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In this article, electrography for diagnosis and screening of fifteen dogs for cardiac diseases were done. ECG waveform measurement and interpretation was performed using standard bipolar (Lead I, II & III) and augmented limb leads (aVR, aVL & aVF). The ECG waveform measurements revealed significant (p, {"references":["Aptekmann K. P., Vailati M. F., Fortuna T. M., Schwartz D. S. (2010). Prevalence of cardiac arrhythmias and conduction disturbances in dogs and cats in Botucatu, Brazil (2003–2007). J Vet Res An Sci 47: 371–79.","Chen Y.J., Chen S.A., Chang M.S., Lin C.I. (2000). Arrhythmogenic activity of cardiac muscle in pulmonary veins of the dog: Implication for the genesis of atrial fibrillation. Cardiovasc Res 48, 265–273.","Chiavegato D., Borgarelli M., D'Agnolo G., Santilli R. A. (2009). Pulmonary hypertension in dogs with mitral regurgitation attributable to myxomatous valve disease. Vet Radiol Ultrasound 50: 253– 258.","Cote E., (2010). Electrocardiography and cardiac arrhythmias. In: Ettinger, S. J., Feldman, E. C., (eds): Textbook of Veterinary Internal Medicine, Edn. 7th, W. B. Saunders Co., Philadelphia: 1159– 1187.","DeFransesco. (2001). Advanced discussions in the diagnosis of heart failure. In a publication on \"Advances in management of cardiac patients\" Waltham and Merial, USA: 3–11.","Ettinger, S. J. and Feldman E.C. (2006). In \"Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat\" 6th Ed. W. B. Saunders Company, Philadelphia, USA.","Gugjoo M. B., Hoque M., Saxena A. C., Samsuz Zama M. M., (2014a). Reference values of sixlimb- lead electrocardiogram in conscious Labrador retriever dogs. Pak J Biol Sci 17(5): 689–695.","Gugjoo M. B., Hoque., M., Saxena A. C., Shamsuz Zama, M. M., Dey, S. (2014b). Reference values of M-mode echocardiographic parameters and indices in conscious Labrador retriever dogs. Iran J Vet Res 15(4): 341–346.","Kraus M. S., Gelzer A. R. M., Moise S. (2008). Treatment of cardiac arrhythmias and conduction disturbances. Manual of canine and feline cardiology, Edn. 4th, W. B. Saunders Co., Philadelphia, USA: 315–32.","Liu S.K., Barry J. M., Lawrence P.T. (1979). Hypertrophic cardiomyopathy in the dog. Am J Path 94: 497–508.","Neto, G. B. P., Brunetto, M. A., Sousa, M. G., Carciofi, A. C., Camacho, A. A. (2010). Effects of weight loss on the cardiac parameters of obese dogs. Pesq Vet Bras. Rio De Janeiro 30:2.","Saini N. (2014). Diagnosis and Therapeutic Management of Myocardial and Valvular Diseases in Dogs. Ph.D. Dissertation, Guru Angad Dev Veterinary and Animal Sciences University Ludhiana, India","Tilley L. P. (1992). Essentials of canine and feline electrocardiography. 3rd Edn. Lea and Fabiger, Philadelphia 1–252.","Tilley L., Smith F. (2016). Electrocardiography. Manual of canine and feline cardiology 5th Edn. W.B Saunders, Philadelphia, USA: 49–76.","Velhankar RD. (2013). Two dimensional echocardiographic studies on dilated cardiomyopathy in dog. Ph.D. Thesis. Maharashtra Animal and Fishery Sciences University, Nagpur, India","Ware W. A. (2000). Pericardial diseases. In: Abbott A. J. (ed.) Small Animal Cardiology Secrets. Hanley and Belfus, Philadelphia: 276–285.","Ware W A. (2009). Cardiovascular system disorder. In: Nelson R. W. and Couto C. G. (Eds). Small Animal Internal Medicine, 4th Edn. Mosby Elsevier: 1–95.","Wess G., Schulze A., Simak J., Killich M., Keller L. J., Maeurer J. and Hartmann K. (2010). Prevalence of dilated cardiomyopathy in Doberman Pinschers in various age groups. J Vet Intern Med 24(3): 533–38."]}

Highlights • Acute abdomen is any acute abdominal condition requiring a quick response. • The abdominal discomfort associated with extra-abdominal pathologies could mimic acute abdomen. • Cardiac tamponade is a medical emergency. • The differential diagnosis could be kept in mind to avoid a delayed treatment., Introduction Acute abdomen is any acute abdominal condition requiring a quick response. The incidence varies according to age and disease aetiology. The abdominal discomfort associated with extra-abdominal pathophysiology and thoracic conditions could mimic acute abdomen. In this case we report a rare case of a young patient with cardiac tamponade masquerading as acute abdomen. Presentation of case A 25-years-old African man presented to the Emergency Department with abdominal pain. An EKG was performed, which revealed sinus tachycardia, with electrical alternans and borderline reduced voltage. At the time of the admission to our unit, he had a clinical worsening and a CT scan of abdomen was performed, which demonstrated hepatomegaly, abundant pericardial effusion and thin right pleural effusion at the lung bases. An echocardiogram confirmed a circumferential pericardial effusion with initial collapse of the right ventricular free wall. It was decided to immediately transport the patient to the Cardiosurgery Unit of another hospital to undergo pericardiocentesis. Discussion Our experience with this case underlines the important point that patients with a large pericardial effusion may present with the clinical features of acute abdomen and peritonitis. Abdominal pain was the primary symptom that prompted this patient to seek medical attention. Conclusion Acute abdomen is any acute abdominal condition requiring a rapid, often surgical, treatment. Cardiac tamponade is a medical emergency. The differential diagnosis could be kept in mind by any emergency physician, surgeon and anaesthesiologist, because an incorrect diagnosis and therefore an incorrect treatment or a delay in pericardial evacuation can be life-threatening.

ECG of patients with Wolf Parkinson White (WPW) syndrome may simulate other entities such as myocardial infarction, ventricular premature complexes, ventricular bigeminy, accelerated idioventricular rhythm, intermittent bundle branch block or electrical alternans. On the other hand, the opposite can also occur where these other conditions may simulate WPW. We present the case of a young patient referred for WPW ablation showing an incessant accelerated idioventricular rhythm mimicking preexcitation.

Two cases are described of iatrogenic traumatic perforation of an ICD electrode through the myocardium in the right ventricle and to the pericardium. The diagnostic gold standard gated CT was not necessary in either case. In the first case the lead insertion was difficult, time-consuming, and complicated by the PostCardiac Injury Syndrome and a slowly accumulating hemorrhagic pericardial effusion causing cardiac tamponade, diagnosed by the clinical picture, elevated CRP, ECG with low voltage and electrical alternans, chest X-ray revealing enlarged cardiac silhouette and echocardiography a large effusion, treated with pericardiocentesis and drainage. In the other case there was painful pericardial irritation and extracardiac pacing and ICD failure with loss of capture, no diagnostic changes in ECG, chest X-ray, and echocardiography; diagnosed by fluoroscopy during replacement at the lead, which went without complications and without pericardial effusion.

RationalePatients with ischemic cardiomyopathy (ICMP) are at high risk for malignant arrhythmias, largely due to electrophysiological remodeling of the non-infarcted myocardium. The electrophysiological properties of the non-infarcted myocardium of patients with ICMP remain largely unknown.ObjectivesTo assess the pro-arrhythmic behavior of non-infarcted myocardium in ICMP patients and couple computational simulations with machine learning to establish a methodology for the development of disease-specific action potential models based on clinically measured action potential duration restitution (APDR) data.Methods and ResultsWe enrolled 22 patients undergoing left-sided ablation (10 ICMP) and compared APDRs between ICMP and structurally normal left ventricles (SNLVs). APDRs were clinically assessed with a decremental pacing protocol. Using genetic algorithms (GAs), we constructed populations of action potential models that incorporate the cohort-specific APDRs. The variability in the populations of ICMP and SNLV models was captured by clustering models based on their similarity using unsupervised machine learning. The pro-arrhythmic potential of ICMP and SNLV models was assessed in cell- and tissue-level simulations. Clinical measurements established that ICMP patients have a steeper APDR slope compared to SNLV (by 38%, p < 0.01). In cell-level simulations, APD alternans were induced in ICMP models at a longer cycle length compared to SNLV models (385–400 vs 355 ms). In tissue-level simulations, ICMP models were more susceptible for sustained functional re-entry compared to SNLV models.ConclusionMyocardial remodeling in ICMP patients is manifested as a steeper APDR compared to SNLV, which underlies the greater arrhythmogenic propensity in these patients, as demonstrated by cell- and tissue-level simulations using action potential models developed by GAs from clinical measurements. The methodology presented here captures the uncertainty inherent to GAs model development and provides a blueprint for use in future studies aimed at evaluating electrophysiological remodeling resulting from other cardiac diseases.

A phenomenon called alternans, which is a beat-to-beat alternation in action potential (AP) duration, sometimes precedes fatal cardiac arrhythmias. Alternans-suppressing electrical stimulus protocols are often represented as perturbations to the dynamics of membrane potential or AP duration variables in nonlinear models of cardiac tissue. Controllability analysis has occasionally been applied to cardiac AP models to determine whether different control or perturbation strategies are capable of suppressing alternans or other unwanted behavior. Since almost all previous cardiac controllability studies have focused on low-dimensional models, we conducted the present study to assess controllability of a higher-dimensional model, specifically the Luo Rudy dynamic (LRd) model of a cardiac ventricular myocyte. Higher-dimensional models are of interest because they provide information on the influence of a wider range of measurable quantities, including ionic concentrations, on controllability. After computing modal controllability measures, we found that larger eigenvalues of a linearized LRd model were on average more strongly controllable through perturbations to calcium-ion concentrations compared with perturbations to other variables. When only membrane potential was adjusted, the best time to apply perturbations (in the sense of maximizing controllability of the largest alternans eigenvalue) was near the AP peak time for shorter cycle lengths. Controllability results were found to be similar for both the default model parameters and for an alternans-promoting parameter set. Additionally, we developed several alternans-suppressing state feedback controllers that were tested in simulations. For the scenarios examined, our controllability measures correctly predicted which strategies and perturbation timings would lead to better feedback controller performance.

Absztrakt: Akut légzési elégtelenség miatt felvett 70 éves férfi betegnél a felvételi EKG pitvari tachycardiát és makro-T-hullám-alternánst mutatott, amely a sinusrhythmus helyreállása után megszűnt. Az EKG-jelenséget sem QT-megnyúlás, sem heveny ischaemia nem kísérte. Az eset arra hívja fel a figyelmet, hogy makro-T-hullám-alternáns jelentkezhet pitvari tachycardia következtében is, amely esetünkben akut respiratoricus insufficientia miatt lépett fel. Orv Hetil. 2020; 161(7): 275–277.

Using a probabilistic reachability-based approach, we present a multi-parameter bifurcation analysis of electrical alternans in the two-current Mitchell–Schaeffer (MS) cardiac-cell model. Electrical alternans is a phenomenon characterized by a variation in successive Action Potential Durations generated by a cardiac cell or tissue. Alternans are known to initiate re-entrant waves and are an important physiological indicator of an impending life-threatening arrhythmia such as ventricular fibrillation. The multi-parameter bifurcation analysis we perform identifies a bifurcation hypersurface in the MS model parameter space, such that a small perturbation to this region results in a transition from highly likely alternans to highly likely non-alternans behavior. Our approach to this problem rests on encoding alternans-like behavior in the MS model as a five-mode, multinomial hybrid automaton. To perform multi-parameter bifurcation analysis of cardiac alternans, we first treat the parameters in question as bounded random variables. We then apply a sophisticated guided-search-based probabilistic reachability analysis to compute a bounded bifurcation region (possibly very tight) that contains the bifurcation hypersurface (BH). Our probabilistic reachability analysis uses a technique that combines a δ-decision procedure with statistical tests. In the process of computing the bifurcation region, we further partition the parameter space into two more regions such that any valuation chosen from one of the regions will either produce alternans or non-alternans behavior with a probability greater than a user-defined threshold.

Mechanical alternans (MA) is a powerful predictor of adverse prognosis in patients with heart failure and cardiomyopathy, but its use remains limited due to the need of invasive continuous arterial pressure recordings. This study aims to assess novel cardiovascular correlates of MA in the intact human heart to facilitate affordable and non-invasive detection of MA and advance our understanding of the underlying pathophysiology. Arterial pressure, respiration, and ECG were recorded in 12 subjects with healthy ventricles during voluntarily controlled breathing at different respiratory rate, before and after administration of beta-blockers. MA was induced by ventricular pacing. A total of 67 recordings lasting approximately 90 s each were analyzed. Mechanical alternans (MA) was measured in the systolic blood pressure. We studied cardiovascular correlates of MA, including maximum pressure rise during systole (dPdtmax), pulse arrival time (PAT), pulse wave interval (PI), RR interval (RRI), ECG QRS complexes and T-waves. MA was detected in 30% of the analyzed recordings. Beta-blockade significantly reduced MA prevalence (from 50 to 11%, p

Background The use and utility of novel oral anticoagulants has been increasing in clinical practice due to their relatively lower incidence of side effects such as intracranial haemorrhage, particularly in the elderly, when compared with vitamin K antagonists. Rivaroxaban is a factor Xa and prothrombinase inhibitor indicated for stroke and venous thromboembolism prophylaxis in non-valvular atrial fibrillation as well as treatment of venous thromboembolism. Case summary A patient with history of paroxysmal atrial fibrillation on Rivaroxaban presented with generalized malaise, lightheadedness, and dizziness. The patient was found to be in profound cardiogenic shock despite unremarkable cardiac enzymes. Electrocardiogram revealed rate controlled atrial fibrillation and T-wave inversions in the inferolateral leads without associated electrical alternans. Bedside echocardiogram revealed a large pericardial effusion consistent with cardiac tamponade physiology. Following anticoagulation reversal, the patient underwent urgent pericardiocentesis yielding haemorrhagic fluid, with subsequent improvement in haemodynamic status. Despite the presence of retroperitoneal lymphadenopathy on previous computed tomography of the abdomen and concern for underlying malignant effusion secondary to lymphoma, cytology of the fluid revealed no evidence of malignant cells and follow-up flow cytometry and bone marrow biopsy were unremarkable. Discussion While hemopericardium is not listed as a known side effect of Rivaroxaban, previous cases of hemopericardium secondary to Rivaroxaban have been described in the literature secondary to pre-disposing risk factors including CYP450 drug interactions or cardiac device implantations. In this case, the patient experienced a spontaneous hemopericardium on Rivaroxaban without any previously elucidated risk factors or evidence of malignancy.

The detection of Paroxysmal Atrial Fibrillation (PAF) is a fairly complex process performed manually by cardiologists or electrophysiologists by reading an electrocardiogram (ECG). Currently, computational techniques for automatic detection based on fast Fourier transform (FFT), Bayes optimal classifier (BOC), k-nearest neighbors (K-NNs), and artificial neural network (ANN) have been proposed. In this study, six features were obtained based on the morphology of the P-Wave, the QRS complex and the heart rate variability (HRV) of the ECG. The performance of this methodology was validated using clinical ECG signals from the Physionet arrhythmia database MIT-BIH. A feedforward neural network was used to detect the presence of PAF reaching a general accuracy of 97.4%. The results obtained show that the inclusion of the information of the P-Wave, HRV and QR Electrical alternans increases the accuracy to identify the PAF event compared to other works that use the information of only one or at most two of them.

AimsWe investigate mechanisms for potential pro-arrhythmic effects of hydroxychloroquine (HCQ) alone, or combined with azithromycin (AZM), in Covid-19 management supplementing the limited available experimental cardiac safety data.MethodsWe integrated patch-clamp studies utilizing In Vitro ProArrhythmia Assay (CiPA) Schema IC50 paradigms, molecular modelling, cardiac multi-electrode array and voltage (RH237) mapping, ECG studies, and Ca2+ (Rhod-2 AM) mapping in isolated Langendorff-perfused guinea-pig hearts with human in-silico ion current modelling.ResultsHCQ blocked IKr and IK1 with IC50s (10±0.6 and 34±5.0 μM) within clinical therapeutic ranges, INa and ICaL at higher IC50s, leaving Ito and IKs unaffected. AZM produced minor inhibition of INa, ICaL, IKs, and IKr,, sparing IK1 and Ito. HCQ+AZM combined inhibited IKr and IK1 with IC50s of 7.7±0.8 μM and 30.4±3.0 μM, sparing INa, ICaL and Ito. Molecular modelling confirmed potential HCQ binding to hERG. HCQ slowed heart rate and ventricular conduction. It prolonged PR, QRS and QT intervals, and caused prolonged, more heterogeneous, action potential durations and intracellular Ca2+ transients. These effects were accentuated with combined HCQ+AZM treatment, which then elicited electrical alternans, re-entrant circuits and wave break. Modelling studies attributed these to integrated HCQ and AZM actions reducing IKr and IK1, thence altering cell Ca2+ homeostasis.ConclusionsCombined HCQ+AZM treatment exerts pro-arrhythmic ventricular events by synergetically inhibiting IKr, IKs with resulting effects on cellular Ca2+ signalling, and action potential propagation and duration. These findings provide an electrophysiological basis for recent FDA cardiac safety guidelines cautioning against combining HCQ/AZM when treating Covid-19.

One of the most common causes of pericardial effusion in the Western world is malignancy. Emergency physicians must maintain vigilance in suspecting pericardial effusion and tamponade in patients with known or suspected malignancy who present with tachycardia, dyspnea, and hypotension. Diagnosis can be expedited by key physical examination, electrocardiogram, and sonographic findings. Unstable or crashing patients with tamponade must undergo emergent pericardiocentesis for removal of fluid and pressure to restore cardiac output.

Em fisiologia cardíaca, alternans elétrica _e um fenômeno caracterizado pela alternância entre potenciais de ação longos e curtos que dá origem a complexos comportamentos espaço-temporais em tecido. Experimentos e medições clínicas indicam que alternans pode ser um precursor de perigosas arritmias, como fibrilação ventricular ou morte súbita. Apesar da importância do alternans no estudo de doenças cardíacas, muitos modelos matemáticos para a eletrofisiologia de células cardíacas não são capazes de reproduzir este fenômeno. Como um potencial remédio para esta deficiência, introduzimos curtos atrasos de tempo em algumas formulações de modelos preexistentes para células cardíacas que são baseados em Equações Diferenciais Ordinárias (EDOs). Vários processos em células cardíacas envolvem atrasos de sensibilidade e de resposta a mudanças em variáveis fisiológicas. Além disso, equações diferenciais com atraso (DDEs) são conhecidas por dar origem a complexas propriedades dinâmicas em modelos matemáticos. Em modelagem biológica, DDEs têm sido aplicadas em epidemiologia, dinâmica populacional, imunologia e redes neurais. Portanto, DDEs podem representar mecanismos que resultam em dinâmicas complexas tanto no nível celular, quanto no nível do tecido. Nesta tese, propomos formulações baseadas em DDEs para modelos de canais iônicos descritos pelo formalismo de Hodgkin-Huxley. Tais formulações são capazes de induzir alternans em simulações celulares envolvendo vários modelos encontrados na literatura. Nós também mostramos que essas modificações podem desestabilizar e quebrar ondas espirais em simulações bidimensionais de propagação elétrica, o que é típico de fibrilação cardíaca. Entretanto, as formulações propostas introduzem novos desafios computacionais devido à necessidade de armazenar e recuperar valores passados de variáveis. Deste modo, nós apresentamos novos métodos numéricos para superar tais desafios e permitir a eficiente simulação de modelos baseados em DDEs no nível do tecido cardíaco. Os métodos propostos foram capazes de diminuir o uso de memória em até 95% em comparação aos algoritmos largamente utilizados na solução numérica de DDEs. Assim, os novos modelos baseados em DDEs e os eficientes métodos numéricos propostos nesta tese contribuem para o estudo de arritmias cardíacas fatais através de modelagem computacional. In cardiac physiology, electrical alternans is a phenomenon characterized by long-short alternations in the action potential duration of cardiac myocytes that give rise to complex spatiotemporal dynamics in tissue. Experiments and clinical measurements indicate that alternans can be a precursor of life-threatening arrhythmias, such as cardiac _brillation. Despite the importance of alternans in the study of cardiac disease, many mathematical models developed to describe cardiac electrophysiology at the cellular level are not able to produce this phenomenon. As a potential remedy to this de_ciency, we introduce short time-delays in some formulations of existing cardiac cell models that are based on Ordinary Di_erential Equations (ODEs). Many processes within cardiac cells involve delays in sensing and responding to changes. In addition, delay di_erential equations (DDEs) are known to give rise to complex dynamical properties in mathematical models. In biological modeling, DDEs have been applied to epidemiology, population dynamics, immunology, and neural networks. Therefore, DDEs can potentially represent mechanisms that result in complex dynamics both at the cellular level and at the tissue level. In this thesis, we propose DDE-based formulations for ion channel models based on the Hodgkin-Huxley formalism that can induce alternans in single-cell simulations in many models found in the literature. We also show that these modi_cations can destabilize spiral waves and produce spiral breakups in two-dimensional simulations, which is a typical model of cardiac _brillation. However, the new DDE-based formulations introduce new computational challenges due to the need for storing and retrieving past values of variables. Therefore, we present novel numerical methods to overcome these challenges and enable e_cient DDE-based studies at the tissue level in standard computational environments. We _nd that the proposed methods decrease memory usage by up to 95% in cardiac tissue simulations compared to straightforward history management algorithms available in widely used DDE solvers.

A chronic heart failure (CHF) rat underwent epicardial programmed electrical stimulation (PES). Ventricular tachycardia (VT) developed during PES. Mechanical alternans was noted despite fixed tachycardia cycle length. Anti-tachycardia pacing attempts initiated a second VT that generated pulse intermittently and then degenerated into pulseless VT with electrical alternans.To our knowledge electrical and mechanical alternans have not been recorded in animal models of CHF during VT. The distinct events of mechanical alternans and electrical alternans may be indicative of progressively worsened calcium handling in the compromised cardiomyocytes.Although ion channel differences between rodents and humans exist, this work attempts to demonstrate this rat model's usefulness in understanding cardiac electrophysiology in CHF.

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

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: The diagnosis of lung malignancy can often be incidental. We present a hemodynamically unstable patient with COVID-19 and pericardial effusion, subsequently diagnosed with metastatic adenocarcinoma of the lung. CASE PRESENTATION: A 54-year-old male with no significant medical history was diagnosed with COVID-19 two weeks prior to presentation. He had dyspnea on exertion since that time and presented to the hospital after having an abnormal CXR and leukocytosis on out-patient testing. His blood pressure was 95/68 with a heart rate of 129. EKG revealed atrial fibrillation and electrical alternans. He had mildly elevated BNP and troponin, with lactic acidosis. Bilateral opacities were noted on CXR. A large effusion concerning for tamponade was noted on bedside echo. He underwent immediate pericardiocentesis and had 2L serosanguinous fluid drained. After initial stabilization, he was found to have extensive bilateral lower extremity DVT and PE.Repeat TTE showed residual effusion with tamponade physiology observed. Despite the findings on imaging, a pericardial window was not pursued due to concerns of anesthesia induction in the setting of a new PE. He underwent placement of a pericardial drain instead. After the procedure, heparin drip was initiated with an IVC filter placed soon after. The patient eventually had a pericardial window placed. His arrhythmia was chemically converted back to sinus rhythm. On POD5, the drains were removed.Autoimmune workup of the fluid was within normal limits, but cytology resulted in a diagnosis of adenocarcinoma positive for TTF-1. Thus, he was diagnosed with stage IV adenocarcinoma of the lung. CT revealed multiple lytic lesions with diffuse lymphadenopathy. MRI showed no evidence of brain metastasis. He was transitioned to apixaban at discharge, with out-patient oncology follow-up. DISCUSSION: A small study of 31 patients showed pericardial effusion was an independent risk factor predicting severity of COVID-19 infection, with reports of the virus being detected in pericardial fluid.[1,2] While virus infection can cause pericardial effusion, other causes should not be ignored in the workup. With hemodynamic instability, immediate intervention is warranted despite the risk involved with pericardiocentesis. In patients with large volume of pericardial effusion extracted, 5% of them will suffer from paradoxical hemodynamic instability and pulmonary edema afterwards, a condition known as pericardial decompression syndrome.[3] The increased venous return after decompression will compress the LV, based on the principle of ventricular coupling, reducing the cardiac output. Treatment for this condition is supportive. CONCLUSIONS: While COVID-19 is known to cause pericardial effusion, other causes, such as malignancy, should not be forgotten and should always remain in our differential. The risk involved with immediate pericardiocentesis goes beyond cardiac injury. REFERENCE #1: Chen Q, Xu L, Dai Y, et al. Cardiovascular manifestations in severe and critical patients with COVID -19. Clin Cardiol. 2020;43(7):796-802. REFERENCE #2: Farina A, Uccello G, Spreafico M, Bassanelli G, Savonitto S. SARS-CoV-2 detection in the pericardial fluid of a patient with cardiac tamponade. Eur J Intern Med. 2020;76:100-101. REFERENCE #3: Prabhakar Y, Goyal A, Khalid N, et al. Pericardial decompression syndrome: A comprehensive review. World J Cardiol. 2019;11(12):282-291. DISCLOSURES: No relevant relationships by Rumon Chakravarty, source=Web Response No relevant relationships by Vernon Chan, source=Web Response

Introduction Muscular connections between the coronary sinus (CS) and left atrium probably impact distribution of electrical activity. Double atrial potentials (DP) may be their presentation. The aim was to investigate the presence of DP in CS recordings during atrioventricular reentrant tachycardia (AVRT) and its contribution to the occurrence of paroxysmal atrial fibrillation (AF). Methods A group of 247 patients with accessory pathways (AP) were screened for DP. The patients with DP during AVRT were compared to those without DP. Results DP during AVRT were found only among the left sided AP (AP-L). Patients with AP-L were divided into Group 1 (n = 17) with DP during AVRT and Group 2 (n = 108) without DP. Patients in Group 1 had higher incidence of AF in history (47.1% vs. 23.1%; p = 0.0376), AF induced during electrophysiological (EP) study (70.6% vs. 25%; p = 0,0002). Group 1 had higher heart rate (HR) during AVRT in the EP study (197.2±27 vs. 175.1±26.3 bpm; p = 0,0019), but HR of clinical AVRT (208.5 ±30.8 vs. 191.6 ±27.8 bpm) was not significant different (p = ns). Additionally, electrical alternans of QRS amplitude during AVRT in the EP study was more frequent in Group 1 (52.9 vs. 20.4 %; p = 0,0048). Conclusion Patients with DP and left-sided AP were more prone to develop AF. The presence of DP was associated with faster AVRT rate. The direction of atrium depolarization during AVRT may be different in the presence of DP and probably plays a role in development of AF in this group of patients. This article is protected by copyright. All rights reserved