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Lee and Chandraratna provide evidence of dry gangrene in the right foot of a 62-year-old man and evidence of a mobile arch atheroma. They suggest that thromboembolism from atheroma is an important cause of stroke and peripheral embolism. We agree. However, we would suggest that this is not a case of "thromboembolism," as it is characterized in the second paragraph. The presence of both the dorsalis pedis and posterior tibial pulses in the affected foot suggests that there has not been a fibroplatelet embolic event. Indeed, this constellation is more suggestive of cholesterol crystal embolization -how else to explain the preserved pulses? Also, single-vessel infrapopliteal occlusion typically does not cause intermittent claudication, much less gangrene. We suggest that the transesophageal echocardiogram reveals a ruptured plaque and substrate for cholesterol emboli, not thromboembolism. Burke AP, FarbA, Malcom GT, Liang YH, Smialek J, Virmani R. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med 1997;336:1276-82. 2. Kolodgie FD, Narula J, Burke AP, et al. Localization of apoptotic macrophages at the site of plaque rupture in sudden coronary death. Am J Pathol 2000;157:1259-68. 3. Kolodgie FD, Petrov A, Virmani R, et al. Targeting of apoptotic macrophages and experimental atheroma with radiolabeled annexin-V: a technique with potential for noninvasive imaging of vulnerable plaque. Circulation 2003;108:3134-9. 4. Hofstra L, Liem IH, Dumont EA, et al. Visualisation of cell death in vivo in patients with acute myocardial infarction.

Monitoring MEPs is a highly reliable technique to assess spinal cord ischemia during TAAA repair. A surgical protocol including cerebrospinal fluid drainage, left heart bypass, and monitoring of MEPs can reduce the paraplegia rate significantly. Adjusted hemodynamic and surgical strategies induced by changes in MEPs could restore spinal cord ischemia in most patients, preventing early and late paraplegia in all type I patients. In type II patients, early paraplegia occurred in 4.2% and delayed neurologic deficit in 2.9%. Despite all available measures, complete prevention of paraplegia in type II aneurysms seems to be unrealistic.

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Summary Background Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke. Methods We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602. Findings Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19–2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95% CI 1·20–1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82–3·29) for intracranial haemorrhage and 1·23 (1·08–1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95% CI 3·08–6·72] for intracranial haemorrhage vs 1·47 [1·19–1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36–9·05] vs 1·43 [1·07–1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69–15·81] vs 1·86 [1·23–2·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48–84] per 1000 patient-years vs 27 intracranial haemorrhages [17–41] per 10...