Quality of life after acute type B dissection in the era of thoracic endovascular aortic repair.

BACKGROUND: Conservative management of acute type B aortic dissection is currently being challenged by primary thoracic endovascular aortic repair. Aim was to assess outcome and quality of life after these different approaches using an adjusted standard population as benchmark. PATIENTS AND METHODS: Observational study of a prospectively collected (January 2000 to December 2005) consecutive series of 87 patients with acute type B aortic dissection. Patients were 63 +/- 13 years old and 68 were men (78.2 %). Seventy-two were managed conservatively (83 %) and 15 invasively (12 by endovascular aortic repair). Follow-up was 36 +/- 19 months. Endpoints were early and late morbidity and mortality, and long-term quality of life as assessed by the Short Form health survey questionnaire. RESULTS: Patient cohorts were similar regarding age, risk profile and local disease. In the conservative cohort, four patients died during early (5.6 %) and eight during long-term follow-up (cumulative four years survival rate 79 %). Thirty-two patients needed secondary surgical management (44 %), i.e. delayed aortic repair (n = 11), or interventions on adjacent aortic sections or major branches (n = 21). In the surgical cohort no patient died, and no repeated interventions were necessary after the peri-operative period. Long-term quality of life scores were 100 (69-115) in conservatively and 94 (75-124) in invasively managed patients. Normal scores range from 85 to 115. CONCLUSIONS: Primary endovascular management of uncomplicated acute type B dissection is safe and leads to excellent long-term results, whereas secondary interventions were required with high incidence after initial conservative management. Long-term quality of life, however, returned to normal with any successful treatment strategy.

Incidence and clinical implications of stent fractures of the Xpert self-expanding nitinol stent in infrainguinal arteries.

BACKGROUND: Different stents in infrainguinal arteries have recently been associated with stent fractures and unfavorable clinical outcome, although data is limited regarding fractures of the Xpert selfexpanding nitinol stent. Thus, purpose of the present investigation was to evaluate its incidence and clinical implications in lower limb arteries. PATIENTS AND METHODS: Fifty-three consecutive patients (53 limbs) with peripheral arterial disease underwent secondary Xpert stent implantation due to suboptimal primary balloon angioplasty (PTA). Median age was 76 years. Stent fractures were evaluated by plain X-ray at median follow-up of 16 months. Stent patency was assessed by duplex ultrasound and sustained clinical improvement was defined as improvement of the ABI of > or = 0.10 together with improvement of at least one Rutherford class above the baseline finding throughout follow-up. RESULTS: Median length of femoropopliteal and infrapopliteal lesion was 3.0 and 2.3 cm, respectively. Sixtyfive stents were implanted in 43 limbs with femoropopliteal and 10 stents in 10 limbs with infrapopliteal lesion, respectively. Stent fractures occurred in 3 of 43 limbs (7.0%) of patients with femoropopliteal lesion with stent-based fracture rate of 4.6%. All fractured stents showed multiple struts fractures and occurred in the distal and middle superficial femoral artery. No stent fracture was observed in infrapopliteal lesions. The fractured stents were not associated with any clinical deterioration. Sustained clinical improvement was 71.0% and 54.6% for femoropopliteal and infrapopliteal lesions, respectively. Stent patency assessed by duplex was 65.2 and 63.9% for femoropopliteal and infrapopliteal lesions, respectively. CONCLUSIONS: Fractures of the Xpert stent were seldom and not associated with unfavorable clinical outcome at midterm follow-up.

Current evidence and prospects for medical treatment of abdominal aortic aneurysms.

Abdominal aortic aneurysm (AAA) is a potentially fatal condition with risk of rupture increasing as maximum AAA diameter increases. It is agreed upon that open surgical or endovascular treatment is indicated if maximum AAA diameter exceeds 5 to 5.5 cm. Continuing aneurysmal degeneration of aortoiliac arteries accounts for significant morbidity, especially in patients undergoing endovascular AAA repair. Purpose of this review is to give an overview of the current evidence of medical treatment of AAA and describe prospects ofpotential pharmacological approaches towards prevention of aneurysmal degeneration of small AAAs and to highlight possible adjunctive medical treatment approaches after open surgical or endovascular AAA therapy.

[Stents in the treatment of supraaortic vessel stenosis]. / Stents zur Behandlung von Stenosen hirnversorgender supraaortaler Gefässe.

We describe and discuss our experience of more than 500 endovascular procedures for revascularisation of acute or chronic occlusion and stenosis of supraaortic vessels using stents in 171 cases. Whereas endovascular treatment of the innominate, subclavian and vertebral arteries are routinely used in atherosclerotic occlusive lesions, carotid stenting is currently being investigated as an alternative treatment to carotid endarterectomy and seems to offer a less invasive, less traumatic and less cost expensive alternative to achieve the goal to prevent stroke. In a subgroup of high surgical risk patients carotid artery stenting with simultaneous embolic protection of the cerebral blood flow by filter systems was even superior to the endarterectomy-treated patients in a prospective, randomized multi-center study (SAPPHIRE): at 30-day follow up the major event rate for the stented group of 156 patients was 5.8% versus 12.6 for the 151 endarterectomy-treated patients.

[Vascular protection with estrogen. In-vitro and in-vivo effects--mechanisms and clinical implication]. / Gefässprotektion durch Ostrogen. Wirkungen in vitro und in vivo--Mechanismen und klinische Implikationen.

Myocardial infarction is the major cause of death in the western world. Men are more prone to develop coronary artery disease than women of the same age, in whom coronary disease is rare before menopause. Epidemiological data have shown that estrogens are vasoprotective--especially in the coronary circulation--but the underlying mechanisms have been investigated more thoroughly only in recent years. Only up to half of the protective effect of estrogen replacement therapy an be attributed to its positive effects of the lipid profile. However, a large part of this protection is caused by mechanisms distinct from lipid metabolism. It is now known that estrogens also exert effects on vascular function and structure of the vessel wall involving numerous cellular and molecular mechanisms. Actions of natural estrogens on human vascular cells and arteries will be discussed. Estrogens modulate vascular function by increasing nitric oxide production via stimulation of endothelial nitric oxide synthase (eNOS) and decreasing endothelin-1 levels in vivo. Furthermore, 17-beta estradiol is a potent inhibitor of vascular smooth muscle cell proliferation and migration, which play a major role in atherosclerotic vascular disease and in the remodeling process. 17-beta estradiol also acutely affects vascular tone in human arteries and attenuates constriction induced by contractile agonists. Finally, clinical studies showed that 17-beta estradiol can acutely and chronically ameliorate vascular function in women with and without vascular disease. In conclusion, results from clinical and in vitro studies showed positive effects of natural estrogens on vascular function which could explain in part their protective actions against coronary heart disease. Thus, primary prevention of coronary heart disease by estrogen replacement therapy after menopause appears to be a new approach to reduce cardiovascular mortality in women.

17 beta-estradiol inhibits proliferation and migration of human vascular smooth muscle cells: similar effects in cells from postmenopausal females and in males.

OBJECTIVES: Cardiovascular disease is rare in premenopausal women, but increases after the menopause when hormone replacement therapy reduces coronary events. Vascular smooth muscle cell (SMC) proliferation and migration occur in atherosclerosis, restenosis and venous graft disease. We studied the effects of 17 beta-estradiol on SMC proliferation and migration. METHODS: SMC were cultured from saphenous veins of postmenopausal women and age-matched men. Cell growth was determined by 3H-thymidine incorporation and cell counting. Migration of SMC was assessed in 4-well chambers. SMC were seeded in one corner and PDGF-BB in filter paper glued onto the opposite wall. RESULTS: PDGF-BB (5 ng/ml for 24 h) similarly stimulated 3H-thymidine incorporation in female (511 +/- 57%; n = 8) and male (528 +/- 62%; n = 12) SMC. This was reduced by 17 beta-estradiol (10(-8)-10(-6) M; female 313 +/- 52%; male 337 +/- 54%; P < 0.05). PDGF-BB increased the number of SMC (P < 0.0001 at 10 days) obtained from females (153 +/- 3%; n = 5) and males (150 +/- 4%; n = 5), which was inhibited by 17 beta-estradiol (10(-6) M; female 134 +/- 7%; male 128 +/- 5%; P < 0.05). Similar results were obtained with basic fibroblast growth factor. In contrast to 17 beta-estradiol, another steroid (dexamethasone) had no effects on 3H-thymidine incorporation in these cells stimulated with PDGF-BB, PDGF-BB (0.01-1 ng) stimulated SMC migration (P < 0.05) which was inhibited by 17 beta-estradiol (10(-10)-10(-6) M; n = 5; P < 0.005). CONCLUSION: 17 beta-Estradiol inhibits growth-factor-induced SMC proliferation and migration regardless of gender. These effects of 17 beta-estradiol may contribute to its cardiovascular protective properties in postmenopausal women during replacement therapy.

[Diagnosis of deep venous thrombosis]. / Diagnostik der tiefen Venenthrombose.

The clinical diagnosis of deep venous thrombosis (DVT) is unreliable. Phlebography, an invasive method, has gained wide diffusion and is considered as gold standard, but it has several draw-backs such as elevated costs and x-ray exposure. For these reasons, other, non-invasive techniques for diagnosing DVT have been looked for. Among them, CW-Doppler, occlusion plethysmography and, more recently, colour-Duplex-sonography have gained most acceptance. While the first two methods are able to diagnose with sufficient sensitivity and specificity proximal DVT, they are unreliable for isolated calf vein thrombosis. The colour-Duplex-sonography, on the other hand, produces results similar to phlebography for proximal thrombosis and succeeds in detecting isolated calf vein thrombosis with sufficient accuracy. We propose therefore the following non-invasive proceeding when confronted with the question of DVT: The first investigation to be done is a (colour)-Duplex examination. If one lacks such an infrastructure, an investigation with CW-Doppler or occlusion plethysmography has to be performed. If the results are positive, the patient will be treated. Otherwise, the exam will be repeated after five to seven days for CW-Doppler and plethysmography. If now the result is positive, the patient will be treated, otherwise, as with a negative Duplex study, the suspicion of DVT will be dismissed.