Abstract
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 ventric-ular 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. e 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. ereafter, 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 pulmonary 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 × 10 3 /mm 3. 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 veno-venous hemodialysis. She also developed hemodynamically unstable). Figure. The heart in the patient described. (a) View of dilated right and left ventricles just caudal to the atrioventricular valves. (b) Transverse cuts of the cardiac ventricles. (c) Close-up view of the ventricular septum and right and left ventricular walls. Linear scars are present in the septum and in the posterior wall of the left ventricle. (d) Low-power view of foci of lymphocytes in an area of scar. (e) Low-power view of collections of lymphocytes in areas of scar between muscle bundles. (f) Higher-power view of lymphocytes associated with myofiber necrosis. Hematoxylin and eosin stains. (Photographs by Jong Mi Ko.) a b c d e f
Cite
CITATION STYLE
Garner, W. L., Starling, C., Kuiper, J. J., & Roberts, W. C. (2006). Lymphocytic Myocarditis as a Cause of Fulminant Fatal Heart Failure. Baylor University Medical Center Proceedings, 19(2), 122–123. https://doi.org/10.1080/08998280.2006.11928141
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