Risk Factors For Stroke, Myocardial Infarction, or Death Following Carotid Endarterectomy: Results From the International Carotid Stenting Study.

OBJECTIVES: Carotid endarterectomy (CEA) is standard treatment for symptomatic carotid artery stenosis but carries a risk of stroke, myocardial infarction (MI), or death. This study investigated risk factors for these procedural complications occurring within 30 days of endarterectomy in the International Carotid Stenting Study (ICSS). METHODS: Patients with recently symptomatic carotid stenosis >50% were randomly allocated to endarterectomy or stenting. Analysis is reported of patients in ICSS assigned to endarterectomy and limited to those in whom CEA was initiated. The occurrence of stroke, MI, or death within 30 days of the procedure was reported by investigators and adjudicated. Demographic and technical risk factors for these complications were analysed sequentially in a binomial regression analysis and subsequently in a multivariable model. RESULTS: Eight-hundred and twenty-one patients were included in the analysis. The risk of stroke, MI, or death within 30 days of CEA was 4.0%. The risk was higher in female patients (risk ratio [RR] 1.98, 95% CI 1.02-3.87, p = .05) and with increasing baseline diastolic blood pressure (dBP) (RR 1.30 per +10 mmHg, 95% CI 1.02-1.66, p = .04). Mean baseline dBP, obtained at the time of randomization in the trial, was 78 mmHg (SD 13 mmHg). In a multivariable model, only dBP remained a significant predictor. The risk was not related to the type of surgical reconstruction, anaesthetic technique, or perioperative medication regimen. Patients undergoing CEA stayed a median of 4 days before discharge, and 21.2% of events occurred on or after the day of discharge. CONCLUSIONS: Increasing diastolic blood pressure was the only independent risk factor for stroke, MI, or death following CEA. Cautious attention to blood pressure control following symptoms attributable to carotid stenosis could reduce the risks associated with subsequent CEA.

Stroke in first-degree relatives of patients with cervical artery dissection.

BACKGROUND AND PURPOSE: Patients with ischaemic stroke (IS) caused by a spontaneous cervical artery dissection (CeAD) worry about an increased risk for stroke in their families. The occurrence of stroke in relatives of patients with CeAD and in those with ischaemic stroke attributable to other (non-CeAD) causes were compared. METHODS: The frequency of stroke in first-degree relatives (family history of stroke, FHS) was studied in IS patients (CeAD patients and age- and sex-matched non-CeAD patients) from the Cervical Artery Dissection and Ischemic Stroke Patients (CADISP) database. FHS ≤ 50 and FHS > 50 were defined as having relatives who suffered stroke at the age of ≤50 or >50 years. FHS ≤ 50 and FHS > 50 were studied in CeAD and non-CeAD IS patients and related to age, sex, number of siblings, hypertension, hypercholesterolemia, smoking and body mass index (BMI). RESULTS: In all, 1225 patients were analyzed. FHS ≤ 50 was less frequent in CeAD patients (15/598 = 2.5%) than in non-CeAD IS patients (38/627 = 6.1%) (P = 0.003; odds ratio 0.40, 95% confidence interval 0.22-0.73), also after adjustment for age, sex and number of siblings (P = 0.005; odds ratio 0.42, 95% confidence interval 0.23-0.77). The frequency of FHS > 50 was similar in both study groups. Vascular risk factors did not differ between patients with positive or negative FHS ≤ 50. However, patients with FHS > 50 were more likely to have hypertension and higher BMI. CONCLUSION: Relatives of CeAD patients had fewer strokes at a young age than relatives of non-CeAD IS stroke patients.

[Endovascular treatment for carotid artery stenosis]. / Endovaskuläre Therapie der Karotisstenose - für wen, für wen nicht?

About 10 - 15% of all ischaemic strokes are caused by focal atherosclerosis and consecutive narrowing (stenosis) of the internal carotid artery (ICA). Carotid endarterectomy (CEA) - the standard treatment for carotid stenosis - substantially reduces the risk of recurrent stroke among patients who have had ischaemic symptoms such as stroke or transient ischaemic attack attributable to the stenosis. To a smaller extent, CEA also reduces the risk of first stroke in patients with hitherto asymptomatic carotid stenosis. Endovascular treatment techniques, including balloon angioplasty in the initial years and more recently, carotid artery stenting (CAS), have been developed as an alternative to CEA for treating carotid stenosis without necessitating surgery. The present review compares risks and benefits between CAS and CEA summarising the existing evidence derived from randomised controlled trials. Among patients with symptomatic carotid stenosis, CEA is associated with a lower risk of peri-procedural stroke or death than CAS. CAS reduces the risk of peri-procedural myocardial infarction, cranial nerve palsy and access site haematoma compared with CEA. The excess peri-procedural stroke risk associated with CAS appears to be limited to patients older than 70 years while in younger patients, CAS is as safe as CEA. Both treatments are equally effective in preventing recurrent stroke in the first few years following treatment. However, recurrent stenosis appears to be more common after CAS, and longer-term follow-up of ongoing trials should be awaited to investigate whether restenosis might be associated with recurrent stroke. The best treatment approach for patients with asymptomatic carotid stenosis remains to be determined in ongoing clinical trials.

Anterior pituitary axis hormones and outcome in acute ischaemic stroke.

BACKGROUND: Early and accurate prediction of outcome in acute stroke is important and influences risk-optimized therapeutic strategies. Endocrine alterations of the hypothalamic-pituitary axis are amongst the first measurable alterations after cerebral ischaemia. We therefore evaluated the prognostic value of cortisol, triiodothyronine (T3), free thyroxine (fT4), thyroid-stimulating hormone (TSH) and growth hormone (GH) in patients with an acute ischaemic stroke. METHODS: In an observational study including 281 patients with ischaemic stroke, anterior pituitary axis hormones (i.e. cortisol, T3, fT4, TSH and GH) were simultaneously assessed to determine their value to predict functional outcome and mortality within 90 days and 1 year. RESULTS: In receiver operating characteristic curve analysis, the prognostic accuracy of cortisol was higher compared to all measured hormones and was in the range of the National Institutes of Health Stroke Scale (NIHSS). Cortisol was an independent prognostic marker of functional outcome and death [odds ratio (OR) 1.0 (1.0-1.01) and 1.62 (1.37-1.92), respectively, P<0.0002 for both, adjusted for age and the NIHSS] in patients with ischaemic stroke, but added no significant additional predictive value to the clinical NIHSS score. CONCLUSION: Cortisol is an independent prognostic marker for death and functional outcome within 90 days and 1 year in patients with ischaemic stroke. By contrast, other anterior pituitary axis hormones such as peripheral thyroid hormones and GH are only of minor value to predict outcome in stroke.

Restenosis after carotid endarterectomy: significance of newly acquired risk factors.

BACKGROUND: In patients who had carotid endarterectomy (CEA), the significance of newly acquired cerebrovascular risk factors (CRFs) is unknown. Newly acquired CRFs are defined as CRFs not present prior to CEA (baseline CRFs) but acquired during long-term follow-up. OBJECTIVE: We sought to determine the significance of newly acquired CRFs in CEA patients with regard to progressive ICA disease (> or =50% restenosis; occurrence or progression of contralateral stenosis). METHODS: In a single-center CEA-registry, 361 CEA patients with annual follow-up visits for 7 years were identified. Hazard ratios (HR) were calculated for (i) any baseline CRF (hypertension, diabetes, hypercholesterolemia, coronary heart disease (CHD), peripheral artery disease (PAD), smoking), (ii) any newly acquired CRF, and (iii) for the use of statins and antihypertensives. RESULTS: No baseline CRF was associated with progressive ICA disease (unadjusted analysis). After adjustment for age and gender, smoking (HR 1.52, 95%CI 1.02-2.26), diabetes (HR 1.64, 95%CI 1.00-2.68), and hypercholesterolemia (HR 1.61, 95%CI 1.03-2.52) were weakly related to progressive ICA disease. Newly acquired hypertension (HR 2.44, 95%CI 1.57-3.79), CHD (HR 2.73, 95%CI 1.81-4.11), diabetes (HR 2.30, 95%CI 1.39-3.80), and PAD (HR 3.94, 95%CI 2.69-5.76) were associated with progressive ICA disease; also, after adjustment for baseline CRFs. Acquisition of at least one new CRF was related to progressive ICA disease (HR(adjusted) 8.07, 95%CI 4.97-13.12). Neither statins nor antihypertensive drugs did alter the odds for progressive ICA disease. CONCLUSION: CRFs acquired during long-term follow-up after CEA may independently contribute to progressive ICA stenosis after endarterectomy. Newly acquired CRFs might be more hazardous than CRFs present prior to CEA.

Alpha-1-antitrypsin deficiency alleles are not associated with cervical artery dissections.

The authors searched for the presence of alpha-1-antitrypsin (AAT) deficiency alleles PiZ and PiS in 74 patients with spontaneous cervical artery dissections (sCADs) and in 74 healthy control subjects. In both groups, the authors found four carriers of deficiency alleles. The connective tissue morphology of one additional patient with sCAD with PiZM genotype and her relatives was studied in skin biopsies. The PiZ allele did not segregate with morphologic alterations of the dermal connective tissue in the family. Therefore, AAT deficiency alleles may not play a role in the etiology of sCAD.

Antiplatelet therapy for preventing stroke and other vascular events after carotid endarterectomy.

BACKGROUND: Antiplatelet drugs are effective and safe in a wide variety of patients at high risk of vascular ischaemic events. Among patients undergoing vascular surgical procedures, these agents significantly reduce the risk of graft or native vessel occlusion. In this context we wished to examine their effects in patients after carotid endarterectomy (CEA). OBJECTIVES: The objective of this review was to evaluate whether antiplatelet agents are safe and beneficial after endarterectomy of the internal carotid artery. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched: 1 October 2002). In addition we performed comprehensive searches of the Cochrane Controlled Trials Register (Cochrane Library Issue 3, 2002), MEDLINE (January 1966 to September 2002) and EMBASE (January 1980 to September 2002), and checked all relevant papers for additional eligible studies. SELECTION CRITERIA: We selected randomised, controlled, unconfounded trials comparing antiplatelet agents with control after carotid endarterectomy in symptomatic or asymptomatic carotid stenosis of different degrees. Treatment duration had to be at least 30 days after CEA. Follow-up should be at least three months. DATA COLLECTION AND ANALYSIS: Two reviewers selected trials for inclusion, assessed trial quality, and extracted data independently from each other. From each trial we extracted, first the number of patients originally allocated to each treatment group, and, second the number of patients who met the criteria for each outcome (intention-to-treat analysis). We calculated a weighted estimate of the odds for each outcome event across studies using the Peto odds ratio method. MAIN RESULTS: Six trials involving 907 patients were identified. For 'death (all causes)' the Peto odds ratio of 0.77 with a 95% confidence interval (CI) of 0.48-1.24 did not show a statistically significant difference between both treatment groups. For 'stroke (any)' the Peto odds ratio of 0.58 (95%CI: 0.34-0.98) indicated a statistically significant benefit in favour of antiplatelet drugs (p=0.04). Concerning the secondary outcome events 'vascular death', 'stroke or vascular death', 'serious vascular events', 'death or dependency', 'myocardial infarction', 'major extracranial haemorrhage', 'local haemorrhage requiring surgery', 'restenosis', 'TIA or amaurosis fugax', neither any benefit nor any hazard of antiplatelet drugs could be shown. For the outcome events 'intracranial haemorrhage', 'ischaemic stroke' and 'occurrence or progression of contralateral stenosis', data were either too sparse for meaningful analyses, or not available at all. REVIEWER'S CONCLUSIONS: Our results may indicate that antiplatelet drugs did not significantly change the odds of 'death' but reduce the outcome 'stroke of any cause' in patients undergoing carotid endarterectomy. However, it can not be excluded that the beneficial effect in reducing stroke is due to chance. There is a suggestion that antiplatelets may increase the odds of haemorrhage, but there are currently too few data to quantify this effect.