Upgrade to CRT in Patients with CS
CS has a complex etiology with granulomatous inflammation of the heart, and the pathogenesis includes the activation of the macrophages or lymphocytes, granuloma development, and fibrosis.1 The published data regarding the outcome of CRT therapy in patients with CS is limited,11-13 and the efficacy of an upgrade to CRT from a pacemaker or ICD in patients with CS is still controversial.11, 12 The echocardiographic response in patients with CS (groups 1 and 2) was lower than that in those with other etiologies (group 3). The possible mechanism was that the progression or fixation of the myocardial fibrosis from sarcoidosis exceeded the improvement in the cardiac function from the CRT therapy in patients with CS. Also, the echocardiographic response to an upgrade to CRT was the lowest in group 1. Corticosteroids are beneficial for suppressing inflammation from CS but have a potential to promote fibrotic changes in the myocardium.14 It is notable that a defect area in the lateral LV was more often seen in group 1 than group 2. The greater fibrotic changes in the lateral LV area would interfere with appropriate bi-ventricular pacing and affect the echocardiographic CRT response. This could explain the lowest echocardiographic response being observed in group 1.