ABSTRACT
Our study was planned to assess the value of plasma NO as an early marker for endothelial injury and to detect its relation to the severity of coronary artery disease and its relation to restenosis after PCI. This study included [51] patients; [14] were normal control group [Group I]; and [37] patients were diseased [Group II], whom classified into three subgroups; subgroup [A] patients with single vessel disease [15 patients], subgroup [B] patients with two vessels disease [15 patients], subgroup [C] multi-vessels disease included [7 patients]. All patients subjected to coronary angiography with or without intervention [PTCA only, PTCA + stent or without stent]. [21] Patients accepted and respected follow-up by coronary angiography after 4 months. NO serum level was done before PCI and after 4 months in those accepted follow-up. Mean NO serum level on control group was 83 micro mol/L, while mean plasma NO serum level in subgroup [A] [34.8 +/- 10.3 micro mol/L], [17.5 +/- 3.5 micro mol/L] in subgroup [B]; and [8.9 +/- 2.2 micro mol/L in subgroup [C]. This revealed a highly significant decrease than control group, with P-value <0.05, <0.0005 and <0.0005 respectively when compared mean NO serum level in control group with each subgroup. On comparing the mean values of plasma NO level of subgroups [A, B, C]; to each other there was more or less gradual mathematical decrease in NO serum level between the subgroups, with highly significant P-values. Comparing the mean level of plasma NO of restenosis cases before and after PCI in each subgroup [A, B and C], we found a significant decrease in plasma NO level after PCI than before PCI. Endothelial dysfunction is an important contributing factor in CAD and it is associated with NO deficiency which can be considered as one of the endothelial markers for CAD. The more the degree of endothelial dysfunction, the more the deficiency of NO, the more the severity of CAD. Restenosis is a multi-factorial subject requiring a lot of work and lack of NO is related at least in part to the development of restenosis after angioplasty. We can suggest that if plasma NO level after PCI is reduced at least 30% of its initial level before PCI, most probably restenosis has occurred