Acute or chronic? Failing left ventricle in a 34 year old

Submission content Introduction: An unusual case of a very young patient without previously known cardiac disease presenting with severe left ventricular failure, detected by a point of care echocardiogram. Main Body: A 34 year old previously well man was brought to hospital after seeing his general practitioner with one month of progressive shortness of breath on exertion. This began around the time the patient received his second covid-19 vaccination. He was sleeping in a chair as he was unable to lie flat. Abnormal observations led the GP to call an ambulance. In the emergency department, the patient required oxygen 5L/min to maintain SpO2 >94%, but he was not in respiratory distress at rest. Blood pressure was 92/53mmHg, mean 67mmHg. Point of care testing for COVID-19 was negative. He was alert, with warm peripheries. Lactate was 1.0mmol/L and he was producing more than 0.5ml/kg/hr of urine. There was no ankle swelling. ECG showed sinus tachycardia. He underwent CT pulmonary angiography which demonstrated no pulmonary embolus, but there was bilateral pulmonary edema. Troponin was 17ng/l, BNP was 2700pg/ml. Furosemide 40mg was given intravenously by the general medical team. Critical care outreach asked for an urgent intensivist review given the highly unusual diagnosis of pulmonary edema in a man of this age. An immediate FUSIC Heart scan identified a dilated left ventricle with end diastolic diameter 7cm and severe global systolic impairment. The right ventricle was not severely impaired, with TAPSE 18mm. There was no significant pericardial effusion. Multiple B lines and trace pulmonary effusions were identified at the lung bases. The patient was urgently discussed with the regional cardiac unit in case of further deterioration, basic images were shared via a cloud system. A potential diagnosis of vaccination-associated myocarditis was considered,1 but in view of the low troponin, the presentation was felt most likely to represent decompensated chronic dilated cardiomyopathy. The patient disclosed a family history of early cardiac death in males. Aggressive diuresis was commenced. The patient was admitted to a monitored bed given the potential risk of arrhythmia or further haemodynamic deterioration. Advice was given that in the event of worsening hypotension, fluids should not be administered but the cardiac centre should be contacted immediately. Formal echocardiography confirmed the POCUS findings, with ejection fraction <35%. He was initiated on ACE inhibitors and beta adrenergic blockade. His symptoms improved and he was able to return home and to work, and is currently undergoing further investigations to establish the etiology of his condition. Conclusion(s): Early echocardiography provided early evidence of a cardiac cause for the patient's presentation and highlighted the severity of the underlying pathology. This directed early aggressive diuresis and safety-netting by virtue of discussion with a tertiary cardiac centre whilst it was established whether this was an acute or decompensated chronic pathology. Ultrasound findings: PLAX, PSAX and A4Ch views demonstrating a severely dilated (7cm end diastolic diameter) left ventricle with global severe systolic impairment.

Autoimmune pulmonary alveolar proteinosis in an adolescent girl with rapidly progressive dyspnea

Autoimmune pulmonary alveolar proteinosis (PAP) is a rare disease, especially in pediatrics, but important to consider, as it may avoid unnecessary and/or invasive investigations and delayed diagnosis. This case report highlights an adolescent girl with rapid onset dyspnea but an unremarkable physical exam and initial testing. However, due to a high index of suspicion, a chest computed tomography (CT) scan was done, revealing a "crazy paving" pattern, which then prompted expedited assessment. This finding, however, is not as specific as often discussed and has a broad differential diagnosis, which will be reviewed in detail as part of this case. Furthermore, this report demonstrates a diagnostic approach for PAP that avoids lung biopsy, previously considered to be required for diagnosis of PAP, but is increasingly becoming unnecessary with more advanced blood tests and understanding of their sensitivity and specificity. Additionally, management strategies for PAP will be briefly discussed.Copyright © 2022 Canadian Thoracic Society.

Severe Acute Hemolytic Anemia Post Covid Vaccination

Case Report: A 26-year-old woman with a history of warm autoimmune hemolytic anemia, immune thrombocytopenia, triple positive antiphospholipid syndrome, and chronic migraine presented to the emergency department with worsening generalized fatigue for one week associated with headache, dyspnea on exertion, nausea, vomiting and lightheadedness. Of note, she had received her second dose of mRNA COVID-19 vaccine 4 days prior to presentation. On admission, patient was found to be severely anemic with a hemoglobin of 4.3g/dL which is decreased from her baseline hemoglobin of 9-10.5g/dL;however, W-AIHA precluded the administration of blood product until adequate blood with the appropriate antibodies could be acquired. During the hospitalization, hemoglobin decreased to 3.3g/dL. Patient was then administered the most compatible blood product which she tolerated well. Hematology was consulted who started the patient on hydroxychloroquine, high dose methylprednisolone, and Intravenous Immunoglobulin (IVIG). Throughout the admission, the patient remained asymptomatic. After 2 days of IVIG, three days of high dose glucocorticoids, and one unit of packed red blood cells, the patient's hemoglobin increased to 7.2g/dL. Patient was discharged home on prednisone taper and hydroxychloroquine. Conclusion(s): Episodes of hemolytic anemia after either the first or second dose of mRNA COVID vaccines are rare and have occurred in patients with known hematological pathology as well as patients without any history of hematologic or immunologic disorders. When taking the history of patients presenting with hemolytic anemia, it is important to query recent vaccinations as, while rare, mRNA COVID vaccine may well be the etiology. While this ultimately will likely not change patient management, this information would be beneficial for further study.

Cardiopulmonary long-term effects in patients after hospitalization due to COVID-19 infection

Background: Multiple studies have described acute effects of the Covid-19 infection on the heart, but little is known about the long-term cardiac and pulmonary effects and complications after recovery. The aim of this analysis was to deliver a comprehensive report of symptoms and possible long-term impairments after hospitalization because of Covid-19 infection as well as to try to identify predictors for Long-Covid. Method(s): This was a prospective, multicenter registry study. Patients with verified Covid-19 infection, who were treated as in-patients at our dedicated Covid hospital (Clinic Favoriten), have been included in this study. In all patients, testing was performed approximately 6 months post discharge. During the study visit the following tests and investigations were performed: Detailed patient history and clinical examination, transthoracic echocardiography, electrocardiography, cardiac magnetic resonance imaging (MRI), chest computed tomography (CT) scan, lung function test and a comprehensive list of laboratory parameters including cardiac bio markers. Result(s): Between July 2020 and October 2021, 150 patients were recruited. Sixty patients (40%) were female and the average age was 53.5+/-14.5 years. Of all patients, 92% had been admitted to our general ward and 8% had a severe course of disease, requiring admission to our intensive care unit. Six months after discharge the majority of patients still experienced symptoms and 75% fulfilled the criteria for Long-Covid. Only 24% were completely asymptomatic (figure 1). Echocardiography detected reduced global longitudinal strain (GLS) in 11%. Cardiac MRI revealed pericardial effusion in 18%. Furthermore, cardiac MRI showed signs of former peri-or myocarditis in 4%. Pulmonary CT scans identified post-infectious residues, such as bilateral ground glass opacities and fibrosis in 22%. Exertional dyspnea was associated with either reduced forced vital capacity measured during pulmonary function tests in 11%, with reduced GLS and/or diastolic dysfunction, thus providing evidence for a cardiac and/or pulmonary cause. Independent predictors for Long-Covid were markers of a more severe disease course like length of in-hospital stay, admission to an intensive care unit, type of ventilation as well as higher NT-proBNP and/or troponin levels. Conclusion(s): Even 6 months after recovery from Covid-19 infection, the majority of previously hospitalized patients still suffer from at least one symptom, such as chronic fatigue and/or exertional dyspnea. While there was no association between fatigue and cardiopulmonary abnormalities, impaired lung function, reduced GLS and/or diastolic dysfunction were significantly more prevalent in patients presenting with exertional dyspnea. On chest CT approximately one fifth of all patients showed post infectious changes in chest CT including evidence for myo-and pericarditis as well as accumulation of pericardial effusions.

Post covid 19 radiological changes in pediatric patients

Background: Introduction: Coronavirus disease (COVID-19) is a global problem. The COVID-19 pandemic has infected millions of people and the number of patients who have been exposed to postcovid implications are increased. Postcovid changes are more investigated in adults, although information is scarce in pediatric patients. Method(s): The aim of the study was to evaluate the radiological changes of respiratory system in peaditric patients after acute mild and severe covid infections. Research subjects: 259 pediatric patients (age: 10 months -18 years) recovered from Covid-19 and had a negative PCR test were examined. All patients underwent X-ray examinations. Patients were divided into 3 subgroups. Patients (46%) recovered from severe or moderate covid pneumonia and had non-respiratory symptoms upon arrival at the clinic: weakness, mild fatigue, drowsiness. Patients (28%) recovered from covid infection and had respiratory symptoms: cough, shortness of breath during exercise, respiratory failure;Patients (26%) with a fever upon entry to the hospital. The statitical analysis was done using SPSS 12.0 software. Result(s): Patients, whose had (69.9% ) the severe Covid pneumonia and postcovid respiratory symptoms (cough 78.4%), which was the cause of abnormal changes in the cardiovascular system were onserved in 48.6% of patients. Unlike other types of viral infections, the changes continue in the postcovid period. Severe course of the disease does not always mean detection of postcovid syndrome and vice versa. However, in case of mild disease the possibility development of various degrees of polyorgan damage was 26.9%. Conclusion(s): The radiological changes are manifested during 4th week from recovery and may last for a longer period of time, however the radiological changes do not always indicator a severity of the disease.

Structural Valve Dysfunction As An Atypical Presentation Of Cardiac Sarcoidosis

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

An 81-Year-old Woman With Proximal Weakness

An 81-year-old woman developed progressive proximal weakness and myalgias several months following a COVID-19 infection. She was admitted to her local hospital for progressive weakness, peripheral edema, and exertional dyspnea. Neurology evaluation noted proximal arm and leg weakness. She had creatine kinase 740 U/L, white blood cells 21,000/mL (with abnormal differential), and abnormal antibody serologies. Additional diagnostic testing obtained included a thigh MRI and muscle biopsy. During her COVID-19 admission, a mediastinal mass had been detected, which was increased in size on this current admission. Notably, she had a remote history of an incidentally discovered mediastinal mass, which had been incompletely resected 18 years prior. At neuromuscular follow-up one month later, she reported improvement in peripheral edema and dyspnea but ongoing weakness. Strength exam noted symmetric Medical Research Council grade 4 weakness in neck flexion/extension, shoulder abduction, elbow flexion/extension, wrist extension, hip flexion/abduction/extension, and knee flexion. She had no fatiguability and no facial or bulbar weakness. Remainder of her neuromuscular examination was unremarkable. Her white blood cell count differential remained abnormal but had improved from her initial presentation. Her recent muscle biopsy slides were reviewed again. Bone marrow biopsy and mediastinal mass biopsy were obtained. A unifying diagnosis was made, and she was started on therapy with resolution of her weakness, myalgias, and abnormal cell counts.

Cardiopulmonary exercise testing and ventilatory efficiency in long COVID-19: 15 months follow-up

Long COVID-19 is defined as persistency of symptoms, such as exertional dyspnea, twelve weeks after recovery from SARS-CoV-2 infection;its pathophysiology still needs to be fully understood. We investigated exercise tolerance and ventilatory efficiency using cardiopulmonary exercise testing (CPET) in patients with long COVID-19. Methods. One hundred patients admitted to our hospital from March to August 2020 for a moderate to critical COVID-19 were enrolled in our long COVID-19 program. Medical history, physical examination and chest HRCT were obtained at hospitalization (T0), at 3 (T3) and 15 months (T15). All HRCTs were revised using a semiquantitative CT severity score (Pan, F. et al. Radiology 2020;295(3):715-721). Pulmonary function tests (PFTs) were obtained at T and T . CPET was performed at T15 in twenty patients (10 male/10 female;mean age 62 years) with residual respiratory symptoms (e.g., exertional dyspnea) and/or an impairment in PFTs, DLCO and/or KCO . Results. At CPET, peak oxygen uptake (VO2 -peak) and ventilatory efficiency (VE /VCO2 slope) were 95.9+/-18.4 SD %pred and 31.4+/-3.9 SD, respectively. Of notice, significant correlations between VE/V'CO2 slope and CT score (T0 ) (r=0.403;p=0.039), CT score (T3) (r=0.453;p=0.022) and DLCO (T3 ) (r=-0.465;p=0.019) were observed. Conclusions. At fifteen-months from COVID-19 pneumonia, a significant number of subjects (20%) still complains of exertional dyspnea. At CPET this may be explained by reduced ventilatory efficiency (i.e., increase in VE/VCO2), possibly related to the degree of lung parenchymal involvement in the COVID-19 acute phase, likely reflecting a damage in the interstitial/pulmonary capillary structure.

Case report of an antimelanoma differentiationassociated protein 5 antibody-associated amyopathic dermatomyositis

Autoantibodies against melanoma differentiation-associated protein 5 (MDA5) associated with dermatomyositis have recently been described in Asians with rapidly progressive respiratory disease. Here we report the case of a middle-aged white woman with anti-MDA5 antibody-associated amyopathic dermatomyositis with interstitial lung disease (ILD), which is stable with minimal immune suppression. A 55-year-old woman was referred to a virtual dermatology clinic during the COVID-19 pandemic suspected of having widespread eczema involving the chest, face, arm and hands on the background of atopy. On direct questioning, she admitted to having constitutional symptoms, exertional dyspnoea, joint pain and symptoms of proximal muscle weakness. On clinical suspicion of possible connective tissue disorder, she was urgently reviewed in the hospital, where she was found to have a photodistributed rash involving cutaneous ulceration and violaceous plaques. Hand examination showed mechanic's hand mimicking hand eczema, ragged nail cuticles and acute tenosynovitis in the left index finger. Her upper and lower limb muscle power was normal and respiratory examination revealed bi-basal fine end-expiratory crepitation. Her repeated biochemical, haematological and muscle enzymes remained normal. Skin biopsy taken from photosensitive rash over the wrist showed hypergranulosis, Civatte body formation, colloid bodies and dyskeratotic keratinocytes, in keeping with severe lichenoid eruption. Superficial dermis showed patchy red-cell extravasation, perivascular chronic infiltration, dermal oedema and serum on the surface, in keeping with ulceration secondary to severe inflammatory processes. There were no eosinophils and eccrine coils were free of inflammation, raising the suspicion of a drug eruption. Her antinuclear antibody and double-stranded DNA were repeatedly negative. Myositisspecific antibody panel was performed owing to a high clinical suspicion of photosensitive dermatoses, both clinically and histologically. Histology revealed positive anti-MDA5 antibodies;repeated positive testing confirmed this. Although lung function was normal, computed tomography revealed evidence of ILD. We made a diagnosis of anti-MDA5 antibodyassociated amyopathic dermatomyositis with ILD. Her malignancy screening was negative. The patient was started on lowdose prednisolone and hydroxychloroquine 200 mg twice daily, with topical steroid applications, which resulted in remarkable clinical improvement. Anti-MDA5 associated dermatomyositis has characteristic cutaneous lesions consisting of skin ulceration and tender palmar papules, mechanic's hands, inflammatory arthritis and rapidly progressive ILD, which is frequently fatal. Although our patient had ILD, she was relatively stable on minimal immunosuppression. It is important for clinicians to have an increased awareness of this disease as it could have a highly variable clinical presentation in the white population.

Patient-reported outcome measures 3 and 6 months after pulmonary rehabilitation following COVID-19

Recent studies have suggested that pulmonary rehabilitation (PR) improves patient-reported outcome measures (PROMs) in patients recovering from COVID-19. Yet, there are hardly any studies that report the further course of recovery after PR. Therefore, we assessed PROMs regarding exertional dyspnea, fatigue, depression, anxiety, and quality of life (QoL) of 224 patients (Oage: 54.3+/-10.4;42% female) who were admitted to a three-week inpatient PR between 4/2020 and 4/2021 due to COVID-19. Data were assessed at the beginning (T1) and at the end (T2) of PR as well as 3 months (T3) and 6 months (T4) afterwards. Repeated measures ANOVAs were calculated to reveal significant changes. In line with previous results, we found significant reductions in symptom severity regarding all PROMs over the course of PR (dT1-T2 =0.910 to dT1-T2=1.538) and a significant increase in QoL (dT1-T2=-1.238). While the improvements in exertional dyspnea and QoL persisted after PR (PT2-T3 =0.321 and pT2-T3=0.358), each other variable significantly deteriorated again at T3 (dT2-T3=-0.386 to dT2-T3=-0.933). However, significant improvements between T1 and T4 could be detected in each variable (dT1-T4=0.567 to dT1-T4=0.696) except for anxiety (pT1-T4=0.708). The improvements were associated with an increase in QoL (dT1-T4=-1.010). Our results suggest that PR leads to significant improvements in clinically relevant PROMs. In most variables, the improvements may also persist after PR. Since we found no improvements in the further course, we conclude that the improvements were predominantly due to PR rather than to the natural course of recovery after COVID-19.

Right ventricular myocardial dysfunction in patients (pts) after severe coronavirus disease (COVID-19)

Aim: To study the systolic function (SF) and diastolic function (DF) of the heart and to assess subclinical myocardial right ventricular (RV) dysfunction in pts after severe COVID-19. We examined 23 males aged 46-70 years (mean age - 58.8 +/- 12.6 yrs) discharged after COVID-19 (50-75% of the parenchymal damage) with exertional dyspnea. We performed transthoracic echocardiography (TTE) with assessment of RV global longitudinal strain (RV-GLS) and right ventricular free wall longitudinal strain (RVLS) using speckle tracking echocardiography. Result(s): The SF of the RV assessed by the excursion of the tricuspid valve ring (TAPSE) was preserved (2.1 +/- 0.6 cm) in all pts under study after severe COVID-19. The left ventricular (LV) ejection fraction was also preserved (62.1 +/- 4.7%) in all pts. TTE revealed normal ventricular and atrial dimensions: LV end-diastolic volume index (62.5 +/- 8.4 ml/m2) and RV end-diastolic diameter (2.7 +/- 0.6 cm), left atrial (LA) volume index (26.7 +/- 3.1 ml/m2) and right atrial (RA) volume index (20.2 +/- 4.5 ml/m2). LV DD was also detected: Grade I in 17 (74%) pts, and Grade II in 6 (16%) pts. Moderate pulmonary hypertension (PH) was present in all pts (time of acceleration of systolic flow in the pulmonary artery (AcT - 85.0 +/- 7.9 msec) as a consequence of significant pulmonary parenchymal involvement. We found reduced RV-GLS (-17.4 +/- 2.7%) and free wall RVLS (-18.9 +/- 3.1%) in 23 (100%) pts. Conclusion(s): Preserved LV and RV SF with Grade 1 and Grade 2 LV DD and moderate PH were established in pts after severe COVID-19. RV wall motion abnormalities with reduced RV-GLS and free wall RVLS were found, indicating the presence of subclinical RV myocardial dysfunction.

Persistent exertional dyspnea post COVID-19: potential mechanisms

Background: Patients recovered from COVID-19 often present with reduced exercise capacity and persistent exertional breathlessness, yet the mechanisms are still poorly understood. Method(s): We aimed to test patients formerly hospitalized for COVID-19 pneumonia with normal chest computed tomography (CT) at 6-month follow up but with persistent exertional breathlessness. Spirometry, chest CT, incremental cycle exercise test with arterial line, resting echocardiography and ventilation/perfusion (V/Q) scan were performed. Result(s): Data represents one patient and 4 healthy controls (CTRL) used for comparison. Patient (age: 41 vs. average 41.5 years in CTRL) was never smoker with FEV1 of 86 %predicted, normal chest CT and normal resting echocardiogram. Patient reported significant activity-related dyspnea (baseline dyspnea index score: 7). During exercise, peak work rate, ventilation, and oxygen update were within normal. Yet, patient had greater dyspnea intensity, ventilatory requirements and ventilatory equivalent for CO during exercise, with 4% drop in O2 saturation, 2 figure. Patient and CTRL had similar tidal volume (VT), rest-to-peak change in dead space/VT, and O2 pulse. V/Q scan showed multiple perfusion defects. Conclusion(s): Preliminary data shows that reduced ventilatory efficiency during exercise, suggesting pulmonary vascular abnormalities, could possibly explain persistent breathlessness in patients recovered from COVID pneumonia.

Respiratory symptomatology of Covid-19 in healthcare workers

Introduction: Health personnel are particularly exposed to the risk of contamination by SARS-CoV2. Various symptoms, particularly respiratory, have been described in this population. Objective(s): Determine the socio-professional, clinical and paraclinical characteristics of healthcare workers with Covid-19. Method(s): Descriptive cross-sectional study with health staff at Rabta hospital, suffering from Covid-19. The information was collected using a questionnaire administered by the doctor during the return to work consultation. Result(s): Our population included 418 health workers and was predominantly female (75.4%) with an average age of 41.5 +/- 10.5 years. They belonged to medical services in 40.1% of cases and held the position of nurse in 33.7% of cases. Contamination was intra-hospital in 45.7% of cases. A history of allergic asthma was noted in 7.4% of health workers. Respiratory symptoms were present in 63.9% of cases, mainly consisting of cough (45.9%) and dyspnea (28.9%). It was a moderate form in 24.2% of cases. A chest computed tomography was performed in 10.3% of cases, objectifying interstitial lung disease in 49% of cases. Hospitalization was necessary for 5.7% of staff with an average duration of 7.9 days. It was significantly related to the presence of respiratory signs (p<=10-3). On returning to work, 14.6% of affected personnel reported the persistence of exertional dyspnea. Conclusion(s): The respiratory signs of Covid-19, dominated by cough and dyspnea, were widely represented in our population and statistically associated with the need for hospitalization.

CHRONIC THROMBOEMBOLIC DISEASE AFTER ACUTE PULMONARY EMBOLISM RELATED TO SARSCoV-2

During SARS-CoV-2 infection, acute pulmonary embolism (PE) worsens the patient's clinical status. However, after resolution of the acute phase, the impact of residual thrombotic lesions in pulmonary vasculature remains unknown. In this line, chronic thromboembolic disease (CTD) consists of persistent thrombotic lesions and involves long-term functional limitations, including those for patients with a CTD with or without chronic thromboembolic pulmonary hypertension (CTEPH). The aim of this study was to evaluate the prevalence of CTD after hospitalization for SARSCoV-2 pneumonia and PE. Also, we evaluated the clinical and functional characteristics of these patients. Forty-two patients diagnosed of PE in the course of SARS-CoV-2 pneumonia were included. In all patients, CT angiography (n=35) and/or pulmonary V/Q scan (n=19) was obtained between 3 to 4 months after discharge. Remaining symptoms, pulmonary function and exercise capacity also were evaluated. Eleven patients (26%) showed persistent thrombotic lesions without residual SARS-CoV-2 pneumonia images. Within this former group, 36% (n=4) had exertional dyspnea as expression of CTD. Only one patient (9%) developed CTEPH. The only related factor with persistent thrombotic lesions was older age (>70 years). Exercise capacity and pulmonary function were not significantly different between symptomatic and non-symptomatic patients. Residual thrombotic lesions are a frequent finding after SARS-CoV-2 infection, however the prevalence of CTD and CTEPH are similar to SARS-CoV-2 non-related acute pulmonary embolism. In this patients, the current recommendations for pulmonary embolism monitoring after discharge could be applied.

Symptoms persisting after hospitalization for COVID-19: 12 months interim results of the CO-FLOW study

After COVID-19 long-term sequelae are frequently reported. We aimed to longitudinally assess persistence and clusters of symptoms up to 12 months after hospitalization for COVID-19, and to assess determinants of the main persistent symptoms. In this multicenter prospective cohort study patients with COVID-19 are followed up at 3, 6, and 12 months after hospital discharge;we present interim results for persistent symptoms up to 12 months. Symptoms were clustered into physical, respiratory, cognitive, and fatigue symptoms. Of the 492 patients included, 97%, 95.5%, and 92.5% had at least 1 persisting symptom at 3, 6, and 12 months after discharge, respectively (p=0.010). Muscle weakness, exertional dyspnea, fatigue, and memory and concentration problems were the most prevalent symptoms at follow-up (>50%). Over time, muscle weakness, hair loss, and exertional dyspnea decreased significantly (p<0.001). Only the physical (p=0.025) and respiratory (p<0.001) symptom cluster declined significantly over time. Female gender was the most important predictor of persistent symptoms and co-occurrence of symptoms from all clusters. Shorter hospital stay and treatment with steroids were related to decreased muscle weakness;comorbidity and being employed were related to increased fatigue;and shorter hospital stay and comorbidity were related to memory problems. The majority of patients experienced COVID-19 sequelae up to 12 months after hospitalization. Only the physical and respiratory symptoms showed slow gradual decline. This finding stresses the importance of finding the underlying causes and effective treatments for post-COVID condition, beside adequate COVID-19 prevention.

Subacute Rhinovirus Myocarditis Complicating Nonischemic Alcohol-Induced Dilated Cardiomyopathy: Unusual Mixed Etiologies of Biventricular Heart Failure

Background Dilated cardiomyopathy (DCM) is caused by many conditions, including ischemia, genetics, infection, chemotherapy, or idiopathic. Clinical suspicion is needed to identify reversible etiologies. Case A middle-aged truck-driver presents with exertional dyspnea, cough, lower extremity edema, and low-grade fever for 2 weeks. He had 20-pack-year smoking history and 3-4 alcoholic drinks weekly. Chest x-ray showed pulmonary congestion. BNP was elevated. ECHO showed severely dilated ventricles with LVEF < 10% and no wall abnormalities. Decision-making Perfusion stress test showed no inducible ischemia. Coronary angiogram showed no epicardial disease. Cardiac MRI (CMR) showed severely dilated biventricular failure, pericardial thickening, circumferential pericardial effusion, epicardial involvement suggestive of subacute myopericardial inflammation and scarring with delayed gadolinium-enhancement and RVEF < 5%. Liver ultrasound showed no cirrhosis. Viral PCR was positive for rhinovirus, negative COVID-19. He was treated medically requiring inotropes then transferred to heart failure center for assist device evaluation. Conclusion Our patient reported moderate alcohol use, which alone would not explain the myopericardial changes seen on CMR. Given the findings, his DCM was attributed to alcohol complicated by possible subacute rhinovirus myocarditis. Our association is further supported by recent respiratory viral prodrome along with exclusion of other etiologies. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Effusive Constrictive Pericarditis, a Heart Failure Mimicker

Background Effusive constrictive pericarditis can initially mimic heart failure and ultimately result in cardiogenic shock. Case Patient is a 57-year-old female with history of recent massive pulmonary embolism status post systemic alteplase, chronic diastolic heart failure, and history of COVID-19 infection presenting with increasing dyspnea on exertion and weakness despite compliance to outpatient diuretics. Patient was noted to be hypotensive, and fluid overloaded on exam. Decision-making Due to concern for constriction right heart catheterization (RHC) was completed and showed cardiac index of 1.1 with elevated filling pressures, discordant variation of right ventricle (RV) and left ventricle (LV) pressure tracings, diastolic equalization of pressure, and dip and plateau pattern of RV and LV diastolic tracing suggestive of constrictive physiology. Transesophageal echocardiogram showed no pericardial effusion with increased echo-density of the pericardium. Cardiac MRI showed mild diffuse thickening and subtle enhancement of the pericardium with septal bounce and no significant pericardial effusion consistent with constrictive pericarditis. Due to persistent hypotension requiring milrinone infusion, the patient underwent pericardiectomy with improvement of hemodynamics and symptoms. Conclusion Effusive constrictive pericarditis can mimic heart failure and should be ruled out in those with evidence of low cardiac output to avoid cardiovascular morbidity and mortality. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Persisting exertional dyspnea and perceived exercise intolerance after mild Covid-19: a critical role for breathing dysregulation?

Background: After mild Covid-19, a subgroup of patients reports post-acute sequelae of Covid-19 (PASC), in which exertional dyspnea and perceived exercise intolerance are common. Underlying pathophysiological mechanisms remain incompletely understood. We studied outcomes from cardiopulmonary exercise test (CPET) in these patients. Method(s): In this observational study, we included patients referred for the analysis of PASC after mild Covid-19 in whom CPET was performed after standard clinical work-up turned out unremarkable. Cardiocirculatory, ventilatory and metabolic response to, and breathing patterns during exercise at physiological limits were analyzed. Result(s): Twenty-one patients (76% female, mean age 40y) who reported severe fatigue (CIS-fatigue >= 35), dyspnea (mMRC 2 (IQR1-2)) and disability in physical role functioning (SF-36) underwent CPET at 32 weeks (IQR 22-52) after Covid-19. Mean peak oxygen uptake was 99% (SD13) of predicted with normal anaerobic thresholds at 62% (SD11) of predicted oxygen uptake. No cardiovascular or gas exchange abnormalities were detected. Twenty out of the 21 patients (95%) demonstrated breathing dysregulation, existing of ventilatory inefficiency (29%), abnormal course of breathing frequency and tidal volume (57%), and acute or chronic respiratory alkalosis in resting blood gases (67%). Conclusion(s): In the absence of deconditioning, breathing dysregulation may explain the experienced exertional dyspnea and exercise intolerance in patients with PASC after mild Covid-19.