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Intro: The spike protein of the SARS-CoV-2 virus targets the human cell receptor of angiotensin-converting enzyme (ACE2), including the myocardium and heart's conduction system. Patients diagnosed with COVID-19 have also been found to exhibit cardiac arrhythmia. Here, a whole-genome sequencing analysis using long-read sequencing was proposed to evaluate the virus genome in a patient who presented with AVNRT as a main presentation of COVID-19. Method(s): The sample was recovered from nasopharyngeal and oropharyngeal swab specimens of a 46-year-old female with no comorbidities who presented with palpitation, and ECG showed typical AVNRT features. The RT-qPCR of SARS- CoV-2 was confirmed positive with a CT-value of 15.82. The total RNAs were extracted and proceeded for RT-qPCR and proceeded with Oxford Nanopore Flongle sequencing. The genomics data of the virus was deposited in GISAID (EPI_ISL_3241561) and further analysed using online bioinformatics tools such as Nextclade CLI 2.3.0. Ethical approval (IREC 2021-080) for the study was obtained from IIUM Research Ethics Committee. Finding(s): Here, we reported a total of 29,775 bp near-complete whole-genome belonging to clade 21J (Delta) of AY.79 lineage (also known as B.1.617.2.79), which formed a dominant variant in Malaysia during the time of sampling. Discussion(s): While a previous study showed an association between Delta variant infection with fulminant myocarditis, the present study reported the benign AVNRT as the main presentation of SARS-CoV-2 infection. Furthermore, we observed the presence of the C3037T mutation previously described in the endomyocardial biopsy of a patient with persistent arrhythmia. Conclusion(s): Even though SARS-CoV-2 targets the respiratory tract, the present study supports the evidence that the ACE2 receptors are present in the heart. In addition, COVID19 is causing more and more damage to heart tissue, and viral transcription has been confirmed on cardiomyocytes. Further functional studies are needed to explore the associated mutations and their relation to cardiac manifestation.Copyright © 2023
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Case Presentation: Term male infant born to SARS-CoV-2 positive mother with infant testing negative. ECG for perinatal bradycardia revealed ventricular pre-excitation. Echocardiogram showed asymmetric LV hypertrophy with prominent trabeculations, subaortic narrowing with no pressure gradient, and normal biventricular systolic function. Rapid increase in RV pressure estimates and NT-proBNP in first week if life concerning for diastolic dysfunction. Anti-arrhythmic therapy initiated for SVT with subsequent resolution. Later, developed progressive LV dilation and systolic dysfunction. Myocardium showed regions resembling non-compaction and others concerning for infiltrative process. Cardiac MRI showed no obvious tumors, but rhabdomyomas could not be ruled out given similar appearance to myocardium. Due to worsening heart failure, everolimus therapy initiated to target potential rhabdomyomas while awaiting genetic testing for tuberous sclerosis. Subaortic narrowing and LV hypertrophy improved within days, and LV appearance became more consistent with non-compaction. Genetic testing revealed a TSC2 gene variant consistent with tuberous sclerosis. Systolic function improved, and patient discharged on afterload reduction. Echocardiogram 6 months post-discharge shows continued LV dilation and mild systolic dysfunction. Discussion(s): Although outflow obstruction and arrhythmias are common with cardiac rhabdomyomas and can cause dysfunction, our patient developed progressive dysfunction in the absence of outflow tract gradient or prolonged arrhythmia. As rhabdomyomas subsided, it became clearer that he had an underlying cardiomyopathy. We suspect that rhabdomyomas in the setting of abnormal myocardium led to abnormalities in myocardial contractility and compliance causing combined systolic and diastolic dysfunction. After complete resolution of rhabdomyomas, cardiac function has improved. However, he continues to have ventricular dilation and mild dysfunction attributable to cardiomyopathy. It is unlikely that mother's SARS-CoV-2 infection played a role as infant tested negative and clinical picture was not consistent with myocarditis.
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COVID-19 is a highly transmissible disease with severe course especially in patients with nephrogenic hypertensive disease and chronic kidney disease due to a higher incidence of all-type infections than in the general population. The aim of the study is to describe a clinical case of SARS-CoV-2 infection complicated by nephrogenic pulmonary edema and COVID-associated pneumonitis, alveolitis. Description of the case. Patient K.S., born in 1975, was hospitalized 24 hours after symptom onset at emergency hospital due to complaints of increased blood pressure up to 180-200/110-120 mm Hg, temperature up to 38.7degreeC, dry cough, feeling of heaviness in the chest, change in urine color. PCR smear for SARS-CoV-2 was positive. Computed tomography revealed a pattern of bilateral COVID-associated pneumonitis, alveolitis, with 75% involvement. The electrocardiogram revealed signs of left ventricular myocardial hypertrophy. Ultrasound examination showed numerous cysts in the kidneys. Urinalysis at admission: leukocytes - 499, erythrocytes - 386. Glomerular filtration rate (CKD-EPI: 29 ml/min/1.73 m2) and corresponds to stage IV of chronic kidney disease. Coagulogram: fibrinogen: 32.3 (1.6-4.0) g/l, D-dimer: 663 (0-250). Despite the treatment, the patient's condition worsened, the phenomena of cardiopulmonary and renal insufficiency increased, which led to a fatal outcome. During a virological study of sectional material: SARS-CoV-2 coronavirus RNA was found in the lung and kidneys. Signs of bilateral COVID-associated pneumonitis, alveolitis with diffuse cellular infiltrates in combination with changes in the alveolar apparatus, signs of pulmonary edema were revealed. Heart-related signs - swelling of the interstitium, fragmented muscle fibers, some of them hypertrophied, a wave-like deformation of cardiomyocytes, blurring of the transverse striation. Arteries with thickened sclerosed walls. In the kidneys - diffuse damage to the proximal tubules of the nephron with areas of cortical and proximal necronephrosis, areas of fibrinoid swelling. Conclusion. The cause of death of a 45-year-old patient was a severe course of bilateral COVID-associated pneumonitis, alveolitis, which contributed to the development of renal medullary hypoxia and type 1 cardiorenal syndrome, which led to early nephrogenic pulmonary edema.Copyright © 2023 Saint Petersburg Pasteur Institute. All rights reserved.
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An association between SARS-CoV-2 infection and myopathy was suspected early in the pandemic: patients with severe COVID-19 showed increased levels of creatine kinase that could not be solely explained by cardiac affection. On the other hand, myalgia and muscle weakness are frequent symptoms in patients with mild or moderate COVID-19 - as with many other viral infections -and subsets of infected patients report persistent muscular weakness and fatigue even months after the initial infection. We performed a case-control autopsy comparing patients with severe COVID-19 to patients with other critical illnesses and assessed inflammation of skeletal muscle tissue by quantification of immune cell infiltrates, expression of major histocompatibility complex (MHC) class I and class II antigens on the sarcolemma. Relevant expression of MHC class I antigens on the sarcolemma was present in 23 of 42 specimens from patients with COVID-19 (55%) and upregulation of MHC class II antigens in 7 of 42 specimens from patients with COVID-19 (17%), but neither were found in any of the controls. In a subset of patients, MHC class I and MHC class II expression showed a clear perifascicular pattern. Signs of degenerating and necrotic fibers could also be found, however there was no statistically significant difference in the frequency of occurrence when compared to non-COVID-19 critically ill patients. We interpreted this as non-specific signs of muscular damage in critically ill patients. Numbers of macrophages, lymphocytes and natural killer cells were found to be increased in muscles from patients with COVID-19. Interestingly, no relevant expression of MxA on myofibers could be found by immunohistochemistry, but in some cases, expression of MxA was found on capillaries. Ultrastructural analysis of selected muscles with perifascicular MHC-expression did not show tubuloreticular inclusions. However, capillaries of the analyzed samples showed basement membrane alterations and signs of ongoing regenerative processes. In addition, we evaluated inflammation of cardiac muscles by quantification of immune cell infiltrates in the same patients, and found that skeletal muscles showed more inflammatory features than cardiac muscles. Moreover, inflammation was most pronounced in patients with COVID-19 with chronic courses. In some muscle specimens, SARS-CoV-2 RNA was detected by reverse transcription-polymerase chain reaction, but no evidence for a direct viral infection of myofibers was found by immunohistochemistry or electron microscopy. This suggests that SARS-CoV-2 may be associated with a postinfectious, immune-mediated myopathy.
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The data of the modern literature describing the long-term consequences of infection of the body with SARS-CoV-2 on the cardiovascular system in the framework of postcovid syndrome are analyzed. To date, postcovid syndrome refers to a condition in which symptoms continue to persist for more than 12 weeks from the moment of diagnosis of COVID-19. Various complaints of patients after undergoing a new coronavirus infection are described, the distinguishing feature of which is their versatility, where cardiovascular manifestations are assigned one of the leading roles. Postural orthostatic tachycardia syndrome, cardiac arrhythmia and conduction disorders are considered. The role of SARS-CoV-2 in the formation of de novo and decompensation of pre-existing cardiovascular diseases has been demonstrated. The possibility of developing heart failure in patients with COVID-19 as an outcome of inflammation of the heart muscle is shown. Particular attention is paid to the analysis of the incidence of myocarditis after 3 months or more from the diagnosis of COVID-19, as well as thrombotic complications, in the genesis of which the main role belongs to the formation of endothelial dysfunction resulting from the interaction of SARS-CoV-2 with vascular endothelial cells. The autoimmune component of the pathogenesis of damage to the cardiovascular system as a result of the formation of endothelial dysfunction in COVID-19 is also considered. The authors present a laboratory-instrumental algorithm for determining cardiovascular complications in people who have undergone COVID-19, including the determination of the N-terminal fragment of the brain natriuretic peptide B-type prohormone, the level of anticardial antibodies, electrocardiography, echocardiography, as well as magnetic resonance imaging of the heart with contrast.
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Introduction: Cardiac sarcoidosis (CS) classically manifests as a restrictive cardiomyopathy or conduction abnormalities, though the full scope of phenotypes may be underrecognized. We present an atypical case of mitral regurgitation (MR) and aortic regurgitation (AR) attributed to CS. Case Presentation: A 33-year-old woman with a history of hypertension, tobacco use, and COVID-19 infection two months prior presented with worsening dyspnea on exertion, orthopnea and lower extremity edema. Initial work up revealed elevated pro-BNP and troponin, and a CXR with pulmonary edema. A prior CTA showed mediastinal and hilar lymphadenopathy. Echocardiogram was notable for mildly dilated LV, severe hypokinesis of the basal inferior myocardium, LVEF 50-55%, moderate MR and moderate AR. cMR revealed multiple foci of predominantly mid-wall late gadolinium enhancement (LGE) in the LV, including a focus adjacent to the posteromedial papillary muscle (Fig. 1). Cardiac PET showed extensive patchy, focal hypermetabolic activity in the LV inferobasal, anterobasal and anterolateral walls. With high suspicion for CS, the patient opted for treatment with steroids and follow-up PET over extracardiac lymph node biopsy due to procedural risk. Discussion(s): Isolated CS is underdiagnosed and can present with a wide range of symptoms. Detection is limited by current diagnostic criteria, namely difficulty ascertaining affected tissue, which may limit recognition of the full range of presentations. Diagnosis and treatment vary widely among institutions but there is consensus on starting immunosuppression and pursuing follow-up cardiac PET for suppression of inflammatory activity in cases of high clinical suspicion. Our patient plans to undergo repeat PET and have ongoing discussion about lymph node biopsy. COVID-19 myocarditis remains on our differential, however given the patchy nature of LGE on cMR which correlated with the FDG uptake on PET, CS is considered the most probable diagnosis. Conclusion(s): CS should be considered in the differential diagnosis for young patients with structural valve abnormalities, even in the absence of arrhythmias or cardiomyopathy. High clinical suspicion may justify early immunosuppressive treatment to prevent irreversible myocardial injury and/or fatal arrhythmias. Whether this treatment will result in resolution of the structural defects remains to be seen and further investigated.Copyright © 2022
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Introduction: Atrial fibrillation (AF) is one of the most common forms of arrhythmia in the clinic. There are about 10 million AF patients in China, of which 1/3 are paroxysmal AF, and the remaining 2/3 are persistent or permanent AF. Long-term AF impairs cardiac function and leads to heart failure and thromboembolism. Moreover, AF increases the risk of mortality and ischemic stroke. Drug therapy and radiofrequency catheter ablation (RFCA) are still the mainstream treatment for AF patients. However, drug therapy has its drawbacks because of the high recurrence rate and side effects. Therefore, the current antiarrhythmic drugs could not meet all the clinical needs of patients with AF. RFCA is superior to antiarrhythmic drugs in maintaining sinus rhythm, improving symptoms and exercise tolerance, and improving quality of life. The role of RFCA in the treatment of persistent AF has gradually been recognized and affirmed. Although RFCA has been progressively used in the treatment of AF, there is still a high recurrence rate of AF after RFCA, especially in patients with persistent AF. Hence, it is meant to solve the high recurrence rate of AF after RFCA. Shensong Yangxin (SSYX) capsule has been proven to treat arrhythmia both in animal studies and clinical research. SSYX capsule could regulate multi-ion channels, improve cardiomyocyte metabolism and regulate autonomic nervous function. In addition, randomized, double-blind, multicenter clinical research indicated that the SSYX capsule exhibited good clinical efficacy in treating ventricular premature beats and paroxysmal AF. However, the effect of SSYX on recurrence after RFCA for patients with persistent AF remains unclear. High-level randomized controlled trials (RCTs) could offer clinicians high-quality evidence regarding the usage of SSYX capsule, especially in persistent AF patients who received RFCA. Hence, the RCTs aim to evaluate the effect of SSYX capsules on the prognosis in patients with persistent AF after RFCA through multicenter, double-blind RCTs. Method(s): This trial will be conducted with a total of 920 participants diagnosed with persistent AF who received RFCA. The participants will be randomized (1:1) into groups receiving either SSYX or Placebo for 1 year. The primary endpoint includes the recurrence of AF within 1 year after RFCA. The secondary outcome measures include changes of AF load at 3 months, 6 months, 9 months, and 1 year after treatment, the time of first atrial flutter/AF, the incidence of cardioversion 1 year after treatment, changes of transthoracic echocardiographic parameters 1 year after treatment, the incidence of stroke and thromboembolism at 6 months and 1 year after treatment, the score of SF-36 within 1 year after treatment. Application: The trial is ongoing. The trial started in September 2019 and recruiting patients. Data collection will be completed after all participants have completed the treatment course and follow-up assessments (expected in 2022, pending COVID-19). Next Steps/Future: The SS-ADJUST study is a randomized control study of TCM in persistent AF after RFCA. It will determine the place of SSYX capsule as a new treatment approach and provide additional and innovative information regarding TCM and the specific use of SSYX in persistent AF after RFCA.
ABSTRACT
Myocarditis is an important cardiovascular complication of COVID-19, a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has been observed that hospitalized patients with pre-existing cardiac disease are at higher risk for the development of this complication. It is predominantly male, with the most affected population being adults over 50 years of age and pediatrics;however, its incidence and prevalence are not completely known. This disease is caused by direct and indirect lesions caused by SARS-CoV-2 infection to the myocardiocyte and other cells. Clinical manifestations vary from mild, such as fatigue and dyspnea, to severe, such as cardiogenic shock. Tests for the detection of this pathology are laboratory, imaging and histological. In this article we briefly review SARS-CoV-2 myocarditis in epidemiology, pathophysiology, clinic, diagnosis, treatment, as well as vaccination myocarditis.Copyright © 2023 Sociedad Espanola de Cardiologia
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Background SARS-CoV-2 infection, the cause of COVID-19, has been associated with myocarditis. Fulminant myocarditis (FM) is rare. Case A 30-year-old male with a past medical history of SARS-CoV-2 infection 7 months prior, presented with a 2-week history of malaise, cough, dyspnea, and signs of cardiogenic shock. He was fully vaccinated 9 months prior. Respiratory viral PCR testing, including SARSCoV-2, was negative. HS-troponin was >20,000 ng/L (NR: 0-53 ng/L). An echocardiogram revealed a dilated cardiomyopathy with an EF of 15-20%. Cardiac catheterization revealed no CAD. Workup for an autoimmune etiology was unrevealing. His condition worsened and he required inotropic support, eventual placement of an LVAD, and initiation of ECMO. He was not able to tolerate cardiac MRI or endomyocardial biopsy. Ultimately, he underwent orthotopic heart transplantation. Pathologic examination of the explanted heart confirmed lymphocytic myocarditis. Decision-making Myocardial injury due to the cardiotropic nature of SARS CoV-2 has been increasingly reported. There has been a 42% increase in viral myocarditis, and the risk is 16 times greater with a history of COVID-19. Symptomatic myocarditis typically manifests within weeks of infection. Such a delayed presentation has not been described. Data from autopsies of deceased COVID-19 patients revealed a 25% to 50% detection rate of SARS-CoV-2 mRNA in the myocardium. One case report described a deceased FM patient with multiple negative SARS-CoV-2 PCR tests, including bronchial lavage samples, having confirmed SARS-CoV-2 within the myocardium postmortem. Hence SARS-Cov-2 can persist in the heart after the resolution of respiratory infection, possibly leading to ongoing inflammation and myocardial damage. This may explain why our patient presented 7 months after a resolved infection. Conclusion SARS-CoV-2 is cardiotropic and can cause fulminant myocarditis even in the absence of a detectable respiratory infection. Hence closer monitoring of post-COVID-19 patients, including screening for subclinical myocarditis, may be prudent. Further research on monitoring and an evaluation of the clinical utility of medical therapy, is also warranted.Copyright © 2023 American College of Cardiology Foundation
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The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected — asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki–Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. Сo-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome. © 2022 Saint Petersburg Pasteur Institute. All rights reserved.
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Background Left Ventricular Non-Compaction Cardiomyopathy (LVNC) is a rare genetic, developmental disorder when the left apical chamber of the heart contains bundles or pieces of muscle that extend into the chamber called trabeculations. These trabeculations are a sponge-like network of muscle fibers that typically become compacted to transform heart muscle to become smooth and solid during a normal development process. Those who have LVNC most commonly are asymptomatic. Those who are symptomatic present with syncope, palpitations, dizziness, dyspnea, fatigue and/or unexplained weight gain or swelling. LVNC has also been suggested as a rare cause of embolic stroke, in our patient's case, "due to sluggish blood flow in deep intertrabecular recesses." Case We present a 29 year old African American female, G2P0011, with a history of cleft palate repair, and recent pregnancy complicated by COVID-19 who reported to ED after having a fall the day before, leg weakness and numbness, unable to walk, headache and a left facial droop on day of admission. No family history of SCD or other cardiac disease was noted. On assessment, was found to have NIHSS of 7 with rate lateral gaze palsy, left facial palsy, and decreased strength and sensation of LUE and LLE. TPA was not given due to being outside the therapeutic window. CT head and MRI brain were consistent with acute right MCA stroke. Secondary stroke workup with TTE revealed reduced LVEF 15-20%, loosely arranged myocardium with suspected LVNC and RV apical thrombus. Cardiac MRI showed increased trabeculations consistent with LVNC. Decision-making Currently, there are no ACC/AHA guidelines on anticoagulation in the setting of LVNC. Cardiology and Neurology had an extensive multidisciplinary discussion on the need for anticoagulation specifically with Warfarin. The patient was educated extensively on the need for medical adherence with anticoagulation and guideline directed medical therapy. Conclusion The patient was started on guideline directed medical therapy for cardiomyopathy and was started on Warfarin after bridging from Lovenox. She continued with physical therapy and was noted to have improvement in residual deficits at her outpatient follow up.Copyright © 2023 American College of Cardiology Foundation
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Background Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is an extremely rare disorder. Case A 20-year-old, 36-week pregnant female (G1P0) presented with acute shortness of breath, sharp chest pain and fever. She was COVID-19 positive and required BiPAP. Echocardiogram showed 40% EF, dilated LV with global hypokinesis and moderate mitral regurgitation (MR). She was hypotensive and on oxygen despite diuresis, emergent cesarean and COVID-19 treatment. Left heart catheterization showed anomalous takeoff of the left main coronary artery (LCA) from the dilated pulmonary artery (PA) with coronary steal (Figure 1). She had ALCAPA repair with LIMA to LAD bypass grafting. Decision-making Differential diagnoses included peripartum cardiomyopathy, Covid-myocarditis, pulmonary embolism, and spontaneous coronary artery dissection. LHC was performed only when symptoms failed to improve and troponin kept rising. ALCAPA has two major clinical subtypes - Infantile type and adult type. Adult type presents as dyspnea, chest pain, reduced exercise ability, and sudden cardiac death. Despite having good RCA to LCA collaterals, adult patients can still have ongoing ischemia of the LV myocardium, causing ischemic MR, malignant ventricular dysrhythmias. Diagnosis was delayed due to pregnancy and COVID-19 infection. Conclusion ALCAPA is a lethal coronary disorder. Elevated troponin and dilated cardiomyopathy with acute MR should raise suspicion of ALCAPA in young adults. [Formula presented]Copyright © 2023 American College of Cardiology Foundation
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A good proportion of patients complain of cardiopulmonary symptoms even after COVID recovery. Post-COVID symptoms were reported most often as mild and self-limiting. On the other hand, severe post COVID cardiopulmonary complications had also been reported. Therefore, the status of extent and severity of underlying cardiopulmonary disease in this group of patients is very mysterious. Evaluation of underlying disease in such patients is extremely essential. Whereas evaluation is a tough challenge during this COVID pandemic due to the high epidemiological burden of symptomatic post COVID patients. Therefore a systemic review was conducted, collecting and compiling all the literature related to post COVID cardiopulmonary symptoms to understand their pathophysiology and severity of underlying disease. At the same time, an attempt was initiated to derive an approach and strategy for evaluation. During analysis, we obtained useful information as described below. Post COVID cardiopulmonary symptoms can arise due to causes like cardiac, pulmonary, psychogenic, neurogenic, and endocrine, etc. COVID manifests a spectrum of post COVID cardiopulmonary sequelae like myocarditis (2/3rd cases), pericarditis (3% cases), pericardial effusion (5% cases), LV dysfunction (12% cases), pulmonary fibrosis (20% cases), pulmonary function abnormalities (40% cases) etc., which can manifest cardiopulmonary symptoms in post COVID patients. However, the extent and severity of cardiopulmonary involvement is very limited. Reported abnormalities during cardiopulmonary evaluation were found to be mild and self-limiting. However, there is higher chance of developing life threatening complications like pulmonary embolism, acute coronary syndrome, left ventricular failure and arrhythmia in a few rare post COVID cases due to the persistence of hyper inflammatory and hypercoagulable states. Stratification of cases based on past history, records during acute COVID period, clinical findings and biomarkers, can guide in identifying high risk cases. A selective, systemic, and step wise clinical and laboratory approach can help in proper evaluation of patients. However, exclusion of other non COVID related causes is extremely essential, before designating symptoms as post COVID symptoms.
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Background: Most common cardio vascular disease events after COVID-19 were hypertension, pulmonary embolism, acute coronary syndrome, myocarditis, stress-Cardiomyopathy, arrhythmias, carcinogenic shock, and cardiac arrest. Aim: To evaluate cardio vascular disease events in patients recovered from COVID-19 in central Indian population Methods: This retrospective observational study was carried out in the department of medicine in a tertiary care hospital, central India. Asses all the participants for post covid cardio vascular events, detailed history, clinical examination and all necessary investigation was done Results: in our study Post COVID 19 cardio vascular events was occur in 17.6%. Majority of the patient was male (69.3%), most common age group were 51-60 years. Higher incidence of cardio vascular disease was reported in obese person. Common cardio vascular diseases found after COVID 19 infection were, hypertension (35.3%), pulmonary embolism (23.5%), Myocarditis (20.6%), myocardial infection (11.8%) and Arrhythmias were in 8.8% cases. Conclusion: Overall observations indicate an increased incidence of hypertension and CVDs post recovery from COVID-19. A dual therapy of ARBs was the preferred choice for management of hypertension. Regular follow-up and close monitoring of symptoms to prevent further CV complications in COVID-19 recovered patients is recommended.
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Background Many patients with COVID-19, particularly from the pandemic's early phase, have been reported to have evidence of cardiac injury such as cardiac symptoms, troponinemia, or imaging or ECG abnormalities during their acute course. Cardiac magnetic resonance (CMR) has been particularly useful to assess myocardial abnormalities given its comprehensive characterization of structure, function, and tissue. Overall, findings have varied, and long term impact of COVID-19 on myocardial structure and function needs further elucidation. Methods We performed TTE and 3T CMR with gadoterate meglumine (Clariscan, GE Healthcare) in survivors of the initial stage of the pandemic without preexisting cardiac disease and matched controls at long-term follow up?>6 months after infection, using an array of techniques to comprehensively evaluate the myocardium. Chi square tests for categorical and t tests for continuous variables were used. P <0.05 was considered significant. Results Our study population consisted of 40 COVID survivors and 12 controls of similar age, sex and race-ethnicity distribution with median age 46, 50% female, 48% Hispanic, 28% Black, mean BMI 27. None had presented with thromboembolism, myocarditis, or ischemia;35% had been hospitalized with 28% intubated. Imaging was performed median 308 days after initial infection. We found no difference in echo characteristics including measures of LV and RV structure and systolic function, valvular abnormalities, or LV diastolic function with median LVEF 60% v 58%, LVEDD 4.0 v 4.4, E/e' ~6, and no RWMA in either group. Using CMR, we confirmed no differences in LV and RV structure and function including median LVEF 57% v 58%, RVEF 53% v 53%, LVEDVi 74 v 72, and RVEDVi 77 v 74. We found no significant differences in T1 (1305 v 1280), T2 (46 v 47), ECV (29 v 30), or LGE mapping. With analysis stratified by patient hospitalization status as an indicator of COVID severity, no differences were uncovered. Conclusion Multimodal imaging of a diverse cohort of COVID-19 survivors who had not presented with acute cardiac pathology reveals no distinct features indicating long-lasting structural or functional damage or inflammation of the myocardium.Copyright © 2023 American College of Cardiology Foundation
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Background Primary cardiac lymphoma (PCL) is an extranodal lymphoma involving only the heart and/or pericardium. PCL accounts for 2% of primary cardiac tumors and 0.5% of extranodal lymphomas. Its diagnosis is usually delayed due to rarity and non-specific findings. Case A 77-year-old man with Alzheimer dementia, atrial fibrillation on apixaban, and COVID-19 illness 3-weeks prior, who presented to the hospital with diffuse abdominal discomfort, fatigue, anorexia, and hypoactivity. Patient was tachycardic and normotensive with pronounced jugular venous distention, non-collapsing with respiration. ECG revealed sinus tachycardia, first degree atrioventricular (AV) block and chronic LBBB. Cardiac troponins were mildly elevated without significant delta. An abdominopelvic CT revealed an incidental, large pericardial effusion (PE). Bedside echocardiogram confirmed a large hemodynamically significant PE as well as a mass-like echogenicity encasing and infiltrating the pericardium and myocardium at the basal aspect of the right ventricle free wall. Decision-making In view of recent COVID-19 infection, he was started on indomethacin and colchicine for suspected viral or neoplastic pericarditis. Pericardiocentesis drained 900ml of amber to serosanguineous fluid with quick hemodynamic improvement. Fluid analysis was non-diagnostic for neoplasia. Subsequently, he developed symptomatic bradycardia with an intermittent complete AV block with junctional escape rhythm, transitioning to a second-degree AV block after removal of beta-blocker. Awaiting permanent pacemaker implant, he developed ventricular fibrillation with sudden cardiac death that required prolonged unsuccessful ACLS. Autopsy revealed an extensive infiltrative tumor, predominantly right-sided, consistent with primary cardiac B-cell lymphoma. Conclusion PCL should be part of the working diagnosis in patients presenting with a pericardial effusive process in combination with a right sided myocardial mass. Early cardiac MRI/PET scan or biopsy should be considered when the diagnosis is not certain. Prompt diagnosis could allow for treatment that potentially prolongs survival.Copyright © 2023 American College of Cardiology Foundation
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Novel coronavirus (nCoV-19) infection has been declared a pandemic by WHO. More than 223 countries are under the attack of this emergency situation. Primarily, pneumocytes encountered by the nCoV-19 via ACE-2 receptor cause pulmonary edema, damage to alveolar cells, production of inflammatory cells, and hypoxia. It has been found that patients with co-existing cardiovascular diseases are more prone to the infection, and severe cardiovascular dysfunction was further observed when infected with nCoV-19. There is no substantial mechanism available for the pathogenesis of this cardiovascular dysfunction;therefore, we herein present a possible mechanistic approach of cardiotoxicity by nCov-19 infection. The hypothesis of this study is based on immunopathology of nCoV-19 in pneumocytes, presence of ACE-2 on cardiomyocytes membrane, cytokine storm, genomic analysis of virus in cardiac tissue, and several reports published on the cardiovascular complications in nCoV-19 across the globe. We have also analyzed the cardiotoxic profile of recently used repurposed and investigational drugs and highlighted their possible cardiotoxic consequences and drug interactions with cardiovascular medicines, such as statins and anti-coagulants.Copyright © 2021 Bentham Science Publishers.
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The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected — asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki–Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. Сo-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome.
ABSTRACT
The COVID-19 pandemic is a worldwide problem. The clinical spectrum of SARS-CoV-2 infection varies from asymptomatic or paucity-symptomatic forms to conditions such as pneumonia, acute respiratory distress syndrome and multiple organ failure. Objective was to describe a clinical case of SARS-CoV-2 infection in the patient with sarcoidosis and cardiovascular pathology developing acute respiratory syndrome and lung edema. Material and methods. There were analyzed accompanying medical documentation (outpatient chart, medical history), clinical and morphological histology data (description of macro- and micro-preparations) using hematoxylin and eosin staining. Results. Lung histological examination revealed signs of diffuse alveolar damage such as hyaline membranes lining and following the contours of the alveolar walls. Areas of necrosis and desquamation of the alveolar epithelium in the form of scattered cells or layers, areas of hemorrhages and hemosiderophages are detected in the alveolar walls. In the lumen of the alveoli, a sloughed epithelium with a hemorrhagic component, few multinucleated cells, macrophages, protein masses, and accumulated edematous fluid were determined. Pulmonary vessels are moderately full-blooded, surrounded by perivascular infiltrates. Signs of lung sarcoidosis were revealed. Histological examination found epithelioid cell granulomas consisting of mononuclear phagocytes and lymphocytes, without signs of necrosis. Granulomas with a proliferative component and hemorrhage sites were determined. Giant cells with cytoplasmic inclusions were detected - asteroid corpuscles and Schauman corpuscles. Non-caseous granulomas consisting of clusters of epithelioid histiocytes and giant Langhans cells surrounded by lymphocytes were detected in the lymph nodes of the lung roots. Hamazaki-Wesenberg corpuscles inside giant cells were found in the zones of peripheral sinuses of lymph nodes. In the lumen of the bronchi, there was found fully exfoliated epithelium, mucus. Granulomas are mainly observed subendothelially on the mucous membrane, without caseous necrosis. Histological examination of the cardiovascular system revealed fragmentation of some cardiomyocytes, cardiomyocyte focal hypertrophy along with moderate interstitial edema, erythrocyte sludge. Zones of small focal sclerosis were determined. The vessels of the microcirculatory bed are anemic, with hypertrophy of the walls in small arteries and arterioles. Virological examination of the sectional material in the lungs revealed SARS-CoV-2 RNA. Conclusion. Based on the data of medical documentation and the results of a post-mortem examination, it follows that the cause of death of the patient R.A., 50 years old, was a new coronavirus infection COVID-19 that resulted in bilateral total viral pneumonia. So-morbidity with competing diseases such as lung sarcoidosis and cardiovascular diseases aggravated the disease course, led to the development of early ARDS and affected the lethal outcome. Copyright © 2022 Saint Petersburg Pasteur Institute. All rights reserved.
ABSTRACT
Background. Intrauterine myocardial injury/infarction (MI) is exceedingly uncommon and the few reported cases occur most commonly with congenital cardiac anomalies, particularly anomalous coronary arteries. Here we present a case of MI in a fetus resulting in intrauterine fetal demise (IUFD). A 36-year-old G3 P1011 mother with a history of methylenetetrahydrofolate reductase (MTHFR) mutation (double heterozygote;may lead to a procoagulable state) on prophylactic aspirin and recent COVID-19 infection during pregnancy (5 weeks prior, recovered) presented at 28 weeks gestational age with one day of decreased fetal movement, at which time IUFD was diagnosed. Method(s): Induction of labor with misoprostol was performed, and the fetus was delivered stillborn vaginally without complications. A full autopsy including histologic examination (including placental histopathology and immunohistochemistry) was performed. Result(s): Autopsy examination of the fetus revealed normal development, including a structurally normal heart. However, histologic examination of the heart demonstrated a discrete region of intramyocardial fibrosis, dystrophic calcification, and giant cell reaction involving a large portion of one ventricle, consistent with MI (Fig 1). Immunostains for infectious causes of myocarditis (including COVID, cytomegalovirus, herpes simplex virus, parvovirus, adenovirus, and toxoplasmosis) were negative. Histologic examination of all other organs was unremarkable. Gross examination of the placenta was remarkable for a hypercoiled umbilical cord, and histologic examination revealed a hypoplastic umbilical artery with partial smooth muscle necrosis as well as a single, nonoccluding stem villus thrombus, without histologic evidence of downstream fetal vascular malperfusion. Conclusion(s): The cause of demise was concluded to most likely be due to fetal myocardial injury, but the etiology is unclear. The differential diagnosis includes a thromboembolic phenomenon possibly leading to infarction (given maternal history of MTHFR mutation and recent COVID infection), myocarditis (possibly burned- out phase), coronary artery abnormalities that were not appreciated on fresh dissection of the heart, and ventricular dysplasia/aneurysm (least likely given histologically normal surrounding myocardium). This rare case is an example of a lethal myocardial injury in an otherwise structurally normal fetal heart.