Edmund Pabst

Cystic adventitial degeneration of the popliteal artery — the diagnostic value of duplex sonography

Cystical adventitial degeneration of the popliteal artery is a disorder which is difficult to diagnose, due to the similarity of the symptoms of people presenting with peripheral arterial occlusive disease (PAOD) or popliteal entrapment syndrome. The only thing that differs from patients suffering from PAOD is the lack of typical risk factors for arteriosclerosis. Typical diagnostic procedures like conventional angiography or magnetic resonance Imaging angiography can be negative, too and therefore misleading. The only which is crucial in the diagnosis of cystic adventitial degeneration of the popliteal artery is to know the morphological background of this disorder, namely that it is a cyst of the adventitia of the artery which leads to a dynamic exercise-dependent flow inhibition. We present a 57-year old white male who had a weeks history of intermittent claudication in his left calf. He was lacking of typical risk factors for arteriosclerosis and on first examination all pulses in both lower extremities were palpable and Doppler index on both legs was >1. Only duplexsonography revealed a cystic formation impressing the left popliteal artery in the hight of the rift in the popliteal joint.

The angiotensin-converting-enzyme insertion/deletion polymorphism is not a risk factor for peripheral arterial disease

BACKGROUND An insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting-enzyme (ACE) is associated with ACE plasma levels and activity. Conflicting results have been reported about the relevance of this polymorphism for atherosclerotic vascular disease. The aim of the present study was to analyze the role of this polymorphism for peripheral arterial disease (PAD). METHODS The study was designed as a case-control study including 522 patients with documented PAD and 522 sex- and age-matched controls. ACE genotype was determined by size-analysis of polymerase chain reaction products. RESULTS ACE genotype frequencies were similar between patients (II: 23.4%; ID: 44.8%; DD: 31.8%) and controls (II: 23.8%; ID: 48.3%; DD: 27.9%, P=0.37). The adjusted odds ratio of carriers of the DD genotype for PAD was 1.29 (95% confidence interval 0.95-1.75). The polymorphism was furthermore not associated with age at onset of PAD (P=0.56), Fontaine stage of the disease (P=0.68) or ankle/brachial index of patients (P=0.86). CONCLUSION The ACE I/D polymorphism is not a significant risk factor for PAD.

Prothrombotic Risk Factors in Patients with Thrombangitis Obliterans

XIII Histological findings in arteries of patients with TAO show that the segmental inflammatory process in the vessel wall is accompanied by a thromSince its first description in 1908 by Leo botic occlusion in the arteries. Therefore, the purBuerger, not very much has changed about pose of our study was to evaluate if prothrombotic the principal insight into the pathogenesis, risk factors can be found in patients suffering from diagnosis and treatment of thrombangitis obliterTAO at a higher level than in a control group ans (TAO) or Buergeŕs disease [1–11]. It is defined lacking venous or arterial disease. From the clinical as a segmental inflammatory occlusive disease point of view, the thrombotic occlusion might be which primarily affects small or medium-sized arthe reason for the worsening of the chronic course teries and veins in the extremities of young of the disease. The pathomechanism for the occuradults [1]. rence of the thrombotic occlusion is unclear. It Characteristically TAO begins relatively early in might be either the inflammatory process of the life, usually between the ages of 25 and 35, and is vessel wall itself or might be caused by a hypercoamore common in men than women with a prevagulable state enhanced by prothrombotic risk lence up to 10:1. There is an intimate relationship factors. between smoking and TAO. Typically all other risk factors for peripheral arterial occlusive disease 1. Patients and Methods (PAOD) like hypercholesterinemia, hypertension or diabetes mellitus are lacking at the time of diag1.1. Patients nosis [3]. Concerning other risk factors or predisposing Twenty-eight patients (17 male and 11 female) with factors, only a few are found in the literature [4–7]. a history of TAO were enrolled in our study. The These papers show a possible relationship of an mean age was 43.8 6 8.8 years. They were diagMHC Class I chain-related gene A (MICA) polynosed with TAO between 1990 and 1998. At the time of diagnosis all of them had been smoking heavily and the diagnosis of TAO was made acAbbreviations: Thrombangitis obliterans, TAO; MHC Class I cording to the following clinical criteria: onset bechain-related gene A, MICA; polymorphism, MICA 1.4; peripheral arterial occlusive disease, PAOD. fore the age of 50, history of smoking, absence Corresponding author: Dr. Marianne Brodmann, Division of Anof arteriosclerotic risk factors other than smoking, giology, Department of Internal Medicine, Karl Franzens Univerinfrapopliteal arterial occlusive lesions, and either sity, Graz A-8036, Graz, Austria. Tel:143 (316) 385 2911; Fax: 143 (316) 385 3788; E-mail: ,marianne.brodmann@kfunigraz.ac.at.. upper-limb involvement or phlebitis migrans.

Osteomyelitis of the Spine and Abscess Formation in the Left Thigh after Stent-Graft Implantation in the Superficial Femoral Artery

Purpose: To present a rare case of abscess formation around a covered stent in the superficial femoral artery. Methods and Results: Two weeks after balloon dilation of a left superficial femoral artery (SFA) occlusion, during which a Hemobahn covered stent had been placed to treat dissection, a 77-year-old nondiabetic male developed intolerable pain and swelling of his left thigh. An abscess had formed around the stent, which was patent; intravenous antibiotic therapy quelled the symptoms, and the patient discontinued his oral antibiotic regimen weeks after discharge. General septicemia ensued. Acute lower limb ischemia and excruciating back pain prompted readmission. The SFA stent-graft occlusion required femoropopliteal bypass; the abscess and spondylodiskitis that had developed in the T12 and L1 vertebrae responded to intravenous antibiotics. The patient is without signs of infection at 6 months. Conclusions: Local and systemic infections associated with intraluminal prostheses are rare, and prophylactic antibiotic therapy is not commonly employed. Balloon- or device-induced arterial injury may expose the arterial wall to bacterial colonization, suggesting that patients receiving lengthy stents or experiencing arterial injury during angioplasty should receive antibiotics as a precautionary measure.

Pulmonary embolism and intracardiac thrombi - individual therapeutic procedures

Mobile right heart thrombus is a severe but rare presentation of thromboembolic disease and usually coexists with an already massive pulmonary embolism (PE). But looking at the literature there is no clear consensus on therapeutic management. We therefore tried to find possible therapeutic guidelines and to evalute an optimal diagnostic procedure looking at three patients who presented at our department with mobile right heart thrombbus in the last year. The first patient with a small (diameter = 1 cm) thrombus in the right ventricle and peripheral pulmonary embolism underwent successful thrombolytic therapy without any complications. Patients II and III showed large intracardiac masses, in patient III extending into the superior vena cava, with central PE. These two patients underwent pulmonary arteriotomy. The diagnostic line in each case was transthoracal echocardiography followed by a helix lung CT scan. Only patients with small intracardiac thrombi and thrombotic masses in the peripheral pulmonary arteries but with hemodynamically significant PE should be treated with thrombolytic agents.

Crimping and repositioning of a maldeployed balloon-expandable arterial stent using a gooseneck snare.

Purpose: To describe a technique for repositioning a fully deployed iliac stent from the infrarenal aorta into the common iliac artery (CIA). Case Report: A 58-year-old man was undergoing treatment for a significant right CIA stenosis when a 7times24-mm Palmaz Genesis medium stent was mistakenly deployed in the infrarenal aorta. With the stent still over the guidewire, an 8times60-mm balloon catheter was placed coaxially in the stent. Via a left groin access, a 6-F vascular sheath was introduced retrograde, and a 2.5-cm Amplatz gooseneck snare was advanced into the infrarenal abdominal aorta and pulled back over the stent. The snare was tightly closed to crimp the stent onto the collapsed balloon; this maneuver was repeated several times until the stent was contracted along its entire length. The balloon/stent assembly was carefully pulled back into the right CIA, and the stent was deployed across the target lesion, although there was overlap of the left CIA. Color duplex sonography at 1 year showed no signs of significant iliac arterial stenoses on either side. The patient reported no claudication. Conclusions: Using a gooseneck snare, fully deployed balloon-expandable iliac stents can be recrimped on a balloon.

The PLA1/A2 polymorphism of platelet glycoprotein IIIA is not associated with deep venous thrombosis

BACKGROUND Platelet glycoprotein (GP) IIb/IIIa, a fibrinogen and von Willebrand factor binding membrane receptor, has an important role in platelet aggregation. A common leucine33-proline polymorphism (PlA1/A2) of the gene encoding the GP IIIa subunit is associated with platelet reactivity and has been proposed as a risk factor for atherothrombotic disease. The aim of this study was to investigate the role of this polymorphism for deep venous thrombosis (DVT). METHODS We performed a case-control study including 206 patients with documented DVT and a sex- and age-matched group of 310 control subjects. GP IIIa genotypes were determined by restriction fragment analysis of amplimers containing the polymorphic site. RESULTS A1/A1, A1/A2 and A2/A2 genotypes were found in 67.0, 31.6 and 1.5 percent of patients and 72.3, 25.8 and 1.9 percent of controls (p=0.35), PlA2 allele frequencies were 0.17 in patients and 0.15 in controls (p=0.92). Odds ratio of the PlA2 allele for DVT was 1.21 (95 percent CI 0.85-1.71, p=0.29) and remained insignificant after adjustment for factor V Leiden and prothrombin 20210A genotypes (1.22, 95 percent CI 0.86-1.75, p=0.27). CONCLUSIONS Our data suggest that the PlA1/A2 polymorphism of GP IIIa is not associated with DVT.