Background: Only few follow-up studies have compared the long-term risk of such major vascular events (MVE) as myocardial infarction (MI) and/or stroke following transient ischaemic attack (TIA) or minor ischaemic stroke (MIS). Estimates of relative risk and cumulative long-term occurrence of MVE may provide better information and contribute to the optimization of treatment decisions. Methods: In the current post hoc modelling study with unique data from Bulgaria, we analysed 183 consecutive patients with TIA (n = 89) or MIS (n = 94), aged >40 years, who were prospectively followed over 36 months for non-fatal or fatal MVE. The cumulative survival, hazard and risks (with 95% confidence intervals) for MVE (combined or by stratification) were calculated by Kaplan-Meier analysis and adjusted (age, sex) by multivariate Cox proportional hazard models. A set of regression models was then applied to MVE incidence (per 100 patients; 4-month intervals). Results: Median follow-up was 36 months (interquartile range 30.8–36.0); no differences by age or sex were found (p > 0.05). The risk of non-fatal or fatal MVE was approximately 28% (stroke 19.7%, MI 8.2%). The adjusted cumulative risk of stroke was 0.21 versus 0.10 for MI. The odds ratio of TIA versus MIS was 0.75 (95% CI 0.43–1.32), i.e. lower for stroke (0.63, 0.31–1.25) than for MI (1.12, 0.40–3.14). The risk of non-fatal MVE was higher in MIS than in TIA (pBreslow = 0.0497), especially for non-fatal stroke (p = 0.0325). Time series regression models provided best estimates of the different outcome dynamics in TIA versus MIS (R2TIA = 0.969 with bpower = 1.04 vs. R2MIS = 0.989 with blinear = 0.84; p1-tailed = 0.04) over the study period. Conclusions: The age- and sex-adjusted cumulative 36-month hazard of MVE is higher after MIS than after TIA, but MVE fatality was higher after TIA than after MIS. Although stroke incidence was higher (up to 3 times that of MI), with the highest difference between months 8 and 18, MI fatality was always higher in absolute, relative or adjusted terms. The above alarming patterns and increasing, diverging tendencies for MVE indicate a higher long-term cumulative risk after MIS compared with TIA. These results confirm our hypothesis of a differential risk of TIA versus MIS and, at least, point toward equal importance of therapies aimed at preventing MVE in both types of preceding conditions (TIA or MIS) and the increased fatality after MI, in particular in patients with TIA.
Background/Aims: Risk of ischaemic stroke (IS) was associated with total homocysteine (tHCY). On the other hand, serum selenium (Se) exhibited anti-aging and cardiopreventive effects. Se and tHCY showed relationships in animals but these were contradictory or inconclusive in humans; therefore, we searched for such associations in acute IS. Methods: Ninety-four participants aged around 47 years were identified and 39 patients versus 46 healthy controls were analysed. Clinical, laboratory (blinded) and risk factor questionnaire methods were used. Comparison, correlation and multifactorial regression analyses were applied. Results: IS patients were similar to controls concerning age and gender. IS was prevalent in the carotid system (76.9%); 82.1% had a subacute onset. IS patients expressed higher tHCY (14.65 ± 9.79 µmol/l) and lower Se levels (1.3 ± 0.5 µmol/l). Twice as many IS patients (23%) had optimal Se levels of <1.01 µmol/l. Subjects with hyperhomocysteinaemia (tHCY ≧15 µmol/l) showed lower Se levels during IS; Se accounted for 15.4% of tHCY variations (R = –0.393; p = 0.015) with unit change increasing tHCY by 8.25 units. Se remained predictive of tHCY levels after adjustments (vitamin B6, fibrinogen, triglycerides). Conclusions: Lower Se was observed during acute IS, being inversely associated with and predicting increased tHCY levels. Of note, there were more IS patients with suboptimal Se than controls.
Venous Thrombosis -Principles and Practice 130 Table 1. Most important causes of and risk factors associated with cerebral venous sinus thromobosis. Reproduced with the written permission from the paper by Stam (2005).In the prospective International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVST) cohort of 624 adults with CVST, women comprised 465 (75%) of the patients. Compared with men, women had significantly lower mean age (42 vs 34 years). Furthermore, a gender specific risk factor -oral contraceptives, pregnancy, puerperium, and hormone replacement therapy -was identified in 65% of the women. CVST is more common in neonates than it is in infants, children or adults. In adults, CVST affects patients who are younger on average than those with arterial types of stroke. In the ISCVST, the mean age of patients with CVST was 39 years, and only 8% of them were older than 65 years (Ferro & Canhao, 2011). Topographically, the most frequent occurrence of CVST has been observed in the superior sagitral sinus (62%) followed by the transverse (lateral) sinus (41-45%) (Figure 1). www.intechopen.comCerebral Venous Sinus Thrombosis -Diagnostic Strategies and Prognostic Models: A Review Reproduced with the written permission from the paper by Saposnik et al. (2011) as derived from data on 624 patients in the International Study on Cerebral Venous and Dural Sinuses Thrombosis as reported by Manolidis & Kutz (2005).The pathogenesis of CVST remains incompletely understood because of the high variability in the anatomy of the venous system, and the paucity of experiments in animal models of CVST. However, there are at least two different mechanisms that may contribute to the clinical features of CVST: a) thrombosis of cerebral veins or dural sinus leading to cerebral parenchymal lesions or dysfunction; and b) occlusion of dural sinus resulting in decreased cerebrospinal fluid (CSF) absorption and elevated intracranial pressure. (Figure 2). Obstruction of the venous structures may result in increased venous pressure, decreased capillary perfusion pressure, and increased cerebral blood volume. Dilatation of cerebral veins and recruitment of collateral pathways play an important role in the early phases of CVST and may initially compensate for changes in pressure. The increase in venous and capillary pressure leads to blood-brain barrier disruption, causing vasogenic edema, with leakage of blood plasma into the interstitial space. As intravenous pressure continues to increase, mild parenchymal changes, severe cerebral edema, and venous hemorrhage may occur due to venous or capillary rupture. The increased intravenous pressure may lead to an increase in intravascular pressure and a lowering of cerebral perfusion pressure, resulting in decreased cerebral blood flow (CBF) and failure of energy metabolism. In turn, this allows intracellular entry of water from failure of the Na+/K+ ATPase pump, and consequent cytotoxic edema (Ferro & Canhao, 2011).www.intechopen.com Ferro & Canhao (2011).Advances in our understanding of ...
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