Background and Purpose-It has been shown previously that cerebral microemboli may occur frequently in patients with a normal mechanical heart valve (MHV) without prior history of stroke. Some arguments strongly suggest that these microemboli have a gaseous origin. In other circumstances such as extracorporeal circulation or decompression in divers, it has been demonstrated that cerebral microbubbles could lead to some deterioration in cognitive functions. Therefore, we have studied attention and memory, which are among the most impaired cognitive functions as demonstrated in previous studies, in patients with an MHV. Methods-Three groups of 12 volunteers each were composed of patients with an MHV and embolic signals in the cerebral circulation (group 1), patients with biological prostheses (group 2), and healthy subjects (group 3). Groups were carefully matched for age and verbal intellectual abilities. For each group, a transcranial Doppler examination was performed and a set of cognitive tests assessing sustained and selective attention and episodic and working memory was administered. Results-The mean embolic rate was 29 per hour in patients with an MHV. No embolus was detected in the other 2 groups.Episodic memory was significantly modified in both groups 1 and 2 compared with the control group for tasks that required high-processing resources. Working memory performance was significantly decreased in MHV patients. No between-groups differences were observed for the other parameters. Conclusions-Alteration of episodic memory can be attributed to a long-term effect of the surgical procedure.Deterioration of working memory can be related to the presence of cerebral microemboli in MHV patients. (Stroke. 1998;29:1821-1826.)

Background and Purpose: Cervical artery dissection (CAD) accounts for 10–20% of ischemic strokes in young adults. Although trauma and preexisting disorders of the arterial wall are the main predisposing factors, most CADs are considered ‘spontaneous’. We hypothesized that CAD could originate in systemic vascular disease bound to the intima–media interface without clinical signs. If this hypothesis is true, endothelium-dependent vasodilation would be impaired in response to a physiological stimulus such as an increase in blood flow. Methods: Flow-mediated arterial dilation was studied in 65 consecutive patients with spontaneous CAD: 26 with carotid artery dissection (ICAD), and 39 with vertebral artery dissection (VAD). CAD patients with vascular risk factors, trivial or obvious cervical trauma, or connective tissue disease were excluded. Twenty-three patients with ischemic stroke of unknown cause were included as controls. Using high-resolution ultrasonography, brachial artery diameter was measured at rest, during post-ischemic hyperemia (flow-mediated endothelium-dependent dilation), and after sublingual glyceryl trinitrate spray (endothelium-independent dilation). Results: The mean ± SD values of the flow-mediated vasodilation index were 5.7 ± 6.2% in ICAD, 5.0 ± 9.3% in VAD and 13.2 ± 6.5% in controls (p < 0.0005), without any difference between ICAD and VAD. Endothelium-independent dilation mean values were 21.5 ± 9.5% in ICAD, 25.1 ± 12.5% in VAD, and 20.8 ± 8.4% in controls, without a significant difference between groups (p = 0.49). Conclusions: These results give evidence of impaired endothelium-dependent vasodilation in CAD patients that is not the result of stroke, and suggest that an underlying abnormality of the arterial wall layers may predispose to CAD.

Classically, cold induced plasma volume reduction is explained by an increased diuresis which is generated by an inhibition of antidiuretic hormone release. However, most of the haemoconcentration appears to be reversible during rewarming. This observation weakens the former statement. The aim of this study was to clarify the mechanisms involved in the reversal of the cold induced haemoconcentration. Six young males, resting in a dorsal reclining position, were exposed successively to a thermoneutral environment (30 min), a cold environment (1 degrees C; cold) or thermoneutrality (control) for 120 min, and during a 60-min recovery period in thermoneutral conditions. During cold stress, a reduction of 15% (i.e. 510 ml) of the plasma volume was observed, and osmolality was unchanged. After the 60-min recovery under thermoneutral conditions, plasma volume variation between the Cold and the Control experiments was reduced and reached 3% (i.e. 100 ml). This volume equalled the increased amount of urine production observed during the cold stress experiment. Haemoconcentration cannot be explained by increased urinary water loss (+/- 100 ml) alone. Therefore a transient shift of plasma water from vascular to interstitial spaces, due to an increase of blood pressure, could be involved in the reduction of plasma volume.

Exposure to cold causes a vasoconstriction and a tachycardia, both resulting in a rise of blood pressure and cardiac work. This last effect may have a deleterious influence on people suffering from ischaemic heart disease (IHD). Moreover, coronary artery spasm could occur if vasoconstriction extends to the heart vessels. Epidemiologic studies have shown that mortality from IHD was correlated to the ambient temperature. There will be more deaths per day in the winter, and fewer in the summer. However, the daily number of deaths also increases during the heat waves. During a cold test, the coronary blood flow remains normal or slightly increased in normal subject. There is never a coronary artery spasm. Subjects who suffer from angina but have normal coronary arteries behave in the same way as normal subjects. Patients with IHD show a decrease in coronary blood flow. In a few cases, those patients may exhibit a coronary spasm with chest pain and even myocardial infarction. It is concluded that people with normal cardiovascular function are unaffected by cold stress whereas those with IHD may be crippled, although rarely, by exposure to cold, especially if they perform a physical work.

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