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Background: The infection caused by the SARS-CoV-2 continues affecting millions of people worldwide and vaccines to prevent the coronavirus disease (COVID-19) are considered the most promising approach for curbing the pandemic. Otherwise, cardiovascular and neurological complications associated with the vaccines were speculated and some few case reports were published. Objective(s): We describe a case of postural orthostatic tachycardia syndrome (POTS) after viral vector COVID-19 vaccination and the possible autoimmune process of the syndrome. Method(s): A 35-year-old female, without previous symptoms or comorbidities, developed intermittent palpitation, intense fatigue and dyspnea, compromising her daily activities, triggered by upright position, seven days following the second dose of the Oxford vaccine. Physical examination was normal, except for a heart rate (HR) increase of 33 beats/min from supine to standing position, with no significant change in blood pressure and reproduction of symptoms. Result(s): A 24-hour Holter monitoring revealed episodes of spontaneous sinus tachycardia correlated with palpitation and fatigue. Extensive diagnostic investigations excluded primary cardiac, endocrine, infectious and rheumatologic etiologies. The patient underwent an autonomic function test which demonstrated normal baroreflex sensitivity, as well as normal cardiovagal and adrenergic scores. Head-up tilt test showed persistent orthostatic tachycardia (HR increase from a medium of 84 beats/min in supine position to 126 beats/min during upright tilt), without hypotension, consistent with the diagnostic criteria for POTS. According to the current guidelines, general behavior recommendations, pharmacotherapy with low dose of propranolol associated with the autonomic rehabilitation were oriented. Along three months of follow-up, the patient reported a gradually improvement in her symptoms. Conclusion(s): POTS is a heterogeneous disorder of the autonomic nervous system characterized by orthostatic tachycardia associated with symptoms of orthostatic intolerance. Although the physiopathology of COVID-19 vaccine and autonomic disorders remains speculative, autoimmune response is one of the possible mechanisms. Based on clinic presentation, the time frame of symptom onset is consistent with other well-known post-vaccination syndromes, which may be an indicator of an autoimmune process induced by immunization. Further studies are needed to assess causal relationship between immunization and autonomic dysfunction.Copyright © 2023
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Methods: Out-hospital clinic patients (pts) recovered from COVID-19 were prospectively recruited and underwent cardiac magnetic resonance (CMR) examination with a protocol including: Edema, hyperemia, and necrosis or scar-derived from signal intensity assessment in T2-weighted, early gadolinium enhancement (EGE) and late gadolinium enhancement (LGE) CMR images. Result(s): A total of 702 patients (mean age 50+/-12 years, 62% female) were included. The median (IQR) time interval between COVID-19 diagnosis and CMR was 13 (8-22) weeks. In none pts signs of edema, hyperemia and necrosis derived from signal intensity assessment in T2-weighted and early gadolinium enhancement was found. LGE was found in 152 (22%). LGE+ patients had significantly lower left ventricular (LV) ejection fraction (58.5+/-7.7 vs 61.1+/-7.9%, p<0.001) and greater LV end-diastolic (117.0+/-52.2 vs 103,0+/-36.3 ml, p=0.023) and end-systolic (50.3+/-28.0 vs 41.0+/-17.5 ml, p=0.010) volumes when compared with LGE- patients. In the resting electrocardiogram (ECG) fragmented QRS was observed significantly more frequently (46% vs 25%, p<0.001) in LGE+ group, whereas in 24h Holter ECG neither single premature, nor complex ventricular extrasystole burden did not differ between groups (p>0.05). There were observed no differences between symptoms of COVD-19 and comorbidities between LGE+ and LGE- pts. In the multivariable logistic regression analysis: Fragmented QRS [OR and 95% CI: 2.85 (1.93-4.21)] and any ST-T segment deviation in resting ECG [OR: 1.93 (1.15-3.25)] were identified as independent predictors of LGE, even after adjustment for comorbidities and COVID-19 symptoms. Conclusion(s): 1. In patients with fibrosis after COVID-19 reduced left ventricular ejection fraction and greater volume of the heart was found. 2. Fragmented QRS and ST-T abnormalities were independent predictors for LGE in patients after COVID-19.
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Background: The COVID-19 disease is known for its severe respiratory complications, however it was found to have some cardiovascular complication in post COVID-19 patients. The heart rate variability (HRV) is a non invasive, objective and reliable method for assessment of autonomic dysfunction in those recovered patients. Purpose(s): We aimed to evaluate the cardiac autonomic function by using valid HRV indices in subjects who recovered from mild to moderate acute COVID-19 but still symptomatic. Method(s): The study Group composed of 50 subjects with confirmed history of mild to moderate post COVID 19. All subjects underwent routine 2D echocardiography assessment in addition to 2D speckle tracking and 24 hours Holter monitoring for HRV analysis. Result(s): The mean age of the study population was 42+/-18 years, symptoms were reported as follows 27 (54%) had Dyspnea, 17 (34%) had palpitations, 7 (14%) had dizziness. Time domain parameters SDNN, SDANN and rMSSD were diminished with mean SDNN value being markedly impaired in 12 (24%) patient, while frequency domain parameters as assessed by LF/HF ratio with mean of 1.837 with 8% of patients being impaired. SDNN was significantly reduced in elderly patients (p=0.001), smokers (p=0.019) and hypertensive (p=0.016) and those complaining mainly of palpitation (p=0.006). SDNN was significantly reduced in patient with impaired LV diastolic function (p=0.009), in patients with reduced MAPSE (p=0.047), reduced TAPSE (p=0.00) and impaired Global longitudinal strain (0.000). Conclusion(s): Patients with post COVID-19 syndrome have abnormalities in the HRV which indicates some degree of dysfunction in the autonomic nervous system and consequently impaired parasympathetic function in this population, however this have been also correlating with subtle impairment of the left ventricular systolic function.We believe that this preliminary research can serve a starting point for future research in this direction.
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Introduction: Pheochromocytoma is a rare neuroendocrine tumor that originates from the adrenal medulla, less commonly from extraadrenal chromaffin cells (paraganglioma). In about 90% of cases, the tumor produces abnormal amounts of catecholamines. Pheochromocytomas are usually benign, but in rare cases can be malignant. Typical clinical manifestations are the result of the haemodynamic and metabolic effects of catecholamines and usually include paroxysmal hypertension with the classic triad (headache, excessive sweating, palpitations), carbohydrate disorders, etc. Elevated levels of catecholamine metabolites (metanephrine and normetanephrine) tested in plasma or in 24-hour urine confirm the diagnosis. Surgical removal of the tumor is the only radical treatment. Follow-up of patients postoperatively should be lifelong and performed by a multidisciplinary team in a specialized center of expertise. Case report: A 36-year-old female patient referred to the clinic for decompensated diabetes mellitus. Detailed history revealed paroxysmal hypertension and the classic triad of pheochromocytoma. The diagnosis was confirmed by high urinary metanephrine levels and an abdominal CT scan, showing a tumor in the right adrenal gland with features typical of pheochromocytoma. Surgical removal of the pheochromocytoma and normalization of catecholamine levels led to normalization of blood pressure and reversal of diabetes mellitus. Conclusion(s): Pheochromocytoma is a difficult diagnosis in endocrinology practice as it can mimic many other diseases. Early detection and surgical removal of the tumor are crucial to avoid complications caused by elevated serum catecholamine levels.Copyright © 2022 Medical Information Center. All rights reserved.
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Background: Coronavirus disease 2019 (COVLD-19), the global pandemic that has spread throughout the world, is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Given the limited scientific evidence on the manifestations and potential impact of this virus on pregnancy, we decided to report this case. Case presentation: The patient was a 38 year-old Iranian woman with a triplet pregnancy and a history of primary infertility, as well as hypothyroidism and gestational diabetes. She was hospitalized at 29 weeks and 2 days gestational age due to elevated liver enzymes, and finally, based on a probable diagnosis of gestational cholestasis, she was treated with ursodeoxycholic acid. On the first day of hospitalization, sonography was performed, which showed that biophysical scores and amniotic fluid were normal in all three fetuses, with normal Doppler findings in two fetuses and increased umbilical artery resistance (pulsatility index [PI] > 95%) in one fetus. On day 4 of hospitalization, she developed fever, cough and myalgia, and her COVID-19 test was positive. Despite mild maternal symptoms, exacerbated placental insufficiency occurred in two of the fetuses leading to the rapid development of absent umbilical artery end-diastolic flow. Finally, 6 days later, the patient underwent cesarean section due to rapid exacerbation of placental insufficiency and declining biophysical score in two of the fetuses. Nasopharyngeal swab COVID-19 tests were negative for the first and third babies and positive for the second baby. The first and third babies died 3 and 13 days after birth, respectively, due to collapsed white lung and sepsis. The second baby was discharged in good general condition. The mother was discharged 3 days after cesarean section. She had no fever at the time of discharge and was also in good general condition. Conclusion(s): This was a complicated triplet pregnancy, in which, after maternal infection with COVID-19, despite mild maternal symptoms, exacerbated placental insufficiency occurred in two of the fetuses, and the third fetus had a positive COVID-19 test after birth. Therefore, in cases of pregnancy with COVID-19 infection, in addition to managing the mother, it seems that physicians would be wise to also give special attention to the possibility of acute placental insufficiency and subsequent fetal hypoxia, and also the probability of vertical transmission.Copyright © 2022 Goldstein and Associates. All rights reserved.
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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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Background and Aim: Cardiac involvement is seen in the majority of cases with multisystem inflammatory syndrome in children (MIS-C). Various rhythm and conduction disturbances, as well as repolarization abnormalities, have been described by more than 50% of the patients, while there are few cases with complete heart block or with asystole. Method(s): Case report Results: 8-year old girl presented with a 5-day history of fever, cough, headache, and abdominal pain. Because of the critical con-dition, with respiratory insufficiency and heart failure symptoms, the child was intubated and started on inotropic support. ECG showed complete AV-block with a ventricular rate of 75/min and with ST-T changes;echocardiography revealed dilated left ventricle with reduced contractility, CT-scan of the lungs showed bilateral pneumonia, the inflammatory markers were elevated, in combination with high troponin levels, and positive SARS-CoV2-IgG antibodies. The diagnosis MIS-C was made and treatment with immunoglobulins, antibiotics, corticosteroids, and anticoagulants was initiated. During the next 2 days, the cardiac function deteriorated further, and while still on mechanical ventilation and inotropic support, extreme bradycardia with a ventricular rate of 35/min was regis-tered, and the patient was indicated for temporary emergency pac-ing. Upon induction of anesthesia, the child became asystolic, requiring extensive resuscitation. After circulation recovery, the ECG showed nodal tachycardia with a heart rate of 140-170/min. A temporary transvenous pacemaker (PM) was inserted, and the patient was started on intravenous amiodarone which resulted in a slower ventricular rate of 70/min. 3 days later sinus rhythm was restored, with first-degree AV-block, which allowed removal of the PM 5 days after its insertion. Left ventricular dimensions were normalized and contractility remained low-normal (EF 56%). During the 6-month follow-up, the ECG and the Holter-monitoring showed sinus rhythm with first-degree AV-block. Magnetic resonance imaging (MRI) on day 15 of the hospital stay demonstrated scattered areas of myocarditis and ischemia predominantly in the left ventricle, as well as thickening of the basal septum. Six months later the MRI changes were reduced but still persistent. Conclusion(s): MIS-C can present with serious and life-threatening rhythm and conduction disturbances in children;this is why extensive cardiac monitoring is obligatory by all patients.
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Background and Aim: The European Medicines Agency has approved mRNA vaccines developed by Pfizer/BioNTech and Moderna for the vaccination of adolescents against the SARS-CoV-2 infection. Cases of myocarditis and pericarditis have been described as rare postvaccination complications. We describe the Latvian experience with adolescents suffering from myocarditis following COVID-19 vaccination. Method(s): From June to December 2021 four cases consistent with postvaccination myocarditis were admitted to the Children's Clinical University Hospital, which is the only centre with special-ized paediatric cardiology care in Latvia. The Pfizer/BioNTech vaccine had been used in all. An ECG, Holter monitoring and ECHO was done, HS Troponin I levels checked, the most common infectious causes of myocarditis were excluded, and a cardiac MRI was performed in all cases. Result(s): Case 1: 12-year-old girl, developed chest pain on postvac-cination day Nr 4 (PVD4) after the 1st dose. Holter monitoring revealed rare non-sustained ventricular tachycardia (NSVT), ECHO showed moderate mitral insufficiency, and a hyperecho-genic papillary muscle, troponin level peaked at 5339 pg/ml (PVD6), MRI (PVD 7) showed widespread myocardial oedema, transmural fibrosis. Symptoms resolved in 1 day, metoprolol suc-cinate and lisinopril were prescribed. Mitral insufficiency persists 5 months later. Case 2: 15-year-old boy, developed chest pain after the 2nd dose on PVD2 and lasted for 7 days, he was admitted on PVD11 with a peak troponin level of 19pg/ml. MRI (PVD15) showed widespread myocardial oedema. Metoprolol succinate was prescribed. Case 3: 15-year-old boy, developed chest pains on the day of the 1st dose and persisted for 35 days, he was admitted on PVD24 with peak troponin level 15ng/ml. MRI (PVD29) showed mild myocardial oedema, myocardial and pericardial fib-rosis. Case 4: 13-year-old boy, developed chest pain on PVD2, which lasted for 65 days, he had an episode of syncope. Holter monitoring showed frequent PVCs, and NSVT, on PVD34 tro-ponin level was 2,5pg/ml. The child received a course of NSAIDs and was referred to us on PVD68. MRI (PVD69) revealed wide-spread myocardial oedema, fibrosis, and pericarditis. Methylprednisolone was given, and betaxolol was prescribed. Conclusion(s): Our case series show that some cases of postvaccination myocarditis develop complications requiring long-term treatment.
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Ischaemic strokes secondary to atrial fibrillation (AF) have a high morbidity and mortality thus, detection of AF post stroke is crucial for secondary prevention. Cardiology services were already struggling to provide timely Holter monitoring and the COVID-19 pandemic resulted in further delays. We collaborated with an external company to deliver adhesive ambulatory electrocardiographic monitors (AECG) to patient's homes which ensured compliance with infection control measures to reduce investigation wait times. We conducted a retrospective study looking at AF detection rates when changing from a traditional 24-hour Holter monitor to a 7-day AECG which was delivered and collected from patients' homes during the pandemic. 78 patients were included in this study. 37 patients had a 24-hour Holter monitor applied and removed by a health care professional in an outpatient setting. 41 patients had a 7-day AECG posted to their home where it was self-administered, removed and collected by a courier. AF was detected in a total of 7 patients. 1 out of 37 (1.2%) patients were found to have AF in the 24-hour Holter monitor group. 6 out of 41 patients (7.7%) were found to have AF when using AECG monitors. We conclude that 7-day AECG monitoring is more effective at detecting AF than 24-hour Holter monitoring. The model of a self-administered monitoring device with a longer observation period helps to reduce wait times for ambulatory monitoring whilst improve the detection rate of AF when used during the COVID-19 pandemic and may be beneficial for use in the future.
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Introduction: The connection of a number of inherited arrhythmias with febrile body temperature is proved. Due to connection between fever and clinical manifestations (including ECG changes) of inherited arrhythmias there are additional opportunities for diagnostics of these life-threatening arrhythmias in infectious patients (including Covid -19). Methods: 3584 ECGs of children with infectious diseases (average age 8.5±5.3 years old;boys - 57.5%, girls - 42.5%) were analyzed. Patients (pts) with QTc>440 ms or QTc<320 ms, complete right bundle branch block, left bundle branch block or its branches, atrioventricular block, ST elevation in the right precordial leads were given additional examination depending on the intended diagnosis (inherited arrhythmias): daily 12-channel Holter ECG monitoring, stress test, echocardiography. The family history was also clarified (cases of sudden cardiac death, syncope). The diagnosis was made on the basis of generally accepted diagnostic criteria and confirmed by molecular genetic analysis. Results: ECG changes, which are typical for Brugada syndrome (BrS), type 1, were detected in 2 pts (0.05%). Long QT syndrome (LQTS) was detected in 2 pts too. Mutations in the SCN5A gene (exon 16 Arg893Cys, R878H) were identified in pts with BrS and in the KCNQ1 (exon 9 Trp379Ter) with LQTS. In pts with LQTS, sinus tachycardia was registered with the background of increased body temperature, which allowed to reveal long QT interval. 1 pt with LQTS is a female athlete. 1pt with BrS had been previously observed by a cardiologist in connection with grade I atrioventricular block. An increase in body temperature leads to disruption of the sodium ion channels which underlie the development of the BrS. In the case of LQTS, in our study, the increase in the QTc is most likely due to a change in heart rate rather than a direct effect of an increase in body temperature on the ion channels. Conclusions: 1. BrS (type 1) was detected in 2 pts (0.05%) and LQTS in 2 pts (0.05%) at first. We consider that when taking an ECG from pts with fibril body temperature, this percentage may be higher. 2. ECG registration in pts with fever (including athletes) raises the probability of timely inherited arrhythmias diagnosis.
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Background: In young adults and adolescent males, myocarditis has been described as a rare complication of SARS-CoV-2 mRNA-vaccination. Reported findings include chest pain, elevated troponin levels, and cardiac MRI abnormalities. ECG abnormalities include ST-elevation but to our knowledge, ventricular arrhythmia has not been yet described. In the vast majority of reported cases, symptoms were relatively mild and patients recovered fully. Method: Here, we report two male adolescents (15 resp. 13 years old) admitted to our hospital with nonsustained (ns) VT and chest pain (patient no. 1) and near syncope (patient no. 2) after receiving an mRNA-SARS-CoV-2 vaccine (patient no. 1: 4 days after the second dose and patient no. 2: 15 days after days after the first dose). Further workup included family history, standard 12 lead ECG, the Holter monitoring, heart catheterization, myocardial biopsy, invasive programmed RV stimulation, and cardiac MRI. Results: Both patients did not have elevated troponin levels nor specific ECG findings. Family history was free for cardiac diseases, sudden cardiac death, or syncopal episodes. The Holter monitoring showed recurrent ns VT in one patient. Cardiac MRI and myocardial biopsy in both patients did not show evidence of myocarditis, but both patients showed severe thickening of the arterioles in myocardial biopsy. Invasive RV-stimulation did not trigger VT. Ultimately, both patients did not meet diagnostic criteria for myocarditis and β-blockers were started for ns VT. As of today, four more patients in age group 12 to 17 years were diagnosed with vaccine-associated myocarditis in our institution and one male with COVID-19 associated myocarditis. Notably, none of these patients had ventricular tachycardia or other cardiac arrhythmia. Conclusion: We observed ventricular tachycardia after SARS-CoV-2-mRNA vaccination in two adolescent males. This manifestation seems to be distinct from the well-described vaccine-associated myocarditis. Interestingly in both patients, perivascular thickening of arterioles was noted in biopsy. The mechanism and causality of ventricular arrhythmia in association with SARS-CoV-2 mRNA vaccines remain unclear and requires further observation.
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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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During the pandemic, several studies were carried out on the short-term effects of acute SARS-CoV-2 infection in athletes. As some cases of young athletes with serious complications like myocarditis or thromboembolism and even sudden death were reported, strict recommendations for return to sport were published. However, we have less data about athletes who have already returned to high-intensity trainings after a SARS-CoV-2 infection. Athletes underwent cardiology screening (personal history, physical examination, 12-lead resting ECG, laboratory tests with necroenzyme levels and echocardiography) 2 to 3 weeks after suffering a SARS-CoV-2 infection. In case of negative results, they were advised to start low intensity trainings and increase training intensity regularly until achieving maximal intensity a minimum of 3 weeks later. A second step of cardiology screening was also carried out after returning to maximal intensity trainings. The above mentioned screening protocol was repeated and was completed with vita maxima cardiopulmonary exercise testing (CPET) on running treadmill. If the previous examinations indicated, 24h Holter ECG recording, 24h ambulatory blood pressure monitoring or cardiac MR imaging were also carried out. Data are presented as mean±SD. Two-step screening after SARS-CoV-2 infection was carried out in 111 athletes (male:74, age:22.4±7.4y, elite athlete:90%, training hours:14.8±5.8 h/w, ice hockey players:31.5%, water polo players:22.5%, wrestlers:18.9%, basketball players:18.0%). Second screenings were carried out 94.5±31.5 days after the first symptoms of the infection. A 5% of the athletes was still complaining of tiredness and decreased exercise capacity. Resting heart rate was 70.3±13.0 b.p.m., During CPET examinations, athletes achieved a maximal heart rate of 187.3±11.6 b.p.m., maximal relative aerobic capacity of 49.2±5.5 ml/kg/min, and maximal ventilation of 138.6±31.2 l/min. The athletes reached their anaerobic threshold at 87.8±6.3% of their maximal aerobic capacity, with a heart rate of 93.3±3.7% of their maximal values. Heart rate recovery was 29.9±9.2/min. During the CPET examinations, short supraventricular runs, repetititve ventricular premature beats + ventricular quadrigeminy and inferior ST depression were found in 1-1 cases. Slightly higher pulmonary pressure was measured on the echocardiography in 4 cases. Hypertension requiring drug treatment was found in 5.4% of the cases. Laboratory examinations revealed decreased vitamin D3 levels in 26 cases, decreased iron storage levels in 18 athletes. No SARS-CoV-2 infection related CMR changes were revealed in our athlete population. Three months after SARS-CoV-2 infection, most of the athletes examined had satisfactory fitness levels. However, some cases of decreased exercise capacity, decreased vitamin D3 or iron storage levels, arrhythmias, hypertension and elevated pulmonary pressure requiring further examinations, treatment or follow-up were revealed.
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Background: COVID-19 was first considered a pandemic on the 11th of March of 2020 by the World Health Organization. Its impact comprised not only the direct consequences of the disease but a decrease in the follow-up and interventions of patients with cardiovascular (CV) disease. In Portugal and the World, the consequences of this complex paradigm shift on emergent pacemaker implantation rates during and after this pandemic is largely unknown. Purpose: We sought to analyse the impact of COVID-19 pandemic on emergent pacemaker implantation rate and patient profile in a tertiary hospital during the first Portuguese lockdown and subsequent post-lockdown period. Methods: We retrospectively reviewed the clinical profile of patients who had pacemakers implanted in our hospital in an urgent/emergent setting from March 18, 2020 to May 17, 2020 (lockdown) and May 19 to July 17, 2020 (post-lockdown). This data was then directly compared to the homologous periods from the year before (H1 and H2, respectively). Results: A total of 180 patients submitted to emergent pacemaker implantation were included. The cohort was comprised of 29 patients who had a pacemaker implanted during lockdown, 60 post-lockdown, 38 in H1 (+31% vs lockdown) and 53 in H2. Average age and gender proportion were similar for all groups. When comparing lockdown and post-lockdown periods, the number of cases significantly increased in the second period (+106.9%) and there was a tendency for a higher number of temporary pacemaker use (3.4% vs 16.7%;p=0.076). Patients admitted during lockdown were 7.57 times more likely to present with hypotension/shock (odds ratio (OR) 7.57;p=0.013). Regarding lockdown and its homologous 2019 period, there was a decrease in the number of patients admitted (-23.7%). Again, there was a higher tendency for hypotension on presentation during lockdown (p=0.054). In comparison to its homologous 2019 period, post-lockdown saw a slight increase in the number of patients (+13.2%) and more patients presented with bradycardia (16.7% vs 3.8%;p=0.026). Also of note, no patients were admitted to the emergency department during lockdown for anomalies detected on ambulatory tests (Holter, electrocardiogram or implanted loop recorder). Conclusion: During lockdown, clinical presentation was generally more severe, with a greater number of patients presenting with hypotension/ shock. In addition, there appears to be a lockdown effect on emergent bradyarrhtmias admissions in the post-lockdown period with a profound impact: higher admission rates and more severe presentations including a higher need of temporary pacemaker. Patients with symptoms suggestive of bradyarrhythmias should be advised to present promptly regardless of the pandemic. (Figure Presented).
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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).