High Risk Of Infarction Research Articles

Capsular warning syndrome—a case of atrial fibrillation and corona radiata infarct

BackgroundCapsular warning syndrome (CWS) is a rare clinical syndrome characterised by recurrent and transient episodes of focal neurological deficits with high risk of infarction. The exact physiological mechanism of CWS remains unclear but is most commonly believed to be a result of haemodynamic insufficiency in diseased, small penetrating vessels. There are no defined treatment guidelines or established effective therapy.Case presentationWe describe the case of a 65-year-old man who presented to the emergency department with recurrent episodes of dysarthria coupled with right facial droop and right-sided weakness. Symptoms recurred a total of ten times within a span of 3 h. He had new onset atrial fibrillation. An initial cerebral angiogram showed mild intracranial atherosclerotic disease with no proximal large vessel occlusion or acute infarct. Magnetic resonance imaging 1 h later demonstrated an infarct in the left corona radiata.ConclusionsThis case illustrates an uncommon etiology of CWS. We will also discuss the lack of consensus in treatment options for CWS to mitigate a complete stroke.

Comparing transvenous coiling and transarterial embolization with Onyx/NBCA for cavernous sinus dural arteriovenous fistulas: A retrospective study in a single center

BackgroundEndovascular management is the gold standard for cavernous sinus dural arteriovenous fistulas (CS-dAVFs) in patients with signs of ophthalmoplegia, visual defects, or intolerable clinical symptoms. Although the efficacy of embolization has been confirmed, complications during post-endovascular management have not been compared in a more extensive CS-dAVFs case series. Therefore, we compared the effectiveness and peri-procedural complications of transvenous coiling with those of transarterial embolization (TAE) using liquid embolic agents. MethodsWe reviewed 71 patients with CS-dAVFs in one medical center from 2005/7 to 2016/7. We performed seventy-seven procedures on 71 patients, including six recurrent cases. We compared the efficacy and peri-procedural complications of transvenous coiling and TAE. ResultsThe complete occlusion rate for transvenous coiling was 79.2%, and that for TAE was 75.0%. Findings revealed (1) similar ophthalmoplegia complication rates (p = 0.744); (2) more frequent and permanent CN5 or CN7 neuropathy with liquid embolic agent use (p = 0.031 and 0.028, respectively); and (3) a higher risk of infarction or ICH (p = 0.002 and 0.028, respectively) in response to aggressive TAE. ConclusionTransvenous cavernous sinus coiling resulted in a similar occlusion rate and lower complication risk than transarterial Onyx/n-butyl cyanoacrylate (NBCA). We can access via an occluded inferior petrosal sinus (even contralateral), and direct transorbital puncture was a safe alternative. TAE with Onyx/NBCA was helpful in cases of oligo-feeders, but multidisciplinary treatment and multi-session TAE were usually needed for patients with multiple feeders and complex fistulas.

Comparison of classification methods for tissue outcome after ischaemic stroke

In acute ischaemic stroke, identifying brain tissue at high risk of infarction is important for clinical decision-making. This tissue may be identified with suitable classification methods from magnetic resonance imaging data. The aim of the present study was to assess and compare the performance of five popular classification methods (adaptive boosting, logistic regression, artificial neural networks, random forest and support vector machine) in identifying tissue at high risk of infarction on human voxel-based brain imaging data. The classification methods were used with eight MRI parameters, including diffusion-weighted imaging and perfusion-weighted imaging obtained in 55 patients. The five criteria used to assess the performance of the methods were the area under the receiver operating curve (AUCroc ), the area under the precision-recall curve (AUCpr ), sensitivity, specificity and the Dice coefficient. The methods performed equally in terms of sensitivity and specificity, while the results of AUCroc and the Dice coefficient were significantly better for adaptive boosting, logistic regression, artificial neural networks and random forest. However, there was no statistically significant difference between the performances of these five classification methods regarding AUCpr , which was the main comparison metric. Machine learning methods can provide valuable prognostic information using multimodal imaging data in acute ischaemic stroke, which in turn can assist in developing personalized treatment decision for clinicians after a thorough validation of methods with an independent data set.

Transit time homogenization in ischemic stroke – A novel biomarker of penumbral microvascular failure?

Cerebral ischemia causes widespread capillary no-flow in animal studies. The extent of microvascular impairment in human stroke, however, is unclear. We examined how acute intra-voxel transit time characteristics and subsequent recanalization affect tissue outcome on follow-up MRI in a historic cohort of 126 acute ischemic stroke patients. Based on perfusion-weighted MRI data, we characterized voxel-wise transit times in terms of their mean transit time (MTT), standard deviation (capillary transit time heterogeneity – CTH), and the CTH:MTT ratio (relative transit time heterogeneity), which is expected to remain constant during changes in perfusion pressure in a microvasculature consisting of passive, compliant vessels. To aid data interpretation, we also developed a computational model that relates graded microvascular failure to changes in these parameters. In perfusion–diffusion mismatch tissue, prolonged mean transit time (>5 seconds) and very low cerebral blood flow (≤6 mL/100 mL/min) was associated with high risk of infarction, largely independent of recanalization status. In the remaining mismatch region, low relative transit time heterogeneity predicted subsequent infarction if recanalization was not achieved. Our model suggested that transit time homogenization represents capillary no-flow. Consistent with this notion, low relative transit time heterogeneity values were associated with lower cerebral blood volume. We speculate that low RTH may represent a novel biomarker of penumbral microvascular failure.

Factor V Q506 (Resistance to Activated Protein C) and Prognosis after Acute Coronary Syndrome

Factor V:Q506 causing resistance to activated protein C (APC-resistance), is a risk factor for venous thrombosis. Some studies have indicated an association with arterial disease, especially in women. We investigated the prevalence of the FV:Q506 allele prospectively in 295 patients with acute coronary syndrome. Mortality and myocardial infarction rate were evaluated after 30 days and after 2 years. The FV:Q506 allele was found in 38 patients. In a Cox proportional hazards model, smokers carrying FV:Q506 had a higher risk of infarction or death within 30 days, compared to non-smokers with a normal genotype (relative risk 2.9 [95% CI 1.2-7.0]). The difference remained significant after 2 years (relative risk 2.8 [95% CI 1.2-6.5]). The effect of the FV:Q506 allele on clinical outcome in acute coronary syndrome has not previously been described. Our results demonstrate a gene-environment interaction between smoking and the FV:Q506 allele, with an increased risk of early complications after an acute ischemic event.

Delayed protection of the ischemic heart--from pathophysiology to therapeutic applications.

Preconditioning the heart with brief episodes of ischemia paradoxically increases its resistance to subsequent ischemic episodes, and markedly limits infarct size. Although preconditioning is now considered as the most powerful antiischemic intervention known, its beneficial effects are short-lived since they are lost if the reperfusion period after preconditioning is extended past 2-3 h. There is, however, some evidence of a delayed phase of protection, manifest 24 h after the initial preconditioning stimulus, associated with a decrease in infarct size, a prevention of postischemic contractile dysfunction (stunning) and a reduction in endothelial injury. The delayed beneficial effects of preconditioning resemble those induced by prior heat stress, and might be related to the expression of stress proteins (heat shock proteins or HSP). Evidence for a role of HSP derives from observations showing that brief ischemia is a potent stimulus for HSP expression. Moreover, transfection of isolated cells with HSP or overexpression of HSP in transgenic mice renders the myocytes more resistant to ischemia. Once produced, HSP are believed to facilitate protein synthesis, stabilize newly formed proteins and repair denatured ones. Alternatively, delayed preconditioning may be mediated by antioxidant enzymes such as superoxide dismutase or catalase, which are also upregulated by ischemia and this could lead to a lesser production of oxygen-derived free radicals during reperfusion. Indeed, in isolated myocytes, prevention of hypoxia-induced expression of superoxide dismutase (using an antisense oligonucleotide) abolished the delayed protective effect of preconditioning. Importantly, recent in vivo evidence suggests that the delayed protection may be mediated by adenosine, through activation of A1-receptors, and by stimulation of protein kinase C. Finally, although the exact mechanisms by which preconditioning induces delayed protection are still mostly unknown, the fact that the expression of protective proteins such as HSP can be induced by many other means than ischemia suggests that it is possible to pharmacologically stimulate this expression and thus possibly mimic the endogenous protective pathway. This could lead to the development of new pharmacological interventions which induce delayed myocardial protection in clinical situations such as angioplasty, coronary bypass surgery or even in patients at high risk of infarction.

Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management.

Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management.

The clinical role of PET in cerebrovascular disease

In normal subjects cerebral oxygen metabolism and blood flow are closely coupled, both grey and white matter extracting about 40% of their arterial oxygen supply. During acute ischaemia blood flow falls and oxygen extraction rises to 100% so that cerebral metabolism becomes totally blood flow dependent. Once acute infarction has occurred both cerebral oxygen metabolism and arterial oxygen extraction fall to low levels, while blood flow often paradoxically rises--the state of luxury perfusion. Once luxury perfusion becomes established the use of pharmacological or surgical methods to increase cerebral blood flow is inappropriate. PET will measure regional cerebral metabolism and blood flow non-invasively in man. Using PET ischaemic tissue can be distinguished from infarcted tissue, and the presence of luxury perfusion can be confirmed. In this way strokes in evolution can be detected, and the use of revascularisation procedures rationalised. Not only are regional cerebral metabolism and blood flow closely coupled, but blood volume is also coupled to blood flow. When greater than 60% stenosis of extracranial arteries occurs, reactive vasodilation of the distal circulation with an increase in rCBV results in order to reduce vascular resistance. By monitoring rCBV with PET, haemodynamically compromised regions of brain can be detected. It has been shown that patients with local areas of raised rCBV due to carotid artery stenosis are at a higher risk of infarction. PET will identify such patients and follow the haemodynamic effects of endarterectomy or EC-IC bypass. Finally PET can look at the distant functional effects of lacunar infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of survival analysis to determine the clinical significance of new Q waves after coronary bypass surgery.

There are few data on the long-term effects of new Q waves on survival and morbidity after coronary bypass graft surgery (CABG). We followed 1340 patients who underwent CABG in 1978 at 10 hospitals participating in the Coronary Artery Surgery Study (CASS). The incidence of perioperative Q-wave infarction was 4.76% (range 0.0-10.3% by hospital). The rate of infarction was higher in patients who had an increased left ventricular end-diastolic pressure or cardiomegaly on the preoperative chest radiograph. Patients who received more grafts or who had longer cardiopulmonary bypass time were also at higher risk of infarction. In a stepwise discriminant analysis of 44 clinical, angiographic and surgical variables, cardiopulmonary bypass time, topical cardiac hypothermia and cardiomegaly entered the stepwise selection of variables. Long-term survival was adversely affected by the appearance of new postoperative Q waves. The hospital mortality was 9.7% in the 62 patients who had new postoperative Q waves and 1.0% in the 1278 patients who did not (p less than 0.001); the 3-year cumulative survival rates were 85% and 95%, respectively (p less than 0.001). In patients who survived to hospital discharge, the presence of new postoperative Q waves did not adversely affect 3-year survival (94% and 96%, respectively). The survival rates were worse in patients who had a history of infarction or who had impaired left ventricular function preoperatively. The number of readmissions to hospital after CABG among the patients who had a transmural perioperative infarction was similar to to that among patients who did not. We conclude that the appearance of new Q waves after CABG adversely affects survival. The major impact on mortality occurs before hospital discharge. Patients who are destined to have a perioperative infarct cannot be predicted from commonly measured preoperative and angiographic variables.