Viral infection is the most common cause of myocarditis in developed countries, but other etiologies include bacterial and protozoal infections, toxins, drug reactions, autoimmune diseases, giant cell myocarditis, and sarcoidosis. Acute injury leads to myocyte damage->activation of immune system->severe inflammation.
Figure 1. Study Population and Rates of Obstructive Coronary Artery Disease. ACC-NCDR denotes American College of Cardiology National Cardiovascular Data Registry, ACS acute coronary syndrome, AMI acute myocardial infarction (MI), CABG coronary-artery bypass grafting, CAD coronary artery disease, and PCI percutaneous coronary intervention.
Acute myocarditis presentation: highly variable, ranging
from subclinical disease to fulminant heart failure
Of 3055 adult patients with suspected acute or chronic
32% had chest pain,
72% had dyspnea
18% had arrhythmias
Patients with fulminant myocarditis typically present
with severe heart failure symptoms that may rapidly lead
to cardiogenic shock
Patients with Giant Cell Myocarditis commonly present
with heart failure symptoms that relentlessly progress to
probable early death despite optimal treatment
Most patients: immune reaction downregulates and the
Some: persistent myocardial inflammation leads to ongoing
myocyte damage and relentless symptomatic heart failure or
Diagnosis: clinical presentation and noninvasive imaging
Therapy: standard heart failure therapy
mechanical circulatory support or heart transplantation is indicated for
Prognosis in acute myocarditis generally good
except in patients with giant cell myocarditis.
Persistent, chronic myocarditis usually has a progressive course but may
respond to immunosuppression.
CMR is of potential use in patients with chest pain, elevated troponin and normal
coronary arteries, where it was shown to identify myocarditis in more than 30% of
Expected tissue pathology in active myocarditis includes intracellular and
interstitial edema, capillary leakage, hyperemia and – in more severe cases - cellular
necrosis and subsequent fibrosis
Cardiac MRI: T2-weighted imaging sensitively detects tissue edema using the
long T2 of water-bound protons as the contrast-generating mechanism resulting in
a high signal intensity of edematous tissue
Increased blood volume in the inflamed area -> increased uptake of contrast agents
during the early vascular phase. Contrast-enhanced fast spin echo T1-weighted MR
after contrast administration can be used to assess experimentally induced
myocardial hyperemia and to detect muscular inflammation..
After inflammatory clearance of necrotic regions, a mesh of fibrocytes with a
large interstitial component replaces formerly viable tissue, again increasing the
volume of distribution for gadolinium into this extracellular space during the late
Transient increase of
wall thickness during
Decrease of LV mass
during the course of
with edema as assessed
by T2-weighted CMR
Transient increase of LV
NCDR CathPCI Registry is a large, voluntary registry of
clinical data and in-hospital outcome data associated with
diagnostic cardiac catheterization and percutaneous
coronary intervention, collected from more than 800 U.S.
Study for whom there were complete data on diagnostic
cardiac catheterization for January 2004-April 2008 :
39.2% of the patients had no coronary artery
disease (<20% stenosis in all vessels).
Study Population and Rates of Obstructive Coronary Artery Disease.
Patel MR et al. N Engl J Med 2010;362:886-895.
Predictors of Obstructive Coronary Artery Disease.
Patel MR et al. N Engl J Med 2010;362:886895.
J Am Coll Cardiol. 2009 April 28; 53(17): 1475–1487: Cardiovascular Magnetic Resonance in Myocarditis: A JACC
White Paper Matthias G. Friedrich et al, for the International Consensus Group on Cardiovascular MR in Myocarditis
Progress in Cardiovascular Diseases: Volume 52, Issue 4, January–February 2010, Pages 274–288 Unusual
Cardiomyopathies Myocarditis Lori A. Blauwet, Leslie T. Cooper
Low Diagnostic Yield of Elective Coronary Angiography: Patel et al. N Engl J Med 2010; 362:886-895 March 11,
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