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Lymphocytic myocarditis

Discussion in 'Cardiology' started by Valery1957, Feb 23, 2019.

  1. Valery1957

    Valery1957 Famous Member

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    Proc (Bayl Univ Med Cent). 2006 Apr; 19(2): 122–123.
    Papers

    PMCID: PMC1426171
    PMID: 16609736
    Lymphocytic myocarditis as a cause of fulminant fatal heart failure
    William Lance Garner, MD, MS,1 Cherry Starling, MD,1 Johannes Jacob Kuiper, MD,1 and William Clifford Roberts, MD1
    Author information Copyright and License information Disclaimer

    This article has been cited by other articles in PMC.

    A 63-year-old Hispanic woman with prior systemic hypertension was well until 39 days before death when she fainted in her kitchen and was hospitalized. An electrocardiogram and telemetry monitoring disclosed sinus bradycardia (50 beats per minute) with first-degree atrioventricular block, left bundle branch block, frequent atrial and ventricular premature complexes, and sinus pauses up to 8 seconds. An echocardiogram showed mitral regurgitation (2+/4+) and an ejection fraction of 60%. An angiogram disclosed normal coronary arteries. The left ventricular and aortic pressures were normal. During her 3 days in the hospital, she had recurrent sinus pauses with associated syncope, and a permanent atrioventricular sequential pacemaker was implanted.

    Thereafter, she felt well and was active until 22 days before she died, when exertional dyspnea appeared and progressed, prompting rehospitalization 20 days before death. Her blood pressure was 120/75 mm Hg, her paced heart rate was 80 beats per minute, and her temperature was normal. A grade 2/6 apical systolic ejection murmur and a third heart sound were audible. She had diffuse pulmonary rales and decreased breath sounds at both lung bases. A chest radiograph showed pulmonary vascular congestion, cardiomegaly, and bilateral pulmory effusions. An electrocardiogram disclosed atrioventricular sequentially paced rhythm with no ST-T changes. Her serum troponin I level was 6.6 ng/mL,and her creatine phosphokinase level was 189 U/L with an MB fraction of 39 ng/mL. Her brain natriuretic peptide level was 2570 ng/L,and her white blood cell count was 10.7 × 103/mm3 . An echocardiogram showed severe global hypokinesis with an ejection fraction of 35%.

    Over the subsequent 19 days in the hospital, the patient's status progressively deteriorated, requiring intravenous inotropic support, mechanical ventilation, and continuous venovenous hemodialysis. She also developed hemodynamically unstable atrial fibrillation and had multiple electrical cardioversions. Right-sided heart catheterization a day before death showed the following pressures (in mm Hg): right atrial mean, 15; right ventricle, 25/10; pulmonary artery, 30/20. The cardiac output was 2.1 L/min and the cardiac index, 1.1 L/min/m2. She was transferred to Baylor University Medical Center 12 hours before death, which resulted from inadequate perfusion of multiple body organs.

    At necropsy, the heart weighed 470 grams. The quantity of subepicardial adipose tissue was increased. The coronary arteries were widely patent with no identifiable plaques. All 4 cardiac chambers were dilated (Figure). The 4 valves were anatomically normal. Multiple myocardial lesions were present grossly in the left ventricular wall and ventricular septum, and histologically numerous foci of lymphocytic infiltrates were present with associated myocardial cell necrosis and foci of replacement fibrosis (Figure)
     

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  2. Valery1957

    Valery1957 Famous Member

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    Chronic lymphocytic myocarditis confirmed by electrogram-guided endomyocardial biopsy
    https://doi.org/10.1093/ehjci/jey288
    Published:

    25 January 2019

    A 52-year-old female patient presented with 6-month history of dyspnoea on exertion. Electrocardiogram showed sinus rhythm and N terminal-proB-type Natriuretic Peptide was elevated (1056 pg/mL) whereas Creatine Kinase-Muscle/Brain and troponin-T were normal. Echocardiography revealed biventricular dysfunction (Left Ventricular Ejection Fraction: 33%). Coronary computed tomography angiography showed no significant stenotic lesions. Cardiac magnetic resonance imaging showed multifocal delayed enhancement on septum (Panel A, red dotted area) with increased native T1 (1329 ms) and slightly increased T2 (41 ms) and extracellular volume values (36%), suggesting multifocal fibrosis suspicious for myocarditis.

    For diagnostic workup, we performed endomyocardial biopsy (EMB) which targeted on biopsy site based on the voltage and...
     

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