Myocarditis and Infectious Diseases

Pericarditis and Myocarditis

Pericarditis

• Non-specific inflammation of the pericardium, a rare emergent condition
• Pericardial effusion: accumulation of fluid in the pericardial space, which can be serous, purulent, fibrinous, or hemorrhagic
• Cardiac tamponade: impairment of ventricular filling due to fluid in the pericardial space, an emergent condition

Pericardial Physiology

• Two layers: parietal (thick, collagenous, stiff) and visceral (thin, closely adherent to epicardial surface)
• Pericardial fluid: normally 15-60 cc, prevents friction, prevents infection, augments atrial filling, and maintains normal pressure-volume relationship
• No physiological consequence to absent pericardium

Pericardial Innervation

• Parasympathetic (vagus, left recurrent laryngeal nerve)
• Sympathetic (stellate, first thoracic ganglia)
• Little somatic sensory innervation, resulting in visceral nature of chest pain

Etiology of Pericarditis

• Viral (most common, e.g., enteroviruses, HIV)
• Bacterial (e.g., streptococcus, staphylococcus, gram-negatives, anaerobes, TB, Lyme disease)
• Traumatic
• Malignant (e.g., lung, breast, lymphoma, leukemia, melanoma)
• Post-irradiation
• Post-MI (e.g., Dressler's syndrome)
• Collagen vascular disease (e.g., RA, SLE)
• Drug-induced (e.g., SLE-like syndrome, procainamide, hydralazine, methyldopa, reserpine, doxorubicin)

Viral Pericarditis

• Most common cause of pericarditis
• Mechanism of injury: direct viral cytotoxicity and indirect auto-antibody-mediated effects
• Syndrome may be immediate or develop 2-4 weeks post-viral illness
• Symptoms: chest pain, pericardial friction rub, fever, tachycardia, tachypnea, dyspnea, and diaphoresis

ECG in Pericarditis

• 4 stages of evolution over 3-4 weeks
• Only 50% of patients have all 4 phases
• Stage 1: diffuse ST elevation, PR depression, and reciprocal ST depression
• Stage 2: ECG transiently normal, some T-wave flattening
• Stage 3: T-wave inversion, deep and uniform
• Stage 4: return to normal, some patients with residual T-wave inversion

Management of Pericarditis

• Treat underlying cause
• Colchicine (1-2 mg PO OD) for pain and inflammation
• Steroids (only if NSAID-resistant)
• Admit if cannot rule out MI, pain control, or if effusion suspected

Myocarditis

• Inflammation of the myocardium
• Etiology:
  • Viral (most common, e.g., enteroviruses, adenovirus, influenza)
  • Bacterial (e.g., S. aureus, streptococcus, mycoplasma, diphtheria)
  • Spirochetal (e.g., Lyme disease)
  • Mycotic (e.g., candida, aspergillus)
  • Rickettsial (e.g., Rocky Mountain Spotted Fever)
  • Helminthic (e.g., trichinosis, schistosomiasis)
  • Protozoal (e.g., Chagas disease)
  • HIV
  • Drugs (e.g., cocaine, emetine, doxorubicin, HIV treatment)
  • Systemic diseases (e.g., collagen vascular disease, sarcoidosis, Kawasaki's disease)

Pathophysiology of Myocarditis

• Three major mechanisms:
  1. Myocardial necrosis from direct invasion
  2. Autoimmune destruction (e.g., beta myosin chain and coxsackie B share 50% same amino acid sequences)
  3. Endotoxins produced by pathogens

Clinical Features of Myocarditis

• VERY NON-SPECIFIC!
• Tachycardia out of proportion to fever
• Severe myalgias
• Non-anatomical ECG changes
• Continued pain with no ECG evolution
• Global (vs segmental) wall motion abnormalities on echo
• Unexplained CHF or dysrhythmias in previously healthy patient

Diagnosis of Myocarditis

• MRI (contrast-enhanced, shown to be useful, maybe the future?)
• Antimyosin scintigraphy (Indium-111, binds to exposed myosin in damaged myocardium)
• Endomyocardial biopsy (gold standard, Dallas criteria used to standardize diagnosis)

Treatment of Myocarditis

• ED treatment:
  • Bed rest
  • Cardiac monitoring
  • Management of arrhythmias
  • CHF treatment (cautious, aggressive preload or afterload reduction may cause cardiogenic shock)
  • Anticoagulation (if intracardiac thrombi detected on echo)
• Definitive treatment: treat specific cause if possible (e.g., Chagas disease, Lyme disease)

Test your knowledge on myocarditis, its causes, mechanisms, and relationships with various diseases. From viral causes to autoimmune destruction and treatment options, assess your understanding of this critical topic.