Does nitric oxide overproduction derived from inducible nitric oxide synthase increase cardiomyocyte apoptosis in human atrial fibrillation?
Levels of hs-CRP were far more enhanced in patients with PmAF compared to the controls. Plasma levels of NO(X) were significantly lower in PmAF patients than SR patients, but the production of NO(X) in the local right atrium increased obviously. Furthermore, iNOS and 3NT expressions increased dramatically in the right atrium in PmAF patients, whereas the expression of eNOS did not change apparently. In addition, when patients were further divided into a higher hs-CRP group (> or =5 mg/L) and a lower hs-CRP group (<5 mg/L) according to the hs-CRP level, significant upregulation of iNOS was found in the higher hs-CRP group. Apoptosis index and caspase 3 staining were also prominently enhanced in PmAF patients compared with SR patients. More importantly, we demonstrated in this study that a higher expression of 3NT was associated with an increased expression of iNOS/eNOS (r=0.74, P<0.05) and an enhanced apoptosis index (r=0.69, P<0.05). In conclusion, the results presented novel evidence that imbalanced expression of iNOS/eNOS could contribute to protein nitration and cardiomyocyte apoptosis in human AF, in which condition inflammation may be an important participant.
Patients with CAD without a previous diagnosis of DM had a high prevalence of abnormal glucose tolerance. Post-challenge hyperinsulinaemia was associated with the number of diseased coronary arteries and the presence of previous MI. The insulin response to the glucose challenge test requires further investigation as a potential risk factor for CAD and a potential target for intervention.