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ISSN: 1734-1922
Archives of Medical Science
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vol. 16
Letter to the Editor

Arguable ICD placement in a sarcoidosis patient with extensive cardiac involvement

Hanna Jankowska
Karolina Dorniak
Marcin Hellmann
Anna Dubaniewicz
Maria Dudziak

Department of Noninvasive Cardiac Diagnostics, Medical University of Gdansk, Gdansk, Poland
Department of Pulmonology, Medical University of Gdansk, Gdansk, Poland
Arch Med Sci 2020; 16 (3): 707–708
Online publish date: 2019/07/18
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Sarcoidosis is a systemic inflammatory disease of unclear etiology, with non-caseating granuloma formation most typically in the lungs and pulmonary lymph nodes. However, many organs can be involved, including the skin, the eyes, the brain and the heart. Cardiac involvement is the major cause of mortality in sarcoidosis. Death may result from either arrhythmia, heart block or heart failure [1, 2].
The diagnosis and management of cardiac involvement can be challenging. A 42-year-old man with a 10-year history of stage 2 pulmonary sarcoidosis confirmed by scalene biopsy presented with new onset dyspnea following an 8-year post-steroid remission. Computed tomography (CT) scan revealed lung disease progression. Two months later he was admitted for symptoms of cerebellar stroke. No atherosclerotic lesions were found on carotid Doppler. However, enlarged left ventricle (LV) with moderately reduced left ventricular ejection fraction (LVEF) and apical as well as basal inferolateral akinesia were found on echocardiography. On top of standard treatment for LV dysfunction, predni-sone 80 mg daily was initiated for suspected cardiac involvement, based on 24-hour ECG monitoring (episodes of nsVT, multifocal ventricular ectopy), echocardiography (LVEF 40%, LVEDD 62 mm), and subsequent cardiac magnet-ic resonance (CMR) findings (LVEF 36%, LVEDD 66 mm, areas of patchy or focal transmural late gadolinium en-hancement (LGE), suggestive of sarcoid lesions). Cardiac magnetic resonance findings also included extensive suben-docardial involvement in the apex and mid-anterior as well as basal postero-lateral wall and transmural involvement of the basal inferior wall, which required differential diagnosis for coronary artery disease (CAD). However, no angio-graphically detectable atherosclerosis was found on subsequent coronary angiography. Standard 12-lead ECG was normal. Highlights from 24-hour ECG, echocardiography, CMR and coronary angiography are compiled in Figure 1.
At 1-year follow-up, LV parameters remained largely unchanged (LVEF 39%, LVEDD 63 mm). Additionally, re-gional LV function assessment with speckle tracking revealed markedly reduced global longitudinal strain (GLS) of –12%, with deformation abnormalities noted in the vast majority of LV segments. Both standard LV parameters and strain abnormalities were unchanged on echocardiography repeated 6 months later. Moreover, multiple episodes of nsVT were recorded on repeated 24-hour ECG. Follow-up CMR...

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