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  1. 1. Myocarditis ECM, 2/7/14
  2. 2. Clinical presentation Acute myocarditis presentation: highly variable, ranging from subclinical disease to fulminant heart failure Of 3055 adult patients with suspected acute or chronic myocarditis    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
  3. 3. Background…  Most patients: immune reaction downregulates and the myocardium recovers.  Some: persistent myocardial inflammation leads to ongoing myocyte damage and relentless symptomatic heart failure or even death.  Diagnosis: clinical presentation and noninvasive imaging findings.  Therapy: standard heart failure therapy  mechanical circulatory support or heart transplantation is indicated for some.  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.
  4. 4. Findings CMR  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 patients  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 washout period.
  5. 5. Morphological abnormalities  Transient increase of wall thickness during myocarditis Decrease of LV mass during the course of uncomplicated myocarditis associated with edema as assessed by T2-weighted CMR Transient increase of LV volumes
  6. 6. LHC 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. sites. 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).
  7. 7. Study Population and Rates of Obstructive Coronary Artery Disease. Patel MR et al. N Engl J Med 2010;362:886-895.
  8. 8. Predictors of Obstructive Coronary Artery Disease. Patel MR et al. N Engl J Med 2010;362:886895.
  9. 9. References 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,