities in patients with mild-moderate SARS-CoV-2 infection, suggesting ongoing myocardial inflammation. Patients (n = 278, 43 ± 13 years, 70.5% female) with post-acute sequelae of SARS-CoV-2 cardiovascular syndrome (PASC-CVS) were included prospectively into the Vienna POSTCOV Registry between March 2021 and March 2023 (clinicaltrials.gov NCT05398952). Clinical, laboratory, and CMR findings were recorded. Patients with abnormal CMR results were classified into isolated chronic pericardial (with/without pleural) effusion, isolated cardiac function impairment, or both (myopericarditis) groups. Medical treatment included a nonsteroidal anti-inflammatory agent (NSAID) for pericardial effusion and a condition-adapted maximal dose of heart failure (HF) treatment. Three months after medical therapy, clinical assessment and CMR were repeated in 82 patients. Laboratory analyses revealed normal hematological, inflammatory, coagulation, and cardiac biomarkers. CMR abnormalities were found in 155 patients (55.8%). Condition-adapted HF treatment led to a significant increase in the left ventricular ejection fraction (LVEF) in patients with initially reduced LVEF (from 49 ± 5% to 56 ± 4%, p = 0.009, n = 25). Low-moderate doses of NSAIDs for 3 months significantly reduced pericardial effusion (from 4/3;5.75/mm to 2/0;3/mm, median/interquartile ranges/p < 0.001, n = 51). Clinical symptoms improved markedly with a decrease in CMR abnormalities, which might be attributed to the maintenance of NSAID and HF medical treatment for PASC-CVS.

Our case demonstrated that thrombotic complications such as coronary thrombosis and left ventricular clot could occur even in coronavirus disease 2019 (COVID-19) patients with nonspecific symptoms which indicates the mysterious face of COVID-19. This complex process highlights the necessity of screening patients for COVID-19 disease even with nonspecific cardiac symptoms.

Inflammatory plays a key role in the development of coronary artery disease (CAD). Colchicine as an anti-inflammatory treatment for CAD has attracted much attention, its efficacy and safety are controversial and deserved further exploration.

To evaluate the efficacy and safety of colchicine for patients with CAD, relevant randomized controlled trials (RCTs) were identified by searching several databases including PubMed, Web of Science, and EMBASE from January 1992 to May 2022. Fourteen eligible trials of colchicine therapy include populations with chronic coronary syndrome (CCS) (N = 2), acute coronary syndrome (ACS) (N = 5), and percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) (N = 7), and involve a total of 13,235 patients which include 6654 subjects in colchicine group and 6581 subjects in the respective control arms. The outcome was reported as odds ratio (OR) and 95% confidence interval (CI), as the relative measure of association. Overall, the incidences of major adverse cardiovascular events (MACEs) (OR 0.65; 95% CI 0.54-0.77, p < 0.01), new ACS (OR 0.68; 95% CI 0.57-0.81, p < 0.01), coronary revascularization (OR 0.65; 95% CI 0.53-0.78, p < 0.01), and stroke (OR 0.51; 95% CI 0.32-0.82, p < 0.01), were lower in the colchicine group than in the placebo arm. We did not find a significant reduction in the incidence of atrial fibrillation (OR 0.84; 95% CI 0.68-1.04, p = 0.11), all-cause mortality (OR 1.06; 95% CI 0.83-1.35, p = 0.83), cardiovascular mortality (OR 0.77; 95% CI 0.52-1.15, p = 0.21). However, we found that colchicine did increase non-cardiovascular mortality (OR 1.44; 95% CI 1.04-2.01, p = 0.03). Although the incidence of gastrointestinal events in the colchicine treatment group was higher than that in the placebo arms (OR 2.08; 95% CI 1.39-3.12, p < 0.01), the symptoms disappeared rapidly after drug withdrawal and could be tolerated by most patients. Colchicine did not increase the incidence of infections (OR 1.42; 95% CI 0.82-2.46, p = 0.22), pneumonia (OR 1.55; 95% CI 0.58-4.18, p = 0.39), cancers (OR 0.98; 95% CI 0.79-1.22, p = 0.88), bleeding (OR 1.14; 95% CI 0.41-3.14, p = 0.80).

Colchicine is an effective, relatively safe drug that could be considered for the treatment of CAD. However, we need to pay attention to the increasing occurrence of non-cardiovascular mortality and infection especially pneumonia possibly caused by colchicine. Efficacy and safety of colchicine for patients with CAD. CAD coronary artery disease; RCTs randomized controlled trials; OR odds ratio; MACEs major adverse cardiovascular events; ACS acute coronary syndrome; NNT number needed to treat; NNH number needed to harm.

Acute pericarditis occasionally requires invasive treatment, and may recur after discharge. However, there are no studies on acute pericarditis in Japan, and its clinical characteristics and prognosis are unknown.

This was a single-center, retrospective cohort study of clinical characteristics, invasive procedures, mortality, and recurrence in patients with acute pericarditis hospitalized from 2010 to 2022. The primary in-hospital outcome was adverse events (AEs), a composite of all-cause mortality and cardiac tamponade. The primary outcome in the long-term analysis was hospitalization for recurrent pericarditis.

The median age of all 65 patients was 65.0 years [interquartile range (IQR), 48.0-76.0 years], and 49 (75.3 %) were male. The etiology of acute pericarditis was idiopathic in 55 patients (84.6 %), collagenous in 5 (7.6 %), bacterial in 1 (1.5 %), malignant in 3 (4.6 %), and related to previous open-heart surgery in 1 (1.5 %). Of the 8 patients (12.3 %) with in-hospital AE, 1 (1.5 %) died during hospitalization and 7 (10.8 %) developed cardiac tamponade. Patients with AE were less likely to have chest pain (p = 0.011) but were more likely to have symptoms lasting 72 h after treatment (p = 0.006), heart failure (p < 0.001), and higher levels of C-reactive protein (p = 0.040) and B-type natriuretic peptide (p = 0.032). All patients complicated with cardiac tamponade were treated with pericardial drainage or pericardiotomy. We analyzed 57 patients for recurrent pericarditis after excluding 8 patients: 1 with in-hospital death, 3 with malignant pericarditis, 1 with bacterial pericarditis, and 3 lost to follow-up. During a median follow-up of 2.5 years (IQR 1.3-3.0 years), 6 patients (10.5 %) had recurrences requiring hospitalization. The recurrence rate of pericarditis was not associated with colchicine treatment or aspirin dose or titration.

In acute pericarditis requiring hospitalization, in-hospital AE and recurrence were each observed in >10 % of patients. Further large studies on treatment are warranted.

Pericarditis complicates pregnancy planning, pregnancy, or the postpartum period, and the management approach requires special considerations. Here, we aim to summarize the latest research, diagnostic, and treatment strategies.

Physiologic cardiovascular (CV) adaptations occurring during pregnancy complicate diagnosis, but for most patients, an electrocardiogram (ECG) and transthoracic echocardiogram (TTE) are sufficient to diagnosis pericarditis in the appropriate clinical context. Aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) can be used until 20 weeks gestation as needed. The use of colchicine is encouraged at any time point to reduce the risk of recurrence. Glucocorticoids may be used at the lowest possible dose for the least amount of time throughout pregnancy and breastfeeding. For incessant, recurrent, or refractory pericarditis, or when the above therapies are contraindicated, there may be a consideration of the use of IL-1 inhibition during pregnancy, recognizing the limited data in pregnant patients. Finally, we encourage the use of a multidisciplinary team approach including OB-GYN, cardiology, and rheumatology when available. The diagnosis and treatment of pericarditis in female patients of reproductive age require special considerations. Although highly effective treatment options are available, there is a need for greater data and larger international registries to improve treatment recommendations.

Pericarditis is the inflammation of the pericardial layers. Myopericarditis is diagnosed when this inflammation involves the myocardium, which is marked by elevated serum cardiac enzymes. With these two pathologies sharing overlaps in etiology, we present a case of a young patient with a recent history of COVID-19 infection who presented with pleuritic and positional chest pain with troponin I elevation and serial ECG changes attributed to myopericarditis as a post-viral sequela of severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection. This case demonstrates the importance of identifying and managing the potential cardiac complications in coronavirus disease 2019 (COVID-19) patients, regardless of age or symptom onset.

We report a case of gonococcal pericarditis, which was unexpected due to its extremely unusual occurrence. A 42-year-old man presented with fever, chest pain, dyspnea, and tachycardia. He was initially stable but rapidly deteriorated, developing pericardial effusion with tamponade requiring a pericardial window. Incompletely decolorized gram stain of the pericardial fluid initially suggested the presence of gram-positive diplococci, which wrongly directed treatment toward possible pneumococcal infection. Because cultures were negative, identification of the causative organism was attempted by molecular and genotyping analysis. These techniques identified Neisseria gonorrhoeae-multi-antigen sequence type 14994 (por 5136/tbpB 33) as the etiology, which has been associated with disseminated gonococcal disease. Real-time polymerase chain reaction showed no evidence of mutations within the N. gonorrhoeae penA gene responsible for causing ceftriaxone resistance. This was crucial in guiding antibiotic treatment, in light of the high prevalence of multi-drug-resistant N. gonorrhoeae. This case highlights the utility of diagnostic molecular techniques in identifying N. gonorrhoeae as the etiology of an exceedingly rare case of pericarditis.

We review the pathophysiology, diagnosis, and contemporary treatment for recurrent pericarditis, with focus on interleukin-1 (IL-1) inhibitors.

Recurrent pericarditis occurs in about 15-30% of patients who have acute pericarditis. With increased understanding of the autoinflammatory pathophysiology of recurrent pericarditis, IL-1 inhibitors including anakinra, canakinumab, and rilonacept have been applied to this condition with great promise. In particular, the RHAPSODY trial found rilonacept significantly improves pain and inflammation, while also reducing recurrence with few adverse events. The next IL-1 inhibitor on the block for pericarditis, goflikicept, is also discussed. Understanding the role of the inflammasome via the autoinflammatory pathway in pericarditis has led to incorporation of IL-1 inhibitors in the treatment of recurrent pericarditis, with proven efficacy and safety and randomized trials. This will lead to increase uptake of this agent which demonstrated lower rates of recurrence and faster time to resolution.

Awareness of gender differences in cardiovascular disease (CVD) has increased: both the different impact of traditional cardiovascular risk factors on women and the existence of sex-specific risk factors have been demonstrated. Therefore, it is essential to recognize typical aspects of ischemic heart disease (IHD) in women, who usually show a lower prevalence of obstructive coronary artery disease (CAD) as a cause of acute coronary syndrome (ACS). It is also important to know how to recognize pathologies that can cause acute chest pain with a higher incidence in women, such as spontaneous coronary artery dissection (SCAD) and myocardial infarction with non-obstructive coronary arteries (MINOCA). Coronary computed tomography angiography (CCTA) and cardiac magnetic resonance imaging (CMR) gained a pivotal role in the context of cardiac emergencies. Thus, the aim of our review is to investigate the most frequent scenarios in women with acute chest pain and how advanced cardiac imaging can help in the management and diagnosis of ACS.

Pericardial disease includes a variety of conditions, including inflammatory pericarditis, pericardial effusions, constrictive pericarditis, pericardial cysts, and primary and secondary pericardial neoplasms. The true incidence of this varied condition is not well established, and the causes vary greatly across the world. This review aims to describe the changing pattern of epidemiology of pericardial disease and to provide an overview of causative etiologies. Idiopathic pericarditis (assumed most often to be viral) remains the most common etiology for pericardial disease globally, with tuberculous pericarditis being most common in developing countries. Other important etiologies include fungal, autoimmune, autoinflammatory, neoplastic (both benign and malignant), immunotherapy-related, radiation therapy-induced, metabolic, postcardiac injury, postoperative, and postprocedural causes. Improved understanding of the immune pathophysiological pathways has led to identification and reclassification of some idiopathic pericarditis cases into autoinflammatory etiologies, including immunoglobulin G (IgG)4-related pericarditis, tumour necrosis factor receptor-associated periodic syndrome (TRAPS), and familial Mediterranean fever in the current era. Contemporary advances in percutaneous cardiac interventions and the recent COVID-19 pandemic have also resulted in changes in the epidemiology of pericardial diseases. Further research is needed to improve our understanding of the etiologies of pericarditis, using the assistance of contemporary advanced imaging techniques and laboratory testing. Careful consideration of the range of potential causes and local epidemiologic patterns of causality are important for the optimization of diagnostic and therapeutic approaches.

Cardiac tamponade is a medical emergency caused by the progressive accumulation of pericardial fluid (effusion), blood, pus or air in the pericardium, compressing the heart chambers and leading to haemodynamic compromise, circulatory shock, cardiac arrest and death. Pericardial diseases of any aetiology as well as complications of interventional and surgical procedures or chest trauma can cause cardiac tamponade. Tamponade can be precipitated in patients with pericardial effusion by dehydration or exposure to certain medications, particularly vasodilators or intravenous diuretics. Key clinical findings in patients with cardiac tamponade are hypotension, increased jugular venous pressure and distant heart sounds (Beck triad). Dyspnoea can progress to orthopnoea (with no rales on lung auscultation) accompanied by weakness, fatigue, tachycardia and oliguria. In tamponade caused by acute pericarditis, the patient can experience fever and typical chest pain increasing on inspiration and radiating to the trapezius ridge. Generally, cardiac tamponade is a clinical diagnosis that can be confirmed using various imaging modalities, principally echocardiography. Cardiac tamponade is preferably resolved by echocardiography-guided pericardiocentesis. In patients who have recently undergone cardiac surgery and in those with neoplastic infiltration, effusive-constrictive pericarditis, or loculated effusions, fluoroscopic guidance can increase the feasibility and safety of the procedure. Surgical management is indicated in patients with aortic dissection, chest trauma, bleeding or purulent infection that cannot be controlled percutaneously. After pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be considered to prevent recurrence and effusive-constrictive pericarditis.

Purulent pericardial effusion is a rare but potentially deadly condition that demands immediate medical attention. When left untreated, it can have catastrophic consequences. While bacterial infection is the most common cause of this condition, it usually occurs in individuals with weakened immune systems or in those undergoing dialysis or thoracic surgery. This case report presented here is unique as it chronicles the uncommon experience of a 58-year-old male with a normally functioning immune system who suffered from purulent pericardial effusion, endocarditis, and pneumonia, all linked to septic arthritis of his knee caused by Streptococcus pneumoniae. The diagnosis and management of this condition require a swift and comprehensive approach, and any delay in treatment can have dire outcomes. This case highlights the significance of early detection and prompt treatment of purulent pericardial effusion to prevent severe complications and improve patient prognosis.

Cardiovascular involvement is an uncommon but severe complication of Epstein-Barr virus (EBV) infection caused by direct damage and immune injury. Recently, it has drawn increasing attention due to its dismal prognosis. It can manifest in various ways, including coronary artery dilation (CAD), coronary artery aneurysm (CAA), myocarditis, arrhythmias, and heart failure, among others. If not treated promptly, cardiovascular damage can progress over time and even lead to death, which poses a challenge to clinicians. Early diagnosis and treatment can improve the prognosis and reduce mortality. However, there is a lack of reliable large-scale data and evidence-based guidance for the management of cardiovascular damage. Consequently, in this review, we attempt to synthesize the present knowledge of cardiovascular damage associated with EBV and to provide an overview of the pathogenesis, classification, treatment, and prognosis, which may enhance the recognition of cardiovascular complications related to EBV and may be valuable to their clinical management.