MioAtlas
G7: Infections and inflammation

Myocarditis

Inflammatory disease of the myocardium (most frequently triggered by viral infections such as enterovirus, parvovirus B19, human herpesvirus type 6, adenovirus, or SARS-CoV-2, or mediated by autoimmune processes or drug toxicity) characterized by myocyte infiltration.

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Definition

Inflammatory disease of the myocardium (most frequently triggered by viral infections such as enterovirus, parvovirus B19, human herpesvirus type 6, adenovirus, or SARS-CoV-2, or mediated by autoimmune processes or drug toxicity) characterized by inflammatory myocyte infiltration, interstitial edema, and cardiomyocyte necrosis, resulting in acute depression of ventricular contractile function and arrhythmias, frequently associating inflammation of the overlying pericardium (myopericarditis) [C2] [G7-09].

Severity criteria

  • Mild (L): Left ventricular ejection fraction (LVEF) ≥ 50 % (preserved global systolic function with localized segmental hypokinesia); normal end-diastolic myocardial wall thickness (< 11 mm); hemodynamic stability without decompensated heart failure.
  • Moderate (M): LVEF 40–49 % (mildly reduced systolic function); myocardial wall thickening due to interstitial edema (11–13 mm); elevated left ventricular filling pressures (PCWP 15–20 mmHg); clinical heart failure in NYHA functional class II–III [C2] [G7-09].
  • Severe / Fulminant (G): LVEF < 40 % (or acute cardiogenic collapse with LVEF < 30–35 %); marked diffuse myocardial wall thickening (> 13–15 mm) secondary to massive acute inflammatory edema (not chronic hypertrophy); requirement for inotropic support or mechanical circulatory assist [G7-09] [C2].
  • Pericardial effusion: Frequent presence of mild-to-moderate serous pericardial effusion (diastolic anechoic separation < 10–15 mm) [C2].

Findings by layer

Hemodynamics

  • LV ejection fraction (left ventricular ejection fraction): L ≥ 50 %, M 40–49 %, G < 40 % [C2].
  • Pulmonary capillary wedge pressure / LV end-diastolic pressure (mean pulmonary capillary wedge pressure / lvedp): Elevated in moderate and severe stages (15–24 mmHg) [C2] [G7-09].
  • Systemic cardiac output: Marked reduction in the fulminant severe form (< 3.5 L/min).

Rhythm

  • Default rhythm: Sinus tachycardia, often disproportionate to body temperature [C2] [G7-09].
  • Alternative rhythms / associated arrhythmias: Frequent ventricular premature beats (PVC), monomorphic ventricular tachycardia, or variable degrees of atrioventricular conduction disturbances [C2] [G7-09].

ECG

  • Sinus tachycardia.
  • Diffuse repolarization abnormalities: Diffuse upwardly concave ST-segment elevation, flattening or asymmetric T-wave inversion in precordial and limb leads [C2] [G7-09].
  • If pericarditis component coexists: Possible subtle PR-segment depression [C2].
  • In severe forms: Reduced QRS complex voltage (low voltage) due to profuse interstitial myocardial edema [G7-09] [E1].

Heart sounds and murmurs

  • Third heart sound (protodiastolic S3 gallop): Cardinal auscultatory sign in moderate and severe forms, originating from deceleration of ventricular filling into a dysfunctional ventricle with elevated end-diastolic pressure [B1] [C2].
  • Fourth heart sound (S4): Present in sinus rhythm due to atrial contraction into an edematous and inelastic myocardium [B1].
  • Functional systolic murmur: Soft apical mid-systolic or early systolic murmur (grade 1–2/6) of functional mitral regurgitation due to annular dilation or papillary dyssynchrony [B1].
  • Pericardial friction rub: Possible triphasic rub audible at the left sternal border if serofibrinous pericarditis coexists [C2].

Arterial pulse

  • Rapid and weak peripheral pulse (relative parvus et celer), with reduced pulse pressure in low cardiac output states [B4].

Jugular venous pulse

  • Moderate jugular venous engorgement with central venous pressure elevation in biventricular dysfunction stages [B3].

Maneuvers

  • Valsalva and standing: Decrease stroke volume and attenuate the functional murmur [B1].
  • Squatting: Increases venous return, transiently increasing stroke volume and third sound intensity [B1].

Simulator severity grades

Simulator severity grades: Mild, Moderate, Severe
Baseline rhythm: Sinus Tachycardia

Also known as: Acute myocarditis · Inflammatory cardiomyopathy · Myocardial inflammation · Infectious myocarditis · Myocarditis

Other pathologies in this group

Sources

  1. [B1] Bedside diagnosis of systolic murmurs . N Engl J Med (1988) . DOI: 10.1056/NEJM198806163182404 PubMed: 2897627
  2. [B3] The jugular venous pressure revisited . Cleve Clin J Med (2013) . DOI: 10.3949/ccjm.80a.13039 PubMed: 24085809
  3. [B4] The Carotid Pulse . Clinical Methods: The History, Physical, and Laboratory Examinations (1990) . PubMed: 21250154
  4. [C2] 2025 ESC Guidelines for the management of myocarditis and pericarditis . Eur Heart J (2025) . DOI: 10.1093/eurheartj/ehaf192 PubMed: 40878297
  5. [E1] AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the International Society for Computerized Electrocardiology . Circulation (2009) . DOI: 10.1161/CIRCULATIONAHA.108.191097 PubMed: 19228820
  6. [G7-09] Recognition and Initial Management of Fulminant Myocarditis: A Scientific Statement From the American Heart Association . Circulation (2020) . DOI: 10.1161/CIR.0000000000000745 PubMed: 31902242