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Cerebral angiography is associated with a small but definite risk of neurological complications with an unknown incidence of clinically silent embolism. We assessed the neurological complication rate compared with the frequency of silent embolism after angiography We used diffusion-weighted magnetic resonance imaging (MRI) before and after angiography to assess embolic events. 100 consecutive angiographies (66 diagnostic and 34 interventional procedures) were done on 91 patients. Patients underwent neurological assessment before, immediately after, and 1 day after angiography. Before angiography, no abnormalities were seen on diffusion-weighted MRI. Diffusion-weighted MRI showed 42 bright lesions in 23 patients after 23 procedures (17 diagnostic, six interventional) in a pattern consistent with embolic events. There was no new neurological deficit after any angiographic procedure. After diagnostic angiography in patients with a history of vasculopathy, the frequency of lesions was significantly higher than in patients without vascular risk factors (12 [44%] of 27 vs five [13%] of 39 patients, p=0·03). In diagnostic angiography, the appearance of lesions was significantly correlated with whether vessels were difficult to probe (p=0·01), amount of contrast medium needed (p<0·01), fluoroscopy time (p<0·01), and use of additional catheters (p=0·02). After diagnostic and interventional cerebral angiography, embolic events are more frequent than the apparent neurological complication rate. In diagnostic procedures, the incidence of embolism is closely related to a vascular risk profile.

Until recently, atherosclerotic disease of the aortic arch was not regarded as a source of cerebral emboli 1 . We have reported on the basis of autopsy studies that the presence of ulcerated plaques in the aorta is an independent risk factor for ischemic stroke, particularly in patients with strokes of unknown cause, and that ulcerated plaques are predominantly found in patients who are 60 years of age or older 2 . The advent of transesophageal echocardiography has made it possible to detect protruding atherosclerotic plaques in the aortic arch and descending aorta 3 , 4 . Although a causal link between pedunculated and . . .

Summary Background Atherosclerotic lesions are heterogeneous and prognosis cannot easily be predicted, even with intracoronary ultrasound and angioscopy. Serial angiographic and necropsy studies suggest that the risk of plaque rupture correlates only weakly with the degree of stenosis. Most ruptured plaques are characterised by a large pool of cholesterol or necrotic debris and a thin fibrous cap with a dense infiltration of macrophages. The release of matrix-digesting enzymes by these cells is thought to contribute to plaque rupture. Other thromboses are found on non-ruptured but inflamed plaque surfaces. We postulated that both types of thrombotic events may be predicted by heat released by activated macrophages either on the plaque surface or under a thin cap. Methods To test the hypothesis, we measured the intimal surface temperatures at 20 sites in each of 50 samples of carotid artery taken at endarterectomy from 48 patients. The living samples were probed with a thermistor (24-gauge needle-tip; accuracy 0-1°C; time contrast 0·15 s). The tissues were then fixed and stained. Findings Plaques showed several regions in which the surface temperatures varied reproducibly by 0·2-0·3°C, but 37% of plaques had substantially warmer regions (0·4-2·2°C). Points with substantially different temperatures could not be distinguished from one another by the naked eye; such points could also be very close to one another (<1 mm apart). Temperature correlated positively with cell density ( r=0·68, p=0·0001) and inversely with the distance of the cell clusters from the luminal surface ( r=-0·38, p=0·0006). Most cells were macrophages. Infrared thermographic images also revealed heterogeneity in temperature among the plaques. Interpretation Living atherosclerotic plaques show thermal heterogeneity, which raises the possibility that an infrared catheter or other techniques that can localise heat or metabolic activity might be able to identify plaques at high risk of rupture or thrombosis.

Antiphospholipid antibodies have been suggested as markers for a high risk of recurrent cardiovascular events in young survivors of an acute myocardial infarction. However, there are few data to confirm or refute this hypothesis. In a cohort study, we have measured anticephalin (aCEPHA) and anticardiolipin (aCL) antibodies in a group of patients surviving an acute infarct. Of 597 patients studied, 13·2% were IgG or IgM aCEPHA positive compared with 4·4% of a reference population (n=158; p=0·002). In a multivariate analysis, adjusted for major cardiovascular risk factors, neither aCEPHA (IgG or IgM) nor aCL (IgG or IgM) was an independent risk factor for mortality, reinfarction, or non-haemorrhagic stroke. Although an increased proportion of survivors of a myocardial infarction have antiphospholipid antibodies, the presence of such antibodies is not a risk factor for subsequent coronary or cerebrovascular thrombosis.

Cervical artery dissection (CAD) accounts for up to one fifth of ischemic strokes occurring before 45 years. Their increasing recognition is probably due to an increased clinical awareness of this condition in patients with painful ischemic events. The internal carotid artery is the most commonly affected vessel. Cerebral ischemia is the most serious consequence of a CAD. It may be due to hemodynamic factors or emboli. The enlargement of the artery may lead to a direct compression of the lower cranial nerves. CAD typically occurs in young adults with a mean age of 40 years with a male:female ratio of 1.5. After exclusion of traumatic cases, the average annual incidence rate of CAD is 2.6 per 100,000, but the reported incidence figures in the literature are likely to be an underestimation of the incidence of CAD. A spontaneous dissection is assumed when no or only minor trauma preceded the onset. However, the differentiation between spontaneous and traumatic dissections is artificial because of a continuum between both forms. The pathogenesis of dissections remains unknown in most cases. However, traumas and primary diseases of the arterial wall are the main predisposing factors. The clinical presentation of spontaneous dissections of the internal carotid artery includes cerebral ischemia, cervical or cranial pain, Homer’s syndrome and cranial nerve palsy; CAD may also be silent. Brainstem ischemic deficits and occipital pain are the most common findings in vertebral artery dissections, but these features may be biased because the most benign and the most severe cases may escape detection. The favorable natural history of CAD emphasizes the need for a noninvasive approach to the detection, monitoring and follow-up. This noninvasive approach can be obtained by means of CT scan, MRI, magnetic resonance angiography and ultrasonography, although angiography remains the gold standard for the diagnosis of arterial dissections. Follow-up studies suggest a fairly good overall prognosis in adults and in children. In many centers, CAD are treated by heparin at the acute stage, although the benefit of such a potentially dangerous treatment has never been proven by a randomized trial.

Keywords: Cardiopulmonary bypass, adverse effects, Cerebral embolism, etiology, Cerebral embolism, physiopathology, Embolism, fat

More and more cardiac disorders are now known to predispose to embolic stroke, but cardioembolic strokes are among the most preventable causes of brain ischaemia. Advances in cardiac imaging techniques and the use of antithrombotic therapy to prevent and treat strokes are discussed.

Cerebral angiography is associated with a risk of neurological complications and air embolism may contribute towards this risk. To test this hypothesis, transcranial doppler ultrasonography was used to monitor the presence of air emboli in the middle cerebral arteries of 7 patients undergoing cerebral angiography. Doppler signals consistent with numerous air emboli were noted during each injection of radiographic contrast. This phenomenon was studied further in sheep. Radiographic contrast medium was injected into the carotid artery while a major carotid branch was insonated transorbitally. Embolic signals similar to those seen in patients were noted. Air was introduced at two points. First, at the time of drawing up the contrast into the syringe, especially with more viscous media. Standing the media before injection resulted in a highly significant reduction of air embolism, reducing the total mean duration of emboli from 1·32 (SD 0·60) s after immediate injection to 0·04 (0·05) s after ten minutes standing for iohexol 340 mg/mL (p<0·001). Second, air was introduced at the time of injection, possibly by the formation of cavitation bubbles under pressure. This occurred most prominently with the less viscous contrast media and with saline, and was significantly reduced by slow injection (mean duration of emboli for saline 2·85 [2·43] s with fast injection compared with 0·32 [0·37] s with slow injection, p=0·004). Air embolism may contribute towards neurological dysfunction after angiography. Measures should be taken to reduce this by allowing contrast media to stand prior to injection, and by flushing catheters with saline injected slowly.

In patients with an occluded internal carotid artery, the carotid stump syndrome is a potential source of microemboli that pass through the ipsilateral external carotid artery and the ophthalmic artery to the territory of the middle cerebral artery. Thus, the syndrome is associated with carotid territory symptoms although the internal carotid artery is occluded. Surgical exclusion of the internal carotid artery associated with endarterectomy of the external carotid artery has been described as the gold standard of treatment by many authors. This report is the second case, to our knowledge, of endovascular treatment of the carotid stump syndrome with the use of a stent-graft.