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Upward titration of beta-blockers in patients with chronic heart failure(CHF) is often limited by bradycardia. It is, however, controversial whether we should implant a pacemaker solely to achieve higher doses of beta-blockers or to give up the upward titration because conventional ventricular pacing causes asynchronous contraction. Therefore, we studied the prognosis in stable CHF patients treated with beta-blockers and who had bradycardia before or during the upward titration. A total of 20 CHF patients(NYHA class II-III) with bradycardia were retrospectively reviewed and were devided into two groups: In 11 patients, upward titration of beta-blockers was stopped due to bradycardia(B group). In 9 patients, pacemakers were implanted before or during upward titration(P group). All patients had a left ventricular ejection fraction of 40% or less and were followed up for 12-40 months(mean 23months). The baseline characteristics of the patients were similar in the two groups. The final doses of beta-blockers were higher in P group than in B group. The rate of hospitalization for worsening heart failure was significantly higher in P group than in B group although there is no difference in all-cause mortality between two groups.Conclusions:(1) The beneficial effects of beta-blockers may not overcome unfavorable effects of conventional ventricular pacemakers in mild to moderate CHF patients. (2) Cardiac resynchronization therapy may be a good option for CHF patients with bradycardia.

Recent studies have suggested that the administration of erythropoietin (EPO) elicits cardio-protective effects in myocardial ischemia and reperfusion (I/R). We investigated whether endogenous EPO signals mediated by EPO receptors (EPOR) expressed in the non-hematopoietic lineage play a role in the protection against I/R injury using transgene-rescued EPOR null mutant mice (RESCUE), which express EPOR exclusively in the hematopoietic lineage. Left coronary artery was occluded for 30 minutes and then reperfused.The infarct size (% area at risk) was assessed 24 hours after I/R by triphenyltetrazolium chloride staining.The cardiac function and structure were evaluated by echocardiography 3 weeks after I/R. The hematocrit, cardiac structure and function were similar in RESCUE and wild-type (WT) mice in the baseline condition. The infarct size in RESCUE (n=8) was larger than that in WT (n=7) (52 ± 4 vs 39 ± 4 %; p < 0.05).The left ventricular (LV) end-diastolic dimension was significantly increased (5.0 ± 0.2 vs 3.8 ± 0.2 mm; p < 0.01), and the LV fractional shortening was reduced (0.15 ± 0.01 vs 0.26 ± 0.05; p < 0.01) in the RESCUE (n=8) compared with WT (n=6) 3 weeks after I/R. In conclusion, a deficiency of endogenous EPO-EPOR signal in the non-hematopoietic lineage may deteriorate the survival of cardiomyocytes after I/R, and accelerate the development of LV remodeling. The endogenous EPO-EPOR system in the non-hematopoietic lineage may play a crucial role in the protection against I/R injury.