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.