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• W3033888930 abstract "Coronavirus disease (COVID-19) is a serious illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The symptoms of the disease range from asymptomatic to mild respiratory symptoms and even potentially life-threatening cardiovascular and pulmonary complications. Cardiac complications include acute myocardial injury, arrhythmias, cardiogenic shock and even sudden death. Furthermore, drug interactions with COVID-19 therapies may place the patient at risk for arrhythmias, cardiomyopathy and sudden death. In this review, we summarise the cardiac manifestations of COVID-19 infection and propose a simplified algorithm for patient management during the COVID-19 pandemic. Coronavirus disease (COVID-19) is a serious illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The symptoms of the disease range from asymptomatic to mild respiratory symptoms and even potentially life-threatening cardiovascular and pulmonary complications. Cardiac complications include acute myocardial injury, arrhythmias, cardiogenic shock and even sudden death. Furthermore, drug interactions with COVID-19 therapies may place the patient at risk for arrhythmias, cardiomyopathy and sudden death. In this review, we summarise the cardiac manifestations of COVID-19 infection and propose a simplified algorithm for patient management during the COVID-19 pandemic. Coronavirus disease (COVID-19) originated in the Wuhan province of China in late 2019 and is a serious illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is genetically related to the coronavirus responsible for the SARS outbreak in 2002 [[1]Wilder-Smith A. Chiew C.J. Lee V.J. Can we contain the COVID-19 outbreak with the same measures as for SARS?.Lancet Infect Dis. 2020; 20: e102-e107Abstract Full Text Full Text PDF PubMed Scopus (264) Google Scholar]. The infection has spread globally and was declared a pandemic by the World Health Organization (WHO) on 11 March, 2020. The number of confirmed cases and deaths continue to rise daily. The clinical manifestations of COVID-19 may range from asymptomatic or mild respiratory symptoms to severe life threating respiratory and cardiac failure (Tables 1 and 2, Figure 1) [2Wu Z. McGoogan J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention.JAMA. 2020; https://doi.org/10.1001/jama.2020.2648Crossref Scopus (4569) Google Scholar, 3Bhatraju P.K. Ghassemieh B.J. Nichols M. Kim R. Jerome K.R. Nalla A.K. et al.Covid-19 in critically ill patients in the Seattle Region — case series.N Engl J Med. 2020; 382: 2012-2022Crossref PubMed Scopus (772) Google Scholar, 4Siddiqi H.K. Mehra M.R. COVID-19 illness in native and immunosuppressed states: a clinical-therapeutic staging proposal.J Heart Lung Transplant. 2020; 39: 405-407Abstract Full Text Full Text PDF PubMed Scopus (397) Google Scholar, 5Wu C. Chen X. Cai Y. Xia J.A. Zhou X. Xu S. et al.Risk factors associated with acute respiratory distress syndrome and death in patients with coronavirus disease 2019 pneumonia in Wuhan, China.JAMA Intern Med. 2020; https://doi.org/10.1001/jamainternmed.2020.0994Crossref Scopus (2125) Google Scholar, 6Song J.-Y. Yun J.-G. Noh J.-Y. Cheong H.-J. Kim W.-J. Covid-19 in South Korea — challenges of subclinical manifestations.N Engl J Med. 2020; 382: 1858-1859Crossref PubMed Scopus (10) Google Scholar]. Among 72,314 patients with COVID-19 in China, the clinical severity was reported as mild in 81.4%, severe in 13.9% and critical in 4.7% of patients [[2]Wu Z. McGoogan J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention.JAMA. 2020; https://doi.org/10.1001/jama.2020.2648Crossref Scopus (4569) Google Scholar]. In a recent study from New York, the most common presenting symptoms were cough (79.4%), fever (77.1%), dyspnoea (56.5%), myalgias (23.8%), diarrhoea (23.7%), and nausea and vomiting (19.1%) [[7]Goyal P. Choi J.J. Pinheiro L.C. Schenck E.J. Chen R. Jabri A. et al.Clinical characteristics of Covid-19 in New York City.N Engl J Med. 2020; 382: 2372-2374Crossref PubMed Google Scholar]. The primary cause of death in COVID-19 infection is respiratory failure but cardiac manifestations may contribute to overall mortality and even be the primary cause of death in these patients (Table 3) [[3]Bhatraju P.K. Ghassemieh B.J. Nichols M. Kim R. Jerome K.R. Nalla A.K. et al.Covid-19 in critically ill patients in the Seattle Region — case series.N Engl J Med. 2020; 382: 2012-2022Crossref PubMed Scopus (772) Google Scholar,7Goyal P. Choi J.J. Pinheiro L.C. Schenck E.J. Chen R. Jabri A. et al.Clinical characteristics of Covid-19 in New York City.N Engl J Med. 2020; 382: 2372-2374Crossref PubMed Google Scholar, 8Shi S. Qin M. Shen B. Cai Y. Liu T. Yang F. et al.Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China.JAMA Cardiol. 2020; (Published online March 25)https://doi.org/10.1001/jamacardio.2020.0950Crossref PubMed Scopus (1036) Google Scholar, 9Mehra M.R. Ruschitzka F. COVID-19 illness and heart failure: a missing link?.JACC Heart Fail. 2020; 8: 512-514Crossref PubMed Scopus (39) Google Scholar, 10Yang J. Zheng Y. Gou X. Pu K. Chen Z. Guo Q. et al.Prevalence of comorbidities in the novel Wuhan coronavirus (COVID-19) infection: a systematic review and meta-analysis.Int J Infect Dis. 2020; 94: 91-95Abstract Full Text Full Text PDF PubMed Scopus (866) Google Scholar, 11Huang C. Wang Y. Li X. Ren L. Zhao J. Hu Y. et al.Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.Lancet. 2020; 395: 497-506Abstract Full Text Full Text PDF PubMed Scopus (11778) Google Scholar]. Concomitant cardiovascular (CV) conditions are present in 8–25% of overall COVID-19 infected population and in a higher proportion of those who die [[7]Goyal P. Choi J.J. Pinheiro L.C. Schenck E.J. Chen R. Jabri A. et al.Clinical characteristics of Covid-19 in New York City.N Engl J Med. 2020; 382: 2372-2374Crossref PubMed Google Scholar,[10]Yang J. Zheng Y. Gou X. Pu K. Chen Z. Guo Q. et al.Prevalence of comorbidities in the novel Wuhan coronavirus (COVID-19) infection: a systematic review and meta-analysis.Int J Infect Dis. 2020; 94: 91-95Abstract Full Text Full Text PDF PubMed Scopus (866) Google Scholar,12Li B. Yang J. Zhao F. Zhi L. Wang X. Liu L. et al.Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China.Clin Res Cardiol. 2020; 109: 531-538Crossref PubMed Scopus (500) Google Scholar, 13Fang Z. Yi F. Wu K. Lai K. Sun X. Zhong N. Liu Z. Clinical characteristics of coronavirus pneumonia 2019 (COVID-19): an updated systematic review.medRxiv. 2020; https://doi.org/10.1101/2020.03.07.20032573Crossref Scopus (0) Google Scholar, 14Guan W.-j. Ni Z.-y. Hu Y. Liang W.-h. Ou C.-q. He J.-x. et al.Clinical characteristics of coronavirus disease 2019 in China.N Engl J Med. 2020; 382: 1708-1720Crossref PubMed Scopus (7794) Google Scholar, 15Zheng Y.-Y. Ma Y.-T. Zhang J.-Y. Xie X. COVID-19 and the cardiovascular system.Nat Rev Cardiol. 2020; 17: 259-260Crossref PubMed Scopus (914) Google Scholar, 16Clerkin K.J. Fried J.A. Raikhelkar J. Sayer G. Griffin J.M. Masoumi A. et al.Coronavirus disease 2019 (COVID-19) and cardiovascular disease.Circulation. 2020; 141: 1648-1655Crossref PubMed Scopus (372) Google Scholar]. A meta-analysis of eight studies from China (46,248 patients) showed a higher prevalence of hypertension (17±7%) and diabetes mellitus (8±6%) followed by cardiovascular disease (5±4%) in COVID-19 patients [[10]Yang J. Zheng Y. Gou X. Pu K. Chen Z. Guo Q. et al.Prevalence of comorbidities in the novel Wuhan coronavirus (COVID-19) infection: a systematic review and meta-analysis.Int J Infect Dis. 2020; 94: 91-95Abstract Full Text Full Text PDF PubMed Scopus (866) Google Scholar]. In another analysis of 44,672 cases from the Chinese Center for Disease Control and Prevention, a higher case fatality rate was noted among patients with pre-existing comorbid conditions (10.5% for CV disease, 7.3% for diabetes, 6.3% for chronic respiratory disease, 6% for hypertension, and 5.6% for cancer) compared to the overall case-fatality rate of 2.3% in the entire cohort [[2]Wu Z. McGoogan J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention.JAMA. 2020; https://doi.org/10.1001/jama.2020.2648Crossref Scopus (4569) Google Scholar]. Medications used for the treatment of COVID-19 infection can also increase overall cardiovascular risk [[12]Li B. Yang J. Zhao F. Zhi L. Wang X. Liu L. et al.Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China.Clin Res Cardiol. 2020; 109: 531-538Crossref PubMed Scopus (500) Google Scholar].Table 1Stages of COVID-19 infection.StagesPathogenesisSymptomsSignsProposed Therapeutic StrategiesBased on Limited Data1Viral response/early infectionConstitutional RespiratoryGastrointestinalMild leukopaenia, lymphopenia. Elevated PT, D dimer, LDH, CRP; ferritin; IL6.Procalcitonin may be normalAntimicrobial therapyReduce Immunosuppressants if needed2Inflammatory phase/pulmonary phaseShortness of breathHypoxia: PaO2/FiO2 ratio < 300Increasing Inflammatory markers including cardiac biomarkers (Troponin, BNP)Abnormal CT chestSupportive care.Restrictive IV fluid strategy.Antimicrobials,Immunotherapy per ID.3Hyperinflammatory phase/Cytokine release stormARDSSIRS, SepsisCardiac failureMultiorgan dysfunction,Shock, DICMarkedly elevated inflammatory markers, cardiac biomarkersAntimicrobial,Immunotherapy per ID.Supportive care including vasoactive drips if indicated.Abbreviations: PT, prothrombin time; LDH, lactate dehydrogenase; CRP, C reactive protein; IL6, interleukin 6; CT, computed tomography; ID, infectious disease; IV, intravenous; ARDS, acute respiratory distress syndrome; SISI, systemic inflammatory response syndrome; DIC, disseminated intravascular coagulation. Open table in a new tab Table 2Clinical features and management tool.COVID like mild symptoms Stay at home and monitor vitals if able Self-quarantine 14 days if testing not feasible Avoid ER if haemodynamically stable and no clinical worsening. Supportive care till more definitive treatment recommendationDiagnostic tests:•CBC: Lymphopaenia, thrombocytopaenia•CMP: Elevated liver function tests•Coagulation: PT/INR, D dimer•LDH, CRP; fibrinogen, ferritin, procalcitonin•Infection: viral panel, blood, urine, sputum cultures, symptom specific cultures and imaging.•Cardiac biomarkers: Troponin, BNP•Telemetry: Continuous QTc monitoring on high risk therapy or pathology•ECG to assess ischaemia, myopericarditis, QTc, rhythm•Echocardiogram if clinically indicated (symptoms, BNP troponin elevation, ECG changes, shock)•Cortisol level (if persistent hypotension)•CT chest without contrast for pneumonia evaluation, with contrast to rule out PE in suspected cases with significant D dimer elevation or atrial arrhythmiasFollow-up tests: as needed•ECG: Repeat if QTc prolonging medications.•ESR, CRP, LDH, ferritin, D dimer, IL-6, procalcitonin•Troponin; NT ProBNP•Mixed/central venous saturation (daily if shock)Supportive therapy:•Supplemental oxygen to maintain oxygen saturation 90–96%•Early intubation/ARDS lung protective strategy•Avoid aerosolisation. Do not disconnect from ventilator without following the precautionary steps even during code.•Avoid unnecessary transportation; encourage bedside procedure when feasible with full PPE.Day 1–5: Early viral prodrome STAGE 1: Observe or Admit if risk factors or COVID+ and more than mild symptoms Observe at home if haemodynamically stable or admit if increased risk assessment score like SOFA, patients with comorbidities (age >65, male, hypertension, chronic disease, diabetes, immunocompromised, malignancy) or haemodynamically unstableDay 5–10 Inflammatory pulmonary phase STAGE 2: Admit if: Cardiopulmonary: Increased shortness of breath, hypoxia or other unstable vitals, ECG changes, worsening labs.Day> 9: Hyperinflammatory/cytokine release STAGE 3: ICU level care Sepsis Hypoxia/ARDS Cardiac failure Multiorgan dysfunction Shock Disseminated intravascular coagulationAbbreviations: CBC, complete blood count; CMP, complete metabolic profile; NTpBNP, N terminal pro brain natriuretic peptide; ESR, drythrocyte sedimentation rate; ICU, intensive care unit; SOFA, Sequential Organ Failure Assessment; PE, pulmonary embolism; PPE, personal protective equipment; LDH, lactate dehydrogenase; ECG, electrocardiograph; CT, computed tomography; INO, inhaled nitric oxide. Open table in a new tab Table 3Summary of cardiovascular disease management in COVID-19 patients.Clinical FeaturesSuggested ManagementIschaemic heart disease, myocarditis, myocardial injury NSTEMI•Check ECG and troponin if clinical suspicion of acute coronary syndrome (ACS)•Guideline directed medical therapy: aspirin, heparin, statin, beta blocker (if no bradycardia or cardiogenic shock)•Assess drug interaction of antiplatelet or anticoagulants•Cardiac catheterisation if high clinical suspicion of acute coronary occlusion•Coronary CT angiogram in haemodynamically stable NSTEMI STEMI•Activate STEMI team per hospital protocol•Primary PCI for STEMI, thrombolytic therapy is controversial, use for low risk STEMI only if interventional cardiologist unavailable•Bedside echocardiogram if any clinical uncertainty•If no angiographic disease- monitor and treat myocarditis sequalae-heart failure; arrhythmia; thromboembolism and risk factor modification. Myocardial injuryMyocarditisStress induced Cardiomyopathy•Echocardiogram to assess LV function•Troponin trend to differentiate from Type I MI and assess prognosis along with BNP•Monitor for arrhythmia, consider EP consult if malignant arrhythmia•Inotropes and vasopressor support if haemodynamic instability with LV dysfunction.•Discuss antiviral and anti-inflammatory therapies approved to use.•Guideline directed medical therapy for cardiomyopathy•Exercise limitation for 3–6 months to prevent sudden cardiac death. Cardiac arrest•Address goals of care early and periodically in all patients•Follow standard ACLS protocol•Consider mechanical CPR device if available•Use proper PPE per hospital protocol prior to initiating resuscitative efforts•Minimise code team size to prevent exposure to health care providersHeart failure and cardiogenic shock Heart Failure•BNP, troponin and echocardiogram to assess new onset HF•Telemetry for arrhythmia detection and monitoring•Standard HF management with daily weight, intake/output, diuresis, monitoring electrolytes and renal function•Limited fluid and blood product administration due to high risk of cardiopulmonary decompensation. Concentrate drips when able.•Avoid nonsteroidal anti-inflammatory agents•Continue ACEI/ARB/ARNI in otherwise stable patients who are at risk for, being evaluated for, or with Covid-19 unless hypotensive or renal failure.•Coronary CT angiogram for ischemic workup for new LV dysfunction if no ongoing ischaemia.•Cardiac catheterisation if HF suspected due to acute coronary syndrome. Shock•SBP<90 for >15 mins with impaired organ perfusion, Urine output <30 m/hr.•Recognise delayed presentation of mechanical complications of myocardial infarction or peritonitis from bowel ischaemia related to low perfusion state.•Check mixed venous saturation to differentiate different types of shock.•Conservative fluid resuscitation, crystalloid preferred over colloid.•Norepinephrine to stabilise shock; transition to inotrope when clinically indicated.•Inhaled pulmonary vasodilators (INO preferred) should only be administered through a closed system to prevent risk from aerosolisation.•Evaluate alternate aetiologies of shock if haemodynamics not improving.•Discuss with interventional cardiology regarding activating shock team.•ECMO and mechanical circulatory support device in highly selected cases. Transplant patientImmunosuppression•Discuss with heart transplant or cardiology team regarding reducing immunosuppression especially anti metabolites due to risk of infections.•Stress dose steroids for adrenal insufficiency for those on chronic steroidsArrhythmia Prolonged QTc•Telemetry monitoring and at least daily QT assessment•EP evaluation if QTc >450 msec in the absence of bundle branch block or >500 with bundle branch block if being started on antiarrhythmic or other QT prolonging medication.•Monitor electrolytes; Keep K >4.5, Mg >2.2•Monitor for QT prolongation if on QT prolonging medications•QTc=QT/√RR interval (in sec, Bazett correction). QTc will approximately be equal to QT if HR 60–70 bpm.Key thresholds:•If QTc ≥470 ms in males and ≥480 ms females but <500 ms: close surveillance and stop QT prolonging medications•If QTc >500ms or >550 ms with BBB or increase in QTc >60 ms after drug initiation: place pacer pads, stop QT prolonging medication and maintain HR >80 bpm with isoproterenol or dobutamine. Polymorphic VTSustained VTVentricular fibrillationTorsades de Pointes (TdP)•Advanced cardiac life support protocol if haemodynamic compromise•Follow guideline recommended antiarrhythmic therapy for specific conditions. Discussion with cardiology/electrophysiology team.•Amiodarone bolus 150 mg IV in non-code setting; Isoproterenol + Lidocaine or temporary pacing if bradycardia induced torsade de pointes.•Monitor electrolytes: Keep K >4.5, Mg>2.2•VT: Amiodarone 150 mg bolus then infusion 1 mg/min if QTc<450 ms (300 mg IV if code); Avoid amiodarone if QTc markedly prolonged.•VT: Lidocaine if QTc>550 ms: bolus 75–100 mg then infusion 0.5–2 mg/min, avoid if poor hepatic function or severe heart failure•Discuss antiarrhythmic drug choice if QTc borderline (450–550 msec) with cardiology/EP.•TdP/polymorphic VT: Maintain heart rate of >80 bpm (may need beta agonist such as dobutamine, isoproterenol or epinephrine; transvenous pacing).•Magnesium IV 2–4 gm for Torsade de Pointes•Limited bedside Echo for LV dysfunction evaluation.•Non-sustained polymorphic VT requires immediate patient assessment as cardiac arrest may follow. SVT including AF/AFL with heart rate > 150 bpm•ACLS protocol if haemodynamically unstable.•Lenient rate control, allow permissive tachycardia.•SVT: Adenosine 6–12 mg IV push in acute management•SVT, AF/AFL: beta blocker may be preferred over calcium channel blocker depending on LV function•AF: if rhythm control desired, may use amiodarone.•Cardiology or EP consult before considering class Ic antiarrhythmics (flecainide, propafenone)•Discuss with cardiology if QTc>450 ms on a QT prolonging drug or QTc>500 ms or QTc increase after started on a QT prolonging drug.•Assess interaction of oral anticoagulant with antivirals. Bradycardia•Follow standard bradycardia guidelines (AHA, ACLS) if patient unstable.•Discontinue AV nodal blocking agents.•Assess medication interaction with antivirals (Table 5).Abbreviations: PCI, percutaneous coronary intervention; LV, left ventricle; HF, heart failure; SVT, supraventricular tachycardia; AF, atrial fibrillation; AFL, atrial flutter; EP, electrophysiology; ACLS, advanced cardiac life support; AKI, acute kidney injury; SBP, systolic blood pressure; BBB, bundle branch block; ms, milliseconds; ECMO, extracorporeal membrane oxygenation; VT, ventricular tachycardia; AHA, American Heart Association; AV, atrioventricular. Open table in a new tab Abbreviations: PT, prothrombin time; LDH, lactate dehydrogenase; CRP, C reactive protein; IL6, interleukin 6; CT, computed tomography; ID, infectious disease; IV, intravenous; ARDS, acute respiratory distress syndrome; SISI, systemic inflammatory response syndrome; DIC, disseminated intravascular coagulation. Abbreviations: CBC, complete blood count; CMP, complete metabolic profile; NTpBNP, N terminal pro brain natriuretic peptide; ESR, drythrocyte sedimentation rate; ICU, intensive care unit; SOFA, Sequential Organ Failure Assessment; PE, pulmonary embolism; PPE, personal protective equipment; LDH, lactate dehydrogenase; ECG, electrocardiograph; CT, computed tomography; INO, inhaled nitric oxide. Abbreviations: PCI, percutaneous coronary intervention; LV, left ventricle; HF, heart failure; SVT, supraventricular tachycardia; AF, atrial fibrillation; AFL, atrial flutter; EP, electrophysiology; ACLS, advanced cardiac life support; AKI, acute kidney injury; SBP, systolic blood pressure; BBB, bundle branch block; ms, milliseconds; ECMO, extracorporeal membrane oxygenation; VT, ventricular tachycardia; AHA, American Heart Association; AV, atrioventricular. SARS-CoV-2 contains four structural proteins, namely spike (S), envelope (E), membrane (M), and nucleocapsid (N) proteins of which S protein mediates the viral entry into host cells [[17]Tai W. He L. Zhang X. Pu J. Voronin D. Jiang S. et al.Characterization of the receptor-binding domain (RBD) of 2019 novel coronavirus: implication for development of RBD protein as a viral attachment inhibitor and vaccine.Cell Mol Immunol. 2020; 17: 613-620Crossref PubMed Scopus (321) Google Scholar,[18]Nikolich-Zugich J. Knox K.S. Rios C.T. Natt B. Bhattacharya D. Fain M.J. SARS-CoV-2 and COVID-19 in older adults: what we may expect regarding pathogenesis, immune responses, and outcomes.GeroScience. 2020; 42: 505-514Crossref PubMed Scopus (7) Google Scholar]. The virus exhibits strong binding to cell-associated and soluble angiotensin converting enzyme (ACE) 2 receptors expressed in many organs such as the heart, kidneys, intestine, lung, brain and liver [[19]Kuba K. Imai Y. Ohto-Nakanishi T. 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• W3033888930 created "2020-06-12" @default.
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• W3033888930 date "2020-07-01" @default.
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• W3033888930 title "SARS-CoV-2 Infection and Cardiovascular Disease: COVID-19 Heart" @default.
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