SUMMARY Five hundred patients referred to the Cerebrovascular Clinic of the Johannesburg Hospital were examined by a battery of noninvasive tests and angiography. Thirty four occlusions of the internal carotid artery were found in 32 patients. These patients were prospectively evaluated, including clinical examination, analysis of risk factors and subsequent management. This group of patients was followed up for a mean period of 18 months, and the clinical and laboratory findings and follow up data of this group were compared to an age and sex matched group of patients with matched presenting symptoms, but with patent internal carotid arteries on angiography. Four clinical patterns emerged in the patients with occluded carotid arteries; asymptomatic (3), TIA's (17), initial fixed stroke (7), and TIA with subsequent stroke (5). Follow up of the occluded group revealed 19 patients (59%) with no further symptoms and no indication for surgical intervention. Nine patients required surgery; 4 external carotid endarterectomies (ipsilateral), 4 internal carotid endarterectomies (contralateral), and one extracranial to intracranial bypass. Two were lost to follow up and one died. After 18 months mean follow up 29 patients (91%) were well and asymptomatic. Follow up for a similar period of the non-occluded group revealed three deaths, three late strokes and three myocardial infarctions. None were lost to follow up. After 19 months mean follow up 26 patients (81%) were well with no new neurological symptoms. The prognosis of appropriately treated patients with total occlusion of the internal carotid artery does not appear to be worse than in patients with similar presenting features and patent carotid arteries. The role of surgery in preventing further emboli despite the presence of a total internal carotid occlusion is highlighted.

SUMMARY A battery of simple noninvasive tests consisting of directional Doppler ultrasound and carotid phonoangiography has been used to detect carotid stenosis in 700 patients. Forty four carotid occlusions in 42 patients were confirmed on angiography, and this study examines the accuracy of this noninvasive battery in predicting the presence of an occluded internal carotid artery. Although the sensitivity of the battery described has been 70% for occlusion, with a specificity of 98% (only five false positives), this relatively low sensitivity and the uniform requirement for surgery in the false positive group have led us to conclude that this battery should not be used as a substitute for angiography when the diagnosis of internal carotid occlusion requires to be confirmed. Nevertheless, these noninvasive tests do have a role in alerting the physician to the presence of carotid occlusion and contralateral carotid artery stenosis, allowing more specific planning of any subsequent arteriography required.

The effects of amlodipine on blood pressure profiles, cardiac hypertrophy, and beta-adrenergic signal transduction were studied in transgenic hypertensive TGR(mREN2)27 rats (TGRs), which are characterized by an inverse circadian blood pressure rhythm. Cardiovascular parameters were monitored by radiotelemetry; beta-adrenoceptor density and function were measured by radioligand binding and by determination of beta-adrenergic stimulation of adenylyl cyclase. Ventricular weight and the activity of cardiac sarcolemmal 5-nucleotidase were used as measures of hypertrophy. Acute i.p. injection of amlodipine (1, 3, 10 mg/kg body weight) either at 8:00 or at 20:00 h dose-dependently reduced blood pressure irrespective of the dosing time. For long-term treatment, TGRs were divided into three groups: untreated; amlodipine, once-daily, 5 mg/kg; and amlodipine, twice daily, 2.5 mg/kg. Both treatment schedules resulted in decreased 24 h means in systolic and diastolic blood pressure and a reduction in ventricular hypertrophy but had no effects on cardiac beta-adrenergic signaling. Once-daily dose of amlodipine at 8:00 h decreased blood pressure predominantly during the daily resting period of the rats, whereas twice-daily dosing induced a bimodal blood pressure pattern. However, even after 5 weeks of treatment, typical circadian profiles could not be observed with either treatment, indicating a short duration of action of amlodipine in rats. Thus it remains an open question whether pharmacologic normalization of the circadian blood pressure pattern in TGRs will more effectively reduce myocardial hypertrophy and restore beta-adrenergic signaling than a reduction in 24-h blood pressure per se.

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