Some patients show such an important clinical improvement and reverse remodelling after cardiac resynchronization therapy (CRT) that anatomy and function approach normal. These patients have been called ‘super-responders’. The aim of our study was to identify predictors of becoming a super-responder after CRT. Eighty-seven consecutive patients who underwent CRT were prospectively studied. Before CRT and 6 months after, clinical and echocardiographic evaluation was performed. Patients with a decrease in New York Heart Association functional class ≥1, a two-fold or more increase of left ventricular ejection fraction (LVEF) or a final LVEF >45%, and a decrease in LV end-systolic volume >15% were classified as super-responders. There were 12% super-responders. At baseline, there were no significant differences between super-responders and the other patients, except for the fact that super-responders had significantly smaller mitral regurgitation and LV end-diastolic diameter (LVEDD) and a shorter duration of heart failure symptoms. Mitral regurgitation jet area, LVEDD, and duration of heart failure symptoms were correlated with this super-response. Moreover, an evolution of symptoms for <12 months was an independent predictor of super-response to CRT. Patients in earlier phases of the cardiomyopathy, with a less altered ventricular geometry, seem to have a greater probability of becoming super-responders.

Diabetic patients have a significantly worse prognosis after an acute myocardial infarction (AMI) than their counterparts. Previous studies have shown that the number of circulating endothelial progenitor cells (EPCs) significantly increase early after an AMI in normoglycemic patients. However, it is well known that type 2 diabetes mellitus (DM) is associated with impaired function and reduced circulating EPCs levels. Nonetheless, few studies have analyzed EPCs response of diabetics to an AMI and the EPC response of pre-diabetic patients has not been reported yet. Therefore, we hypothesized that in the acute phase of an AMI, diabetic and pre-diabetics have lower circulating EPCs levels than patients with normal glucose metabolism. We also evaluated the possible capacity of chronic antidiabetic treatment in the recovery of EPCs response to an AMI in diabetics.

Background: T cells have been implicated in the development and progression of inflammatory processes in chronic heart failure (CHF). Cardiac resynchronization therapy (CRT) has beneficial effects on symptoms and cardiac remodeling in CHF. However, its impact on the inflammatory immune response remains controversial. We aimed to study the impact of CRT on T cells in heart failure (HF) patients. Methods: Thirty-nine HF patients were evaluated before CRT (T0) and six months later (T6). Quantification of T cells, their subsets, and their functional characterization, after in vitro stimulation, were evaluated by flow cytometry. Results: T regulatory (Treg) cells were decreased in CHF patients (healthy group (HG): 1.08 ± 0.50 versus (heart failure patients (HFP)-T0: 0.69 ± 0.40, P = 0.022) and remaining diminished after CRT (HFP-T6: 0.61 ± 0.29, P = 0.003). Responders (R) to CRT presented a higher frequency of T cytotoxic (Tc) cells producing IL-2 at T0 compared with non-responders (NR) (R: 36.52 ± 12.55 versus NR: 24.71 ± 11.66, P = 0.006). After CRT, HF patients presented a higher percentage of Tc cells expressing TNF-α and IFN-γ (HG: 44.50 ± 16.62 versus R: 61.47 ± 20.54, P = 0.014; and HG: 40.62 ± 15.36 versus R: 52.39 ± 18.66, P = 0.049, respectively). Conclusion: The dynamic of different functional T cell subpopulations is significantly altered in CHF, which results in an exacerbated pro-inflammatory response. Even after CRT, it seems that the inflammatory condition underlying CHF continues to evolve with the progression of the disease. This could be due, at least in part, to the inability to restore Treg cells levels. Trial registration: Observational and prospective study with no trial registration.