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| [[[[Link title]]]]__NOTOC__
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| {{CMG}} {{AE}} {{mitra}}{{MC}}
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| ==Overview==
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| ==Complications==
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| ===Myocardial injury===
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| ===Acute Coronary Syndromes===
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| ===Heart Failure===
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| ====Pathophysiology====
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| *Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
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| *Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
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| *Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:
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| **Acute exacerbation of chronic heart failure
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| **Acute myocardial injury (which in turn can be caused by several mechanisms)
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| **Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
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| **Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
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| **Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)
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| ====Symptoms and signs====
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| *Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
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| *Lower limb edema
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| *Orthopnea
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| *Paroxysmal nocturnal dyspnea
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| *Confusion and altered mentation
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| *Cool extremities
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| *Cyanosis
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| *Syncope
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| *Fatigue
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| *Hemoptysis
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| *Palpitations
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| *Weakness
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| *Wheezing or cardiac asthma
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| *Distended jugular veins
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| *Crackles on auscultation
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| ====Electrocardiography (ECG)====
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| *There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
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| *The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
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| *These ECG findings may include:
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| **Low QRS Voltage
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| **Left ventricular hypertrophy
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| **Left atrial enlargement
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| **Left bundle branch block
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| **Poor R progression
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| **ST-T changes
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| ====Chest x-ray (CXR)====
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| *The Chest x-ray may show evidence of:
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| **Cardiomegaly
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| **Pulmonary congestion
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| **Increased pulmonary vascular markings.
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| *Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
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| ====Echocardiography====
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| *A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.
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| *To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
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| *In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
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| **Cardiac point-of-care ultrasound (POCUS)
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| **Focused cardiac ultrasound study (FoCUS)
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| **Critical care echocardiography
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| *Cardiac ultrasound can help in assessing the following parameters:
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| **Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
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| **Left ventricular diastolic function
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| **Left ventricular structural abnormalities, including LV size and LV wall thickness
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| **Left atrial size
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| **Right ventricular size and function
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| **Detection and quantification of valvular abnormalities
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| **Measurement of systolic pulmonary artery pressure
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| **Detection and quantification of pericardial effusion
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| **Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia
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| ====Cardiac biomarkers====
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| *Cardiac Troponins:
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| **Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
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| **Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.
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| *Natriuretic Peptides:
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| **Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.
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| **Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
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| **Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
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| **Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.
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| **However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.
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| **Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.
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| ====Treatment====
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| *Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists.
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| *Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include: <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
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| **Fluid restriction
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| **Diuretic therapy
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| **Vasopressors and/or inotropes
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| **Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
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| *Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.
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| *Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.
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| ===Cardiogenic Shock===
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| ===Myocarditis===
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| ===Pericarditis===
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| ===Arrhythmias ===
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| ==== Pathophysiology: ====
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| Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]]. According to a study done in Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had arrhythmias. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 [[pneumocytes]] exhibit ACE 2 receptors in the lung. Studies report that coronary [[endothelial cells]] in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the [[renin-angiotensin system]]. The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and [[Endothelium|endothelial cells]]. [[Hypoxemia|Hypoxia]] and [[Electrolyte disturbance|electrolyte abnormalities]] that are common in the acute phase of severe [[COVID-19]] can potentiate [[Cardiac arrhythmia|cardiac arrhythmias]]. Binding of SARS-CoV-2 to ACE2 receptors can result into [[hypokalemia]] which causes various types of [[Cardiac arrhythmia|arrhythmia]]. Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]]. According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage.
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| ==== Signs and Symptoms: ====
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| Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).
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| *'''Palpitations:''' According to a study done in Hubei province,[[Palpitation|palpitations]] were reported as a presenting symptom by 7.3 percent of patients.
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| *'''Prolong QT Interval:''' According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had [[QT interval|corrected QT interval]] (QTc) >500 milliseconds at the time of admittance. However, in another study that involved 84 patients who got [[hydroxychloroquine]] and [[azithromycin]], the baseline QTc interval was 435 milliseconds before receiving these medications.
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| *'''Atrial Arrhythmia:''' According to a study, among 393 patients with COVID-19, [[Cardiac arrhythmia|atrial arrhythmias]] were more common among patients requiring invasive [[mechanical ventilation]] than noninvasive [[mechanical ventilation]] (17.7 versus 1.9 percent)
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| *'''Ventricular Arrhythmia:''' According to a study done in Wuhan, China. among 187 hospitalized patients with [[COVID-19]], 11 patients (5.9 percent) developed [[Ventricular arrhythmias|ventricular tachyarrhythmias]].
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| *'''Cardiac Arrest:''' According to a Lombardia Cardiac Arrest Registry (Lombardia CARe) of the region Lombardia in Italy. Out of 9806 cases of [[COVID-19]], 362 cases of out-of-hospital [[cardiac arrest]] were reported during the study time frame in 2020. During a similar period in 2019, 229 cases of out-of-hospital [[cardiac arrest]] were reported, which means an increment of 58% was observed in 2020 among [[COVID-19]] patients. According to the records from a tertiary care hospital in Wuhan. Out of 761 patients with severe [[COVID-19]], 151 patients developed in-hospital [[cardiac arrest]]. 136 patients received resuscitation. Out of 136 patients, 119 patients had a respiratory cause. 10 patients had a cardiac cause. 7 patients had other causes. Ventricular fibrillation or pulseless ventricular tachycardia was observed in 8 patients (5.9%), [[Pulseless electrical activity]] in 6 patients (4.4%), and [[asystole]] in 122 [[COVID-19]] patients (89.7%).
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| ==== Diagnostic Testing: ====
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| *'''ECG:''' Most patients with the severe COVID-19, and especially patients who receive QT-prolonging medications, should have a baseline electrocardiogram (ECG) performed at the time of admission to the hospital.The best technique to get the QT interval is with a 12-lead electrocardiogram (ECG). However, to scale back exposure to hospital workers, this could not perpetually be possible. A single-lead ECG might underestimate the QT interval, and there ought to be an effort to use a multiple-lead telemetry system to observe the QT interval.
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| *'''Transthoracic echocardiography:''' Transthoracic echocardiography is recommended for an inpatient with heart failure, arrhythmia, ECG changes, or newly diagnosed cardiomegaly on chest x-ray or CT-chest.
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| ==== Treatment:====
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| * '''Polymorphic Ventricular Tachycardia:''' All patients with torsades de pointes (TdP) should be determined if they are hemodynamically stable or unstable through immediate evaluation of the symptoms, vital signs, and level of consciousness.
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| **
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| ===Out-of-hospital cardiac arrest and Sudden Cardiac Death===
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| ===Spontaneous Coronary Artery Dissection===
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| ==References ==
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| <references />
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