Cardiovascular Manifestations of COVID-19

Acute Cardiac Injury

Definition

Serum levels of cardiac biomarkers (eg, high-sensitivity cardiac troponin I) above the 99th percentile upper reference limit, or new electrocardiographic and echocardiographic abnormalities (Huang, et al., Lancet, 2020; Zhou, et al., Lancet, 2020)

Pathophysiology

May occur directly as consequence of virus-associated Acute Coronary Syndrome, Arrhythmia, Myo/Pericarditis, or Cytokine Release, or indirectly associated with the combination of acute illness and underlying hypertension, coronary artery disease, heart failure, structural heart disease, chronic kidney disease, or diabetes (Bonow, et al. JAMA Cardiology 2020; Thygesen, et al., JACC, 2018)

Diagnostics

Incidence

Prognostic Implications

  • Associated with increased utilization of noninvasive ventilation (38 [46.3%] vs 13 [3.9%]; P < .001) and invasive mechanical ventilation (18 [22.0%] vs 14 [4.2%]; P < .001) (Shi, et al., JAMA Cardiology, 2020)
  • Associated with increased mortality
    • Occured in 59% of non-survivors (N = 32) vs. 1% of survivors (N = 1) (Zhou, et al., Lancet, 2020)
    • Adjusted HR 4.26 [95% CI, 1.92-9.49] p < 0.001) (Shi, et al., JAMA Cardiology, 2020)
    • Mortality 59.6% (n = 31) in individuals with ↑TnT vs. 8.9% (n = 12) with normal TnT; p < 0.001 (Guo, et al., JAMA Cardiology, 2020)
    • Increased mortality was seen with elevated troponin regardless of CVD status, but underlying CVD was also associated with increased mortality without evidence of cardiac injury
      • Mortality 7.62% (8 of 105) among patients without CVD + normal TnT, 13.33% (4 of 30) for underlying CVD + normal TnT levels, 37.50% (6 of 16) for those without underlying CVD + ↑TnT levels, and 69.44% (25 of 36) for underlying CVD + ↑TnT (Guo, et al., JAMA Cardiology, 2020)

Treatment Considerations

Acute Coronary Syndrome

Definition

Pathophysiology

  • Myocardial ischemia as a consequence of atherothrombotic coronary artery disease (eg. plaque disruption, plaque erosion, or thromboembolic phenomenon; Type I MI), mismatch between oxygen supply and demand (Type II MI), in association with cardiac death (eg. Type III MI), related to percutaneous coronary intervention (Type IV MI), or associated with coronary artery bypass grafting (Type V MI)

Incidence

  • As of 3/2020, case reports of acute coronary syndromes (ACS) (Type 1 MI) in the setting of COVID-19 have yet to be published (Driggin, et al., JACC, 2020)
  • Severe respiratory infection has been identified as a risk factor for acute myocardial infarction
    • Incidence ratio [IR] 6.1, 95% CI 3.9-9.5 following influenza; IR 2.8, 95% CI 1.2–6.2 following non-influenza viral illness (Kwong, et al., NEJM, 2018)
  • One case of spontaneous coronary artery dissection (SCAD) reported in France (Courand, JACC Cardiovascular Interventions, 2020)

Diagnostics

Treatment Considerations (SCAI Guidelines)

See Penn Tenecteplase Pathway for ST- Elevation Myocardial Infarction

See Szerlip, et al., Catheterization and Cardiovascular Interventions, 2020 and Welt, et al., JACC, 2020, summarized below:

STEMI

  • Primary PCI for high risk patients (anterior location, hypotension, elevated Killip class, cardiogenic shock, life-threatening, delayed presentation >12 hours)
  • Consider fibrinolysis for low risk patients without contraindications (intracranial hemorrhage, prior stroke, recent trauma/surgery, intracranial malignancy/arteriovenous malformation/aneurysm, active bleeding, uncontrolled hypertension); otherwise consider primary PCI or medical management

NSTEMI

  • Early angiography (<2 hours) for very high risk patients (refractory chest pain, heart failure, cardiogenic shock, life-threatening arrhythmia)
  • Conservative management for non-very high risk patients with antiplatelet therapy, anticoagulation (48 hours), high-intensity statin, beta-blocker, ACE-inhibitor (if indicated)

Arrhythmia

Incidence

Diagnostics

Treatment Considerations

Atrial Fibrillation/Flutter

  • No hypotension/shock: Beta blockade and/or calcium-channel blockade
  • Hypotension/shock: Consider amiodarone infusion

Ventricular Tachycardia

  • Pulseless/Unstable: ACLS, defibrillation/cardioversion
  • Stable: Consider amiodarone or lidocaine infusion
  • Consider stopping QTc prolonging medications in patients who develop torsades in the setting of prolonged QT

Bradyarrhythmia

  • Consider epinephrine, dopamine, isoproteronol, temporary pacemaker

Myo/Pericarditis

Incidence

Clinical Presentation

Myo/Pericarditis may present with a broad spectrum and severity of symptoms including chest pain, palpitations, tachycardia/bradycardia, elevated cardiac biomarkers, or acute-onset heart failure with cardiogenic shock.

Diagnostics

  • Cardiac troponin, NT-proBNP, Ferritin, IL-6, LDH, D-dimer
  • Physical exam may demonstrate pericardial friction rub, signs of heart failure (S3, elevated jugular venous pressure, edema)
  • ECG - case reports of pseudo-STEMI manifestations
    • Diffuse ST-segment elevation with PR-segment depression
  • Consider limited echocardiogram
  • Unclear role of endomyocardial biopsy (to evaluate direct viral effects) and/or cardiac MRI/CT (to evaluate for myocardial inflammation and the presence of underlying coronary artery disease)

Management

  • Supportive treatment
    • Acute Heart Failure: avoid medications with negative chronotropic/inotropic effects (eg. beta-blockers, calcium-channel blockers) if concerned for new heart failure as cardiac output may be dependent on tachycardia; avoid NSAIDs which may lead to fluid retention and myocardial injury. See Cardiomyopathy/Heart Failure/Cardiogenic Shock.
    • Arrhythmia: see Arrhythmia
    • Pericarditis without myocardial involvement: consider colchicine, NSAIDs
  • Consider anti-inflammatory/immunomodulators if concomittant Cytokine Release; Anecdotal/case reports describe treatment with steroids and IVIG

Thromboembolic Disease/Coagulopathy

Incidence

Prognostic Implications

Treatment Considerations

Secondary Hemophagocytic Lymphohistiocytosis/Cytokine Release

Definition

Hyperinflammatory syndrome characterised by macrophage activation and fulminant hypercytokinemia, associated with multiorgan failure and shock.

Clinical Presentation

Incidence

Prognostic Implications

Treatment Considerations

  • Care typically supportive
  • Consideration of IVIG, steroids (may be associated with worsened lung injury), enrollment in clinical trial (or off-label use) of cytokine blockade (IL-6 antagonists [eg. tocilizumab, sarilumab, siltuximab] or IL-1 antagonists [eg. anakinra])

Cardiomyopathy/Heart Failure/Cardiogenic Shock

Incidence

Diagnostics

  • Physical Exam: ↑JVP/CVP, edema, rales/crackles
  • Labs: Cardiac troponin, NT-proBNP, lactate, central/mixed venous oxygen saturation (ScVO2) if available; consider evaluation of Cytokine Release with Inflammatory Biomarkers
  • ECG
  • Chest x-ray
  • Consider limited echocardiogram
    • For patients with cardiogenic shock, echocardiogram may help differentiate the etiology and change management (eg. global hypokinesis vs. regional wall abnormality suggesting ACS, mechanical complications of an untreated MI)

Prognostic Implications

Management

Stable/Chronic

Unstable/Cardiogenic Shock

  • Consider invasive hemodynamic monitoring with arterial and central venous catheters
  • Goals: MAPs 65-75, CVP 6-14, PCWP 12-18, PAD 20-25, SVR 800-1000, SCvO2 > 60%, CI > 2.2 (Note: Achieving MAP goal is first priority, then optimize other parameters)
  • Ensure negative inotropes such as beta blockers, calcium channel blockers and antihypertensives are discontinued.
  • Titration of norepinephrine infusion for goal MAP 65-75
  • Initiate diuretic therapy for CVP > 14, PCWP >18, PAD > 25
  • Consider inotropic support (eg. dobutamine or epinephrine infusions)
  • Consider bedside placement of IABP or ECMO if patients are not responding to medical management alone