Asymptomatic cervical atherosclerosis carries a variable risk of vascular events. We sought to identify patients with asymptomatic cervical bruits who may be at increased risk of developing ischemic events. We conducted a prospective multicenter cohort study of neurologically asymptomatic patients presenting a cervical bruit. Patients had biannual neurologic and carotid duplex evaluation. Association between ultrasonographic findings and vascular events, adjusting for common risk factors, was evaluated. Seven hundred fifteen patients were followed on average for 3.6 years. Mean age was 65 years. At initial visit, 357 subjects had a > or = 50% stenosis. Overall, 237 events occurred in 177 patients. Annual rate of all primary vascular events in patients with > or = 50% stenosis was 11.0% versus 4.2% in those with < 50% stenosis (p < 0.001). Annual rate of stroke and vascular death was 5.5% in the > or = 50% group compared with 1.9% in the < 50% group (p < 0.001). Yearly rate of unheralded ischemic stroke was 4.2% in subjects with > or = 80% stenosis and 1.4% in those with stenosis < 80% (p < 0.001). A stroke or TIA was ipsilateral to a > or = 80% stenosis in 66% of patients. Progression of carotid stenosis particularly to more than 80% was associated both with a higher rate of ipsilateral neurologic events and overall combined vascular events. Our data suggest that severity of carotid stenosis is the main risk factor predicting occurrence of neurologic and other vascular events. Yearly rate of ipsilateral stroke with > or = 50% carotid stenosis is low (1.4%) and most are nondisabling. Progression to > or = 80% or occlusion is associated with worse outcome.

Aspirin did not have a significant long-term protective effect in asymptomatic patients with high-grade (> or = 50%) carotid stenosis.

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Summary:The pathogenesis of U-wave inversion and its clinical value are still not clear, although the U wave was described by Einthoven together with the other electrocardiographic (ECG) waves. Not considered a useful diagnostic clue, it is not usually mentioned in ECG reports. In recent years, stimulated by the long QT syndromes and by the discovery of U-wave changes in some pathologic, mostly cardiac states, this neglected wave has attracted new interest. This review focuses on the negativity of the U wave in ischemic heart disease. The discovery of M cells and their electrophysiology has established the cellular basis for repolarization and has contributed to our knowledge of U-wave genesis. Hemodynamic changes during diastole in acute ischemia also furnish interesting elements for the interpretation of U-wave changes, and some experimental and clinical studies, besides designating stretch as a cause of U-wave changes, have also proved their value for more accurate bedside diagnosis and prognosis. They may indicate the extent of myocardial ischemia, the presence of collateral circulation, and the possible territory and vessel involved. When U-wave changes are the first and only sign of ischemia, they may contribute to a decision regarding the hospital admission of a patient without typical ischemic symptoms. Furthermore, U-wave changes during exercise tests increase their sensitivity.

Physicians were aware of and agreed with the recommendations, so additional large-scale dissemination of the guidelines would be unlikely to improve prescription patterns. However, negative attitudes about beta-blockers and hypolipaemic therapy affected adherence to recommendations for these drugs. Continuing medical education interventions involving local opinion leaders might address some of the obstacles identified.