Recent stents in patients of acute myocardial infarction clinically and angiographic results

Conronary thrombosis plays a major role in the pathogenesis of acute myocardial infarction. Between December 1998 to November 2000. 57 patients with acute myocardial infarction who were admitted at coronary care unit [CCU] of Sayed Galal and Al Housein University Hospital were included in this study. The patients were divided into two groups: G1: they had primary PCI. G2: [25 patients] they had received streptokinase followed by percutaneaus coronary intervention [PCI] within 24hs after failed thrombolysis [Persistent chest pain and/or extension of ST segment elevation]. The primary goal of therapy for acute myocardial infarction is rapid, complete and sustained restoration of infarct related artery [IRA] blood flow. Both fibrinolytic and mechanical restoration of antegrade coronary blood flow in patients have been shown to improve left ventricular function, reduce infarct size and reduce mortality. Although intravenous fibrinolytic therapy is effective in improving outcome after myocardial infarction and can be administered early to a great proportion of patients than is possible with percutaneaus coronary intervention, its effectiveness profile is disappointing to most cardiologists. The advantages of PCI include immediate visual assessment of reperfusion success and identification of the entire coronary and ventricular anatomy. This assessment often obviate the need for noninvasive testing befor hospital discharge and can lead to an accelerated discharge and recovery of low risk patients. The benefit of primary angioplasty seems greatest in elderly and those with high risk characteristics. The presence of the platelet rich thrombus in acute myocardial infarction and the central role of platelet activation in stent thrombosis suggest a potentially, advantagious role for the new class glycoprotein Ilb; llla receptor antagonists during PCI. Stenting in acute MI and in thrombus containing lesion has become a feasible and safer procedure in an expert hands, with new devices, high pressure deployment and with the use of [GPIIbIIIa blockers

Value of serum nitric oxide in patients with coronary artery disease before and after percutaneous transluminal coronary angioplasty with or without stent

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