key: cord-029332-yn603pvb authors: nan title: Full Issue PDF date: 2020-07-15 journal: JACC Case Rep DOI: 10.1016/s2666-0849(20)30838-x sha: doc_id: 29332 cord_uid: yn603pvb nan T he coronavirus disease-2019 (COVID- 19) pandemic has revolutionized clinical practice in recent months unlike any other health emergency in recent years. JACC: Case Reports has taken this challenge very seriously, dedicating to it an entire issue. We have received excellent case reports from across the world. Our goal is to provide a comprehensive report of representative cardiovascular involvement in COVID-19 (Central Illustration). Besides the concern regarding QT interval prolongation with hydroxychloroquine and azithromycin treatment, COVID-19 is strongly associated with the occurrence of sudden unexpected arrhythmias. Given the general ignorance of the pathophysiological mechanisms of the virus at the time of submission of these case reports, it is hard to state with certainty that COVID-19 has been the cause of these arrhythmias, but they surely offer an interesting direction for future research in the field. Included are cases of Brugada type I pattern positivization (1) in the context of fever, one of the most common presenting symptoms of the disease (2); electrical ventricular storm (3); transient atrioventricular block in the absence of myocarditis (4); sinus node dysfunction requiring pacemaker implantation (5) ; and finally a provocative report on the use of amiodarone as a possible treatment for COVID-19 (6) . Overall, the cytokine storm has proved to have a strong impact on the conduction system. The clinical presentation of patients with COVID-19 has ranged from asymptomatic to acute respiratory distress syndrome requiring mechanical ventilation. One cause of sudden respiratory deterioration is the increased risk for venous thromboembolic disease in these patients (7) (Figure 1 ). These events have been noted both early and in the recovery phase of COVID-19. Furthermore, thromboembolic events have occurred despite the use of prophylactic anticoagulation or even full anticoagulation (8) . A majority of patients have elevated levels of D-dimer and laboratory findings consistent with sepsis-induced diffuse intravascular coagulation, suggesting a coagulopathic process, yet no prospective studies have demonstrated the predictive nature of these markers for the occurrence of a thromboembolic event, only a higher risk for mortality (9) . The early recognition and treatment of venous thromboembolic disease has therefore been a dilemma. We therefore provide commentary and suggest treatment algorithms (10) . We received case reports in 4 general categories detailing an increased risk or arterial thrombosis during the COVID-19 pandemic. causing STEMI in infected patients (11, 12) . Second, there were a number of cases of STEMI in patients younger than 30 years without risk factors for atherosclerosis (13) . This phenomenon occasionally occurred before COVID-19, but the increased incidence reminds us to always include myocardial infarction in the differential diagnosis of a younger patient with chest pain and to always consider performing screening electrocardiography. Third, a number of cases of STEMI mimics were submitted, including patients with ST-segment elevation due to myopericarditis, Brugada pattern, takotsubo cardiomyopathy, or endothelial dysfunction due to infection or cytokine storm. As many as 40% of patients with COVID-19 and ST-segment elevation may have normal coronary arteries on angiography, complicating the decision whether to administer fibrinolytic therapy to patients without early access to primary percutaneous coronary intervention. Finally, there were reports of spontaneous thrombosis (14) involving the ascending and descending aorta, the cerebrovascular arteries, the mesenteric and renal arteries, and the peripheral arteries, underscoring an increased systemic risk for arterial thrombosis in patients with COVID-19. The development of heart failure in patients infected with severe acute respiratory syndrome coronavirus-2 has been described to involve 2 different, and overlapping, mechanisms. One is cytokine release resulting in myocardial inflammation (Figure 3) , and affected patients has demonstrated both inflammatory infiltrates and viral particles. The heart failure cases presented in this special issue, however, describe more varied presentations of patients, some with pre-existing heart failure and others with no known cardiac disease prior to becoming ill with infection. In addition to cases of direct myocardial injury, some with pathological evidence, we also present 2 cases of takotsubo cardiomyopathy (16, 17) Two cases highlight the special circumstances faced by patients with left ventricular assist devices (18, 19) , which include the inability to tolerate prone positioning to augment respiratory support because of the mechanical equipment and the hypothesis that mechanical circulatory support may provide a type of protection against the most serious hemodynamic consequences of severe acute respiratory syndrome coronavirus-2 infection. Included also is a case series of pediatric patients who had hemodynamic collapse and cardiac dysfunction (20) , a presentation that has been rare in this younger age group. The now well-recognized thromboembolic disorders encountered with this disease include a case in this issue of massive pulmonary embolism and resultant severe right heart failure (8) . And 2 separate reports describe patients with concomitant noncardiac disease, 1 with human immunodeficiency virus infection (18) and 1 with influenza (21) . All the cases of heart failure represent the investigators' best attempts at providing supportive and emerging therapies at a time when they had no established guidelines and no best practices to follow. From the beginning of the pandemic, we believed that it was very important to publish the "voices" of our frontline colleagues across the world, to help cardiologists to get acquainted with mechanical ventilation (22) , to describe the first evidence of sex differences in COVID-19 (23) , and to discuss the significant changes in health care with telemedicine and virtual clinics. The impact of COVID-19 on African Americans has also recently been described in JACC (Table 1 ) revealed leukopenia, normocytic anemia, thrombocytopenia, and significant increase in C-reactive protein levels. A nasopharyngeal swab sample tested positive for severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) using real time-reverse transcriptionpolymerase chain reaction. The patient had a medical history of bipolar disorder and hypothyroidism. He reported having fever for 1 week. Given the patient's presentation of prolonged asystole, differential diagnosis included metabolic disorders, pharmacologic agents and extracardiac diseases with special attention to thyroid hormone levels. To recognize cardiovascular complications among COVID-19 patients. To demonstrate arrhythmic risk related to COVID-19 disease. To manage sick sinus dysfunction in COVID-19 disease. During the following days, the patient had episodes of asystole associated with hypotension but without loss of cardiac output ( Figure 3 ). Moreover, alternating episodes of bradycardia and tachycardia Note bilateral ground glass opacities. Once reversible causes were excluded, symptoms were related to dysfunction of the intrinsic sinus node, and the patient underwent dual-chamber ratemodulated implantation of a pacemaker (PM) ( Figure 4 ). Because of evidence of sinus tachycardia, bisoprolol was administrated. Further and later PM control showed only this episode. Transthoracic echocardiography was repeated before the patient was discharged and showed no differences from the previous one. In consideration of his progressive clinical improvement, the endotracheal tube was removed, and the patient began to breath spontaneously. On psychiatric indication, therapy for bipolar disorder was reintroduced. This could be due to hypoxia and electrolyte abnormalities, which could lead to episodes of cardiac arrhythmia, or due to central nervous system alterations caused by SARS-CoV-2 disease. Increasing evidence shows that CoVs are not always confined to the respiratory tract but may also invade the central nervous system, inducing neurological diseases (1, 3) , and some CoVs have been shown to be able to spread to the medullary cardiorespiratory center through chemoreceptors and mechanoreceptors in the lung and lower respiratory airways through a synapse-connected route (4) . Considering that most CoVs share a similar viral structure and infection pathway (5) , the infection mechanisms previously found for other CoVs may also be applicable to SARS-CoV-2. Furthermore, the transsynaptic transfer also has been reported for avian bronchitis virus (6) In fact, the intrinsic cardiac nervous system has regional control over different cardiac functions, such as sinus node electrical activation and propagation, as well as atrioventricular nodal conduction, and consists of ganglia composed of afferent, efferent, and interconnecting neurons to other cardiac ganglia. These ganglia coordinate the sympathetic and parasympathetic inputs received from the rest of the cardiac autonomic nervous system. Generally, autonomic dysfunction refers to a disorder of an autonomic nervous system that may arise from intrinsic or extrinsic mechanisms. Intrinsic autonomic dysfunction arises from diseases that directly affect the autonomic nerves, such as diabetes mellitus and the various syndromes of primary autonomic failure. Extrinsic autonomic dysfunction often is secondarily induced by cardiac or other disease (9) . Patients with autonomic dysfunction commonly have poor long-term prognosis, and death can occur from pneumonia, acute respiratory failure, sudden cardiopulmonary arrest, or fatal arrhythmias related, for example, to SSD. Specifically, SSD includes a spectrum of heart rhythm disturbances related to abnormal sinus impulse formation or propagation (10) and has different presentations, such as bradycardia, alternating episodes of bradycardia and tachycardia and sinoatrial block. In some cases, SSD presents with sinus node arrest and prolonged asystole, such as in the present patient. Symptoms related to SSD are generally fatigue and syncope or presyncope, but patients can be asymptomatic in the early phase of the disease. When symptoms are related to dysfunction of sinus node, PM implantation is required. Currently, data regarding the neuroinvasive potential of SARS-CoV-2 with subsequent autonomic dysfunction are less described. Furthermore, to these authors' knowledge, this is the first case in medical literature of SSD related to COVID- 19 infection. An improved understanding is crucial primarily for guiding the need for additional arrhythmia monitoring during hospitalization and after discharge (2) . The present authors believe that recognition by the scientific community of these risks related to COVID-19 disease may be helpful for strict monitoring of affected patients and also for furthering knowledge of such complications for global public health. Diagnostic coronary angiography performed through the right radial approach revealed angiographically normal coronary arteries (Figures 3 and 4) . Ventriculography confirmed the globally mildly reduced ejection fraction. The patient was admitted to a dedicated coronavirus disease-2019 (COVID- 19) intensive care unit. The COVID-19 results became available within 24 h and were positive. His condition continued to improve, and he required minimal supplemental oxygen to maintain arterial saturation. All serial troponin values were negative. Two days later he developed a brief episode of supraventricular tachycardia that was successfully terminated with intravenous adenosine ( Figure 5 ). Four days after the initial presentation, he was doing well without fever. The C-reactive protein level had decreased to 25.4 mg/l, and the ECG demonstrated nearly complete resolution of the initial Brugada-like ECG pattern ( Figure 6 ). The patient was discharged to home after the 1-week hospital stay. Diagnosis and treatment of ST-segment elevation myocardial infarction during the COVID-19 pandemic present multiple diagnostic and logistic challenges (1) . Myocardial injury, myocarditis, acute coronary syndromes, and arrhythmias have all been described in the setting of COVID-19 infection (2) . ST-segment elevation in the right precordial leads and Brugada-like ECG patterns have previously been associated with various conditions (e.g., fever, myocarditis toxicity, metabolic disorders, certain drugs). These Brugada-like patterns usually disappear once the inciting event is removed (3) . A Brugada-like ECG pattern presents an additional diagnostic and therapeutic challenge because it may be seen in patients presenting with chest pain, thus mimicking ST-segment elevation. Atrioventricular nodal re-entrant tachycardia, such as developed in our patient, has similarly been associated with Brugada syndrome (4) . Most recently, COVID-19 infection has been described as unmasking Brugada syndrome in a patient who presented with syncope (5). Our case is important because it demonstrates the need to differentiate between the Brugada syndrome and the Brugada-like ECG configuration. Given that our patient had a COVID-19-associated Brugada ECG pattern with no history of syncope, observation therapy was recommended because the risk of major adverse cardiac events is low (6) . COVID-19 manifests mainly as a respiratory syndrome that includes pneumonia and, in the worst case scenario, acute respiratory distress syndrome (3) . We have also learned that, in a not negligible number of cases, the virus can provoke myocardial ischemia and/or inflammation, with or without an associated respiratory syndrome (4) . There are already numerous cases of COVID-19 manifesting as ST-segment elevation myocardial infarction that have triggered activation of primary percutaneous coronary intervention protocols. The cause of this STsegment elevation is unknown: it has been linked to traditional plaque rupture in those patients who have required coronary angioplasty, but it has been suggested that myocarditis or microvascular thrombosis could be the cause when no obvious thrombus or coronary flow interruption is detected. If all this were not sufficient, here comes Brugada type I pattern, interfering with and complicating the lives of interventional cardiologists. Indeed, in the case reported by Vidovich (2) , the patient presented with shortness of breath, substernal chest pain, and fever. The electrocardiogram showed a Brugada type I pattern in the right precordial leads with no reciprocal changes; the presence of chest pain, shortness of breath, and reduction of systolic left ventricular function, assessed with a 2-dimensional echocardiogram, led to urgent coronary angiography, which excluded an ongoing acute coronary syndrome. No significant electrolyte imbalance was found. Vidovich's (2) conclusion was that the Brugada type I pattern, completely unknown to the patient until this admis- A link between fever and a Brugada type I pattern is very well known and has been described extensively (5) (6) (7) . In fact, the international guidelines on sudden cardiac death recommend lowering body temperature as soon as possible in those patients with an established diagnosis of BS, as well as in carriers of the mutations with a proved inducible Brugada type I pattern (8) . The increase in body temperature has indeed been proven to cause a higher degree of inactivation of sodium channels, both mutated and wild ones: in the subjects who are genetically predisposed, this reduced sodium flow can result in a dangerous transmural heterogeneity that is the basis for phase 2 re-entry ventricular arrhythmias and sudden death (9, 10) . It would also be of interest understand whether the virus itself could interact directly with the myocardial ion channels and provoke the electrocardiographic modification typical of BS. The take-home message is therefore that patients with BS and concomitant COVID-19 infection should be monitored in the intensive care unit or in the telemetry ward until the fever is resolved, regardless of their respiratory conditions. Further research will be needed to help clinicians to navigate this uncharted sea. A 49-year-old man presented to the emergency department with acute-onset high-grade fevers accompanied by dry cough and shortness of breath that had been ongoing for a week before presentation. He denied any associated nausea or vomiting, diarrhea, sore throat, congestion, or skin rash. Of note, he had recently returned from a high-prevalence area for coronavirus disease-2019 (COVID-19) within the United States and was in self-quarantine. He was monitoring his symptoms; however, when his shortness of breath was not improving with his asthma medications (albuterol inhaler and cetirizine), he presented to the emergency department. On arrival, he was noted to be febrile at 102.5 F, he was tachypneic to 22 breaths/min, he was normotensive at 125/75 mm Hg, his heart rate was 75 beats/min, and he was saturating 98% oxygen on room air. Physical examination was remarkable for decreased breath sounds bilaterally. His past medical history was significant for mild intermittent asthma. Our patient's clinical presentation was concerning for viral or bacterial lower respiratory tract infection. An electrocardiogram revealed normal sinus rhythm with normal PR (172 ms) and QRS (94 ms) intervals To anticipate and diagnose conduction disturbances associated with the novel coronavirus. To understand the mechanism responsible for high-degree AV block associated with COVID-19 without evidence of overt myocarditis. ( Figure 1 ). No acute ST-T wave changes were noted. A single-view chest radiograph showed blunted costophrenic angles bilaterally with concern for right middle lobe opacity ( Figure 2 Inflammatory markers were mildly elevated; the ferritin level was 571 mg/ml (normal range 0 to 400 ng/ml), and C-reactive protein was elevated at 1.2 mg/dl (normal range 0 to 0.9 mg/dl). The procalcitonin level was negative at 0.039 ng/ml (normal range 0 to 0.080 ng/ml), and thyroid hormone levels were within normal limits. His nasopharyngeal swab tested positive for SARS-CoV-2 ribonucleic acid. Given the patient's underlying asthma, which predisposed him to an increased risk for pulmonary patients were noted to have cardiac arrhythmias (2) . COVID-19 involvement of the heart has ranged from asymptomatic myocardial injury to acute coronary syndrome, mild to fulminant myocarditis, stress cardiomyopathy, and cardiogenic shock; however, the mechanism of cardiac involvement is not exactly clear (3) . Furthermore, underlying cardiovascular disease or risk factors and myocardial injury have been shown to portend poor prognosis in these patients (4) . In this case, we present a patient with moderate COVID-19 infection who showed evidence of transient conduction disturbances with highdegree atrioventricular (AV) block. High-degree AV block is known to be an uncommon presentation of acute myocarditis in adults, more commonly seen in cardiac sarcoidosis and giant cell myocarditis (5) . However, because our patient did not have any other overt evidence of myocardial involvement, with normal cardiac biomarkers and a normal echocardiogram, his presentation is unusual and interesting. It is possible that COVID-19 may have caused subclinical myocarditis leading to high-degree AV block in this case. ACE2 receptors are abundant in the heart and are present in multiple cell types, including macrophages, endothelial cells, smooth muscle cells, and cardiomyocytes (6) . Further, animal models have shown the presence of ACE2 receptors in sinoatrial nodal cells in rats (7) , and conduction disturbances and ventricular fibrillation have been noted with overexpression of the ACE2 receptor in experimental mice models (8) . Hence, another possibility is that isolated involvement of the AV node and infra-Hisian conduction system by SARS-CoV-2 may have caused transient high-grade AV block. Whether this block is secondary to direct viral involvement or is an autoimmune response is unknown at this time. Our patient did not have a recurrence of these conduction disturbances after he was started on supportive Her medical history included mild asthma, heart failure with preserved ejection fraction, coronary artery disease (percutaneous coronary intervention 2010), paroxysmal atrial fibrillation (AF), hypertension, obesity, and total hip arthroplasty 1-month prior. Her differential diagnosis included bacterial/viral pneumonia, acute on chronic heart failure with preserved ejection fraction, pulmonary embolism, and coronavirus disease-2019 (COVID- 19) . On arrival she was hemodynamically stable: heart rate 62 beats/min, blood pressure 130/84 mm Hg, respiratory rate of 18, and oxygen saturation 98% on 6L nasal canula. Physical examination noted bilateral rales. Chest x-ray showed patchy bilateral consolidations with mild interstitial edema ( Figure 1) . A computed tomography pulmonary angiogram revealed no pulmonary embolism but bilateral interlobular septal thickening and peripheral ground glass opacities most prominent in the posterior and lower zones. Laboratory tests were remarkable for a white blood cell count of 6.0 k/ml, absolute lymphocyte count of 350/ml, The differential for electrical storm in COVID-19 remains broad. Myocarditis and cytokine storm may not be universal drivers of cardiac sequelae in COVID-19. Management of these arrhythmias requires consultation with expert, multidisciplinary teams. hemoglobin 8.8 mg/dl (7.7 mg/dl 1 month prior), hyponatremia to 129 mmol/l, ferritin of 1,167 ng/ml, Nterminal pro-brain natriuretic peptide of 721 pg/ml, and C-reactive protein of 4.9mg/dl (Figure 2A ). Remaining laboratory tests were within normal limits. A nasopharyngeal swab was sent for severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and respiratory viruses, blood cultures were collected, vancomycin and cefepime were started, and the patient was admitted to a negative-pressure room. were mildly elevated at admission and continued to rise with AST, reaching a peak on day 7 of admission. Similarly, ALT peaked on day 9 of admission. By discharge, the transaminase levels were downtrending ( Figure 4 ). An abdominal ultrasound showed normal liver size (15.5 cm) with increased liver echogenicity and a nodular contour suggestive of liver fibrosis, likely due to Fontan Associated Liver Disease (FALD). His CBC was trended with normalization of his platelet count by day 6 of hospitalization. In the emergency room, the patient was hypoxic with oxygen saturations of 86% on right atrium with accompanying dyspnea. He was placed on 4 to 6 l of oxygen via a nasal cannula, which led to an improvement in the oxygen saturations to low 90s. GGT (g-glutamyl transferase) being the most common (12) . This patient had modest transaminitis likely due to the effects of COVID-19 on his underlying FALD (13) . The patient was discharged after a 10-day hospitali- Over the 12-month period preceding the SARS-CoV-2-related stay-at-home order, a total of 4 patients followed by the ACHD service at the University of Washington Medical Center with defects of various severities died in an acute setting. In this report we Unexpected mortality among patients with ACHD appears to have acutely increased at a single academic ACHD center during the SARS-CoV-2 pandemic. The ongoing SARS-CoV-2 pandemic appears to be contributing to increased ACHD mortality by delaying patient contact with health care. Routine follow-up care for high-risk groups, including those with congenital heart disease, during the SARS-CoV-2 pandemic is critical to ensure appropriate triage and care for vulnerable populations. Even with prior clinical stability, these populations remain at risk for acute cardiovascular complications and increased mortality. describe a series of 4 acute-setting ACHD deaths that occurred within a single week at the time of the effective stay-at-home order. Acute-onset death was defined as death that occurred either out of the hospital or within 24 h of presentation to a medical facility. With the exception of 1 patient (case 4) who was called but did not answer the phone 2 days prior to being found dead at home, none of the patients had a missed clinic appointment since the initiation of the stay-at-home order, and none had made contact with the medical system to report concerning symptoms prior to their deaths. A After the procedure, the Impella CP catheter was removed without complications, and the femoral access was closed with the use of 2 Proglide closure systems (Abbott Vascular, Santa Clara, California). The staff allowed to enter the catheterization lab Since its outbreak in Italy in mid-February, COVID-19 has spread rapidly, with over 40,000 cases and more than 3,000 deaths to date. Epidemiologic analysis shows that the presence of comorbidities significantly increases mortality: 10.5% in patients with cardiovascular diseases; 7.3% in patients with diabetics; 6.3% in patients with chronic respiratory diseases; 6% in patients with hypertension; and 5.6% in oncologic patients (7) . Given the high number of infected patients, we often diagnose cardiovascular diseases at different stages during the viral pathology. In this perspective, some selected patients could benefit from treatments that deviate from current guidelines. We report the first case of a patient with COVID-19 and acute coronary syndromes treated in Italy for unprotected LMCA stenosis with protected percutaneous coronary intervention. The use of the Impella CP cardiac assist system to provide left ventricular support during high-risk percutaneous coronary interventions is recommended in such settings, because its efficacy is supported by randomizedcontrolled trials (8) and large registries (9,10). Nevertheless, this case also highlights the importance The patient had no significant medical history. He never smoked. There was no family history of cardiovascular disease (CVD). An early viral panel polymerase chain reaction was negative for multiple respiratory viruses. A severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) nucleic acid amplification test Early and rapid testing is critically necessary in patients with suspected COVID-19 to prevent severe evolution. ECG ST-segment elevations in inferior leads have been described in several COVID-19 patients, with variable clinical significance. An accurate evaluation of the true incidence of acute myocardial injury related to COVID-19 requires a standardized definition, which should include a combination of ECG changes, biochemical markers, and imaging abnormalities. Given the very low pre-test probability for coronary artery disease and the absence of coronary calcifications on the chest CT scan, a coronary CT angiogram was not indicated, and the patient was not referred for invasive coronary angiography. The patient was treated conservatively, without thrombolytic agents or initiation of the acute coronary syndrome management protocol. The COVID-19 pandemic represents the largest worldwide health care challenge to date. Limited but rapidly emerging data have documented the role of CVD in increasing both the risk of infection and the severity of its clinical presentation (1) (2) (3) (4) . In particular, CVD is associated with a sharp increase in overall mortality, which reaches almost 20% of patients hospitalized (5) . However, although such an association can be anticipated to a certain degree (on the basis of existing data from previous outbreaks of influenza and severe acute respiratory syndrome), the incidence of myocardial injury in COVID-19 infection appears to be higher (6) . Furthermore, the definition of COVID-19-associated "myocardial injury" lacks standardization and is based primarily on elevated (and highly variable) serum levels of cardiac-specific troponins as the single most common defining markers. This myocardial injury has been associated with possibilities. Logistically, we now understand that the decision to proceed with angiography carries a significant risk for nosocomial spread of the virus endangering hospital staff. We are also learning that acute kidney injury is quite prevalent and highly associated with mortality in COVID-19 patients (6). One should think twice before administering intravenous contrast medium in these patients. Consensus documents from our professional societies that are based on early COVID-19 observations have resurrected considering the use of fibrinolytic therapy for STEMI (7) . In a setting of limited staffing and resources, and where time to treatment is expected to be significantly delayed, fibrinolytic therapy provides a more rapid and logistically easier approach to reperfusion therapy while reducing staff exposure to infection. However, contraindications to fibrinolytic therapy have to be absent, and STEMI mimics have to be excluded. The fibrinolytic strategy is probably most reasonable for hospitals without PCI capability or immediate availability. At PCI-capable hospitals with adequate staffing, primary PCI is still preferred (8, 9) . Until there is universal availability of rapid testing (<5 min) for both the virus and the antibodies, our approach to STEMI will have to be modified. This is primarily the result of new infection control considerations that will have to be included in our daily workflow. The current door-to-balloon time quality metric should be suspended by hospital quality improvement committees as a measure of system performance because of the current diagnostic and logistical challenges in delivering STEMI care. In the American College of Cardiology National Cardiovascular Data Registry CathPCI Registry reporting form, noting a "system delay" as a reason for a prolonged door-to-balloon time will avoid any external quality of care penalties. We now work in the era of COVID-19 STEMI care. The patient remained asymptomatic, and no confirmatory tests were performed for the same reason as in the first patient. Very late LAD artery stent thrombosis was found, and a new DES was implanted. The patient was asymptomatic, but because the COVID-19 pandemic had reached its peak, a pre-admission polymerase chain reaction test was performed, with a positive result. The patient had a favorable course and was discharged 5 days later. as antiplatelet therapy. Ten days later, prasugrel was replaced by clopidogrel (after antiviral treatment was completed), and the patient was discharged. The COVID-19 pandemic has significantly decreased worldwide interventional cardiology activity. In Spain, cardiac catheterization procedures have been reduced by 48%, with a reduction of 40% for primary angioplasty (2) . Similar data have been reported in We present 1 case of acute stent thrombosis and 3 very late stent thrombosis cases ( Table 1) . Despite no initial COVID-19 testing in 2 cases, symptoms and subsequent testing ( Figures 3A to 3D ) supported that the patients were infected at the time of stent thrombosis ( Table 2) . The patient reported an active lifestyle with a history of playing competitive football and had a body mass ST-segment elevation myocardial infarction with a high thrombus burden can appear as the first and only onset of COVID-19 symptoms. Plaque rupture in predisposed patients with cardiovascular risk factors can be enhanced by severe inflammation and worsened by prothrombotic characteristics of this new infectious disease. In the course of this COVID-19 pandemic, SARS-CoV-2 infection should probably be ruled out in patients with unusual or severe thrombotic and ischemic events, even when there are no symptoms of COVID-19 disease. index of 27 kg/m 2 . He had no significant medical history except for past smoking (20 pack-years), which he had quit 2 years before. He had no family history of cardiovascular disease and was taking no medication or drugs. No diagnosis other than a STEMI was possible. The initial electrocardiogram displayed a sinus rhythm with an anterior ST-segment elevation and Q waves with negative T waves in the inferior leads The patient did not develop heart failure, or heart rhythm disturbances, or other complications of myocardial infarction. Furthermore, he remained free of COVID-19 disease symptoms. In the context of the COVID-19 pandemic, unusual myocardial infarction presentations, such as in young individuals at low cardiovascular risk, should lead to with T-wave inversion in DIII and aVf ( Figure 1 ). The patient had no past medical history and was not on any medications. To describe the management of patients with refractory ARDS requiring coronary angiography. To describe the feasibility of coronary angiography with the patient in prone position. The differential diagnosis included acute myocardial infarction, myocarditis, and takotsubo syndrome. There was no evidence of obstructive coronary disease, and the final diagnosis was myocarditis, although we were not able to perform cardiac magnetic resonance in this highly unstable patient. With a rapid spread worldwide, COVID-19 has become a public health emergency of international concern (1). The clinical course of SARS-CoV-2 infection is mostly characterized by respiratory tract symptoms, including fever, cough, pharyngodynia, fatigue, and complications related to pneumonia and ARDS, often In a patient in prone position, the geometry and orientation of the heart as well as the coronary anatomy do not allow to obtain perfectly symmetric pictures of the coronary arteries using usual views. Consequently, the interpretation of coronary angiography was simply done following the heart's shape. with unchanged cranial/caudal tilts (8, 9) or using the double-inversion technique to normalize all angiographic pictures such as in a left-located heart (10) is usually enough to perform and analyze coronary angiography in such patients. Finally, even though we did not perform percutaneous coronary intervention, performing percutaneous coronary intervention with a patient in prone position would not be a critical issue for an experienced operator. pandemic, the most plausible diagnosis seemed to be a severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. Tables 1 and 2 summarize the biochemical tests and atrial blood gas analysis before, during, and after amiodarone therapy. Figure 1 shows the illness clin- No adverse events were reported. The patient was discharged on day 8. infection in cell cultures and mouse models (4, 5) . Amiodarone is a widely available, low-cost antiarrhythmic drug that in the past has been considered as a possible antiviral medication (6) . Amiodarone and its main metabolite (mono-N-desethyl amiodarone) were shown to inhibit the entry of filoviruses (a family of single-stranded, negative-sense RNA viruses that includes Ebola virus) at the same serum concentration found in patients treated for arrhythmias (7, 8) . Amiodarone also proved able to remain to be investigated, and drug interaction with other treatments (e.g., hydroxychloroquine, lopinavir/ritonavir, atazanavir, and darunavir/cobicistat) are major concerns (10) . Notably, amiodarone toxicity At follow-up visit, 10 days after discharge, the patient was asymptomatic. In this case, amiodarone was given for research purposes in a hospital setting. This is an approach still under investigation. Do not try this at home. To diagnose ACP in patients with SARS-CoV-2-related ARDS. To appreciate potential role of almitrine in improving oxygenation and RV function. To understand SARS-CoV-2-related atypical type of ARDS. Medical history included only an overweight with a body mass index of 38.9 kg/m 2 . The differential diagnosis included pulmo- and septal dyskinesia disappeared ( Figure 1C ). Moreover, RV global longitudinal strain improved from -14.8% to -22.7% ( Figure 1D ). Twelve hours following almitrine infusion, RVSWI decreased from 19.7 to 17.5 g/m/beat/m 2 . The clinical spectrum of SARS-CoV-2-related cardiovascular complication includes myocarditis, pericarditis, vasoplegia, RV failure, and acute coronary syndromes (1, 2) . In this case, we highlight the RV dysfunction Another explanation is the impact of ARDS and mechanical ventilation on the RV. ACP is a well-known complication of ARDS despite a protective ventilation, with an incidence of 25%. Hence, ACP may be related to a high driving pressure, leading to an increased RV afterload (4) . Moreover, the patient was on norepinephrine, which may increase RV afterload. Another explanation is that hypoxia could lead to RV dysfunction in its own right (5). ventilation-to-perfusion ratio (8) . Moreover, previous studies in the 1990s showed that at a low dose, the deleterious effect on pulmonary vascular resistance was negligible, especially when associated with nitric oxide (9) . Hence, we hypothesized that almitrine use in the case of SARS-CoV-2 atypical ARDS might be useful. In the present case, almitrine infusion was associated with RV function improvement and decrease in pulmonary vascular resistance. This is probably due not only to a better oxygenation, but also to a better distribution of pulmonary vascular flow to aerated lung areas. Before almitrine infusion, we observed a high RVSWI with a normal-to-low range of CI, suggesting a hemodynamic disconnection between the RV and left ventricle. The reduction in RV afterload by almitrine infusion resulted in an improvement in this disconnection (decreased RVSWI and improved CI). As almitrine infusion could induce reversible lactic acidosis and hepatic dysfunction (10) To describe high-risk clinical features in a patient on durable LVAD support who developed COVID-19. To illustrate potential complications and clinical dilemmas in managing COVID-19 in a patient supported with a durable LVAD. Reverse transcription polymerase chain reaction results for severe acute respiratory syndrome-coronavirus-2 (SAR-CoV-2) was positive at the initial emergency department visit and at the authors' institution. Serial laboratory and imaging tests are detailed in Table 1 . Several markers of disease severity were abnormal including absolute lymphocyte count, C-reactive protein level, and cardiac enzymes. Chest radiographs showed bilateral infiltrates concerning for atypical pneumonia (Figure 1 ). The patient was quarantined in a negative-pressure intensive care room. The host response to COVID-19 infection is often localized in the lung parenchyma, but a surge in proinflammatory cytokines can occur (3, 4) . Known as a "cytokine storm," this phenomenon is described in dynamics. We should closely monitor for: 1) RV failure and need for inotropic support; 2) drops in LVAD speed or suction events, low flow, or pulsatility index events due to vasoplegia associated with infection. To limit health care workers' exposure to COVID-19, nonessential testing such as echocardiograms, The antimalarial medication hydroxychloroquine, which was chosen as the initial treatment agent for our patient, was shown to reduce in vitro SAR-CoV-2 cell entry, and a retrospective study suggested its clinical benefit in COVID-19 (3, 4) . A major side effect is QTc prolongation, so the present protocol provides monitoring guidance of this complication. Immunomodulatory biological agents such as tocilizumab are reserved for severe COVID-19, defined by the Values in bold are in-hospital values that were consistent with baseline values. *Last visit values were the latest values obtained within the previous 6 months. Baseline LDH, WBC, platelet, absolute polymorphonuclear leukocytes, and absolute lymphocytes were recorded as an average of the previous 3 values measured within 1 year. †This patient was placed on ventilator support on the night of HoD 2 and was given tocilizumab on the evening of HoD 3. ‡This patient experienced pulseless electrical activity arrest after the return of spontaneous circulation. kRelative change is the percentage of increase or decrease from baseline value. ALT ¼ alanine aminotransferase; ARDS ¼ acute respiratory distress syndrome; AST ¼ aspartate aminotransferase; BNP ¼ B-type natriuretic peptide; CK-MB ¼ creatine kinase MB; CVP ¼ central venous pressure (obtained from right heart catherization at baseline, and from central venous line in the hospital); eGFR ¼ estimated glomerular filtration rate; FiO2 ¼ fraction of inspired oxygen; HoD ¼ hospital day; LDH ¼ lactate dehydrogenase; LVAD ¼ left ventricular assist device; MAP ¼ mean arterial pressure (obtained from Doppler or arterial line); PaO2 ¼ arterial partial pressure of oxygen; WBC ¼ white blood cell. presence of both worsening respiratory failure and a cytokine storm as shown by increasing inflammatory markers. Still, caution is warranted as major adverse effects of tocilizumab include infection, infusion reactions, dyslipidemia, neutropenia, and potential malignancy (7) . Patients on LVAD support are particularly vulnerable to infectious complications due to the inherent presence of hardware and driveline Finally, prone ventilation is beneficial in cases of severe ARDS. The maneuver has been effective in improving lung mechanics and gas exchanges, and in some cases, it may prevent the need to escalate to venous-venous extracorporeal membrane oxygenation (8, 9) . Although there are no published outcomes, early experience in Wuhan, China indicates that prone position was widely used in patients with COVID-19-related severe ARDS with possible benefits (9) . Nonetheless, it may be prohibitive in heart failure patients on LVAD support. A 58-year-old woman presented with productive cough, fatigue, fever, and diarrhea for the previous 5 days. Physical Abbreviations as in Figure 2 . (6) . Stress cardiomyopathy has also been reported with viral infections (7) . Histological studies have shown mild inflammatory infiltration (8, 9) , and it is possible that heightened inflammation with viral infections, particularly that seen with COVID-19, may contribute to development of stress cardiomyopathy. Overall, the prognosis of stress cardiomyopathy is favorable, with the majority of patients fully recovering LV function by 2 months (4). Twitter: @FerrasDabbagh1. He had a history of hypertension and was taking lisinopril. The differential diagnosis included SARS-CoV-2 causing severe ARDS and acute cardiac injury from direct viral toxicity (i.e., myocarditis), acute coronary syndrome (ACS), demand ischemia, and stress cardiomyopathy. Prevalence and prognostic implications of cardiac injury (defined as troponin elevation >99th percentile upper reference limit) in COVID-19. Considerations for differentiating causes of cardiac injury in COVID-19. Management strategies for myocarditis and severe ARDS in COVID-19. and mortality benefit in animal models (11) . Improved airway inflammation has also been observed in animals treated with ARIs (12) . Other viral infections such as influenza and respiratory syncytial virus were considered, but the pre-test probability for COVID-19 was high because other residents at the facility had been diagnosed with COVID-19 recently. In the emergency department, the patient was tachypneic with an initial oxygen (O 2 ) saturation 98%. Table 1 lists the results of his initial laboratory testing including normal levels of ferritin, procalcitonin, interleukin (IL)-1, and IL-6. Levels of C-reactive protein, lactate dehydrogenase, and troponin were elevated. There was a reduced white blood cell count without lymphopenia. A chest radiograph had no air space or interstitial infiltrates (Figure 1 ). There was a single low-flow LVAD alarm noted 3 days prior to presentation. Based upon the adequate room air saturation, absence of pulmonary infiltrates, and minimally abnormal inflammatory markers, the patient was classified as having a mild case of COVID-19. Due to persistent breathlessness, hydroxychloroquine was initiated on day 2 with QTc monitoring. To the best of our knowledge, this is the first re- In the current COVID-19 pandemic, lopinavir/ritonavir was studied in a randomized, controlled trial in Table 2) . The patient was discharged to his nursing facility on hospital day 5 once a room was available where he could be quarantined, and he continued to feel well 10 days later. Mahmood et al. To make a diagnosis of fulminant myocarditis concomitant with COVID-19 pneumonia. To understand the value of serial cardiac magnetic resonance after myocarditis due to COVID-19. Sinus tachycardia (100 beats/min) with negative T waves from V 2 to V 4 . To be able to arrive at the differential diagnosis of acute cardiac dysfunction in the setting of severe COVID-19 disease early after heart transplantation. To understand the need for individualized management, balancing risks of infection and rejection in heart transplantation recipients with severe infections early after transplantation. was discharged to isolation at home with pulse oximetry and plans for daily telemedicine assessments. Three days later the patient presented to the emergency department with rapidly progressive respiratory distress and hypoxia. The patient had a history of end-stage non- Figure 1 . The patient reported continued gradual recovery by weekly telemedicine assessments after discharge. He had a history of pityriasis lichenoides chronica. He had no personal or family history of congenital heart disease, immunodeficiency, or autoimmune disease. The differential diagnosis included viralinduced myocarditis or underlying cardiomyopathy unmasked by an acute viral illness. Table 1) . The patient has had no recurrent episodes of CHB since day 4 of admission, and a repeat echocardiogram on day 12 of admission demonstrated lownormal biventricular systolic function. and conduction abnormalities appears to be a rare manifestation of SARS-CoV-2 infection in children (3) (4) (5) . Nonetheless, evaluation for myocardial injury may be warranted in pediatric patients with symptomatic SARS-CoV-2 infection, particularly in patients whose clinical symptoms (e.g., dyspnea, hypoxia) seem out of proportion to chest imaging findings. On autopsy, histopathologic examination of the heart showed mild to moderate myocyte hypertrophy with mild to moderate diffuse interstitial and perivascular fibrosis (Figures 2A and 2B) . The impact of influenza co-infection in this patient with COVID-19 must also be considered because this virus is known to contribute to cardiovascular morbidity and mortality secondary to up-regulation of the inflammatory response and endothelial dysfunction (2) . As such, influenza A likely had significant effects on her cardiac functioning. Coinfection with SARS-CoV-2 is of great concern, with limited data delineating the The patient's medical history showed arterial hypertension, dyslipidemia, and impaired fasting blood sugar. COVID-19 has extrapulmonary and cardiovascular manifestations. COVID-19 may be associated with exaggerated inflammatory response with an abnormal activation of coagulation, so a screening of coagulation setup may be indicated. COVID-19 may show up with Takotsubo syndrome. The differential diagnosis included acute myocardial infarction, Takotsubo syndrome, myocarditis, and coronary embolism. The patient was transferred to our center for an urgent coronary angiography, which revealed nonsignificant coronary atherosclerosis. Figures 5 and 6 , Videos 3 and 4). Our priority was to treat the patient with enoxaparin 7,000 IU twice daily as per the patient's weight. During the first days of hospitalization, and taking into consideration that the patient was hypotensive (systolic blood pressure: 80 mm Hg; mean blood pressure: <65 mm Hg), we treated the patient with Chest radiography was repeated in the following days and showed progressive reduction of interstitial pneumonia. Also, blood test results revealed an improvement of inflammation indexes ( Table 1) . On day 7 of hospitalization, the nasopharyngeal swab was repeated, with a positive result. The first negative result was registered on day 15. On the 14th day, we performed another transthoracic echocardiography, which showed the resolution of the 2 thrombi ( Figure 7) and a complete restoration of LVEF (57%) (Video 5). His past medical history was notable for type 2 diabetes mellitus, remote prostate cancer, and ventricular tachycardia. COVID-19 and concern over prolonged separation from his family. Our service is modeled after previously published "e-consultation" workflow recommendations in "peacetime" prior to the SARS-CoV-2 outbreak (4). In phase 2, we implemented these processes, and all emergent cases were treated as PUIs. As we approach phase 3, our processes continue to undergo iterative improvements and all cases coming to the CCL will be considered PUIs. Our approach to STAT and routine TEE is outlined in Remote monitoring is used for electrophysiology clinic device checks, with patients triaged to present for evaluation if they develop concerning arrhythmias, heart failure alerts, or device-related issues. *VT storm that has failed medical treatment including at least 2 antiarrhythmic drugs (including propranolol), treatment of underlying reversible condition if present (QTc prolongation due to ischemia, medications, or metabolic/electrolyte imbalance), general anesthesia, and left stellate ganglion block (if available). †Not reversible or fails to respond to chronotropic drugs such as isoproterenol, dopamine, and/or scopolamine, and temporary pacing cannot be safely maintained in an intensive care setting. In this scenario a screw-in active fixation lead connected to an externalized generator or an active fixation temporary pacing lead may be considered depending on the patient's clinical condition and could be performed in the intensive care setting under fluoroscopic guidance (if available) or in an operating room with negative airflow capabilities and fluoroscopy. CIED ¼ cardiac implantable electronic devices; EOS ¼ end of service; ERI ¼ elective replacement indicator; VT ¼ ventricular tachycardia. In the wake of this pandemic, formal medical student and trainee didactics were disbanded to allow for social distancing. Additionally, several states expe- Her past medical history included hypertension and diabetes mellitus. The differential diagnosis included communityacquired pneumonia, atypical pneumonia, and coro- Figures 3A and 3B ). The patient was started on therapeutic enoxaparin and was closely monitored for hemodynamic instability. She declined to take hydroxychloroquine, recommended by some experts for management for COVID-19. She remained hemodynamically stable and was transitioned to oral anticoagulant therapy (apixaban) with plans to continue anticoagulation for 6 months. The COVID-19 outbreak is an unprecedented global public health challenge. Since the end of December 2019, when the first cases of SARS-CoV-2 infection were detected in Wuhan, China, the disease has spread exponentially (1). On January 30, 2020, the World Health Organization declared COVID-19, the disease caused by the novel coronavirus, a public health emergency of international concern and later officially upgraded it to a global pandemic. As of April 24, 2020, more than 2,790,000 confirmed cases from more than 180 countries and more than 195,000 deaths have been documented worldwide. The projected U.S. death toll is >240,000, with an estimated total burden of more than 1 million COVID-19 cases. In approximately 88% of cases, fever is the most common presentation, followed by cough (68%), vomiting (5%), and diarrhea (3.8%) (2) . In up to 15% of patients, the natural course of the disease is complicated by severe interstitial pneumonia, which can lead to acute respiratory distress syndrome, multiorgan failure including acute kidney injury, dissemi- To suspect PE early in the disease process in confirmed or suspected COVID-19 patients. To identify high-risk patients early and to offer appropriate therapies while mitigating patient and provider risk. The patient was managed with intravenous unfractionated heparin (UFH) and dobutamine; infection. CDT is associated with early improvement in RV function and hemodynamics in deteriorating patients with lower doses of tPA (8, 9) ; however, PUI approximately 10 times less frequent (15, 16) . Importantly, a substantial proportion of the thrombotic events were diagnosed very early during the hospital stay, suggesting that they had already occurred before admission (15) . In view of the previously mentioned (preliminary) findings, and although it cannot yet be concluded with safety that the thrombosis risk among patients with severe COVID-19 is substantially higher than that of patients with severe infection caused by other bacterial or viral pathogens (19, 20) , thrombotic events are very likely to be a key aspect of COVID-19-associated morbidity and mortality (21) . It is therefore now necessary to make The patient's medical history was notable only for obesity (body mass index 31 kg/m 2 ) and type 2 diabetes. The primary differential diagnosis for the patient's The usual risk stratification schema for acute PE rely on a combination of hemodynamic clinical parameters, such as hypoxemia, tachycardia, and hypotension along with serum biomarkers, such as troponin or brain natriuretic peptide, followed by confirmatory imaging tests (12) . Severe COVID-19-related ARDS may present with many similar hemodynamic and biomarker derangements masking underlying VTE. illness. Figure 2 ). An axillobifemoral bypass was performed, followed by therapeutic anticoagulation with good initial results. The patient died 7 days after surgery from a major hemorrhage. CASE 3. The third patient was a 72-year-old male with history of hypertension, diabetes, and coronary artery disease ( Table 1 ) who was admitted for hypoxic CT angiography of patient 1 shows a nonobstructive thrombus formation of descending aorta (arrow) in an axial view (A) and a sagittal view (B). disease. A recent paper attributes this state "to excessive inflammation, platelet activation, endothelial dysfunction, and stasis" (5) . Others have suggested that formation and polymerization of fibrin are responsible for this hypercoagulability (6) . Therefore, recent recommendations insist on thromboprophylactic measures to prevent thromboembolism (4, 7, 8) . A recent publication found evidence of the presence of virus in endothelial cells (9) . One explanation is that the angiotensin-converting enzyme 2 receptor that the virus uses to infect cells is widely expressed in endothelial cells. This causes endotheliitis, which could explain why COVID-19 patients seem prone to venous and arterial thrombosis. This paper (9) blockade may also be considered (7) . It should be noted that mild ARDS may be managed with noninvasive forms of ventilation. However, during the present pandemic, modifications to usual critical care may be necessary. Given concern for viral transmission, current recommendations advise It is also important to monitor the patient's driving pressure, or difference between the PEEP and plateau pressure, as increased driving pressures have been associated with higher mortality in ARDS (10) . With a basic understanding of these fundamentals, it is possible for all cardiologists to provide safe and effective care for our patients with COVID-19. As many of us prepare to use skill sets long forgotten, it will be important to remember to ask for help when needed. One of the few bright spots in this pandemic has been the resurgence of interdisciplinary team- and is thought to protect against lung injury. These 2 functions may be due to differences in the location of the ACE2 proteins, transmembrane or in the plasma (16) . The ACE2 gene is located on the X chromosome, which suggests that women might have higher ACE2 levels and thus be protected against more severe disease compared to men (17) . There has been recent concern in the cardiology community about the possible negative effect of Italy, as it has done in the past, will improve its health and economic systems after this tragedy. Probably nothing will be like before, and this catastrophe will be a great opportunity to further improve an efficient and effective national universal health system. heroes, we look like prey in heroes' capes. That kind of bravery, that work integrity, is not boundless. No one is so fearless or short-sighted as to discount all risks. When I try to figure out how I feel in this moment, the Italian motto "andrà tutto bene" ("everything will be alright") that has been viral since the onset of the The CCL nursing staff was reinforced to speed up procedures. All noncritical equipment or supplies were removed from the CCL to facilitate cleaning and disinfection procedures. Availability of PPE is a concern, so we created 2 sets of PPE to best manage available resources: a mid-level kit and a fullprotection kit for suspected and confirmed cases. Despite the concern of the medical community, we believe society has largely adhered to the social isolation recommendations, as we are looking at a constant drop in admissions to intensive care units and an increase in patients successfully discharged. The availability of masks for everyone is still not a reality as we are conceiving the first draft of a plan to reduce restriction measures. Subsequently, as we are receiving more papers, we have decided to divide JACC: Case Reports publications into 5 sections: acute coronary syndromes, heart failure, arrhythmias, thromboembolic events, and stories from the front line, in the format of "Voices of Cardiology" papers. All these papers have been highlighted in this issue (4) . Recognizing the value of not overloading our audience with publications, and in an effort to keep the quality high and up to the standards of JACC journals, we accepted approximately 8% to 10% of the manuscripts submitted. We selected the best of the best cases and brought together world-renowned specialists to write editorials. Although we understand that clinical cases have been of crucial importance for our understanding of COVID-19, it is of equal importance that they cannot substitute for large studies and pharmacological trials. Therefore, unless we were dealing with an impressive side effect of a medicine, we have been very cautious in publishing pharmacological evidence, as large trials would prove the benefits and side effects of these medicines currently under trial. Another important task of JACC: Case Reports is that To ease navigation on the ACC COVID-19 Hub, its content was organized into sections on clinical guidance, practice considerations, and frontline perspectives. Given the novelty and rapidity of the COVID-19 pandemic, most of the initial content was based on analyses of frontline experiences and expert opinion. The Hub executive team and SQC worked to ensure that the content struck a balance between reasonable, actionable suggestions and acknowledgment that more rigorous research was needed to better inform the best approach to COVID-19 management. Going forward, the Hub will continue to generate content but now turn its attention to highlighting the growing peer-reviewed research on COVID-19 and CV disease. The ACC has commissioned a task force to promote research in this area, and the Hub will serve as a primary dissemination platform, in conjunction with JACC and other cardiology-focused journals. In addition, the Hub will highlight best practices and frontline experiences from its membership on "reopening" protocols. With projections that COVID-19 will ebb and flow worldwide over the next several years, our membership will need to navigate the best way to continue to treat CV disease during this time. The ACC COVID-19 Hub has proved to be a useful resource to assembling and distributing information broadly during a rapidly evolving pandemic. Lessons learned include the need to build a nimble process to commission, organize, and distribute content, an ability to engage with experts to generate content, a method to closely monitor of member and community needs to inform content development, and an emphasis on highlighting rigorously conducted research and expert consensus over mere opinion and speculation. 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