A rare complication of pericardiocentesis: Pneumopericardium.

Pneumopericardium is the presence of air in the pericardial sac. Pneumopericardium after pericardiocentesis has been rarely reported in the literature. In the present case, we report a patient who presented with tamponade physiology during COVID-19 and developed pneumopericardium after emergency pericardiocentesis. Immediate recognition and treatment are crucial and chest x-ray, thorax computerized tomography, and transthoracic echocardiography (TTE) are used for diagnosis.

Acute pericarditis as a major clinical manifestation of long COVID-19 syndrome.

BACKGROUND: The long COVID-19 syndrome has been recently described and some reports have suggested that acute pericarditis represents important manifestation of long COVID-19 syndrome. The aim of this study was to identify the prevalence and clinical characteristics of patients with long COVID-19, presenting with acute pericarditis. METHODS: We retrospectively included 180 patients (median age 47 years, 62% female) previously diagnosed with COVID-19, exhibiting persistence or new-onset symptoms ≥12 weeks from a negative naso-pharyngeal SARS CoV2 swamp test. The original diagnosis of COVID-19 infection was determined by a positive swab. All patients had undergone a thorough physical examination. Patients with suspected heart involvement were referred to a complete cardiovascular evaluation. Echocardiography was performed based on clinical need and diagnosis of acute pericarditis was achieved according to current guidelines. RESULTS: Among the study population, shortness of breath/fatigue was reported in 52%, chest pain/discomfort in 34% and heart palpitations/arrhythmias in 37%. Diagnosis of acute pericarditis was made in 39 patients (22%). Mild-to-moderate pericardial effusion was reported in 12, while thickened and bright pericardial layers with small effusions (< 5 mm) with or without comet tails arising from the pericardium (pericardial B-lines) in 27. Heart palpitations/arrhythmias (OR:3.748, p = 0.0030), and autoimmune disease and allergic disorders (OR:4.147, p = 0.0073) were independently related to the diagnosis of acute pericarditis, with a borderline contribution of less likelihood of hospitalization during COVID-19 (OR: 0.100, p = 0.0512). CONCLUSION: Our findings suggest a high prevalence of acute pericarditis in patients with long COVID-19 syndrome. Autoimmune and allergic disorders, and palpitations/arrhythmias were frequently associated with pericardial disease.

Rare atypical presentation of a polymicrobial gastropericardial fistula.

We present the unique case of a gastropericardial fistula with a rare, delayed presentation in a man in his 70s. Relevant surgeries include Watchman Left Atrial Appendage Closure device placement 1 year prior to arrival and gastric bypass surgery 20 years prior to arrival. The patient presented to the emergency department with weakness, diarrhoea and left knee pain. He was admitted for cellulitis of the left lower extremity, prosthetic septic arthritis of the left knee and group G streptococcus bacteraemia. His hospital course was complicated by acute chest pain and dyspnoea. Imaging revealed pneumopericardium. Oesophagogastroduodenoscopy visualisation confirmed the diagnosis of gastropericardial fistula. The patient could not be transferred to a tertiary centre for definitive management because of the effect of the COVID-19 pandemic on tertiary hospital volumes. After pericardial drainage and administration of antimicrobials without improvement, the patient was discharged to hospice care at his request and died 1 day after discharge.

Chronic purulent pericarditis: case report.

Purulent pericarditis is an infection of the pericardial space that produces pus that is found on gross examination of the pericardial sac or on the tissue microscopy. In this case report, we will discuss a 31-year-old male who presented with a chief complaint of low-grade fevers, dry cough and difficulty breathing for about two weeks which preceded after removing of dental also two weeks prior. He was admitted and treated as COVID-19 in the isolation ward, he later developed cardiac tamponade and during pericardiocentesis thick pus was discharged. Pus culture and Gene Xpert tests were all negative. After his condition improved, the patient was transferred to the general ward with the pericardial window still discharging pus. Pericardiectomy was chosen as definitive management. The key takeaway in this report is that Empirical treatment with RHZE (rifampin, isoniazid, pyrazinamide, and ethambutol) in resource-limited settings is recommended due to difficulty in identifying the exact cause at a required moment.

Measurement of epicardial adipose tissue using non-contrast routine chest-CT: a consideration of threshold adjustment for fatty attenuation.

BACKGROUND: Epicardial adipose tissue (EAT) is known as an important imaging indicator for cardiovascular risk stratification. The present study aimed to determine whether the EAT volume (EV) and mean EAT attenuation (mEA) measured by non-contrast routine chest CT (RCCT) could be more consistent with those measured by coronary CT angiography (CCTA) by adjusting the threshold of fatty attenuation. METHODS: In total, 83 subjects who simultaneously underwent CCTA and RCCT were enrolled. EV and mEA were quantified by CCTA using a threshold of (N30) (- 190 HU, - 30 HU) as a reference and measured by RCCT using thresholds of N30, N40 (- 190 HU, - 40 HU), and N45 (- 190 HU, - 45 HU). The correlation and agreement of EAT metrics between the two imaging modalities and differences between patients with coronary plaques (plaque ( +)) and without plaques (plaque ( -)) were analyzed. RESULTS: EV obtained from RCCT showed very strong correlation with the reference (r = 0.974, 0.976, 0.972 (N30, N40, N45), P < 0.001), whereas mEA showed a moderate correlation (r = 0.516, 0.500, 0.477 (N30, N40, N45), P < 0.001). Threshold adjustment was able to reduce the bias of EV, while increase the bias of mEA. Data obtained by CCTA and RCCT both demonstrated a significantly larger EV in the plaque ( +) group than in the plaque ( -) group (P < 0.05). A significant difference in mEA was shown only by RCCT using a threshold of N30 (plaque ( +) vs ( -): - 80.0 ± 4.4 HU vs - 78.0 ± 4.0 HU, P = 0.030). The mEA measured on RCCT using threshold of N40 and N45 showed no significant statistical difference between the two groups (P = 0.092 and 0.075), which was consistent with the result obtained on CCTA (P = 0.204). CONCLUSION: Applying more negative threshold, the consistency of EV measurements between the two techniques improves and a consistent result can be obtained when comparing EF measurements between groups, although the bias of mEA increases. Threshold adjustment is necessary when measuring EF with non-contrast RCCT.

Acute Pericarditis: Update.

PURPOSE OF REVIEW: Since 2015, when ESC guidelines for the diagnosis and management of pericardial diseases were published, ongoing research has enhanced the current state of knowledge on acute pericarditis. This review is an update on the latest developments in this field. RECENT FINDINGS: In recurrent acute pericarditis, autoinflammation has been included among causative mechanisms restricting the vague diagnoses of "idiopathic" pericarditis. Cardiac magnetic resonance that detects ongoing pericardial inflammation may guide treatment in difficult-to-treat patients. Development of risk scores may assist identification of patients at high risk for complicated pericarditis, who should be closely monitored and aggressively treated. Treatment with IL-1 inhibitors has been proven efficacious in recurrent forms with a good safety profile. Finally, acute pericarditis has recently attracted great interest as it has been reported among side effects post COVID-19 vaccination and may also complicate SARS-CoV-2 infection. Recent advancements in acute pericarditis have contributed to a better understanding of the disease allowing a tailored to the individual patient approach. However, there are still unsolved questions that require further research.

Is there a relationship between epicardial adipose tissue, inflammatory markers and prognosis in COVID-19 in patients under 65 years?

Aim: This study investigated the prognostic value of epicardial adipose tissue volume (EATV) attenuation (EATA) in patients admitted to the intensive care unit for COVID-19. Materials & methods: C-reactive protein (CRP), fasting blood glucose (FBG), neutrophil and lymphocyte counts, neutrophil-to-lymphocyte ratio (NLR) and lymphocyte-to-CRP ratio (LCR) were recorded. Receiver operator characteristic analysis was performed for EATV and EATA. Results: The study included 190 patients (65 deceased, 125 discharged, mean age 52.01 ± 9.6 years). The deceased group had significantly higher FBG and CRP values and significantly lower platelet count and LCR values. EATA (cut-off: -92.38 HU) and EATV (cut-off: 15.74 cm2) were significantly higher in the deceased group. EATV had a correlation with age, FBG, CRP, neutrophil, NLR and LCR, whereas EATA correlated with involvement on CT scan. Conclusion: EATV is associated with inflammatory parameters, whereas EATA is associated with CT scan involvement and can be used to predict mortality in young adult patients.

Browning Epicardial Adipose Tissue: Friend or Foe?

The epicardial adipose tissue (EAT) is the visceral fat depot of the heart which is highly plastic and in direct contact with myocardium and coronary arteries. Because of its singular proximity with the myocardium, the adipokines and pro-inflammatory molecules secreted by this tissue may directly affect the metabolism of the heart and coronary arteries. Its accumulation, measured by recent new non-invasive imaging modalities, has been prospectively associated with the onset and progression of coronary artery disease (CAD) and atrial fibrillation in humans. Recent studies have shown that EAT exhibits beige fat-like features, and express uncoupling protein 1 (UCP-1) at both mRNA and protein levels. However, this thermogenic potential could be lost with age, obesity and CAD. Here we provide an overview of the physiological and pathophysiological relevance of EAT and further discuss whether its thermogenic properties may serve as a target for obesity therapeutic management with a specific focus on the role of immune cells in this beiging phenomenon.

Association of epicardial adipose tissue with the severity and adverse clinical outcomes of COVID-19: A meta-analysis.

OBJECTIVES: Epicardial adipose tissue (EAT) has been proposed to be an independent predictor of visceral adiposity. EAT measures are associated with coronary artery disease, diabetes, and chronic obstructive pulmonary disease, which are risk factors for COVID-19 poor prognosis. Whether EAT measures are related to COVID-19 severity and prognosis is controversial. METHODS: We searched 6 databases for studies until January 7, 2022. The pooled effects are presented as the standard mean difference (SMD) or weighted mean difference with 95% confidence intervals (CIs). The primary end point was COVID-19 severity. Adverse clinical outcomes were also assessed. RESULTS: A total of 13 studies with 2482 patients with COVID-19 were identified. All patients had positive reverse transcriptase-polymerase chain reaction results. All quantitative EAT measures were based on computed tomography. Patients in the severe group had higher EAT measures compared with the nonsevere group (SMD = 0.74, 95% CI: 0.29-1.18, P = 0.001). Patients with hospitalization requirement, requiring invasive mechanical ventilation, admitted to intensive care unit, or with combined adverse outcomes had higher EAT measures compared to their controls (all P < 0.001). CONCLUSIONS: EAT measures were associated with the severity and adverse clinical outcomes of COVID-19. EAT measures might help in prognostic risk stratification of patients with COVID-19.

Epicardial adipose tissue in contemporary cardiology.

Interest in epicardial adipose tissue (EAT) is growing rapidly, and research in this area appeals to a broad, multidisciplinary audience. EAT is unique in its anatomy and unobstructed proximity to the heart and has a transcriptome and secretome very different from that of other fat depots. EAT has physiological and pathological properties that vary depending on its location. It can be highly protective for the adjacent myocardium through dynamic brown fat-like thermogenic function and harmful via paracrine or vasocrine secretion of pro-inflammatory and profibrotic cytokines. EAT is a modifiable risk factor that can be assessed with traditional and novel imaging techniques. Coronary and left atrial EAT are involved in the pathogenesis of coronary artery disease and atrial fibrillation, respectively, and it also contributes to the development and progression of heart failure. In addition, EAT might have a role in coronavirus disease 2019 (COVID-19)-related cardiac syndrome. EAT is a reliable potential therapeutic target for drugs with cardiovascular benefits such as glucagon-like peptide 1 receptor agonists and sodium-glucose co-transporter 2 inhibitors. This Review provides a comprehensive and up-to-date overview of the role of EAT in cardiovascular disease and highlights the translational nature of EAT research and its applications in contemporary cardiology.

Epicardial adipose tissue thickness is associated with increased COVID-19 severity and mortality.

BACKGROUND: Increased adiposity and visceral obesity have been linked to adverse COVID-19 outcomes. The amount of epicardial adipose tissue (EAT) may have relevant implications given its proximity to the heart and lungs. Here, we explored the role of EAT in increasing the risk for COVID-19 adverse outcomes. METHODS: We included 748 patients with COVID-19 attending a reference center in Mexico City. EAT thickness, sub-thoracic and extra-pericardial fat were measured using thoracic CT scans. We explored the association of each thoracic adipose tissue compartment with COVID-19 mortality and severe COVID-19 (defined as mortality and need for invasive mechanical ventilation), according to the presence or absence of obesity. Mediation analyses evaluated the role of EAT in facilitating the effect of age, body mass index and cardiac troponin levels with COVID-19 outcomes. RESULTS: EAT thickness was associated with increased risk of COVID-19 mortality (HR 1.18, 95% CI 1.01-1.39) independent of age, gender, comorbid conditions and BMI. Increased EAT was associated with lower SpO2 and PaFi index and higher levels of cardiac troponins, D-dimer, fibrinogen, C-reactive protein, and 4 C severity score, independent of obesity. EAT mediated 13.1% (95% CI 3.67-28.0%) and 5.1% (95% CI 0.19-14.0%) of the effect of age and 19.4% (95% CI 4.67-63.0%) and 12.8% (95% CI 0.03-46.0%) of the effect of BMI on requirement for intubation and mortality, respectively. EAT also mediated the effect of increased cardiac troponins on myocardial infarction during COVID-19. CONCLUSION: EAT is an independent risk factor for severe COVID-19 and mortality independent of obesity. EAT partly mediates the effect of age and BMI and increased cardiac troponins on adverse COVID-19 outcomes.

Blood glucose and epicardial adipose tissue at the hospital admission as possible predictors for COVID-19 severity.

PURPOSE: To study the possible association of CT-derived quantitative epicardial adipose tissue (EAT) and glycemia at the admission, with severe outcomes in patients with COVID-19. METHODS: Two hundred and twenty-nine patients consecutively hospitalized for COVID-19 from March 1st to June 30th 2020 were studied. Non contrast chest CT scans, to confirm diagnosis of pneumonia, were performed. EAT volume (cm3) and attenuation (Hounsfield units) were measured using a CT post-processing software. The primary outcome was acute respiratory distress syndrome (ARDS) or in-hospital death. RESULTS: The primary outcome occurred in 56.8% patients. Fasting blood glucose was significantly higher in the group ARDS/death than in the group with better prognosis [114 (98-144) vs. 101 (91-118) mg/dl, p = 0.001]. EAT volume was higher in patients with vs without the primary outcome [103 (69.25; 129.75) vs. 78.95 (50.7; 100.25) cm3, p < 0.001] and it was positively correlated with glycemia, PCR, fibrinogen, P/F ratio. In the multivariable logistic regression analysis, age and EAT volume were independently associated with ARDS/death. Glycemia and EAT attenuation would appear to be factors involved in ARDS/death with a trend of statistical significance. CONCLUSIONS: Our findings suggest that both blood glucose and EAT, easily measurable and modifiable targets, could be important predisposing factors for severe Covid-19 complications.

Pericarditis after SARS-CoV-2 Infection: Another Pebble in the Mosaic of Long COVID?

With the emerging success of the COVID-19 vaccination programs, the incidence of acute COVID-19 will decrease. However, given the high number of people who contracted SARS-CoV-2 infection and recovered, we will be faced with a significant number of patients with persistent symptoms even months after their COVID-19 infection. In this setting, long COVID and its cardiovascular manifestations, including pericarditis, need to become a top priority for healthcare systems as a new chronic disease process. Concerning the relationship between COVID-19 and pericardial diseases, pericarditis appears to be common in the acute infection but rare in the postacute period, while small pericardial effusions may be relatively common in the postacute period of COVID-19. Here, we reported a series of 7 patients developing pericarditis after a median of 20 days from clinical and virological recovery from SARS-CoV-2 infection. We excluded specific identifiable causes of pericarditis, hence we speculate that these cases can be contextualized within the clinical spectrum of long COVID. All our patients were treated with a combination of colchicine and either ASA or NSAIDs, but four of them did not achieve a clinical response. When switched to glucocorticoids, these four patients recovered with no recurrence during drug tapering. Based on this observation and on the latency of pericarditis occurrence (a median of 20 days after a negative nasopharyngeal swab), could be suggested that post-COVID pericarditis may be linked to ongoing inflammation sustained by the persistence of viral nucleic acid without virus replication in the pericardium. Therefore, glucocorticoids may be a suitable treatment option in patients not responding or intolerant to conventional therapy and who require to counteract the pericardial inflammatory component rather than direct an acute viral injury to the pericardial tissue.

Myocardial injury in COVID-19 patients is associated with the thickness of epicardial adipose tissue.

Aim    High sensitive troponin (hs-TnI) levels may increase secondary to Coronavirus disease-2019 (COVID-19), and this increase is associated with cardiovascular mortality in COVID-19 patients. Epicardial adipose tissue (EAT) is associated with myocardial injury directly as a reservoir tissue for coronavirus, and indirectly through mediators it secretes as an apocrine gland. We aimed to evaluate the relationship between myocardial injury secondary to COVID-19 infection and EAT thickness.Material and methods    Thoracic computed tomography (CT) was performed in 73 consecutive patients diagnosed with COVID-19. EAT thickness and volume were calculated by two radiologists blind to the study data. We formed two groups according to hs-TnI concentrations, patients with myocardial damage (hs-TnI ≥11.6 ng / l) and without myocardial damage (hs-TnI<11.6 ng / dl).Results    A total of 46 patients were women (63.0 %). The mean age was 66.4±12.3 yrs in the myocardial injury group and 55.9±9.7 yrs in the group without myocardial injury (p<0.001). There were 20 hypertensive patients (68.9 %) in the injury group, while there were 12 hypertensive patients (27.3 %) in the group without injury (p=0.001). Glucose, C-reactive protein, D-dimer, white blood cell count, neutrophil, and neutrophil / lymphocyte ratio were higher in the injury group (p<0.05, for all variables). The mean EAT thickness was 5.6±1.6 mm in the injury group, whereas it was 4.8±1.8 mm in the group without injury (p=0.031). EAT thickness of 4.85 mm and above was associated with the myocardial injury with 65 % sensitivity and 39 % specificity (AUC=0.65, 95 % CI: 0.52-078, p=0.031).Conclusion    In patients with COVID-19 infection, higher rates of myocardial injury were observed as the EAT thickness increased. Epicardial adipose tissue, contributes to cytokine-mediated myocardial injury either directly or indirectly by acting as a reservoir for coronavirus. Increased EAT thickness is associated with myocardial injury in COVID-19 patients.

Pericardial Cytokine "Storm" in a COVID-19 Patient: the Confirmation of a Hypothesis.

Novel Coronavirus Disease in most cases produces mild symptoms which resolve after a few days. Some authors hypothesized that SARS-CoV-2 infection could trigger excessive cytokine production leading to a severe multi-organ disease requiring intensive care admission. Respiratory and neurological symptoms are the most frequently reported manifestation of the disease. Indeed, cardiac involvement is reported mostly as a part of a systemic disease. Few isolated cardiac manifestations of COVID-19 infection have been described. We report herein a case of SARS-CoV-2 related severe isolated pericardial involvement requiring ICU admission due to cardiac tamponade needing urgent drainage. Analysis of pericardial fluid from drainage demonstrated a higher cytokine concentration than blood values. Other causes of pericardial disease, such as autoimmunity, bacterial or other than COVID-19 infection, neoplasms or acute myocardial infarction were also evaluated, but all tests confirmed negative results. The suspicion of isolated involvement of the pericardium was therefore demonstrated by the analysis of cytokines which strongly support our hypothesis.

Cardiac tamponade and massive pleural effusion in a young COVID-19-positive adult.

COVID-19 has a broad spectrum of cardiac manifestations, and cardiac tamponade leading to cardiogenic shock is a rare presentation. A 30-year-old man with a history of COVID-19-positive, reverse transcription polymerase chain reaction (RT-PCR) done 1 week ago and who was home-quarantined, came to the emergency department with palpitations, breathlessness and orthopnoea. His ECG showed sinus tachycardia with low-voltage complexes, chest X-ray showed cardiomegaly and left pleural effusion and two-dimensional echocardiography showed large pericardial effusion with features suggestive of cardiac tamponade. He was taken up for emergency pericardiocentesis which showed haemorrhagic pericardial fluid. Intercostal drainage insertion was done for left-sided large pleural effusion. After ruling out all the other causes for haemorrhagic pericardial effusion, the patient was started on colchicine, steroids, ibuprofen and antibiotics to which he responded. Both pericardial and pleural effusions resolved completely on follow-up.

COVID-19 and Obesity: Role of Ectopic Visceral and Epicardial Adipose Tissues in Myocardial Injury.

In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the "cytokine storm" and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.