Background-Biventricular pacing has been proposed to improve symptoms and exercise capacity in patients with advanced heart failure and wide electrocardiographic wave complexes. This study investigated the effect of biventricular pacing on reverse remodeling and the underlying mechanisms. Methods and Results-Twenty-five patients with NYHA class III to IV heart failure and electrocardiographic wave complex duration Ͼ140 ms receiving biventricular pacing therapy were assessed serially up to 3 months after pacing and when pacing was withheld for 4 weeks. Tissue Doppler echocardiography was performed using a 6-basal, 6-mid segmental model to assess the time to peak sustained systolic contraction (T S ). There was significant improvement of ejection fraction, dP/dt, and myocardial performance index; decrease in mitral regurgitation, left ventricular (LV) end-diastolic (205Ϯ68 versus 168Ϯ67 mL, PϽ0.01) and end-systolic volume (162Ϯ54 versus 122Ϯ42 mL, PϽ0.01); and improved 6-minute hall-walk distance and quality of life score after pacing for 3 months. The mechanisms of benefits were as follows: (1)
Despite adequate pretreatment with clopidogrel, patients with aspirin resistance as measured by a point-of-care assay have an increased risk of myonecrosis following non-urgent PCI.
Long-term right ventricular apical pacing resulted in a high incidence of myocardial perfusion defects that increased with the duration of pacing. These myocardial perfusion abnormalities were associated with apical wall motion abnormalities and impaired global left ventricular function.
After a median follow-up of 7.8 years, permanent RV apical pacing was associated with HF in 26% of patients. Elderly age at the time of implant, a wider paced QRS duration and the presence of CAD independently predicted new-onset HF. More importantly, HF after RV apical pacing was associated with a higher cardiovascular mortality.
Direct endomyocardial implantation of autologous BM cells significantly improved exercise time, LVEF, and NYHA functional class in patients with severe CAD who failed conventional therapy.
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