Published online Sep 26, 2016. doi: 10.4330/wjc.v8.i9.496
Peer-review started: May 23, 2016
First decision: June 17, 2016
Revised: July 12, 2016
Accepted: July 29, 2016
Article in press: August 1, 2016
Published online: September 26, 2016
Processing time: 120 Days and 8.5 Hours
Cardiac involvement of sarcoid lesions is diagnosed by myocardial biopsy which is frequently false-negative, and patients with cardiac sarcoidosis (CS) who have impaired left ventricular (LV) systolic function are sometimes diagnosed with dilated cardiomyopathy (DCM). Late gadolinium enhancement (LE) in magnetic resonance imaging is now a critical finding in diagnosing CS, and the novel Japanese guideline considers myocardial LE to be a major criterion of CS. This article describes the value of LE in patients with CS who have impaired LV systolic function, particularly the diagnostic and clinical significance of LE distribution in comparison with DCM. LE existed at all LV segments and myocardial layers in patients with CS, whereas it was localized predominantly in the midwall of basal to mid septum in those with DCM. Transmural (nodular), circumferential, and subepicardial and subendocardial LE distribution were highly specific in patients with CS, whereas the prevalence of striated midwall LE were high both in patients with CS and with DCM. Since sarcoidosis patients with LE have higher incidences of heart failure symptoms, ventricular tachyarrhythmia and sudden cardiac death, the analyses of extent and distribution of LE are crucial in early diagnosis and therapeutic approach for patients with CS.
Core tip: Late gadolinium enhancement (LE) in magnetic resonance imaging is a critical finding in the diagnosis of cardiac sarcoidosis (CS), but it is also observed in dilated cardiomyopathy (DCM). We review the significance of LE distribution in comparison with DCM. LE distributed into all ventricular segments and myocardial layers in CS, whereas it was localized predominantly in the midwall of ventricular septum in DCM. Transmural, circumferential, and subepicardial and subendocardial LE were highly specific in CS. Since patients with LE have more adverse cardiac events, the analyses of extent and distribution of LE are crucial for diagnosis and management of CS.