This review presents an update on the diagnosis and management of acute limb ischemia (ALI), a severe condition associated with high mortality and amputation rates. A comprehensive spectrum of ALI etiology is presented, with highlights on embolism and in situ thrombosis. The steps for emergency diagnosis are described, emphasizing the role of clinical data and imaging, mainly duplex ultrasound, CT angiography and digital substraction angiography. The different therapeutic techniques are presented, ranging from pharmacological (thrombolysis) to interventional (thromboaspiration, mechanical thrombectomy, and stent implantation) techniques to established surgical revascularization (Fogarty thrombembolectomy, by-pass, endarterectomy, patch angioplasty or combinations) and minor or major amputation of necessity. Postprocedural management, reperfusion injury, compartment syndrome and long-term treatment are also updated.
The current study analysed the dynamics of oxidative stress markers in patients with acute ST-elevation myocardial infarction treated by primary percutaneous intervention. Excessive reactive oxygen species production is known to induce myocardial reperfusion injury. There are few studies that evaluated oxidative stress markers in the interventional era, the historical papers were all based on thrombolysis as a mean of reperfusion. Thirty-seven patients were included. Peripheral venous blood samples were obtained prior to coronary angioplasty, at 1 hour and 24 hours after that. Plasma malondialdehyde, reduced glutathione / oxidised glutathione ratio and total antioxidant capacity were determined. Malondialdehyde was significantly lower at 1 hour (3.1 ± 0.96 nmol/ml vs 2.68 ± 0.81 nmol/ml, p<0.01) and 24 hours (3.1 ± 0.96 nmol/ml vs 2.15 ± 0.95 nmol/ml, p<0.01). Also, reduced glutathione / oxidised glutathione ratio dropped significantly at 1 hour (3.25 Q1-Q3 2.17-5.19 vs 2.33 Q1-Q3 1.53-2.82, p<0.01) and at 24 hours (3.25 Q1-Q3 2.17-5.19 vs 1.96 Q1-Q3 1.28-2.85, p<0.01). Total antioxidant capacity had non-significant variation. There was no correlation between these markers and time from symptom-onset or left ventricular ejection fraction. Reperfusion of the occluded coronary artery by percutaneous coronary intervention in acute myocardial infarction led to a rapid decrease of reduced glutathione / oxidised glutathione ratio, that may indicate a depletion of antioxidants as a consequence of overproduction of reactive oxygen species in the damaged area. However, the malondialdehyde level significantly decreased after vessel opening. This may suggest low reperfusion injury after angioplasty.
The current study analysed the effect of high-dose statin loading prior to primary percutaneous coronary intervention on oxidative stress markers, in patients with acute ST-elevation myocardial infarction (STEMI). Besides the lipid lowering effect, statins have antioxidant properties that might reduce myocardial ischemia-reperfusion injury. From a total of 37 patients, 18 patients received high-dose statin before coronarography and were included in the statin group, while 19 statin naive patients were included in the control group. Peripheral venous blood samples were obtained before coronary reperfusion, at 1 hour and 24 hours after that. The following markers of oxidative stress were determined from the serum: malondialdehyde (MDA), reduced glutathione to oxidized glutathione ratio (GSH/GSSG) and total antioxidant capacity (TAC). Values are shown as medians and interquartile ranges. MDA concentration and TAC had non-significant differences between the two groups, at all time frames. Before angioplasty, GSH/GSSG ratio was comparable between the two groups: 3.59 (2.13-5.37) in the statin group vs 2.69 (2.15-5.02) in the control group, p=0.49. At 1 hour after reperfusion, values were still similar: 2.26 (1.32-4.28) in the statin group vs 2.33 (1.88-2.50) in the control group, p=0.55. After 24 hours, there was a significant increase of GSH/GSSG ratio in the statin group 2.41 (1.58-3.28) vs 1.56 (1.12-2.03) in the control group, p=0.01. This finding suggest that, in STEMI patients, high-dose statin loading before primary percutaneous coronary intervention significantly reduces oxidative stress burden, early after administration.
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