Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (54 page)

BOOK: Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis
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   Clinical presentation of myocarditis is highly variable with most cases likely asymptomatic. Chest pain most commonly is pleuritic in nature due to concomitant pericarditis, although may mimic chest pain of acute coronary syndromes. Sinus arrhythmias predominate over AV block or ventricular tachycardia.
   Chest symptoms are often preceded by a viral prodrome with tachycardia out of proportion to fever.
   Myocarditis should be suspected when unexplained LV dysfunction or arrhythmias are present, particularly in the young. CAD, valvular disease, congenital abnormalities must be excluded with a careful history of toxin and autoimmune disease taken. Myocarditis associated with autoimmune disease (giant cell myocarditis), unlike most other etiologies, is a rapidly progressive disease that is often fatal. Ventricular arrhythmias are more common with this variant of myocarditis.
   Recent vaccination should raise the possibility of a hypersensitivity myocarditis.
   Laboratory and Other Findings
   ECG: neither sensitive nor specific for diagnosis. Most commonly will reflect changes with pericarditis (see Pericarditis above) but may mimic ST elevation MI. Widened QRS and Q waves carry a poor prognosis, with diffuse low voltage seen with myocardial edema particularly ominous.
   Viral serology should not be used for diagnosis with positive and negative predictive values of 25% and 49%, respectively.
   Core laboratory: Elevation of cardiac biomarkers occurs in less than half of all acute cases but does predict mortality in patients hospitalized with fulminant myocarditis (CK-MB >29 ng/mL sensitivity of 83%). Acute-phase reactants are elevated (ESR, CRP, mild leukocytosis). If clinically appropriate, serology for toxoplasmosis, Chagas disease, trichinellosis, and Lyme carditis may be sent in addition to those for autoimmune disease, fat aspirates for amyloidosis, and ferritin (hemochromatosis).
   
Endomyocardial biopsy
with histopathologic confirmation remains the gold standard for diagnosis but is little used given the mild course of most viral myocarditis. In practice, it is used to differentiate giant cell, lymphocytic, and hypersensitivity myocarditis in fulminant heart failure. A diagnosis of GCM is critical as it can be ameliorated with immunosuppressive therapy and/or transplantation. Biopsy sensitivity for GCM is approximately 85%.
   
Cardiac MRI
is increasingly utilized for diagnosis with sensitivity of 88% and even higher when combined with biopsy. It should be performed only if the CMR result will change management (minority of cases). Proposed diagnostic criteria for myocarditis are based on pattern and distribution of gadolinium enhancement.
   
Stress-induced (Takotsubo) cardiomyopathy
: Acute but rapidly reversible LV dysfunction in the absence of flow-limiting coronary disease. The ventricular pattern of wall motion abnormality in this form of stunning involves distal portion of the LV (apical ballooning) with basal hypercontractility. Typically effects older women and is precipitated by intense psychological stress. ECG may mimic ST elevation MI with low-level troponin positivity. While hemodynamic perturbations and shock may be present, almost all patients recover completely in 1–4 weeks.

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