COVID-19-associated stress cardiomyopathy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2] Sara Zand, M.D.[3]

Synonyms and keywords: Takotsubo syndrome, TTS, Takotsubo cardiomyopathy, broken heart syndrome, Stress cardiomyopathy, left ventricular outflow obstruction ( LVOTO)

Overview

COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020. This disorder is the result of extreme sympathetic stimulation due to the abnormal release of catecholamines and cortisol leading to rapid, severe, reversible cardiac dysfunction, as well as, wall motion abnormality of the left ventricle subtending more than one coronary artery territory, without evidence of significant obstructive coronary artery disease. Few cases of stress cardiomyopathy reported in literature due to direct consequences of covid-19 on the myocardium. However, due to increased psychological, social, economical distress during covid-19 pandemic, the incidence of stress cardiomyopathy in non-covid-19 patients increased significantly compared with prepandemic periods. In general, stress cardiomyopathy may develope in the setting of emotional stress or secondary to infections such as covid-19. The latter may have worse prognosis in terms of mortality compared with emotional trigger.

Historical Perspective

• COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020.

Classification

• Takotsubo cardiomyopathy is classified as follows:

• Primary takotsubo cardiomyopathy: acute cardiac symptoms resulting from emotional or physical stress, main cause of seeking medical attention
• Secondary takotsubo cardiomyopathy: developing in hospitalized patients for other reasons

Apical type	Midventricular type	Basal type	Focal type
Common type (>80%), hypokinesia or dyskinesia of midventricular and apical parts of anterior, septal, inferior and lateral walls of left ventricle associated with hyperkinesia of basal segments	Hypokinesia or dyskinesia of midventricular segments, like a cuff in most cases, with normokinesia or hyperkinesia of basal and apical segments	Inverse takotsubo cardiomyopathy, wall motion abnormality is reciprocal to apical type, hypokinesia or dyskinesia of basal segments, normokinesia or hyperkinesia of midventricular, anterior, antroseptal, and antroapikal segments of left ventricle	Focal hypkinesia or dyskinesia of any segments of the left ventricle , commonly antroseptal wall

Pathophysiology

• Inflammation and cytokine storm are the underlying mechanisms of cathecolamines release in patients with covid-19.
• It is thought that COVID-19-associated stress cardiomyopathy is the result of extreme sympathetic stimulation due to abnormal release of catecholamines such as epinephrine, norepinephrine, dopamine and also high level of cortisol.
• Increase level of cathecolamines and cortisol in patients with covid-19 may cause direct toxic effect on cardiomyocytes and stress cardiomyopathy.
• Direct effect of cathecolamine on cardiomyocytes may lead to myocardial stunning, hyperdynamic contractility, multiple vessles spasm, and/or microvascular dysfunction.
• Increased cortisol level observed in patients with covid-19 may cause isometric tension, reduced relaxasion of papillary muscles, reduced total relaxation time, without any effect on contraction time.
• The mechanisms occurring in COVID-19 patients may lead to myocardial injury and left ventricular dysfunction are:.

  Stress-induced adrenergic discharge as consequence of fever and inflammatory response to infection

  The direct SARS-CoV-2 injury causing endothelial dysfunction, which may cause microvascular vasoconstriction that can manifest in a transient left ventricular apical dysfunction, (apical ballooning).

• Proposed mechanisms that have the potential to cause myocardial injury in acute coronavirus disease 2019 cardiovascular syndrome:
  

Stress Induced Cardiomyopathy

Microvascular/Thrombotic Injury

Cytokine Storm

Pre-existing cardiovascular Disease

Acute Myocardial Injury Characterized by Abnormal Troponin

Viral Myocarditis

Hypoxemia

Hypotension +/- Shock

Ventricular or atrial arrhythmias

Causes

Common causes of stress cardiomyopathy include:

• Physical stressors
• Emotional stressors (anger, argument, surgery, natural disasters, grief, happiness)
• Several medications
• General anesthesia
• Infectious disease
• Novel coronavirus disease 2019

Differentiating COVID-19-associated stress cardiomyopathy from other Diseases

• For further information about the differential diagnosis, click here.
• To view the differential diagnosis of COVID-19, click here.
  

Differentiating diagnosis	Takotsubo cardiomyopathy	STEMI
Stressful trigger	Prominent stressful event (79%)	8%
Elevated troponin on admission	91%	37%
LVEF<40%	Higher incidence of decreased LVEF at presentation (80%)	31%
Symptoms	Chest pain (73%)	Higher rate of chest pain (100%)
Sex	Female	Male
Age	Older age (66 years old)	Mean age 60 years old
Risk factors	Lower incidence of HLP, smoking, diabetes mellitus	HLP, smoking, diabetes mellitus
Coronary angiography	Lower incidence of stenosis> 50% (15%)	Stenosis> 50% in 100%
In-hospital mortality	1.3%	3.6%

Epidemiology and Demographics

• The incidence of stress cardiomyopathyassociated covid-19 is approximately 7.8% of all patients presenting acute coronary syndrome which is higher than pre-pandemic period.
• In critically ill covid-19 patients, the incidence of stress cardiomyopathy is approximitely 2-4%, compared to 1-2% among general population.

Age

• Stress cardiomyopathy is more commonly observed among elderly patients with a mean age of 64.6 years.

Gender

• Male are more commonly affected with stress cardiomyopathy secondary to covid-19.
• Primary stress cardiomyopathy is much more common in women..

Race

• There is no racial predilection for stress cardiomyopathy in covid-19 patients.

Risk Factors

• There are no established risk factors for COVID-19-associated stress cardiomyopathy.
• In general population, secondary stress cardiomyopathy is much more commen in older men , as well as with higher incidence of conventional risk factors including HTN, diabetes mellitus, dyslipidemia, cerebrovascular disease, cardiac arrhythmia.
• Common risk factors in reported takotsubo cardiomyopathy secondary to covid-19 include:

  Older age

  HTN

  DM

  Dyslipidemia

  Prior stroke

• Atrial fibrillation
• Psychiatric illness
• Hypoxia
• Severe covid-19 pneumonia requiring mechanical ventilation support

• Common triggers associated with development of secondary takotsubo cardiomyopathy in severe covid-19 pneumonia include:

  Respiratory condition

  Intubation

  Medication use

  Epinephrine use

  Anxiety

  Betablocker withdraw

Screening

• There is insufficient evidence to recommend routine screening for COVID-19-associated stress cardiomyopathy.

Natural History, Complications, and Prognosis

• There are varied degree of the recovery of patients with stress cardiomyopathy associated covid-19 reported in literature within two months.

• Early clinical features include acute coronary syndrome with chest pain and ECG changes and rise of troponin, acute pulmonary edema, decreased oxygen saturation without response to O2 therapy, hemodynamic instability.
• Patients with stress cardiomyopathy associated with covid-19 had a longer hospital days admission compared with the pre-pandemic period.
• Stress cardiomyopathy in critically ill covid-19 patients may progress to develop cardiogenic shock, pulmonary edema, hemodynamic collapse, and death.
• Patients with secondary takotsubo cardiomyopathy may experience cardiogenic shock, respiratory failure requiring mechanical ventilation support and coagulation disorder. However, in reported patients with takotsubo cardiomyopathy exacerbation of respiratory status may be due to covid-19 complicating takotsubo cardiomyopathy.
• Some patients may recover and have a normalized cardiac function within a few weeks. .
• Prognosis of stress cardiomyopathy associated covid-19 is not clearly described yet, and mortality rate of patients with stress cardiomyopathy without covid-19 infection is approximately 5% during pandemic (similar to pre-pandemic covid-19 period). However, the mortality rate of takotsubo cardiomyopathy secondary to covid-19 pneumonia is 10 times higher than non-covid-19 patients.
• Complications of stress cardiomyopathy include:
  • Severe Heart failure
  • Acute pulmonary edema
  • Cardiogenic shock
  • Dynamic left ventricular outflow tract obstruction (peak gradients >25 mmhg in echo or cath)
  • Hypotension
  • Moderete to severe acute functional mitral regurgitation
  • Bradycardia
  • QT prolongation and ventricular arrhythmias
  • Torsade de pointes
  • Left ventricular mural thrombus
  • Mitral valve dysfunction
  • Pulmonary embolism
  • Systemic embolism, stroke
  • LV free wall rupture
  • Acute renal failure
  • In-hospital death

Diagnosis

• In the development of new hypotension and tachycardia in intubated covid-19 patients with comorbidities ( HTN, dyslipidemia, atrial fibrillation, previous stroke) or the need for vasopressor and presence of hypoxia, investigation about stress cardiomyopathy should be done by taking ECG and check of cardiac biomarkers ( troponin, NT-Pro BNP.
• In the presence of any ECG changes or cardiac biomarkers abnormality, transthoracic echocardiography should be done

Diagnostic Study of Choice

• Echocardiography is the gold standard of diagnosis of takotsubo cardiomyopathy.
• High risk feature of takotsubo cardiomyopathy on echocardiography include: LVEF<45%, Moderate to severe mitral regurgitation, right ventricular involvement.
• The diagnosis of stress cardiomyopathy is made when all 4 of the following diagnostic criteria are met:
  • Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid segments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present.
  • Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
  • New electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin.
  • Absence of pheochromocytoma and myocarditis.
• The diagnosis of COVID-19-associated stress cardiomyopathy is largely the same, but happening in the context of a SARS-CoV2 infection.

History and Symptoms

Symptoms of stress cardiomyopathy can mimic acute coronary syndrome. The most common presenting symptoms are:

• Chest pain or chest tightness
• Shortness of breath
• Vomiting
• Loss of consciousness due to syncope or cardiac arrest in rare cases

• Considering emotional factors such as fear of severity of covid-19, contact with a hospitalized family member, worry about socioeconomic costs, intrusive thoughts about morbidity of covid-19 that may lead to stress cardiomyopathy.

Physical Examination

• The following physical examination findings may be seen in patients with stress cardiomyopathy:

Organ System	Findings	Suggestive Of
General appearance	Patient may be anxious, ill-appearing or diaphoretic
Vital signs	Tachypnea Tachycardia or bradycardia Hypotension	Cardiogenic shock
Cardiac	Murmurs, S3, gallop rhythm, Displaced point of maximal impulse (PMI)	Heart failure
Respiratory	Rales, crackles	Pulmonary edema

Laboratory Findings

• Laboratory findings consistent with the diagnosis of stress cardiomyopathy in covid-19 patients include elevated troponin and Pro-BNP.
• Elevated levels of serum catecholamines may also be found in patients with stress cardiomyopathy.
• Evidence of ongoing COVID-19 disease is required to establish the diagnosis.

Electrocardiogram

The ECG findings are largely the same of the regular stress cardiomyopathy, and are often confused with those of an acute anterior wall myocardial infarction. Findings on ECG include:

• ST elevation in the precordial leads
• T wave inversion
• Q wave formation
• QT prolongation
• New-onset bundle branch block (BBB)
• Rarely, malignant ventricular arrhythmias may be seen

X-ray

Takotsubo refers to a ceramic pot used to trap octopuses in the Japanese language. The typical chest x-ray findings in patients with stress cardiomyopathy include a takotsubo-shaped heart, in which there is apical ballooning and narrowing of the proximal portion near the great vessels.

Echocardiography or Ultrasound

The following echocardiographic findings may be seen in patients with stress cardiomyopathy:

• Apical ballooning
• Apical or mid-segment dyskinesia or akinesia
• Left ventricular systolic dysfunction
• Reduced ejection fraction

CT scan

A cardiac CT scan can also help differentiate between stress cardiomyopathy and acute MI. Regional abnormalities in the wall motion of the heart, along with absence of coronary atherosclerosis support the diagnosis of stress cardiomyopathy over an acute MI.

Chest CT scan may also show findings associated with COVID-19 and they can include:

• Unilateral or bilateral pneumonia
• Mottling and ground-glass opacity
• Focal or multifocal opacities
• Consolidation
• Septal thickening
• Subpleural and lower lobe involvement more likely

MRI

• Cardiac magnetic resonance (CMR) is a useful imaging modality in distinguishing between stress cardiomyopathy and myocarditis or MI. In the case of myocarditis or MI, there is delayed hyper-enhancement of gadolinium. However, absence of gadolinium hyper-enhancement supports the diagnosis of stress cardiomyopathy. Also, stress cardiomyopathy results in regional wall abnormality and its extent can best be documented using cardiac magnetic resonance.
• CMR in stress cardiomyopathy shows absence of irreversible damage and segmental LV dysfunction.

Other findings on CMR include:

• Hypokinetic or dyskinetic areas in the wall of the heart
• Myocardial edema
• Apical thrombi

Other Imaging Findings

Positron Emission Tomography (PET) Scan

In patients with stress cardiomyopathy, a PET scan may be done. Areas of hypokinesia or dyskinesia have reduced glucose utilization compared to normal regions.

Coronary Angiography

• Stress cardiomyopathy can mimic an acute MI, mainly anterior MI, since the clinical presentation, ECG and laboratory findings are similar. Hence, coronary angiography is considered a great diagnostic modality to differentiate between the two diagnoses.
• A normal angiography or absence of substantial coronary stenosis supports the diagnosis of stress cardiomyopathy.

Other Diagnostic Studies

Cardiac Catheterization

When patients with stress cardiomyopathy undergo cardiac catheterization, the following findings are usually reported:

• Normal anatomy of the coronary arteries, without evidence of acute plaque rupture
• Low ejection fraction (EF)
• Minimal or no evidence of coronary vasospasm
• Minimal disturbance of microcirculation

Myocardial Biopsy

• The histological findings on myocardial biopsy in patients with stress cardiomyopathy include:
  • Inflammatory infiltrates, consisting of mononuclear lymphocytes, leukocytes and macrophages
  • Myocardial fibrosis
  • Contraction bands, which may or may not be associated with necrosis

• The combination of inflammatory changes and contraction bands distinguish stress cardiomyopathy from coagulative necrosis seen in MI.

Treatment

Medical Therapy

• The mainstay of therapy of stress cardiomyopathy associated with covid-19 is supportive care.
• In mild TTS without signs of heart failure, beta-blocker and ACEI or ARB are recommended and inotrope agents such as epinephrine, norepinephrine, dobutamine, milrinone, isoproterenol should be avoided.
• In the presence of pulmonary edema without evidence of left ventricular outflow obstruction, administration of ACEI, betablockers, diuretic and nitroglycerin are recommended.
• In the presence of cardiogenic shock and left ventricular outflow obstruction (no heart failure symptoms), short acting betablocker, IV fluide, and placing impella are recommended.
• Diuretic, nitroglycerin, intraaortic ballon pump should be avoided in the evidence of cardiogenic shock and left ventricular outflow obstruction.
• If there is evidence of pump failure in the context of cardiogenic shock, levosimentan, ECMO, impella are considered.
• Arrhythmia such as VT, VF, torsades de pointes, bradycardia, long QT interval should be managed.
• Temporary RV pacing is recommended in the presence of AV block and placement of permanent device is not recommended.
• In the presence of bradycardia and long QTc >500 ms, betablocker should be avoided.
• In the presence of left ventricular clot or large portion of akinesia of left ventricle involving apex, anticougulation therapy is recommende.
• Classic treatment of heart failure including ACEI and betablocker should be kept at least three months or untill recovery of regional wall motion abnormality.
• Treatment of underlying disorders such as coronary artery disease is reasonable by continuing aspirin and statin.

Surgery

• Surgical intervention is not recommended for the management of COVID-19-associated stress cardiomyopathy.

Primary Prevention

• There are no established measures for the primary prevention of COVID-19-associated stress cardiomyopathy.
• Preventive measures should be taken to avoid COVID-19 infection.

Secondary Prevention

• There are no established measures for the secondary prevention of COVID-19-associated stress cardiomyopathy.

References

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