Circumferential Pericardial Effusion Research Articles

786 SYSTOLIC ANTERIOR MOVEMENT OF MITRAL VALVE: NOT ONLY HYPERTROPHIC CARDIOMYOPATHY, BUT ALSO CARDIAC AMYLOIDOSIS

Abstract A 71 years-old man was diagnosed with lambda light chain multiple myeloma evolving from monoclonal gammopathy of unknown significance during hematological follow-up. Serum creatinine and blood urea were normal, but proteinuria was significant. A subsequent renal biopsy showed amyloid deposits in renal glomeruli. He had no comorbidities or previous cardiologic history. To provide a complete diagnostic work-up, an echocardiogram was performed, showing marked and asymmetric left ventricular hypertrophy (interventricular septum diastolic thickness IVSd 15 mm) with dynamic left ventricular outflow tract obstruction (LVOTO) due to an incomplete systolic anterior motion (SAM) of mitral valve. ECG showed sinus rhythm with 1st degree atrio-ventricular block; notably, there was no electrocardiographic sign of left ventricular hypertrophy. Therefore, a Cardiac Magnetic Resonance (CMR) was performed, showing left ventricular hypertrophy (interventricular septum thickness 15 mm) with normal contractility. Mild left atrial enlargement and thickening of the interatrial septum were found, together with mild circumferential pericardial effusion. No perfusion defects were recorded, but late gadolinium enhancement (LGE) pattern was not assessable because of difficult myocardial signal nulling point. These findings were consistent with cardiac amyloidosis (CA). By the time, histological demonstration of amyloid was mandatory, so an endomyocardial biopsy was performed. Amyloid deposits were found to be in the myocardial interstitial space and into the myocardial vessel walls. Immunohistochemical staining revealed diffuse and high reactivity for lambda free light chains and moderate reactivity for kappa chains. No transthyretin was found in the specimens. Finally, a diagnosis of AL amyloidosis with cardiac and renal involvement associated with lambda light chain multiple myeloma was made and chemotherapy with bortezomib, thalidomide and dexamethasone (VTD) was started. During the cardiologic follow-up, three syncope with prodromal symptoms have occurred. In all these circumstances, no arrhythmias were found at prolonged ECG Holter monitoring. Echocardiogram showed a progression of the dynamic outflow obstruction to 80 mmHg and increasing mitral regurgitation associated with complete systolic anterior motion of the valve. Given the echocardiographic features and the clinical events, we performed a genetic blood test which excluded sarcomeric genes mutations. Also, familial screening with ECG and echocardiogram was negative. A better management of pharmacological therapy, together with avoidance of hypovolemia and supportive treatment of anemia finally relieved patient's symptoms. Conclusions we presented this case to underline that, although rare, cardiac amyloidosis can resemble other hypertrophic cardiomyopathies with left ventricular outflow tract obstruction due to SAM of the mitral valve and irregular septal hypertrophy, caused by amyloid deposits. Most of these cases are seen in the senile transthyretin type, but sometimes they are observed in AL patients. Nowadays, it is crucial to diagnose these patients correctly as early treatment is critical for survival in this population.

Abstract 13815: SARS-CoV-2 and Plasmodium Falciparum Co-Infection A Lethal Combination to the Heart

Introduction: COVID-19 pandemic has had an unprecedented impact worldwide, co-infections with neglected tropical diseases like Malaria can occur and affect the heart. Objective: Describe a unique case of Malaria and SARS CoV2 infection occurring concurrently with cardiac complications. Clinical Case: A 69-year-old male, retired canoeing athlete, with well-controlled arterial hypertension, presented odynophagia, cough, and dyspnea on slight exertion for 2 days. On examination, O2 saturation was 91%, blood pressure 100/60 mmHg, regular heart rate of 110 bpm, positive PCR for SARS-CoV-2, elevated D-Dimer, and chest X-ray with evidence of viral pneumonia. He received supplemental oxygen, steroids, and paracetamol. Two days later, he presented with choluria, afternoon episodes of high fever preceded by chills and myalgia, and a thick blood smear showed Plasmodium falciparum (PF) trophozoites. Antimalarial treatment was started with primaquine 15mg, 20 mg of artemether, and 120 mg of Lumefantrine daily with the disappearance of fever until day 14 of onset of symptoms when he presented with acute heart failure (AHF) with a reduced ejection fraction of 45%. NYHA Class IV, arterial hypotension, sudden onset palpitations, and afternoon febrile episode. The electrocardiogram showed atrial fibrillation (AF) with a rapid irregular ventricular response of 120 bpm; The echocardiogram revealed a 7mm circumferential pericardial effusion, right ventricular dysfunction. Treatment with colchicine, enoxaparin, spironolactone, and bisoprolol was started. A new thick smear demonstrated the persistence of PF. A new antimalarial regimen was restarted, with the disappearance of the fever 48 hours after its onset, with the reversion of AF to sinus rhythm. Discussion: A unique case of concurrent COVID-19 and Malaria, which cause challenges to the heart and lead to cardiovascular complications. Conclusion: An exceptional case is presented, the coexistence of SARS-CoV-2 and PF infection-associated complications of myocarditis, pericarditis, new-onset AF, and AHF. This interaction should not go unnoticed, physicians’ awareness is key, and early diagnosis and treatment can be lifesaving, mitigate and offer the best chance of cure.

Abstract 15745: Effusive Constrictive Pericarditis After Covid-19 Vaccination

Case Report: A 42-year-old male with no significant past medical history presented to the emergency department (ED) after a three-week history of myalgias, non-productive cough, and progressively worsening dyspnea accompanied by a two-week history of right-sided chest pain that all started four days after receiving his Pfizer COVID-19 booster vaccine. Chest pain was described as constant, non-radiating, and aggravated by positional changes. On ED arrival, the patient was febrile to 102.9°F and tachycardic with initial labs significant for leukocytosis of 13.6 Thou/uL, C-reactive protein at 17.18 mg/dL, troponins negative x2, and a negative COVID-19 NAAT testing. EKG revealed diffuse T wave inversions and chest x-ray was noncontributory. Transthoracic echocardiogram (TTE) obtained showed a small fibrinous circumferential pericardial effusion with no evidence of cardiac tamponade; however, there was an interventricular septal bounce suggestive of effusive-constrictive pericarditis. This diastolic septal bounce was also seen on cardiac magnetic resonance imaging, along with a pericardial enhancement measuring up to 0.2 cm in thickness. With a negative infectious and autoimmune workup, along with low clinical suspicion for tuberculosis or malignancy, the leading differential was the temporal relationship between receiving the Pfizer COVID-19 mRNA booster vaccine and the development of effusive-constrictive pericarditis (ECP). The patient was started on Colchicine 0.6 mg twice daily, Ibuprofen 400 mg three times daily, and subsequently discharged after symptomatic improvement and being afebrile for 72 hours with plans for close cardiology follow-up. Discussion: ECP is a rare syndrome characterized by a concurrent decrease in pericardial compliance with pericardial effusion and is seen in 4.5% to 6.9% of patients who present with pericardial effusions. To date, less than five other case reports internationally have delineated a relationship between COVID-19 mRNA vaccines and the development of ECP, making recognition of this etiology challenging. In patients who have a mixed hemodynamic picture with subacute features of both cardiac tamponade and constrictive pericarditis, clinicians should have a high index of suspicion for ECP.

Abstract 14547: A Rare Case of Pericardial Effusion Causing Cardiac Tamponade in Preeclampsia

Background: Cardiovascular manifestations of preeclampsia are caused by increased peripheral vascular resistance and systemic endothelial damage causing third spacing of fluids. Usually this presents as lower extremity edema or non-cardiogenic pulmonary edema. Here we report a rare case of third spacing into pericardial space causing cardiac tamponade in a patient with severe pre-eclampsia. To our knowledge, only 2 similar cases have been reported so far. Case presentation: 35-year-old female G1P0A0 presented to the hospital at 36 weeks and 6 days of gestation with complaints of elevated blood pressure, headache, blurring of vision, and shortness of breath. On physical exam, she had blood pressure of 170/85, 3+ bilateral lower extremity edema and labs showed urine protein to creatinine ratio of 13,962. She was diagnosed with severe pre-eclampsia and underwent emergent C-section without any complications. On postoperative day 1, patient continued to complain of shortness of breath and became hypoxic requiring 2 to 3 L of supplemental oxygen. Chest x-ray showed slight pulmonary edema but BNP was 49. She had persistent lower extremity swelling and was empirically diuresed with IV Lasix with some improvement in her symptoms. An echocardiogram showed large circumferential pericardial effusion with early right ventricular diastolic collapse consistent with cardiac tamponade. Her LV function was normal with an EF of 70% without any wall motion abnormalities. She was taken to the Cath Lab for pericardiocentesis and underwent drainage of almost 650 cc of yellowish clear-colored fluid. Analysis of the fluid showed 1186 nucleated cells, pH 7.5, and protein of 2.9 mg/dl. Her ANA and Rheumatoid factor were negative. The pericardial drain was removed after 5 days with no evidence of recurrence of tamponade on repeat echo. Conclusion: Peripartum shortness of breath with leg swelling is a common complain among pregnant women with pre-eclampsia. Although peripartum cardiomyopathy is more common, pericardial effusion with cardiac tamponade is also a potential diagnosis and should be kept in the differential. Echocardiography can differentiate these entities.

Abstract 10781: An Unusual Case of Transient Inflammatory Constrictive Pericarditis: IgG4 Disease

Case Presentation: A 54-year-old male with a past medical history of hypertension presented with chest tightness, shortness of breath, fatigue, and ankle edema. His vital signs were within normal limits but physical exam was significant for jugular venous distension and bilateral peripheral edema. Laboratory studies were unremarkable except for elevated inflammatory markers (C-reactive protein [23.6 mg/dl] and erythrocyte sedimentation rate [34 mm/hour]). Interferon assay, Influenza A/B antigens and anti-nuclear antibody were negative. The patient was diagnosed with constrictive pericarditis (CP). Although the patient was treated appropriately for pericarditis with a steroid taper, colchicine and ibuprofen, his symptoms recurred. Therefore, he underwent a radical pericardiectomy which resulted in a marked clinical improvement. The final pericardial pathology revealed fibrosis and plasma cell infiltrates with >30% of cells positive for IgG4. An echocardiogram revealed a small pericardial effusion with septal bounce, annulus reversus, and a plethoric inferior vena cava consistent with a diagnosis of CP. Cardiac magnetic resonance imaging showed a small circumferential pericardial effusion and respirophasic septal flattening during inspiration with marked pericardial delayed enhancement (DHE). Discussion: CP is commonly caused by viral or idiopathic etiologies, with infection (tuberculosis) being more prominent in developing countries. IgG4 disease is an uncommon cause of CP with only a few cases of IgG4-related CP have been reported. Pathological findings on histology include IgG4-positive lymphoplasmacytic cells and fibrosis. The disease is characterized by steroid-responsive condition but pericardiectomy is pursued with a suboptimal response. Cardiovascular manifestations of IgG4 disease are under explored and our case illustrates the importance of recognizing and treating the pericardial complications of IgG4 disease.

Abstract 9812: Abracadabra Alakazam: Sudden Invasion of the Pericardium by Haemophilus Influenzae

A 25 year old man presented with three days of cough, shortness of breath, and pleuritic chest pain. Initial vital signs in the ED were normal, and exam demonstrated tonsillar erythema without exudate. Labs revealed a leukocytosis of 18.9k/μL, D-dimer of 690 ng/mL, C-reactive protein of 5.7 mg/dL, and lactate elevated to 2.9 mmol/L. High-sensitivity troponin, NT-proBNP, and SARS-CoV-2 RT-PCR were all negative. Presenting electrocardiogram demonstrated PR elevation in aVR with diffuse ST-segment elevation in the inferior and anterolateral leads. Point-of-care echocardiogram demonstrated normal biventricular function without pericardial effusion. CTPA was negative for pulmonary embolism, and he was observed for presumed acute viral pericarditis. Fourteen-hours later, he became febrile to 38.3°C, tachycardic to 133 bpm, and hypotensive to 97/65 mmHg with diffuse abdominal pain. Repeat lactate was 9.0 mmol/L. This prompted an emergent CT scan which now showed a new large pericardial effusion and bilateral pleural effusions ( Panel A ). Repeat echocardiogram confirmed a large circumferential pericardial effusion with early signs of tamponade including right atrial inversion in late diastole ( Panel B ). Emergent pericardiocentesis yielded 560 mL of brown, purulent fluid ( Panel C ) with immediate improvement in hemodynamics. Bacterial gram stain and culture grew Haemophilus influenzae ( Panel D ). Immunodeficiency screening was negative. Transient severe biventricular systolic dysfunction was noted, consistent with sepsis-induced cardiomyopathy. He completed a targeted antibiotic course with partial recovery of his ejection fraction by discharge. Purulent pericarditis is rare in developed countries, and invasive H. influenzae in a young, immunocompetent adult is particularly unusual. This case illustrates the importance of early diagnosis and management of purulent pericarditis given its potential for rapid progression and high mortality.

PRIMARY LUNG ADENOCARCINOMA PRESENTING AS CARDIAC TAMPONADE

PRIMARY LUNG ADENOCARCINOMA PRESENTING AS CARDIAC TAMPONADE

TUBERCULOUS TAMPONADE WITH A TWIST: A CASE OF TB AND COVID-19

TUBERCULOUS TAMPONADE WITH A TWIST: A CASE OF TB AND COVID-19

LOW-PRESSURE CARDIAC TAMPONADE: A RARE COMPLICATION IN THOSE UNDERGOING HEMODIALYSIS WITH KNOWN PERICARDIAL EFFUSION

LOW-PRESSURE CARDIAC TAMPONADE: A RARE COMPLICATION IN THOSE UNDERGOING HEMODIALYSIS WITH KNOWN PERICARDIAL EFFUSION

SQUAMOUS CELL CARCINOMA OF THE LUNG LEADING TO MALIGNANT CARDIAC TAMPONADE DUE TO LARGE CARDIAC METASTASES

SQUAMOUS CELL CARCINOMA OF THE LUNG LEADING TO MALIGNANT CARDIAC TAMPONADE DUE TO LARGE CARDIAC METASTASES

ATYPICAL PRESENTATION OF CARDIAC TAMPONADE SECONDARY TO MALIGNANT THYMIC NEUROENDOCRINE TUMOR MASKED BY OPIOID OVERDOSE

ATYPICAL PRESENTATION OF CARDIAC TAMPONADE SECONDARY TO MALIGNANT THYMIC NEUROENDOCRINE TUMOR MASKED BY OPIOID OVERDOSE

Pericardial Epithelioid Inflammatory Myofibroblastic Sarcoma: An Atypical Presentation

Sarcomas are a diverse group of cancers of mesenchymal origin. Epithelioid inflammatory myofibroblastic sarcoma (EIMS) is an uncommon and hardly reported neoplasm that is a malignant variant of the typically benign inflammatory myofibroblastic tumor (IMS). We discuss an exceedingly rare case of a 53-year-old patient with primary EIMS of the pericardium who presented in impending hemodynamic collapse. A transthoracic echocardiogram revealed a large circumferential pericardial effusion with tamponade physiology and an echogenic intrapericardial mass compressing the right ventricle to near obliteration. She underwent emergent sternotomy with resection and one cycle of chemotherapy with liposomal doxorubicin before having recurrent metastatic pericardial and pleural effusions, ultimately leading to her unfortunate passing.

PERICARDITIS IN A PATIENT ON PEMBROLIZUMAB

TYPE: Case Report TOPIC: Cardiovascular Disease INTRODUCTION: Pembrolizumab, an immune check point inhibitor (ICI) reverses the T-cell suppression and induces antitumor responses. ICIs are associated with varity of immunity-related adverse effects (IRAEs) that can affect multiple organ systems. However cardiotoxicity, hematological complications, venous thromboembolism, and pulmonary toxicity are less well recognized. CASE PRESENTATION: A 44-year male with squamous cell carcinoma of lungs presented with complaints of non-radiating chest pain and shortness of breath on exertion. The patient received 45th cycle of pembrolizumab, two weeks prior to this presentation. Physical examination was within normal limit. Vital signs were stable. Laboratory values revealed normal electrolytes, troponin, and elevated C-reactive protein. Electrocardiogram revealed ST segment elevations in lead I, aVL and V4-V6. Anti-platelet agents were started and cardiac catheterization revealed normal coronary arteries. The echocardiogram showed small circumferential pericardial effusion. He was then started on corticosteroids and colchicine for acute pericarditis. After ruling out other possibilities it was believed to be IRAEs from pembrolizumab. Patient clinically improved with no additional intervention and was discharged on anti-inflammatory agents for acute pericarditis to prevent recurrence. DISCUSSION: The IRAEs are triggered by the activation of autoimmune system by T-cell activation. Pericardial effusion during PD-1 inhibitor treatment of lung cancer is exceedingly rare and has been reported in only about ten cases so far. These reports indicated the reasons for pericardial effusion as pesudoprogression or IRAEs. Most of these patients underwent invasive management and only one case was managed using corticosteroids without requiring invasive intervention. CONCLUSIONS: Pericarditis should be considered in a patient on prebrolizumab preseting with chest pain. DISCLOSURE: Nothing to declare. KEYWORD: Pericarditis

P119 PERI– MYOCARDITIS A RARE CASE OF ESCHERICHIA COLI INFECTION, A BACTERIUM THAT SHOULD NOT BE UNDERESTIMATED

Abstract Myopericarditis is defined as inflammation of the heart muscle and pericardium, which can be caused by infectious agents, toxins, or immunological reactions. The most recognized cases are secondary to cardiotropic viral infections. Escherichia coli rarely causes myopericarditis and is secondary to the septic dissemination of bacteria or myocardial toxicity of endotoxins. We describe a case of bacterial sepsis due to Escherichia coli which caused myocardial damage with pericardial effusion. 32 year old woman without cardiovascular risk factors, suffering from congenital immunodeficiency for IG type A, B–cell NH lymphoma undergoing chemotherapy treatment, Hashimoto‘s thyroiditis. The patient arrives for dyspnoea and fever. The ECG showed mild PR depression and an over diffuse ST in all leads with low voltage QRS and increased TNI. PA 120/70 mmHg, HR 74 b / m, FR of 15 acts / m. ETT showed diffuse hypokinesia with FE40% and moderate, circumferential, corpuscular and hyperechoic pericardial effusion without signs of cardiac tamponade. CRP, ESR, Procalcitonin, Leukocytes were elevated, hypothyroidism and low gamma globulin values. The serology of pericardiotropic viruses is negative. Chest x–ray of mild bilateral pleural effusion. Urine culture was performed for pollakiuria, dysuria, fever: positive for Escherichiacoli. After gamma globulin replacement therapy, levothyroxine and targeted antibiotic therapy, the patient presents clinical and laboratory improvement and improvement in FE with persistence of pericardial effusion. Pericardiocentesis is performed with drainage of 800 ml of serous–looking liquid with coarse fibrin shoots. Cytological examination of the liquid shows a blood serum aspect with a carpet of granulocytic inflammatory elements. The patient was discharged after therapy with colchicine, prednisone, levothyroxine sodium, indomethacin, ramipril, omeprazole. The ECG showed an evolved ischemic type pattern. Conclusion Very rare cases of Escherichia coli cystitis complicated by myo–pericarditis have been described in the literature. Presumably hypothyroidism and congenital IgA immunodeficiency contributed to favoring and worsening the formation of the effusion. However, further studies are still needed to clarify the mechanisms of myocardial damage, although reversible during this type of bacterial infection.

P124 ECOCARDIOGRAPHIC DIAGNOSIS OF TYPE A AORTIC DISSECTION

Abstract Clinical case In August 2021, an 89–year–old woman with no previous cardiovascular history, suffering from systemic arterial hypertension under pharmacological treatment, dyslipidemia and M. di Parkinson came to our observation for syncopal episode. The clinical presentation was characterized by a syncopal episode in the absence of prodromes and reported chest pain upon awakening. At the time of arrival in PS the patient was alert, attentive, and oriented, asymptomatic, hemodynamically stable with PAS 90 mmHg, with normo–iso–sphygmic peripheral pulses. A cardiological evaluation was requested and the transthoracic echocardiography revealed dissection of the proximal ascending aorta with evidence of intimal flap starting from the aortic root and extending to the proximal tract of the aortic arch, moderate aortic valve insufficiency and moderate circumferential pericardial effusion (2 cm), with the presence of blood clots, in the absence of signs of hemodynamic compromise. CT angiography confirmed Stanford type A aortic dissection with intimal flap originating in the supravalvular site (maximum diameter 6 cm), longitudinally extended for about 6 cm at the level of the ascending aorta until the emergence of the epiaortic vessels which were not involved. Consequently, cardiac surgery teleconsultation was required which, based on the patient‘s advanced age, did not allow surgical treatment due to a prohibitive operative risk, considered comparable to the natural course of the disease. The patient was then admitted to intensive care where remained asymptomatic and in cardio–circulatory compensation until death occurred on the third day due to cardio–circulatory arrest from PEA. Conclusions Aortic dissection is a high–mortality condition that requires an immediate diagnostic–therapeutic approach. In the diagnostic process, transthoracic echocardiography represents the most promptly performed examination and not infrequently allows the diagnosis before radiological confirmation by angioTC.

P177 A SHOT TO THE HEART

Abstract We report the case of a 50–year–old man who, during a wild bird hunt, was accidentally fired with a shotgun loaded with pellets which hit the chest, the neck and the face of the hunter. The patient was taken to the emergency room, tachypnoic and suffering from chest pain, systolic blood pressure was 150/70 mmHg, SpO2 88%, analgesic therapy, liquids administration and O2 therapy were performed with moderate response. On physical examination there was a reduced vesicular murmur in middle field on the right, no heart murmurs; noticeable edema of face and neck soft tissues and absence of evident jugular turgor. The ECG showed sinus rhythm, HR 100/min, morphology at the limit for ST slightly rigid in the inferior site. He underwent a total body CT in which a shotgun pellet was found located at the heart base near the right atrium, with associated pericardial fluid, with a maximum thickness of about 10 mm, with blood density. A shotgun pellet was also found in the apical segment of the right upper lung lobe with associated parenchymal ground glass (the pellet site of passage) without pneumothorax and pleural effusion. CT also showed multiple hunting pellets in the soft tissues of the face and of the neck without significant lesions. The echocardiogram confirmed the presence of circumferential pericardial effusion of mild degree, but progressively worsening, mainly represented along the cardiac apex and the inferolateral wall, but without signs of cardiac tamponade (right atrium within limits, absence of significant Doppler variation in blood flow across cardiac valves). The hospital where the patient arrived was at a distance of 30 minutes from the cardiac surgery, therefore the patient was urgently transferred to the cardiac surgery room of the hub (distance of 30 minutes). Fortunately, the patient maintained hemodynamic stability and arrived in the operating room with good blood pressure, but with a pre–tamponade effusion. The man quickly underwentcardiac surgery, the pericardial effusion was drained and the responsible breach was found in at the atrio–caval junction and successfully sutured. The patient was discharged in the 6th day and currently is in good clinical condition.

P297 PERICARDIAL EFFUSION WITHOUT HEMODYNAMIC INSTABILITY: WHEN AND TO WHOM THE PERICARDIOCENTESIS?

Abstract Cardiac tamponade is traditionally considered a clinical diagnosis, but there are pre–tamponating effusions that occur without signs of cardiogenic shock, and in these situations it can be complex to determine when and which patient treat with pericardiocentesis. The clinical case concerns a 90–year–old woman who comes to the emergency room for exertional dyspnea. Upon arrival blood pressure was 150/90 mmhg, heart rate 70 bpm. On chest x–ray, enlargement of the cardiac silhouette was evident (Fig 1). The echocardiogram showed a circumferential pericardial effusion of 2 centimeters with signs of right cardiac chambers compression (Fig 2). Hospitalized in ICU, the clinical situation was complicated by the onset of atrial fibrillation with a high ventricular response (Fig 3) and immediate cardiogenic shock (BP 70/40 mmHg, tachypnea, altered mental status). We proceed with emergency electrical cardioversion, effective in restoring sinus rhythm with almost immediate arrhythmic recurrence; therefore we perform a pericardiocentesis, with regression of the shock status after aspiration of a few cc of serum–haematic pericardial fluid (total 750 cc); spontaneous restoration of sinus rhythm after the procedure. Neoplastic problems were excluded, IgM positivity for influenza A and B on blood tests. The patient presented no further complication, was discharged at home, in sinus rhythm, with negative follow–up so far. This clinical case focuses the question of the indication and timing of pericardiocentesis. We managed a pericardial effusion with ultrasound signs of compression of the right sections, but in the absence of clinical signs of cardiogenic shock / Beck‘s triad. Given the clinical evolution, should we have perform the pericardiocentesis as soon as the patient arrived, in conditions of hemodynamic stability? Interesting are the score index proposed by Halpern et al. and an ESC position statement that serves to identify patients to undergo urgent pericardiocentesis based not only on clinical factors, but also on imaging evaluation. The total score of our case would have been indicative for an immediate pericardiocentesis. In our opinion, the formulation of a triage system for patients with pericardial effusion and hemodynamic stability that can be routinely implemented in clinical practice would be extremely useful.

Cardiac Tamponade Totalis: Unique Phenomenon of Biventricular Tamponade After LVAD Implant

<h3>Introduction</h3> Cardiac tamponade results in obstructive shock due to cardiac chamber compression and impaired cardiac output. This commonly involves the RV due to its lower pressure. We report the first case of biventricular tamponade in a patient with a LVAD. <h3>Case Report</h3> A 30 yr old female (ht 4'7", wt 32 kg, BSA 1.13 m²) with inotrope dependent non-ischemic cardiomyopathy presented for heart transplant evaluation. Right heart catheterization on milrinone 0.375 mcg/kg/min was notable for RA 32 mmHg, PA 51/30 (37) mmHg, PCWP 34 mmHg, CI 1.2 L/min/m², PVR 1.8 Wood units. She was listed for cardiac transplant as her vessels were too small for percutaneous peripheral short term mechanical circulatory support. She decompensated needing VA-ECMO and then HeartWare LVAD implantation (speed 2300 RPM). 7 days post operatively, low flow alarms occurred with hypotension requiring escalating doses of ino-pressors. Echocardiography revealed a large circumferential pericardial effusion resulting in biventricular collapse (Figure A). Emergent surgical drainage was performed with 500 ml blood removal, resulting in re-expansion of both ventricles (Figure B). <h3>Summary</h3> To our knowledge this is the first report of biventricular cardiac tamponade, or as we have termed it, tamponade totalis. In the presence of a pericardial effusion, continuous LV unloading via a LVAD can cause the LV pressure to be lower than the pericardial pressure. Coupled with reduced RV preload from post-operative bleeding, this results in biventricular compression and tamponade. A combination of patient (size, anticoagulation, surgical approach) and pump (RPM) related factors likely lead to the development of tamponade totalis. Diagnosis of tamponade in a patient with a continuous flow LVAD is challenging due to similarities in presentation of right heart failure and atypical signs. Unique clues suggestive of tamponade in patients with a LVAD are respiratory variation of the pulsatilitiy index waveform and pulseless paradoxus. Imaging is key to diagnosis.

Moderna Vaccine Induced Recurrent Myopericarditis

COVID-19 mRNA vaccine-related myocarditis and myopericarditis is a rare complication, with the US Centers for disease Control and Prevention reporting 4.2 per million females aged 12-29 years, dropping to 1.0 per million over 30, and exceptionally rare is recurrent myopericarditis requiring immunosuppressive therapy. We report a case of a 51-year-old female with no significant medical history presented to the emergency department with pleuritic chest pain, and progressive breathlessness 9 days after her first Moderna vaccine. Electrocardiography revealed widespread ST segment elevation with PR depression in the inferior leads. Her inflammatory markers were elevated with a C- reactive protein of 263. Transthoracic echocardiography revealed a moderate circumferential pericardial effusion with a maximum of 1.8cm adjacent to the lateral wall of the left ventricle in the parasternal short axis view and no evidence of tamponade physiology. The patient did not show initial response to anti-inflammatory therapy, and was commenced on steroid therapy, and subsequently immunosuppressive therapy, namely azathioprine, to manage disease activity. This case brings to light a rare but significant side effect of mRNA vaccine, and whilst this case should not impede vaccination efforts, it highlights that whilst the majority of patients get transient self-limiting myocardial inflammation, rare cases of prolonged myopericarditis may occur which may require prolonged immunosuppression.

Ischemic stroke as a comorbidity in a patient with Stanford A aortic dissection: A case report

Background. Aortic dissection is one of the leading causes of death in cardiovascular disease. The clinical course of aortic dissection is often atypical and can mimic a variety of clinical manifestations. Stroke is one of the conditions that can make the management of aortic dissection becoming more complex. Case presentation. A 55-year-old female patient came with complaints of severe chest pain. The patient was diagnosed with Stanford aortic dissection, De Bakey type II, hypertension heart disease, mild mitral regurgitation, mild circumferential pericardial effusion. After the second day of treatment, the patient also complained of sudden slurred speech and weakness on right extremities. The administration of antiplatelet were postponed in consideration of the current patient with aortic dissection. On the 7th day of treatment, the patient experienced a worsening motor strength on the right extremities. We decided to continue antihypertensive therapy on acute phase of ischemic stroke with the consideration that aortic dissection can cause higher mortality. Conclusions. The management of ischemic stroke in a patient with aortic dissection is challenging. In ischemic stroke patient with aortic dissection, anti-hypertensives need to be given to reduce the stress on the aortic wall and prevent expansion of the dissection which has a higher mortality rate.