Metabolic syndrome is associated with different clinical outcome after cardiac resynchronization therapy in patients with ischemic and non-ischemic cardiomyopathy

Abstract

Background: Although association of metabolic syndrome (MS) and ischemic heart disease is strongly established, it is not known whether presence of MS may differently influence clinical responses to cardiac resynchronization therapy (CRT). The aim of this study was to evaluate the associations between obesity and metabolic features and the clinical outcome after cardiac resynchronization with defibrillator therapy (CRT-D), compared to an implantable cardioverter defibrillator (ICD).

Methods: The risk of heart failure (HF) or death and death alone was evaluated in 829 non-obese patients, 156 obese patients without MS, and 277 obese patients with MS (all with left bundle branch block), who were enrolled in the Multicenter Automatic Defibrillator Implanta­tion Trial with Cardiac Resynchronization Therapy (MADIT-CRT).

Results: Obese patients with MS (HR 0.50, 95% CI 0.32–0.77, p = 0.002), obese patients without MS (HR 0.57, 95% CI 0.30–1.06, p = 0.077), and non-obese patients (HR 0.48, 95% CI 0.37–0.62, p < 0.001) had a similar risk reduction of HF/death in response to CRT-D therapy when compared to ICD patients. However, among those with non-ischemic cardiomyo­pathy, obese patients with MS experienced a 90% reduction for HF/death (HR 0.11, 95% CI 0.04–0.32, p < 0.001), whereas obese patients without MS had no reduction (HR 0.98, 95% CI 0.48–1.98, p = 0.951; interaction p < 0.001). The reverse was observed in ischemic car­diomyopathy patients: obese patients with MS had no reduction in the risk of HF/death (HR 0.80, 95% CI 0.48–1.34, p = 0.402), while obese patients without MS showed a significant reduction in the risk of events (HR 0.15, 95% CI 0.04–0.65, p = 0.011; interaction p = 0.036). Similar trends were observed for the endpoint of death.

Conclusions: Presence of MS differentiates the response to CRT in obese patients with is­chemic and non-ischemic etiology for HF.