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Background: Among patients with COVID-19 infection, the risk of adverse cardiovascular outcome, particularly myocarditis and dysrhythmias remain elevated at least up to one year after infection. We present a case of atrial tachycardia and atrial Torsades de Pointes from COVID myocarditis, persisted 6 months after infection, which was successfully managed by ablation. Objective(s): A 25-year-old female presented with mild COVID-19 infection, Omicron variant, in May 2022. One month after, her Covid infection resolved;she presented with symptomatic atrial tachycardia, paroxysmal atrial fibrillation and flutter. ECG showed multiple blocked premature atrial contractions (PAC) (Figure 1A). Holter monitor showed PAC triggered atrial tachycardia degenerating to paroxysmal atrial fibrillation, atrial Torsades de Pointes. She has mild persistent troponin elevation. Echocardiography was normal. Cardiac MRI showed evidence of mild myocarditis with subepicardial late Gadolinium enhancement (LEG) along the lateral mid-apical left ventricular wall and edema. (Figure 1B). She was treated with Colchicine for 2 months. Repeat cardiac MRI 4 months after COVID infection showed resolution of edema and LGE. However, her symptomatic PAC and atrial tachycardia did not respond to betablocker and amiodarone. She underwent electrophysiology study. Activation mapping of PAC using CARTO revealed earliest activation at the right anterior atrial wall, with close proximity to tricuspid valve;unipolar signal showed QS pattern, bipolar signal showed 16 msec pre-PAC (Figure 1C and 1D). Mechanical pressure from ThermoCool SmartTouch ablation catheter (Biosense Webster Inc.) at this site suppressed the PAC. Radiofrequency ablation resulted with an initial acceleration and then disappearance of the PAC. We did not isolate pulmonary veins or ablate cavotricuspid isthmus. Post ablation, PAC and atrial fibrillation were not inducible on Isoproterenol. Method(s): N/A Results: Covid myocarditis can result in dysrhythmia that lingers long after Covid myocarditis has resolved. Covid myocarditis can be caused by direct viral invasion of myocytes or more commonly is inflammatory related to cytokine release and edema. Our case demonstrates that dysrhythmias can persist despite resolution of myocarditis. Catheter ablation can successfully to treat these arrhythmias. Conclusion(s): This case highlights the importance of recognizing cardiac dysrhythmia as possible the long-term cardiac complications of COVID-19, requiring specific treatment such as catheter ablation. [Formula presented]Copyright © 2023
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Background: The coronavirus (COVID-19) pandemic, which affected millions of people worldwide, is associated with a chronic fatigue sequela, also known as long-COVID. While various adverse effects of COVID-19 on the cardiovascular system were reported, the prolonged sequela of COVID-19 on heart rhythm remains unknown. Aim(s): To describe the prevalence of cardiac dysrhythmias among patients who presented with Long Covid following recovery from COVID-19 infection. Method(s): We conducted a prospective study among 87 patients who suffered from Long Covid syndrome following recovery from COVID-19 and were treated in the COVID-19 recovery clinic between December 2020 and June 2021. All patients were referred for transthoracic echocardiography (TTE) and 24-hour Holter examination. Result(s): The mean age was 52+13 years, and 52 (59.8%) patients were females. Seventy-nine (90.8%) of the patients had normal sinus rhythm without evidence of any arrhythmias. Atrial premature beats were recorded in 70 (80.5%) patients with a median of 6/day (interquartile range 3-20/day;maximum: 5180/day). Ventricular premature beats were recorded in 50 (57.5%) patients with a median of 4/day (interquartile range 2-19/day;maximum: 6847/day). Overall, seven patients (8%) had sustained atrial dysrhythmias: One had atrial fibrillation, one had atrial flutter, and five had atrial tachycardia. Sixty-six (75.9%) patients underwent TTE, which was mainly unremarkable as 65 patients had a normal left ventricular function, and three (4.5%) patients had evidence of pulmonary hypertension. Discussion(s): Cardiac arrhythmias are not uncommon among symptomatic COVID-19 recovered patients. Atrial arrhythmias were most common, with an up to 8% incidence rate. These findings may suggest that atrial dysrhythmias may be associated with long-term symptomatic sequela of COVID-19 infection.
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Background Premature atrial contractions (PACs) are usually seen as a relatively benign condition. Data about PACs induced cardiomyopathy and requiring ablation are limited. Case After recovery of COVID-19 infection, an otherwise healthy 39 year old patient presented with palpitations lasting for several months. His blood lab-work was non-significant. Electrocardiogram showed frequent premature beats with both narrow and wide QRS complex. Medical treatment was ineffective. Holter monitoring showed 21% burden of premature beats over 2 days. Transthoracic echocardiogram (TTE) showed ejection fraction (EF) 45% with dilated LV dimension. MRI confirmed a structurally normal heart. Decision-making The patient was diagnosed with arrhythmia-induced cardiomyopathy, so he was referred for electrophysiological study. There was A-V activation pattern confirming atrial origin of all of the premature beats. Intermittent bundle branch block during conduction of the beats with the shortest A-V time caused wide QRS complex. With 3D CARTO mapping system, activation mapping of the right atrium and direct mapping of tricuspid annulus, we were able to reach the origin site of the PACs and apply ablation lesions there. After a month, TTE showed EF 56% with normal LV dimensions. Symptoms resolved and there was no evidence of PACs. Conclusion follow up of patients with frequent PACs is very important for early detection of induced cardiomyopathy. Catheter ablation in these cases leads to excellent results. [Formula presented]Copyright © 2023 American College of Cardiology Foundation
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Ventricular tachycardia (VT) is a type of broad complex tachycardia originating from a focus in the ventricle. It is one of the four important rhythms which can lead to cardiac arrest. Accurate and timely diagnosis of true VT is the cornerstone for proper management in the emergency department (ED). We present an interesting case of an electrocardiographic artifact mimicking VT, which led to a diagnostic dilemma in the ED.Copyright © 2023 Rehman, Albaroudi, Akram, Ahmad, licensee HBKU Press.
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Aim. To carry out comparative analysis of echocardiographic and electrocardiographic (ECG) data of survivors and deceased patients with COVID-19 (sub-analysis of the international register “Dynamics analysis of comorbidities in SARS-CoV-2 survivors”). Material and methods. The study presents the results of a sub-analysis of the international AKTIV registry, which was called AKTIV CARDIO. Data were collected from 9 medical centers in the Russian Federation. AKTIV CARDIO included 973 hospitalized patients, of which 50 patients died during hospitalization. Results. Comparative analysis of echocardiographic parameters revealed that 4 parameters differed in deceased patients compared to survivors: left ventricular ejection fraction (LVEF), right ventricular end diastolic dimension (RV EDD), right atrial (RA) short axis diameter and pulmonary artery systolic pressure (PASP). RA short axis diameter was higher in deceased patients compared with survivors (38,0 [36,0;39,0] versus 35,0 [33,0;38,0] mm, p=0,011). RV EDD was higher in deceased patients than in survivors (3,0 [29,0;33,0] vs 28,0 [27,0;32,0] mm, p=0,019). LVEF was lower in deceased patients compared with survivors (55 [52;55] vs 60 [56;65]%, p<0,001). PASP was higher in deceased patients compared with survivors (25 [21;35] vs 20 [19;25] mm Hg, p=0,006). Correlation analysis found that the largest number of correlations with markers of the infection severity was observed for RA short axis diameter and RV EDD. A comparative analysis of ECG data revealed that in deceased patients, compared with survivors, atrial fibrillation (AF) (21,4% vs 6,06%, p=0,001) and supraventricular premature beats (14,3% vs 3,36%, р=0,004) occurred more often. In addition, deceased patients had longer QTc interval (440 [416;450] vs 400 [380;430] ms, p<0,001). Conclusion. Comparative analysis of echocardiographic data showed that deceased patients have more pronounced right heart remodeling, higher PASP and lower LVEF. Patient survival was related to RV and RA sizes. Right heart enlargement was associated with markers of infection severity. Echocardiographic parameters characterizing the right heart side can probably be independent prognostic factors in the acute COVID-19 period.
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INTRODUCTION The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause multiple cardiologic complications such as myocardial injury, cardiogenic shock and arrhythmias. In patients admitted to an intensive care unit (ICU), sinus tachycardia and atrial fibrillation are the most commonly reported arrhythmias. However, data on the prevalence of arrhythmias after symptomatic SARS-CoV-2 infection is limited. Using 48-hour electrocardiographic (ECG) Holter monitoring, we aimed to analyse the incidence and types of arrhythmias among healthcare workers who recovered from SARS-COV-2 infection. MATERIAL AND METHODS The study involved 34 healthcare workers from the university hospital, who had SARS-CoV-2 infection confirmed by pharyngeal swab up to 4 months before study onset and who did not need an ICU stay due to the illness. Each subject underwent a 48-hour ECG monitoring and completed a questionnaire on the course of the disease. Cardiac magnetic resonance imaging (CMR) was performed and the presence of potential arrhythmias substrate was assessed. RESULTS We recruited 24 women and 10 men (47% were doctors) in the mean age of 37 ± 11 years old who underwent symptomatic SARS-CoV-2 infection, but did not require hospitalization during illness. The mean time from the positive swab test to the start of 48-hour ECG monitoring was 2.9 ± 0.9 months. The most frequently reported (in 100%), though sparse, were supraventricular premature contractions (SVPCs) (mean 46 ± 64 per person/day). Atrial fibrillation or atrial flutter were not recorded, however supraventricular tachycardia (SVT) was found in 18% of subjects, and the range of the highest frequency of SVTs was 124-179 bpm. There were no ventricular tachycardia episodes. Ventricular premature contractions (VPCs) were found in 28% of participants but were usually sparse (mean number per person 98 ± 252/day). Six participants had more than 100 VPCs/day, and in 1 it exceeded 1000/day. No one had QTc interval longer than 438 ms. 48-hour ECG monitoring revealed a tendency towards sinus tachycardia during activity time, however, the daily rhythm modulation was diminished in only 15% of participants. Significantly higher maximal daily heart rate (P <0.05) was observed in 29% of subjects in whom CMR revealed the presence of late gadolinium enhancement (LGE). The presence of LGE or extended T1 and T2 relaxation times from CMR were not predictors of the increased number of VPCs or SVPCs (P >0.05). No significant atrioventricular conduction disturbances were recorded. CONCLUSIONS The prevalence of arrhythmias in the mid-term observation of not-hospitalized COVID-19 survivors is low. During prolonged 48-hour ECG monitoring of healthcare workers, neither life-threatening nor clinically significant arrhythmias were recorded. Therefore, the arrhythmic burden after infection with SARS-CoV-2 should be considered as marginal.
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Purpose: To study clinical features of myocarditis and its possible mechanisms (including persistence of SARS-Cov-2 in the myocardium) in the long-term period after acute COVID-19. Methods: Fifteen patients (8 male and 7 female, mean age 47.8±13.4, 24-65 years) diagnosed with postcovid myocarditis were included in the study. The diagnosis of COVID-19 was confirmed by positive PCR results in 40%, and seroconversion in all patients. The average time of admission after COVID-19 was 4 [3;7] months, from 2 to 9 months. The diagnosis of myocarditis was confirmed by cardiac MRI in 10 patients and by right ventricular endomyocardial biopsy (EMB) in 6 patients. The PCR for cardiotropic viruses and PCR with immunohistochemical study for SARSCov2 detection were used. All patients had study for anti-heart antibodies (AHA), EchoCG, and Holter ECG. Coronary atherosclerosis was excluded in all patients over 40 years (7 coronary angiography, 4 cardiac CT). Results: A clear association of the cardiac symptoms with a previous new coronavirus infection was noted in all patients. The symptoms started 1-5 months following COVID-19. MRI showed subepicardial and intramyocardial LGE, signs of hyperemia, increased T1 relaxation time, edema. AHA levels were increased 3-4-fold in 73%. Two variants of postcovid myocarditis were observed. 1. Arrhythmic variant (n=6) - newly developed frequent supraventricular or ventricular extrasystole, recurrent atrial fibrillation in the absence of systolic dysfunction. 2. Decompensated variant with biventricular heart failure (n=9): the mean LV EF was 34.1±7.8% (23 to 46%), LV EDD 5.8±0.7 cm, EDV 153.8±46.1 ml, pulmonary artery systolic pressure 40.7±11.2 mmHg. In one case, myocarditis was accompanied by IgG4- and ANCA-negative aortitis. SARS-Cov-2 RNA was detected in 4 of 5 myocardial biopsies (in one case the material in the study). The longest period of virus persistence after COVID-19 was 9 months. By using spike and nucleocapsid antibodies, coronavirus was detected in cardiomycytes and macrophages. Data of patients with morphologically proved myocarditis are presented in Table 1. Lymphocytic myocarditis was diagnosed and confirmed immunohistochemically (n=5);giant cell myocarditis with atrial standstill was detected in one more case (Fig. 1). Three patients had also signs of endocarditis, in two cases with parietal thrombosis. Conclusions: COVID-19 can lead to the subacute and chronic myocarditis of varying severity. Post-COVID myocarditis manifests itself in two main clinical forms - isolated arrhythmias and systolic dysfunction with heart failure. Post-COVID myocarditis is characterized by prolonged persistence of coronavirus (up to 9 months in this study, in most patients with decompensated variant) in combination with high immune activity (high titers of AHA), which should be considered as the main mechanisms of its longterm course. Treatment approaches for such myocarditis require investigation. (Figure Presented).