Inhaled Milrinone via HFNC as a Postextubation Cardiopulmonary Elixir: Case Series and Review of Literature

Pulmonary hypertension (PH) often complicates perioperative course following pediatric cardiac surgery, often presenting unique challenges to the attending cardiac anesthesiologist. Apart from difficult weaning from cardiopulmonary bypass, PH can often compound weaning from mechanical ventilation in this postoperative subset. From pathophysiological standpoint, the former can be attributed to concurrent detrimental cardiopulmonary consequences of PH as a multisystemic syndrome. Therefore, with an objective to address the affected systems, that is, cardiac and pulmonary simultaneously, we report combined use of inhaled milrinone (a pulmonary vasodilator) through high-frequency nasal cannula (oxygen reservoir and continuous positive airway pressure delivery device), purported to complement each other's mechanism of action in the management of PH, thereby hastening postoperative recovery. This article additionally presents a nuanced perspective on the advantages of combining the aforementioned therapies and hence proposing the same as a possible postoperative cardiopulmonary elixir.

HIGH-FLOW NASAL CANULA AND INHALED EPOPROSTENOL RESPONSE IN COVID-19

SESSION TITLE: Medications and Pulmonary Rehabilitation in COVID-19 Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: The use of inhaled epoprostenol (iEPO) has demonstrated improvement in outcomes for patients with pulmonary hypertension and right heart failure. iEPO has been used as a rescue therapy for acute respiratory distress syndrome (ARDS) and has been shown to improve oxygenation, reduce shunting, and decrease pulmonary artery pressures. However, pulmonary vasodilators do not improve mortality in patients with ARDS. Furthermore, there is currently little data on the efficacy of iEPO via high flow nasal cannula (HFNC) for ARDS patients. Here, we describe our experience with iEPO in our patients with COVID-19-related ARDS on HFNC in a Northern California county hospital. METHODS: From March 2020 to December 2021, 74 patients with COVID-19 infection and related ARDS were placed on HFNC and received iEPO, at a public tertiary care center. A positive response to iEPO was defined as an increase P/F ratio of 10%, increase in PaO2 of 20%, decrease in FiO2, or reduced flow rate within 24 hours of initiation of iEPO. Non-parametric statistics were used to compare groups. RESULTS: 21 women and 53 men with COVID ARDS ranging from 30-86 years of age (mean age 60.1 ± 13.9) received iEPO while on HFNC. The mean hospital length of stay was 36.3 ± 43 days. All patients received steroids and 83.8% received antibiotics. 55.4% of all patients in the study (n=41) progressed to mechanical ventilation and 58.1% (n=43) survived to discharge, mean age 57 ± 14 years. 20.3% (n=15) of patients showed a response to iEPO. Patients who responded to iEPO were significantly less likely to progress to mechanical ventilation (13% vs 66%, p=0.0003) and more likely to survive to discharge (93% vs 49%, p=0.0021). CONCLUSIONS: Among patients with COVID ARDS on HFNC, patients who respond to iEPO are less likely to progress to mechanical ventilation and more likely to survive to discharge. Our study is limited by small sample size and lack of randomization. Use of iEPO in the right subset COVID ARDS on HFNC may improve outcomes. CLINICAL IMPLICATIONS: Patients on HFNC selected for initiation of iEPO had a poor overall prognosis, with 41.9% not surviving to discharge and 55.4% requiring mechanical ventilation. iEPO response correlates with not requiring mechanical ventilation and with increased likelihood of survival to discharge. DISCLOSURES: No relevant relationships by Heng Duong No relevant relationships by Craig Ivie No relevant relationships by Neharika Khurana No relevant relationships by Connie Park No relevant relationships by Natasha Puri No relevant relationships by Adam Thompson No relevant relationships by John Wehner

UTILIZING COMBINATION THERAPY WITH INHALED EPOPROSTENOL AND LOOP DIURETICS IN ACUTE HYPOXIC RESPIRATORY FAILURE FROM COVID-19

SESSION TITLE: What Lessons Will We Take From the Pandemic? SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/19/2022 11:15 am - 12:15 pm PURPOSE: Inhaled pulmonary vasodilators such as epoprostenol (IE) and nitric oxide have been used to treat refractory hypoxemia due to COVID-19 by improving ventilation-perfusion mismatch. One undesirable consequence of this therapy is increased left atrial pressures and risk of pulmonary edema due to systemic vasodilation. The concomitant use of diuretics could mitigate this side effect thereby optimizing IE’s therapeutic impact. The aim of this study was to assess improvement in oxygenation in spontaneously breathing and mechanically ventilated patients with COVID-19 who received IE alone and those who received both IE and loop diuretic (LD) within 24 hours of each other. METHODS: This is a retrospective case control study approved by the local IRB. Improvement in oxygenation was defined as an improvement in the PaO2/FiO2 (PF) ratio by at least 10% within the 24 hours following therapy. SpO2/FiO2 (SF) ratio was used as a surrogate in cases where arterial blood gas trend was not available. Data was analyzed using SPSS version 26 and chi-square analysis was used to compare the 2 groups. RESULTS: A total of 80 patients with COVID-19, confirmed through RT-PCR, received IE from October 2020 to February 2022. Patients were stratified into 2 groups: combination therapy with IE and LD (IE-LD;n = 34;42.5%) vs IE alone (n = 46;57.5%). Improvement in oxygenation was seen in 82.4% IE-LD patients, which was a statistically significant difference compared to19.6% IE patients (z = 5.568, p <.00001). Hospital length-of-stay was comparable (19.6 days in IE-LD, 25.0 days in IE;p = 0.13) but there was a trend towards decreased in-hospital mortality (64.7% in IE-LD, 82.6% in IE only). The eventual need for mechanical ventilation in spontaneously breathing patients (52.9% in IE-LD, 56.3% in IE;p = 0.85) and mean ventilator days in intubated patients (14.3 days in IE-LD, 16.6 days in IE;p = 0.61) were not statistically different between the 2 groups. CONCLUSIONS: IE is a valuable rescue therapy in cases of refractory hypoxemia due to Covid-19 as previous studies have shown that approximately half of all patients will show improvement in oxygenation. In our study, 43 out of 80 patients had an increase in PF or SF ratio of at least 10% and the majority of these received combination therapy rather than IE alone, suggesting that LD is an effective adjunct to IE. CLINICAL IMPLICATIONS: The role of inhaled pulmonary vasodilators in management of Covid-19 is well-documented as they have been shown to delay intubation in spontaneously breathing Covid-19 patients. Despite the small sample size and retrospective design, our study reports that using LD to minimize inadvertent effects of pulmonary edema when administering IE, can further improve oxygenation in this population. Thus, more studies investigating this combination therapy are warranted. DISCLOSURES: No relevant relationships by Kristine Bessette No relevant relationships by Raj Parikh No relevant relationships by Michael Perkins No relevant relationships by Mari-Elena Pino No relevant relationships by Saimir Sharofi

In it for the long run! Long-Term ECMO as a Bridge to Recovery in Severe COVID-19 ARDS

Introduction: During the pandemic, various guidelines were developed for the utilization of extracorporeal membrane oxygenation (ECMO) for COVID-19 ARDS. However, once patients were cannulated for ECMO, the timeframe for lung recovery and referral for lung transplantation was less clear. To date, there are few reported cases of successful long-term (>28 days) ECMO as a bridge to lung recovery. Method(s): We present three patients who were referred for lung transplantation for severe COVID-19 associated respiratory failure and ultimately achieved successful lung recovery following long-term venovenous ECMO support. Patients presented at different stages of the pandemic, were of different ethnicities, aged 35-54 years old, average BMI of 27.6 and two were male. Prior to cannulation, all patients failed mechanical ventilation, prone positioning, neuromuscular blockade and pulmonary vasodilators. Patients were cannulated within 7 days of intubation, underwent early tracheostomy and participated in ambulatory physical therapy. Complications during ECMO included acute renal failure requiring renal replacement therapy, pneumothorax, right ventricular dysfunction and concomitant bacterial pneumonia with bacteremia. The median duration of ECMO was 104 days (range 84-142 days). Radiographic imaging reported end stage restrictive changes in all patients. Survival to hospital discharge was 100%. All patients had complete renal recovery, resolution of RV dysfunction and functional independence without oxygen. Radiographic changes and pulmonary function continued to improve after decannulation. Conclusion(s): Long-term ECMO is an effective strategy for lung recovery in severe COVID-19 ARDS. Duration of ECMO support and radiographic findings should not be used alone to determine recoverability or need for lung transplantation.

To drain, or not to drain: Diagnostic and therapeutic challenges associated with cardiac tamponade in Right heart sided heart failure and pulmonary hypertension

Background: In clinical practice, cardiac tamponade is not an all-or-none phenomenon, but rather a continuum of hemodynamic impairment. Diagnosis depends on an overall assessment of clinical and echocardiographic findings, hemodynamic measurements, and other corresponding patient-level variables must be considered to make a diagnosis to initiate timely intervention.1 The identification of cardiac tamponade in the presence of severe pulmonary hypertension and right ventricular failure can be even more challenging, because the classic findings are often not observed. Our patient clearly had hemodynamic compromise (orthostatic collapses and then persistent hypotension from a large pericardial effusion but did not exhibit the common features of tamponade on ECHO. This can be explained by the preexisting, markedly elevated right-sided pressures, which prevented typical findings of pulsus paradoxus, right atrial and ventricular diastolic collapse, and equalization of diastolic pressures.1 Case presentation: 44 Years old lady background of Interstitial lung disease, pulmonary artery hypertension, Right heart failure and anti-synthetase syndrome. Recently required Intensive care admission for COVID pneumonitis and was discharged on home oxygen. Now admitted to hospital after she boarded the flight without oxygen and became unwell. She was treated on lines of exacerbation of interstitial lung disease, Right heart failure and moderate pericardial effusion without signs of tamponade in ECHO and was given adequate diuresis and responded very well to it. Her oxygen requirement came down and she clinically improved. Few days after, she developed diarrhea and prerenal Acute kidney injury while in ward and became borderline hypotensive which improved after her diuretic doses were reduced and then held. She then after few days started to develop orthostatic collapses with hypotension and then became persistently hypotensive. Her CT Pulmonary angiogram showed unchanged moderate circumferential pericardial effusion, and no Pulmonary embolism. She was reviewed by Critical care outreach team and an urgent bedside Echocardiogram was performed to rule out features of tamponade which showed moderate pericardial effusion, severely dilated Right heart with massive Right ventricular pressures compressing her Left ventricle. She was urgently reviewed by cardiology and was taken to Intensive care unit for invasive hemodynamic monitoring, where she was given inotropes and inhaled pulmonary artery vasodilators. The decision was taken to cautiously diurese and not to drain the pericardial effusion due to risk of developing further instability by increasing right ventricular expansion causing further collapse and pressure on Left ventricle. Discussion and conclusion: Our case stresses on the importance of Bedside Echocardiogram in timely identifying the atypical features of cardiac tamponade and to understand the different hemodynamics and mechanism of obstructive shock in patients with pre-existing right sided heart failure. After the establishing that patient was in obstructive cardiogenic shock with atypical findings of tamponade, the next most important step was to decide whether to drain the pericardial effusion or not. In our literature search, we found that the drainage of a large pericardial effusion in patients with pulmonary hypertension has been accompanied by catastrophic, sudden hemodynamic collapse and it has been postulated that the presence of pericardial fluid limits right ventricular distension in response to pressure and volume overload. When the pericardial fluid is removed, rapid enlargement of the right ventricle causes: (1) reduced right ventricular systolic function due to muscle fiber distension;and (2) compression of the left ventricle, which leads to impaired diastolic filling and left ventricular outflow track obstruction.1.

Compassionate use of pulmonary vasodilators in acute severe hypoxic respiratory failure due to COVID-19

Introduction: There have been over 200 million cases and 4.4 million deaths from Covid-19 worldwide. In the UK over half a million have required hospitalisation, with over 130,000 deaths. Although most experience a mild illness the mortality can be over 50% for those requiring mechanical ventilation.1 One potential treatment for severe hypoxaemia is inhaled pulmonary vasodilator (IPVD) therapy, either as nitric oxide (NO) or prostaglandin analogues. Despite the lack of robust evidence IPVDs are often considered recue treatments for refractory hypoxaemia.2,3 Given the disease severity in COVID-19 we implemented a protocol for the use of IPVDs on a compassionate basis for patients with severe hypoxaemia receiving otherwise maximal support. In this study we detail our findings and assess differences between survivors and non-survivors. Objectives: The primary outcome of this study was percentage changes in PaO2/FiO2 (PF) ratio and Alveolararterial (A-a) gradient at 2, 6, 12, 24, 48 and 72 hours following initiation of IPVD therapy. Secondary outcomes were differences in characteristics and response to therapy between survivors and non-survivors who received an IPVD. Methods: Data from a prospectively maintained research database of patients with SARS-CoV-2 admitted to the ICU at a large teaching hospital were analysed for the time period 14 March 2020 -11 February 2021. Patients aged 18 years or older who received an IPVD during their admission were eligible for inclusion. An IPVD was considered if the PF ratio was less than 13.3kPa despite rescue therapies (prone positioning, neuromuscular blockade, airway pressure release ventilation). Nitric oxide was commenced at 20ppm and titrated to response. If oxygenation improved Iloprost nebulisers were commenced at 10-30mcg four hourly and NO weaned. Results: Three-hundred eight patients with SARS-Cov-2 were admitted during the study period of whom 59 (19.2%) received IPVD therapy. Patients receiving an IPVD had a lower PF ratio (14.37 vs. 16.37kPa, p=0.002) and higher APACHE-II score (17 vs. 13, p=0.028) at admission compared to those who did not. Survival to ICU discharge was lower in patients receiving an IPVD (55.9% vs. 81.9%, p<0.001). The median PF ratio at commencing IPVD therapy was 11.33kPa (9.93-12.91) with a median of 6 days from admission to receiving an IPVD. At 72 hours the median improvement in PF ratio was 33.9% (-4.3-84.1). In patients receiving IPVDs there were no differences in other therapies received (steroids, prone ventilation, ECMO) between survivors (n=33) and non-survivors (n=26), with the exception of renal replacement therapy. At 72 hours changes in PF ratio (70.8 vs. -4.1%) and reduction in A-a gradient (44.7 vs. 14.8%) differed significantly between survivors and non-survivors (both p <0.001). Conclusion: The response to the compassionate use of IPVDs for patients with acute hypoxic respiratory failure due to Covid-19 differs significantly between survivors and non-survivors. Both NO and inhaled prostaglandins may offer therapeutic options for severe hypoxaemia due to COVID-19, with prostaglandins particularly attractive as they do not require specialist delivery systems. The use of inhaled prostaglandins, and NO where feasible, should be studied in both isolation and combination in adequately powered prospective randomised trials.

Administration of Inhaled Nitric Oxide for COVID and Non-COVID Acute Respiratory Distress Syndrome in the Intensive Care Unit: A Retrospective Cohort Analysis

Rationale: Inhaled nitric oxide (iNO) has been used for several years as an adjunctive therapy for improving oxygenation in adults with acute respiratory distress syndrome (ARDS). Recently, several authors have suggested iNO as a useful therapy in the setting of ARDS secondary to COVID-19. Nevertheless, there remains unclear evidence regarding the utility of iNO in adults with both COVIDand non-COVID-associated ARDS, and still less evidence regarding who might benefit from this costly treatment. We sought to investigate the effect of iNO on oxygenation in adults with ARDS secondary to both COVID and non-COVID etiologies, evaluate the difference in outcomes between patients with and without COVID receiving iNO, and explore the cost associated with the administration of iNO in an intensive care setting. Methods: We conducted a retrospective cohort study in the medical and surgical intensive care units at a tertiary-care academic medical center. All patients with ARDS who received iNO over a two-year period were considered for inclusion. Exclusion criteria included prior pulmonary hypertension already on a pulmonary vasodilator, initiation of iNO prior to arrival at our institution, or lack of an arterial blood gas immediately before and after the initiation of iNO. Outcomes measured included change in PaO2/FiO2, 30-day mortality, and the cost of iNO administration. Results: 177 consecutive patients were evaluated, of whom 108 met criteria for inclusion. Change in PaO2/FiO2 ratio following iNO administration was significantly smaller in patients with COVID than in patients with non-COVID ARDS (22.9% vs 60.4%, p = 0.002). Among COVID patients there was no significant improvement in PaO2/FiO2 following the administration of iNO (95% CI [-64%, 108%]). A response in PaO2/FiO2 (defined as >10% increase) was not associated with 30-day mortality (p = 0.29). The average cost of iNO administration among all patients was $66597.79, and there was a trend toward greater cost in patients deemed P/F responders ($76433 vs $53195, p = 0.07). There was no difference in these outcomes in patients receiving iNO for refractory hypoxia versus patients receiving iNO for RV dysfunction. Conclusions: In this study, iNO administration incurred an average cost of $66597.79 per patient and showed no association with improved PaO2/FiO2 ratio in patients with COVIDARDS. PaO2/FiO2 changes in COVID patients were significantly smaller than in non-COVID patients. An increase in PaO2/FiO2 > 10% was a poor predictor of 30-day mortality but did show a trend toward increased cost burden.

TCTAP C-005 Conundrum of a ‘Primary’ Angioplasty: Provisional Stenting of Left Main Stem / Left Anterior Descending During STEMI With Double Bifurcation

Clinical Information Patient Initials or Identifier Number: R Relevant Clinical History and Physical Exam: A 64-year-old lady with underlying dyslipidemia presented to our emergency department with typical chest pain. Immediate electrocardiogram was performed which showed sinus rhythm, ST elevation at lead 1, aVL and V1, hyperacute T wave at V2 till V3 with ST depression at leads II, III and aVF. Hence a diagnosis of acute anterolateral myocardial infarction, Killip 1 was given and urgent referral to cardiologist was made. Subsequently, she was subjected for primary angioplasty. Relevant Test Results Prior to Catheterization: Blood results showed sodium of 134 mmol/L, potassium of 3.5 mmol/L, urea of 3.2 mmol/L and creatinine of 67 mmol/L. Liver enzymes were within normal limits with aspartate transaminase of 38 U/L and alkaline phosphatase of 91 U/L. Creatinine kinase was 330 U/L but increased to 2861 U/L during subsequent day. In addition, COVID-19 RTK antigen was negative. Relevant Catheterization Findings: Coronary angiogram revealed mild disease at proximal right coronary artery and proximal left circumflex. Minimal disease was noted at distal left main stem, but severe disease was observed from proximal left anterior descending till mid left anterior descending. Heterogenous plague suggesting thrombus was seen at ostial first diagonal as well. [Formula presented] [Formula presented] Interventional Management Procedural Step: Right femoral assess was obtained with 7Fr sheath, and SL 3.5 7Fr guiding catheter was engaged to left coronary artery. Intracoronary heparin and tirofiban were given prior to wiring. First diagonal was wired with Sion Blue while left anterior descending was wired with Runthrough Floppy. Post-wiring both vessels, coronary flow remained TIMI 3 and hence we decided to proceed with IVUS. From IVUS, noted fibrous elastic plague with heavy thrombus burden. Intracoronary streptokinase was given and noted improvement of thrombus from IVUS. BMW wired to left circumflex. Lesion predilated with scoring balloon and associated with no reflow events, resolved post vasodilators. Left main stem was stented with Onyx 3.5 x 26 mm and deployed at 16 atm. Both side branches wires were rewired into same branches via Crusade microcatheter. LMS stent was post dilated with NC Euphora 4.5 mm at nominal pressure. Noted impingement of both ostium diagonal and circumflex branches. Balloon kissing inflation was performed for both LAD/Diagonal bifurcation and LMS/LAD/circumflex bifurcation. POT was performed post balloon kissing inflation with NC Euphora 3.5 mm and 4.5 mm for both LAD and LMS respectively. Next, IVUS was repeated for mid LAD stent length and Onyx 3.0 mm X 15 mm was deployed at nominal pressure. IVUS repeated and noted under-expansion of overlapped segments and post dilated with NC Euphora 3.0 mm at high pressure. [Formula presented] [Formula presented] [Formula presented] [Formula presented] Conclusions: Our clinical vignette demonstrated few learning points including utilization of IVUS during primary angioplasty. Understanding of plague characteristic ensures adequate stents expansion especially with fibro elastic plague. In addition, we also demonstrated several precautions in dealing with bifurcation lesions including usage of double lumen microcatheter for wiring the side branches. Even though we opted for provisional stenting, balloon kissing inflation played pivotal role in preserving flow into side branches.

FIRST REPORTED CASE OF TAKOTSUBO CARDIOMYOPATHY INDUCED BY PERCUTANEOUS CORONARY INTERVENTION

Background: We report an unusual case of Takotsubo cardiomyopathy (TTC) caused by radial spasm during percutaneous coronary intervention (PCI), resulting in a fatal outcome. Case: A 70-year-old Caucasian female presented with an acute anterior myocardial infarction (MI) with anterior ST segment elevation. Coronary angiography showed critical proximal left anterior descending artery stenosis, and she underwent successful PCI via the right radial artery. Post-MI echocardiogram showed anterior wall hypokinesis with a left ventricular ejection fraction (LVEF) of 45%. The right coronary artery (RCA) had 70% stenosis in the mid-vessel and a staged outpatient intervention was planned. Decision-making: The staged procedure was delayed by seven months due to the COVID-19 pandemic. The same right radial access was selected but she developed significant radial spasm. Despite vasodilators, radial spasm persisted, so balloon-assisted tracking technique was used to advance guiding catheter. Fractional flow reserve of the RCA stenosis was positive at 0.76. PCI was then successfully performed using a 3x48 mm Xience stent. Thirty minutes later, she developed severe chest pain with widespread ST segment elevation. Repeat angiography via the right femoral artery showed patent coronary arteries. Echocardiography showed new apical ballooning pattern, typical of TTC with LVEF was 35%. She was discharged after 48 hours, but she re-presented a week later with cardiogenic shock. She had florid pulmonary oedema and an echo showed new torrential mitral regurgitation due anterior mitral leaflet chordal rupture. The apical ballooning that was observed a week earlier had resolved. An intra-aortic balloon pump was inserted, and the patient underwent emergency repair of the mitral valve. The procedure was technically successful, but the patient died on postoperative day one, due to multi-organ failure. Conclusion: We believe that TTC in our patient was caused by radial artery spasm. To our knowledge, this is the first case of TTC caused by radial spasm. Furthermore, chordal rupture secondary to TTC has been reported only once before.

Vasospasm due to eosinophilic coronary periarteritis treated with an anti-IL-5

Background: Vasospasm due to eosinophilic coronary periarteritis (VECP) can cause not only vasospastic angina but also myocardial infarction and sudden cardiac death. It is usually resistant to conventional treatment of coronary disease and responds to systemic corticosteroids. The role that may have the monoclonal antibodies reducers eosinophils is unknown. Method: A 52-year-old female with chronic rhinosinusitis with nasal polyposis, moderate persistent bronchial asthma and Aspirinexacerbated respiratory disease(AERD), without atopy, had been treated with inhaled and intranasal fluticasone, oral montelukast and inhaled formoterol. In July 2019, she arrived at the emergency room with an acute coronary syndrome. Results: The procedures performed revealed high levels of troponin 16717ng/L(0- 47ng/L), and abnormal electrocardiogram (alteration of repolarization in II, III and aVF). Marked eosinophilia of 750cells/ mm3 was noticed. She was treated with oral vasodilators and aspirin, which due to her AERD required rapid desensitization, being effective. However, she continued with recurrent chest pain and electrocardiographic abnormalities. Diagnostic coronary angiography revealed vasospasm in the right coronary artery without atheromatous lesions. Type 2 myocardial infarction secondary to VECP was suspected and prednisone 30mg/day was started with complete resolution of chest pain. She developed a Cushing syndrome and prednisone dose was reduced, but chest pain and eosinophilia(1000/mm3) reappeared, and prednisone 20mg/day was reintroduced. It was decided to discontinue corticosteroids and treatment was begun with anti-IL-5(benralizumab) in May 2020, reducing eosinophilia( 0/mm3) from the first dose. At 6 months we suspended prednisone without new episodes of pain. In August 2020, she was visited due to SARS-CoV-2 infection without symptoms of bronchospasm or pneumonia and received the 4th dose of benralizumab without complications. Conclusion: An acute coronary syndrome refractory to conventional medications with normal coronary arteries and eosinophilia, with a history of chronic rhinosinusitis/polyposis, asthma and/or AERD, VECP should be considered and early treatment with corticosteroids could save lives. This is the first case to our knowledge in which anti IL 5 has been used for VECP to control of the eosinophilic disorder. Likewise, it was administrated during the SARS-CoV-2 infection without complications.

Is this scleroderma lung or COVID-19 lung?

Case report-IntroductionThis is a case of Pakistani female with limited systemic sclerosis and associated mild interstitial lung disease. The lung disease was complicated by SARS-COV-2 related pneumonitis in April 2020 and that led to treatment challenges.She was previously seen in multiple private hospitals and labelled as Rheumatoid arthritis. She was being treated with long term steroids and Methotrexate. After her initial presentation to our Rheumatology services, her diagnosis was correctly revised to Systemic Sclerosis with phenotype of CREST. Her treatment was adjusted to Vasodilators and Mycophenolate due to skin and Lung involvement.Case report-Case descriptionThis is a case of 40-year-old Pakistani female who had been having multiple joint pains since 2010. She also experienced severe Raynaud's.She presented to our Rheumatology clinic in December 2018. Her symptoms included recurrent digital ulcers, tight and tough skin at fingers and Raynaud's worse during winter months. Her examination confirmed peripheral cyanosis with multiple digital ulcers with superimposed infection, marked sclerodactyly and calcinosis. She was started on Vasodilator therapy including calcium channel blocker and PDE5 inhibitor due to severity of ulceration. Infection was managed with prolonged course of antimicrobial therapy. Her immunology showed positive anti nRNP/Sm. Anti-centromere and anti Scl 70 were negative. Her condition fit description of CREST (Calcinosis, RP, Oesophageal dysmotility, telangiectasia). Her management included weaning off Methotrexate and reduction in the dose of corticosteroids.In February 2019, Respiratory work up showed normal Chest radiograph, High resolution CT chest showing no significant abnormality and FEV1 82%, FVC 86%, and DLCO 77%. Her PASP was 25mmHg. Overall, her condition remained stable over the course of next year. Her medication included Cellcept, low dose prednisolone, hydroxychloroquine, and Sildenafil. More importantly, Digital ulcers have been well controlled with combined vasodilator therapy.In April 2020, she developed SARS-CoV-2 with mild respiratory symptoms and was admitted to a different hospital. Fortunately, she responded well to ward based supportive and symptomatic treatment with no need for respiratory support. Subsequently, she has seen a different respiratory physician and had repeat imaging of chest which has led to dilemma whether the ground glass opacities in both lungs is due to scleroderma lung or COVID-19 related lung disease. She was given high dose prednisolone by the respiratory physician which has been reduced in rheumatology clinic. The new findings on chest imaging are sequelae of SARS-COV-2.Case report-DiscussionThis case highlights few important points as below:Systemic sclerosis diagnosis was not made for many years even though she has had severe digital ulcers for a long time. She was being managed as Rheumatoid arthritis. Systemic sclerosis remains a difficult disease to diagnose and is still under recognised.SARS-COV-2 related illness has not affected this patient adversely despite the fact of being on long term maintenance prednisolone of 7.5mg daily dose and Cellcept 2gm. Her cellcept was temporarily stopped during acute illness.We know that viral pneumonitis can present with typical ground glass opacities in bilateral areas of lungs and differential diagnosis does include connective tissue related lung disease but this lady had no significant respiratory involvement prior to COVID-19 illness and follow up scan will help to decide if this is disease progression or related to viral cause.Case report-Key learning pointsThere are multiple learning points in this case:Continuity of care under same primary team can avoid confusion related to diagnosis and diagnosis related complications. This lady had none, or mild subclinical lung involvement related to systemic sclerosis prior to contracting COVID-19 illness. Her CT chest findings after the episode of SARS-COV-2 were attributed to systemic sclerosis as she was seen by different respiratory team. This conti uity is not always possible, but MDT collaboration needs to be improved across hospitals and across various departments.Systemic sclerosis remains an under diagnosed and under recognized complex rheumatic disorder and more primary care physicians need to be educated so they can appropriately refer these cases to Rheumatology services.Multi-disciplinary collaboration between Rheumatology, Respiratory and other specialties is the key point to manage these complex cases.This case also highlights an interesting observation that presence of significant immune disorder and immunosuppressant medication does not always equate to worse outcome if patient contracts SARS-COV-2. Supportive care, appropriate observation, and temporary suspension of DMARD in such cases can avoid any further complications.

Stress myocardial blood flow reduced after severe COVID-19, not related to symptoms

Introduction: Persistent cardiopulmonary symptoms after COVID-19 are reported in a large number of patients and the underlying pathology is still poorly understood. (1) Histopathologic studies revealed myocardial macrophage infiltrates in deceased patients, likely an unspecific finding of severe illness, and increased prevalence of micro- and macrovascular thrombi. (2) We examined whether microvascular perfusion, measured by quantitative cardiac magnetic resonance under vasodilator stress, was altered post COVID-19. Methods: Our population consisted of 12 patients from the Pa-COVID- 19-Study of the Charité Berlin, which received a cardiac MRI as part of a systematic follow up post discharge, 10 patients that presented at the German Heart Center Berlin with persistent cardiac symptoms post COVID-19 and 12 patients from the Kings College London referred for stress MRI and previous COVID-19. The scan protocol included standard functional, edema and scar imaging and quantitative stress and rest perfusion to assess both macro- and microvascular coronary artery disease. The pharmacological stress agent was regadenosone in 20 and adenosine in 13 of the patients. To control for the higher heart rate increase under regadenosone compared to adenosine, we calculated the myocardial blood flow per heartbeat (MBFΔHRi) under stress. Results: The median time between first positive PCR for COVID-19 and the CMR exam was 2 months (Range 0 to 12). None of the 33 patients exhibited signs of myocardial edema. One patient with a previous history of myocarditis had focal fibrosis. Three patients with known coronary artery disease showed ischemic Late Enhancement. Five patients had a small pericardial effusion;one of these four patients showed slight focal pericardial edema and LGE, consistent with mild focal pericarditis. Five Patients had a stress-induced focal perfusion deficit. Mean Stress MBFΔHRi was 32.5±6.5 μl/beat/g. Stress MBFΔHRi was negatively correlated with COVID-19 severity (rho=-0.361, P=0.039) and age (r=-0.452, P=0.009). The correlation with COVID-19 severity remained significant after controlling for age (rho=-0.390, P=0.027). There was no apparent difference in stress MBFΔHRi between patients with and without persistent chest pain (34.5 vs. 31.5 μl/beat/g, P=0.229) Conclusion: While vasodilator-stress myocardial blood flow after COVID- 19 was negatively correlated to COVID-19 severity, it was not correlated to the presence of chest pain. The etiology of persistent cardiac symptoms after COVID-19 remains unclear. (Figure Presented).