Viral Pericarditis Research Articles

CARDIAC TAMPONADE RELATED TO VIRAL RESPIRATORY INFECTION: UTILITY OF PERICARDIOSCOPY

TYPE: Case Report TOPIC: Procedures INTRODUCTION: Recurrent pericardial effusion occur in lung cancer in 5% to 10% and in 60% of viral pericarditis. Recurrence after drainage occur in one third requiring a new pericardial puncture with better prognosis and refractory pericardial effusion a pericardiotomy pericardial cavity inspection is indicated looking for an etiological agent, obtain complete tissue, satisfactory pericardial exploration and, eventually, surgical repair of a bleeding site. CASE PRESENTATION: 42y female arrive to emergency room with cardiac tamponade a hemo pericardial tamponade was diagnoses during initial puncture refractory to treatment and puncture progressive with pleural effusion during hospital stay. The only previous symptoms that referred was a respiratory viral disease two previous weeks, first cytologic examination revel atipic cells, left thoracoscopic approach after dreinage of cavity throw the pericardial cavity ad the internal surface of the parietal pericardium the surface of the heart and the intrapericardial segments of the great vessels was done, macroscopic findigs revel pericardial thickening with a pearly appearence.the final hystopthologic and cultue report no malignant cells and no bacterial grow DISCUSSION: cardiac tamponade and pericarditis can be a manifestation of infection, connective tissue disorders, malignancy, hypothyroidism, trauma, and renal dysfunction, observed in more than half of viral pericarditis. During treatment heart failure improved with a single pericardial drainage but the inflammatory response and recurrence of the pericardial effusion may required a definitive surgical treatment CONCLUSIONS: Pericardioscopy increases the diagnostic sensitivity of surgical pericardial drainage and biopsy without increasing the specific risk, it should keep in mind when the target lesions can't be reach of more standard technique. DISCLOSURE: Nothing to declare. KEYWORD: PERICARDIOSCOPY

Pericardial effusion among children: Retrospective analysis of the etiology and short-term outcome in a referral center in the south of Iran.

Background and AimsWe reinvestigated the causes, symptoms, and management of childhood pericardial effusion (PE) and its gradual changes during recent years in a referral pediatric cardiology center in the south of Iran.MethodsWe retrospectively analyzed the profile of PE patients who were under 18 years old from 2015 to 2020. The patient's demographic, clinical, and paraclinical information was extracted and analyzed using SPSS software.ResultIn general, 150 out of 63,736 admitted patients (0.23% of the total pediatric admissions) were diagnosed with PE (male/female 1:1.17). The median age was 3.25 years (range:\\ 2 days to 18 years; interquartile range: 9.5), and 50% of them were under 3 years of age. 32.6% had moderate to severe PE. Most patients presented with acute symptoms (68%) and respiratory problems, as the most common symptoms (30.6%). Tamponade signs were presented in 2% (n = 3) of the patients, and 80.7% (n = 121) were in a stable hemodynamic condition. In total, renal failure (22%) and parapneumonic effusion were the leading etiologies. Viral (7%) and bacterial (5%) pericarditis were the seventh and eighth causes; however, in severe cases, renal failure (22%) and bacterial pericarditis (14%) were dominant. In total, 14.1% (n = 21) of the patients needed pericardiocentesis that increased to 78.3% (n = 18) in severe cases. Only 6% had persistent PE for more than 3 months.ConclusionChildhood PE is mostly a result of renal failure and noninfectious causes. True pericarditis cases are not common, except in severe cases. It is more common in less than 3‐year‐old patients, and chronicity is rare. Severe cases had a high chance of pericardiocentesis, but other cases were mainly managed by treatment of the underlying causes.

Pericardial effusion caused by viral pericarditis in a patient receiving peritoneal dialysis

BackgroundAcute pericarditis causes acute inflammation of the pericardium. Although most cases of pericarditis are idiopathic with no identifiable cause, its etiology can be infectious, such as viral, bacterial, mycotic, and tuberculous infections, or non-infectious, including post-pericardiotomy, metastatic malignant tumor, connective tissue disease, or uremia. However, there has been no report of pericarditis caused by adenoviral infection in patients undergoing peritoneal dialysis (PD). Herein, we report a case of pericarditis and pericardial effusion caused by adenoviral infection in a patient undergoing PD.Case presentationA 59-year-old man who had been undergoing PD in our department for 3 years had a bout of acute enteritis. He was later admitted to the emergency department of our hospital because of malaise and loss of consciousness due to pericardial effusion. Testing after admission revealed elevated adenovirus antibody titers. Pericardial effusion improved although no changes in his PD prescription were made. The patient was hospitalized and admitted to maintain hemodynamics and prevent hypotension. Since insufficient dialysis volume was ruled out by peritoneal equilibrium tests and dialysis volume assessment, the patient was kept under observation, and no changes were made regarding the method of dialysis. Pericardial effusion and the C-reactive protein level both gradually declined, and the patient’s weight remained steady. The adenovirus antibody titer alone increased to 1:64 at approximately 2 weeks after hospitalization. The final diagnosis was acute pericarditis due to adenoviral infection rather than uremia or dialysis-associated pericarditis.ConclusionsWe treated a patient with a rare case of pericardial effusion caused by viral (adenoviral) pericarditis in a patient undergoing PD. In addition to testing for the usual causes, uremic and dialysis-associated pericarditis must always be ruled out in patients receiving dialysis. In cases of pericarditis with a viral origin, diagnosis and treatment must be comprehensive.

Constrictive pericarditis: rare but reversible cause of protein losing enteropathy.

Constrictive pericarditis is uncommon in children. It results from scarring and consequent loss of the normal elasticity of the pericardial sac and is most commonly seen as a late sequelae of idiopathic or viral pericarditis. Here, we report a case of protein losing enteropathy as a complication of constrictive pericarditis in a 2-year-old child. Pericardial thickening was demonstrated by cardiac MRI and subsequent pericardiectomy led to remarkable improvement and resolution of protein losing enteropathy.

The circRNA circSIAE Inhibits Replication of Coxsackie Virus B3 by Targeting miR-331-3p and Thousand and One Amino-Acid Kinase 2.

Coxsackie virus B3 (CVB3), an enterovirus, is the main pathogen causing viral myocarditis, pericarditis, hepatitis and other inflammation-related diseases. Non-coding RNAs with a closed loop molecular structure, called circular RNAs (circRNAs), have been shown to be involved in multiple virus-related processes, but roles and mechanisms in CVB3 infection have not been systematically studied. In this study, when HeLa cells were infected with CVB3, the expression of hsa_circ_0000367 (circSIAE) was significantly decreased as demonstrated by real-time quantitative PCR assays. We found that circSIAE downregulated the expression of miR-331-3p through direct binding and inhibited the replication of CVB3 in HeLa and 293T cells. The analysis of signals downstream of miR-331-3p suggested that miR-331-3p promotes CVB3 replication, viral plaque formation and fluorescent virus cell production through interactions with the gene coding for thousand and one amino-acid kinase 2 (TAOK2). In conclusion, this study found that circSIAE can target TAOK2 through sponge adsorption of miR-331-3p to inhibit the replication and proliferation of CVB3 virus, providing an early molecular target for the diagnosis of CVB3 infection.

OP01 Withdrawal of infliximab or anti-metabolite therapy in Crohn’s Disease patients in sustained remission on combination therapy: A randomized unblinded controlled trial (SPARE)

Abstract Background Combination therapy with infliximab and anti-metabolites is a standard option for patients with Crohn’s disease (CD). The implications of long term use of combination therapy may lead patients and clinicians to contemplate treatment de-escalation once steroid-free remission has been achieved. The aim of our study was to assess the relapse rates and time spent in remission over 2 years, after withdrawal of infliximab or anti-metabolite compared to continuation of combination therapy. Methods CD patients treated with a combination therapy of infliximab (IFX) and anti-metabolite > 8 months and in sustained steroid-free remission > 6 months were recruited in 64 centers in France, United Kingdom, Belgium, Sweden, Australia, Germany and The Netherlands. Patients were randomized into 3 arms - continuing combination therapy (arm A); stopping IFX (arm B); or stopping anti-metabolite (arm C). In case of a relapse [defined by CDAI and an objective marker of inflammation (CRP or fecal calprotectin)], patients were retreated by resuming infliximab in arm B or the anti-metabolite in arm C, according to a pre-defined scheme, including optimization of IFX up to 10 mg/Kg if necessary in all arms. The two co-primary endpoints were the relapse rate and mean survival time spent in remission over 2 years. A major secondary endpoint was treatment failure (complications or not recapturing remission). Results 254 patients were screened, 211 randomized, 5 withdrew consent and 1 was lost to follow-up, leaving 205 patients for the analysis - 67 randomized to arm A, 71 to arm B and 67 to arm C. Demographic and clinical characteristics are shown in Table 1. The two-year relapse rates were 14% (IC95%: 4–23%) in arm A, 40% (IC95%: 28–51%) in arm B, and 10% (IC95%: 2–18%) in arm C (p=0.0003 arm B vs arm A and <0.0001 arm B vs arm C) (figure 1). The time spent in remission was 1.91 yrs (IC95%: 1.83–1.99), 1.89 yrs (IC95%: 1.82–1.96) and 1.93 yrs (IC95%: 1.86–2.00) in arm A, B and C, respectively. Out of the 39 relapsers, 28 were retreated/optimized. Remission was achieved in 1/2 retreated patients in arm A, 22/23 in arm B and 2/3 in arm C. Treatment failure was observed in 4/67, 4/71 and 3/67 patients, in these three arms, respectively. No malignancy was observed, one tuberculosis in arm C and two severe infections (pneumonia and viral pericarditis) in arm B. Conclusion Infliximab withdrawal, but not antimetabolite withdrawal, was associated with a significantly higher risk of relapse than continuation of combination therapy. Almost all patients who stopped IFX achieved rapid remission when resuming treatment. The time spent in remission over 2 years was similar across groups.

THE STORY OF THE HEART'S WET SUIT: A CASE OF CARDIAC TAMPONADE WITH COVID-19 IN A YOUNG FEMALE

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: COVID-19 has awestruck physicians across the world with its atypical presentations. Often, pericarditis and myocarditis occur with viral infections in young adults. It is rare to see viral infections causing cardiac tamponade, which is a potentially fatal complication. Several cases of pericardial effusions and pre-tamponade physiology have been reported in elderly individuals with an extensive history of cardiac disease. Here, we describe the case of a previously healthy young adult who developed COVID-19 related cardiac tamponade without any preceding respiratory symptoms. CASE PRESENTATION: A 34-year-old female with a past medical history of hypothyroidism had tested positive for the SARS CoV-2 (Severe Acute Respiratory Distress Syndrome Coronavirus-2) one week prior to presentation. She presented with constant, central chest pain radiating to the back for 2 days. While being evaluated for hypotension, the patient broke into convulsions and was consequently intubated and mechanically ventilated. The patient's Brain natriuretic peptide (BNP) was elevated at 2,470 pg/mL (normal range: 0 – 450 pg/mL), and cardiac troponin was mildly elevated at 0.63 ng/mL. Initial electrocardiogram showed a low voltage strip with sinus tachycardia, and electrical alternans, suggestive of pericarditis(1). Computerized tomography (CT) of the chest with contrast revealed a small non-tappable pericardial effusion. CT head was negative. Over the course of a few hours, significant elevation of cardiac troponin to 5.18 ng/mL, and escalation in vasopressor requirements prompted us to obtain bedside echocardiography, which demonstrated a large pericardial effusion with pre-tamponade physiology. Emergent bedside pericardiocentesis was performed and 250cc of serous pericardial fluid was drained. A pericardial window was kept open to watch for re-accumulation. Post-procedural electrocardiogram had normal voltage, showed no electrical alternans and tachycardia had resolved. The patient was gradually weaned from vasopressor support and other supportive treatment. The pericardial drain was removed. An echocardiogram obtained at a 2-month follow-up showed a healthy heart with a normal ejection fraction. DISCUSSION: On initial evaluation, the differential diagnosis for convulsive syncope in a young patient with hypotension and COVID-19 were pulmonary embolism or a thromboembolic stroke. EKG findings and subsequent clinical course pointed towards a possible pericardial effusion. However, pericardial effusions are commonly idiopathic and only a smaller subset of cases stem from infectious disease. Viral pericarditis causes gradual accumulation of transudate leading to a pericardial effusion. Interestingly, in our patient cardiac tamponade was acute. CONCLUSIONS: This case underscores that an index of suspicion should be held for COVID-19 causing cardiac tamponade in young individuals and that prompt intervention is invaluable. REFERENCE #1: Eisenberg MJ, de Romeral LM, Heidenreich PA, Schiller NB, Evans GT Jr. The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG. A technology assessment. Chest. 1996 Aug;110(2):318-24. doi: 10.1378/chest.110.2.318. PMID: 8697827. DISCLOSURES: No relevant relationships by Neha Panchagnula, source=Web Response

FC 130RANDOMIZED, PLACEBO-CONTROLLED, PHASE 3B TRIAL OF TOLVAPTAN IN THE TREATMENT OF CHILDREN AND ADOLESCENTS WITH AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE (ADPKD): 1-YEAR DATA

Abstract Background and Aims Tolvaptan (TOL) is a vasopressin V2 receptor antagonist that inhibits total kidney volume (TKV) growth and kidney function decline in adults with rapidly progressing ADPKD. The therapeutic potential of TOL in pediatric patients at risk of early disease progression has not been previously reported. We conducted a clinical trial of TOL in children and adolescents with early manifesting ADPKD to evaluate pharmacodynamic properties and preliminary efficacy and safety information in this age group. Method This was a Phase 3b, 2-part trial (EudraCT: 2016-000187-42; ClinicalTrials.gov: NCT02964273). Phase A (reported here) was a 1-year, randomized, double-blind, placebo (PBO)-controlled, multicenter trial; Phase B is an ongoing, 2-year, open-label extension. Subjects had to be diagnosed with ADPKD (presence of renal cysts with family history and/or genetic diagnosis), with estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2 and body weight ≥20 kg. The target population was aged 12-17 years; subjects aged 4-11 years were also allowed to enter if eligibility criteria were met. Starting and maintenance TOL/PBO doses were based on body weight. The co-primary endpoints were changes from baseline in spot urine osmolality (Uosm) and specific gravity at Week 1; additional endpoints were the 12-month changes in TKV and eGFR. Safety and tolerability were monitored. In this exploratory trial, outcomes were summarized descriptively, with no statistical comparisons planned between groups. Results Of 91 subjects enrolled (66 aged 12–17 years and 25 aged <12 years), 48 were randomized to TOL and 43 to PBO. Among enrolled subjects, there was a history of hypertension in 23.1%, proteinuria 15.4%, kidney pain 12.1%, and hepatic cysts 6.6%. Mean changes (±SD) from baseline in spot Uosm and specific gravity at Week 1 were greater with TOL vs PBO: -386 (284) vs -93 (332) mOsm/kg and -0.009 (0.007) vs -0.002 (0.008), respectively. In subjects aged 12–17 years (1 subject with tuberous sclerosis and ADPKD excluded as an outlier), the mean % TKV change (±SD) from baseline to Month 12 was 4.6% (9.1) for TOL and 7.7% (9.3) for PBO (Figure 1). Mean change (±SD) in eGFR from Day 7 to Month 12 in subjects ages 12–17 years was 0.4 (10.3) mL/min/1.73 m2 for TOL and -3.5 (10.9) mL/min/1.73 m2 for PBO (Figure 2). The most frequent treatment-emergent adverse events during Phase A were (TOL vs PBO): polyuria (25.0% vs 2.3%), blood creatinine increased (18.8% vs 4.7%), pollakiuria (18.8% vs 0.0%), cough (14.6% vs 11.6%), nocturia (14.6% vs 4. 7%), thirst (14.6% vs 2.3%), abdominal pain (12.5% vs 7.0%), constipation (10.4% vs 2.3%), and orthostatic hypotension (10.4% vs 0.0%). Potentially clinically significant increases in creatinine (>1.5 x baseline) occurred in 4 TOL subjects and no PBO subject. No subject had elevated transaminases or drug-induced liver injury. Serious adverse events were reported in 1 TOL subject (viral pericarditis) and 6 PBO, none considered related to treatment. One subject discontinued due to pollakiuria (TOL) and 1 due to dizziness (PBO). Conclusion TOL demonstrated activity indicative of effective V2 receptor antagonism in children and adolescents with ADPKD. In addition, our trial yielded preliminary results suggestive of efficacy in slowing TKV growth and eGFR decline with acceptable tolerability, warranting further investigation in pediatric patients with ADPKD. The 2-year, Phase B extension to this trial is ongoing. Sponsored by OPDC, Inc.

Subacute idiopathic pericarditis with a large pericardial effusion in a young adult seven months post COVID-19 (SARS-Cov-2) infection

The number of COVID-19 (SARS-Cov-2) cases has risen substantially throughout the world, and consequently we are finding there are several extrapulmonary manifestations associated with this disease. Viral pericarditis and pericardial effusion have been reported several times in COVID-19 patients, however the majority of these cases occurred during active infection or within a relatively short time frame afterwards. The following case is a young female with only a past medical history of COVID-19 pneumonia, seven months prior, presenting with abdominal pain and progressively worsening dyspnea. She was subsequently found to have a large pericardial effusion without tamponade, but requiring a pericardial window. Gross pathology showed fibrinous pericarditis. It is suspected her symptoms and pericardial effusion resulted from a subacute idiopathic pericarditis likely as post-viral complication of COVID-19.

Use of Electrocardiographic Screening to Clear Athletes for Return to Sports Following COVID-19 Infection.

ObjectiveTo quantify the occurrence rate of abnormal electrocardiographic (ECG) findings and symptoms following coronavirus disease 2019 (COVID-19) infection.Patients and MethodsIn this retrospective analysis, we studied adult patients (>18 years old) who were participating in collegiate athletics and previously tested positive for COVID-19 between August 1, 2020, and December 30, 2020. The athletes underwent general examinations and ECG screening prior to being medically cleared for a return to sports following their COVID-19 diagnosis. Predetermined predictors were grouped into categorical variables including (1) sex, (2) symptom severity, and (3) body mass index (normal vs overweight [≥24 kg/m2]). These variables were used to examine differences of abnormal rates that occurred between different predictor categories.ResultsOf the 170 athletes screened, 6 (3.5%) presented with abnormal ECG findings and were referred to cardiologists. We found no evidence that sex, symptom severity, and body mass index category were associated with a higher rate of abnormal ECG findings (all P>.05). Greater severity of COVID-19 symptoms was associated with a higher percentage of ST depression, T-wave inversion, ST-T changes, and the presence of fragmented QRS complex. Loss of smell, loss of taste, headache, and fatigue were the most prevalent symptoms, with 38.8% (66), 36.5% (62), 32.9% (56), and 25.3% (43), respectively, of the 170 athletes reporting each symptom.ConclusionPreliminary findings indicate a low risk of myocardial injury secondary to COVID-19 infection, with less than 4% of the 170 patients in our study presenting with abnormal ECG findings and a total of 16 patients (9.4%) requiring referral to a cardiologist. Although viral myocarditis was not detected in any athlete referred for cardiological assessment, 2 patients experienced effusive viral pericarditis.

Risk Factors for Morbidity and Mortality Following Hospitalization for Pericarditis

BackgroundViral or idiopathic pericarditis is a frequent condition, often considered benign, although prior studies have suggested that pericarditis is associated with both cardiovascular and noncardiovascular disease, for example, malignancy. ObjectivesThis study sought to assess mortality risk and morbidity patterns in patients with incident viral or idiopathic pericarditis. MethodsIn nationwide Danish registries, we identified patients discharged with a first-time diagnosis of pericarditis from 1996 to 2016. Patients with a severe underlying heart condition were excluded. The patients were matched 1:10 with individuals from the general population by sex and year of birth. We assessed 5-year mortality using Kaplan-Meier and Cox proportional hazards models adjusted for baseline comorbidities and identified subsequent hospital admissions. ResultsWe identified 7,988 patients with pericarditis and 79,880 matched control individuals. The absolute 5-year survival probability was 92.9% and 95.8% in the pericarditis and control groups, respectively (adjusted hazard ratio: 1.31; 95% confidence interval: 1.13 to 1.52). The greatest difference in mortality was seen the first year, and it was primarily driven by the female part of the population. The incidence rate per 1,000 person-years of new-onset, admission-required diagnosis was higher in the pericarditis group both for cardiovascular and noncardiovascular diseases. ConclusionsWe observed a higher mortality risk over 5 years in the pericarditis group, especially among the female patients, compared to matched control individuals. Furthermore, we observed a higher frequency of both cardiovascular and noncardiovascular hospital admissions, highlighting the need for focus on underlying morbidity in patients presenting with apparent viral or idiopathic pericarditis.

Abstract 14877: A Never Ending Tale of Pericarditis

Background: The evidence on recurrent pregnancy-related pericarditis is limited, and management strategies are based mainly on case reports and expert opinion. Case: A 25-year-old G2P1, 28-week pregnant female, with a history of presumed viral pericarditis complicated by pericardial tamponade and recurrent colchicine resistant pericarditis which was successfully treated with a prolonged steroid taper in the postpartum period, now 1 year in remission presents with shortness of breath and pleuritic chest pain with elevated inflammatory consistent with prior presentation of myo-pericarditis. A trans-thoracic echocardiogram (TTE) revealed a mild pericardial effusion without evidence of systolic dysfunction, and pericardial tamponade. Decision-Making: Given prior history of pregnancy related colchicine resistant pericarditis which was complicated by pericardial tamponade around her prior delivery time, it was decided by an interdisciplinary team involving rheumatology, cardiology and obstetrics, to initiate prednisone 10 mg daily. Symptoms subsequently subsided with a down trend of cardiac and inflammatory biomarkers. Daily 10 mg prednisone was to be continued up through delivery but within 2 months she presented yet again with a similar clinical picture and was diagnosed with recurrence of disease. Her prednisone was increased to 20 mg daily with symptom resolution. Two weeks later, she went into labor and received stress dose steroids. She had a normal spontaneous vaginal delivery without any complications. She continued the same dose of 20 mg of prednisone until her follow-up with rheumatology when the decision was made to initiate azathioprine and slowly titrate off the steroids. Conclusion: The case highlights not only the rare association between pregnancy and recurrent pericarditis but also the complexity of its management. The case of our patient underscores the importance of family planning, shared-decision making, and management by an interdisciplinary team comprised of rheumatology, obstetrics/gynecology, and cardiology. There are currently no known well controlled trials of therapy for pregnancy related idiopathic recurrent acute pericarditis.

Long-term natural history of transient constrictive pericarditis

Abstract Background In recent years, there has been increasing recognition of a potentially-reversible, transient/ subacute form of constrictive pericarditis (CP). To date, studies have been small with lack of long-term longitudinal follow-up. Purpose We aimed to elucidate the causes and natural history of subacute CP. Methods Patients were included if (1) they had a diagnosis of CP, (2) had cardiac magnetic resonance (CMR) within 12 months of symptom onset with evidence of pericardial delayed enhancement/ inflammation (Figure) (3) received anti-inflammatory medications. Results A total of 78 individuals were included, comprising 61 men (78%) with a mean age of 59±14 years. Causes of subacute CP included idiopathic/ viral pericarditis (58%), post-pericardiotomy (29%), autoimmune (6%), radiation therapy (3%) and others (4%). After median follow-up of 4.4 years, 31 (40%) required pericardiectomy. There were no deaths. Patients who underwent pericardiectomy had longer duration of symptoms at presentation [6 (4–9) vs. 3 (2–5) months, P<0.01], were more likely to be on diuretic therapy (87 vs. 45%, P<0.001), had lower ultra-sensitive C-reactive protein [4.4 (2.6–13.1) vs. 11.95 (1.8–61.55) mg/dl, P<0.001] and lower erythrocyte sedimentation rate [5 (2–10) vs. 25 (6–43 mm/hr), P=0.031] compared to those who were managed medically. There were no other significant differences in clinical characteristics or baseline anti-inflammatory therapy. The presence of elevated inflammatory markers (HR: 0.18; 95% CI: 0.06–0.58, P<0.01) was an independent predictor of freedom from pericardiectomy after adjustment for relevant clinical and imaging parameters. Conclusions We present the original observations of the largest cohort of patients with transient CP to date and demonstrate that increased inflammatory markers were independently associated with long-term freedom from pericardiectomy. Our results suggest that a trial of anti-inflammatory therapy in the setting of elevated inflammatory markers may be appropriate prior to referral for surgery given the possible reversibility. Pericardial delayed enhancement Funding Acknowledgement Type of funding source: None

Cardiac Tamponade in a Patient With Myocardial Infarction and COVID-19: Electron Microscopy

We present the case of a patient with myocardial infarction and COVID-19 disease who developed hemorrhagic pericardial effusion and cardiac tamponade. The differential diagnosis included post-infarction pericarditis and mechanical complications, thrombolysis, Dressler syndrome, and viral pericarditis. The histopathologic examination of the pericardial tissue sample and electron microscopic examination established the diagnosis. (Level of Difficulty: Advanced.)

Acute Pericarditis and Cardiac Tamponade in a Patient with COVID-19: A Therapeutic Challenge.

We report a case of acute viral pericarditis and cardiac tamponade in a patient with COVID-19 to highlight the associated treatment challenges, especially given the uncertainty associated with the safety of standard treatment. We also discuss complications associated with delayed diagnosis in patients who potentially may need mechanical ventilation.LEARNING POINTSLarge pericardial effusion and cardiac tamponade should be considered in patients with COVID-19 who decompensate further after intubation and mechanical ventilation.The characteristics of pericardial effusion in patients with COVID-19 are described.A successful treatment approach for acute pericarditis in a patient with COVID-19 in light of differing opinions over the safety of NSAID use is described.

Management of Acute Idiopathic (Viral) Pericarditis in the Emergency Department: A Review for the Nursing Professional.

Acute pericarditis is an inflammatory disorder that contributes to chest pain admissions in the emergency department (ED). Nursing professionals can play a vital role in the differential, triage and management of acute pericarditis in the ED. First-line pharmacotherapy to specifically treat acute pericarditis of viral or idiopathic origin is paramount in improving patients' quality of life and reducing the risk of further recurrences of pericarditis and consists of combination therapy with aspirin (acetylsalicylic acid [ASA]) or a nonsteroidal anti-inflammatory drug (NSAID), in combination with colchicine. Corticosteroids should not be initiated as first-line therapy in idiopathic (viral) pericarditis, as they increase the risk of recurrences. Nursing professionals are also pivotal in monitoring pharmacotherapy with respect to safety and efficacy. Overall, the nursing professional can facilitate timely administration and monitoring of medications, provide patient education, promote adherence, and assist in transitions of care for patients diagnosed with acute idiopathic (viral) pericarditis in the ED.

Management of Acute Idiopathic (Viral) Pericarditis in the Emergency Department: A Review for the Nursing Professional.

Management of Acute Idiopathic (Viral) Pericarditis in the Emergency Department: A Review for the Nursing Professional.

BACTERIAL PERICARDITIS: AN ODD PRESENTATION OF OBSTRUCTIVE/DISTRIBUTIVE SHOCK

SESSION TITLE: Case Report Semifinalists 6 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Pericarditis represents a small portion of ED chest pain visits (5%) and an even smaller portion of hospital admissions, 0.1%. Depending on the etiology, the prognosis and outcome differ significantly. Purulent pericarditis is an exceedingly rare occurrence (less than 1% of cases of pericarditis) and falls into a high mortality, high-risk group. Here we present a case of rapidly progressive bacterial pericarditis causing cardiac tamponade and shock CASE PRESENTATION: A 58-year old African American male presented to the emergency department with one day of tight radiating chest pain that was relieved with leaning forward. An EKG showed diffuse ST elevations indicative of pericarditis. At this time, there were no systemic signs of infection. NSAIDs and colchicine were started for presumed viral pericarditis. Serum troponins were mildly elevated. An echocardiogram (echo) showed decreased ejection fraction but no pericardial effusion. The patient underwent left and right heart catheterization showing volume overload but no evidence of coronary artery disease. Diuretics were started, but within hours his urine output dropped and he became hypotensive. He was intubated for respiratory failure. His lactate and procalcitonin levels were increased, but without leukocytosis. The patient was started on broad-spectrum antibiotics. Blood cultures grew streptococcus within 24 hours. A bedside ultrasound showed interim development of a large pericardial effusion and possible tamponade physiology. A formal repeat echocardiogram confirmed this finding. The patient underwent emergency pericardiocentesis and pericardial drain placement under fluoroscopy yielding 200cc of purulent pericardial fluid. The patient rapidly deteriorated, expiring less than 48 hours from admission. DISCUSSION: This patient had a very low clinical suspicion for bacterial pericarditis upon initial presentation. He had no evidence of a pericardial effusion on his first echocardiogram. However, his clinical condition rapidly deteriorated due to development of purulent pericardial effusion and cardiac tamponade that was detected on point of care chest ultrasound. The patient underwent pericardial drainage and was started on broad-spectrum antibiotics. Bacterial pericarditis is a rare medical condition with purulent pericardial effusion with cardiac tamponade is a rare medical condition with high mortality. CONCLUSIONS: There are two critical points in this case: first, distributive and obstructive shock can coexist in some cases. Obstructive shock is one of the least frequent causes of shock, especially in the setting of bacteremia and when clinicians gravitate to distributive shock as a primary etiology. Second, bedside ultrasound is a powerful tool that can change quickly management if used wisely. Reference #1: Adler Y et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC). The European Association for Cardio-Thoracic Surgery (EACTS), European Heart Journal, Volume 36, Issue 42, 7 November 2015, Pages 2921–2964, https://doi.org/10.1093/eurheartj/ehv318. Reference #2: Bhaduri-McIntosh, S et al. Purulent Pericarditis Caused by Group A Streptococcus. Tex Heart Inst J. 2006; 33(4): 519–522. Reference #3: Sagristà-Sauleda, J et al. Diagnosis and management of pericardial effusion. World J Cardiol. 2011 May 26; 3(5): 135–143. Published online 2011 May 26. https://doi.org/10.4330/wjc.v3.i5.135 DISCLOSURES: No relevant relationships by Juan Galvis, source=Web Response No relevant relationships by Umair Gauhar, source=Web Response No relevant relationships by Saarik Gupta, source=Web Response

Does Colchicine Substitute Corticosteroids in Treatment of Idiopathic and Viral Pediatric Pericarditis?

Background and Objectives: Recurrence of pericarditis (ROP) is an important complication of the acute pericarditis. The aim of this study was to analyse the influence of aetiology, clinical findings and treatment on the outcome of acute pericarditis. Methods: Data were retrospectively collected from medical records of patients treated from 2011 to 2019 at a tertiary referent heart paediatric center. Results: Our investigation included 56 children with idiopathic and viral pericarditis. Relapse was registered in 8/56 patients, 2/29 (7.41%) treated with nonsteroidal anti-inflammatory drugs (NSAID) and 6/27 (28.57%) treated with corticosteroids (CS) and NSAID. Independent risk factors for ROP were viral pericarditis (p = 0.01, OR 31.46), lack of myocardial affection (p = 0.03, OR 29.15), CS use (p = 0.02, OR 29.02) and ESR ≥ 50 mm/h (p = 0.03, OR 25.23). In 4/8 patients the first recurrence was treated with NSAID and colchicine, while treatment of 4/8 patients included CS. Children with ROP treated with CS had higher median number of recurrence (5, IQR: 2–15) than those treated with colchicine (0, IQR: 0–0.75). Conclusions: Independent risk factors for recurrence are CS treatment, viral aetiology, pericarditis only and ESR ≥ 50 mm/h. Acute pericarditis should be treated with NSAID. Colchicine and NSAID might be recommended in children with the first ROP.

The Role of Corticosteroids in Pediatric Viral and Idiopathic Pericarditis

The Role of Corticosteroids in Pediatric Viral and Idiopathic Pericarditis