Left atrial sarcoidosis as a substrate for peri-mitral atrial flutter: an unusual, underlying atrial disease

Kanae Hasegawa; Kenichi Kaseno; Takayoshi Aiki; Hiroshi Tada

doi:10.1093/eurheartj/ehy150

Hasegawa, Kanae; Kaseno, Kenichi; Aiki, Takayoshi; Tada, Hiroshi

2018-03-15 00:00:00

A 52-year-old man was admitted for treatment of recent-onset heart failure. The electrocardiogram demonstrated atrial flutter (Panel A). Echocardiography disclosed left atrial (LA) dilatation (44.8 mm) and a diffusely hypokinetic left ventricular (LV) wall motion (ejection fraction = 43%). Three-dimensional electroanatomical activation mapping disclosed the flutter was a macro-reentrant, clockwise, peri-mitral flutter (Panel B; Supplementary material online, Videos S1 and S2). Voltage mapping revealed the left atrium, other than the anterolateral wall, was widely damaged (Panel C). No distinct electrograms were recorded from the LA posterior wall or pulmonary veins. Radiofrequency ablation at a site between the posterior wall (scar) and mitral annulus terminated the tachycardia. View largeDownload slide View largeDownload slide F-18-fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET) identified an increased FDG uptake on the LA wall, including the atrial septum, pulmonary veins, hilar lymph node, and liver (Panel D). Strong FDG uptakes were found on the LA anteroseptal and septal walls (arrowheads), which demonstrated a low voltage area. There was a weak uptake on the LA posterior wall (arrows), which demonstrated a scar region. No abnormal uptake was found in the ventricles. The biopsy specimens of the lung and liver revealed non-caseating epithelioid cell granulomas (Panel E). With treatment with prednisolone, the enhanced FDG uptake disappeared from his body (Panel D). The LA diameter and LV ejection fraction improved to 38.7 mm and 67%, respectively. He has done well with no tachyarrhythmias or heart failure during 18 months of follow-up without any antiarrhythmic drugs. Cardiac sarcoidosis could affect only atrial, not ventricular, tissue and become a substrate for supraventricular tachyarrhythmias. Supplementary material is available at European Heart Journal online. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

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European Heart Journal Oxford University Press

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Left atrial sarcoidosis as a substrate for peri-mitral atrial flutter: an unusual, underlying atrial disease

$A 52-year-old man was admitted for treatment of recent-onset heart failure. The electrocardiogram demonstrated atrial flutter (Panel A). Echocardiography disclosed left atrial (LA) dilatation (44.8 mm) and a diffusely hypokinetic left ventricular (LV) wall motion (ejection fraction = 43%). Three-dimensional electroanatomical activation mapping disclosed the flutter was a macro-reentrant, clockwise, peri-mitral flutter (Panel B; Supplementary material online, Videos S1 and S2). Voltage mapping revealed the left atrium, other than the anterolateral wall, was widely damaged (Panel C). No distinct electrograms were recorded from the LA posterior wall or pulmonary veins. Radiofrequency ablation at a site between the posterior wall (scar) and mitral annulus terminated the tachycardia. View largeDownload slide View largeDownload slide F-18-fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET) identified an increased FDG uptake on the LA wall, including the atrial septum, pulmonary veins, hilar lymph node, and liver (Panel D). Strong FDG uptakes were found on the LA anteroseptal and septal walls (arrowheads), which demonstrated a low voltage area. There was a weak uptake on the LA posterior wall (arrows), which demonstrated a scar region. No abnormal uptake was found in the ventricles. The biopsy specimens of the lung and liver revealed non-caseating epithelioid cell granulomas (Panel E). With treatment with prednisolone, the enhanced FDG uptake disappeared from his body (Panel D). The LA diameter and LV ejection fraction improved to 38.7 mm and 67%, respectively. He has done well with no tachyarrhythmias or heart failure during 18 months of follow-up without any antiarrhythmic drugs. Cardiac sarcoidosis could affect only atrial, not ventricular, tissue and become a substrate for supraventricular tachyarrhythmias. Supplementary material is available at European Heart Journal online. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)$

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Left atrial sarcoidosis as a substrate for peri-mitral atrial flutter: an unusual, underlying atrial disease

Left atrial sarcoidosis as a substrate for peri-mitral atrial flutter: an unusual, underlying atrial disease

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Left atrial sarcoidosis as a substrate for peri-mitral atrial flutter: an unusual, underlying atrial disease

Left atrial sarcoidosis as a substrate for peri-mitral atrial flutter: an unusual, underlying atrial disease

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