ESC Guidelines on the diagnosis and treatment of peripheral artery diseases Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries The Task Force on the Diagnosis and Treatment of Peripheral Artery Diseases of the European Society of Cardiology (ESC)

Non-thrombotic PE does not represent a distinct clinical syndrome. It may be due to a variety of embolic materials and result in a wide spectrum of clinical presentations, making the diagnosis difficult. With the exception of severe air and fat embolism, the haemodynamic consequences of non-thrombotic emboli are usually mild. Treatment is mostly supportive but may differ according to the type of embolic material and clinical severity.

Thromboembolic risk was especially high for aortic and mitral valve replacement for 90 days after operation, and overall was increased with lack of anticoagulation, mitral valve location, previous thromboembolism and increasing age. Anticoagulation reduced thromboemboli and appears to be indicated in all patients as early as possible for 3 months and thereafter in those with risk factors, but needs prospective testing.

Fifty per cent of patients with heart failure, ha increased plasma angiotension II despite chronic ACE inhibitor therapy. These patients had higher neurohormonal activation and poor prognosis.

The effect of recombinant hirudin and the dosage of heparin on acute platelet-thrombus deposition during carotid angioplasty in anesthetized pigs was prospectively assessed. Fifty-five animals (mean weight, 33.9 kg) were randomized to one of six heparin dosages: heparin boluses of 35, 50, 100, 150, 200, or 250 units/kg followed by a continuous infusion of35, 50, 100, 150, 200, or 250 units/kg/hr, respectively. Another five pigs received a bolus of 1 mg/kg hirudin (recombinant desulphatohirudin), a specific thrombin inhibitor, followed by an infusion of 1 mg/ kg/hr. Bilateral carotid angioplasty was performed in all pigs 20 minutes after starting the infusion; they were sacrificed 57±12 minutes after the procedure. Deep medial arterial injury was present in approximately 75% of the dilated segments, and subendothelial injury in the remaining 25%. Mean log of number of platelets and molecules of fibrinogen per centimeter squared of deep injury in segments from all the animals treated with heparin were 4.74± 1.03 and 5.02+±0.64, respectively. A regression analysis showed an inverse correlation of the log of platelet deposition with the heparin group (r= -0.56,p=0.0001) with administered total units of heparin (r= -0.55, p =0.0003) and with mean plasma heparin concentration (r= -0.55, p =0.0004) in deeply injured arteries. Similar inverse relations were obtained for fibrinogen. In contrast, the deposition of platelets and fibrinogen in subendothelial injury was very low and independent of the heparin administered. Macroscopic thrombus decreased from 72% of deeply injured arterial segments in the lowest heparin dosage group (activated partial thromboplastin time similar to the animals in the hirudin group) to 10%o in the highest heparin dosage group and to 0% in the animals treated with hirudin. Activated partial thromboplastin times were threefold that of control basal values for animals on the lowest heparin dosage (35 units/kg); a similar prolongation of times was observed in the hirudin group. However, the mean logs of platelet and fibrinogen deposition per centimeter squared of deep injury were significantly lower in the hirudin group than on 35 units/ kg heparin (3.23 ±0.44 vs. 5.44±0.60 and 3.98±0.36 vs. 5.33 ±0.53, respectively; p <0.001) and were also lower in the hirudin group than on the highest dosage (250 units/kg) of heparin (3.8±0.6 and 4.6+0.6, respectively; p < 0.04). In the presence of deep but not subendothelial arterial injury after angioplasty, there is a dose-dependent inhibition by heparin of acute platelet and fibrinogen depositions and the proportion of arterial segments with mural thrombosis. Hirudin was more effective in preventing thrombosis than heparin; this probably reflects the more specific and potent inhibition of thrombin by hirudin.