In clinical practice, biological markers are not available to routinely assess the progression of atherosclerotic disease or the development of restenosis following endarterectomy or catheter based interventions. Endarterectomy procedures provide an opportunity to study mechanisms of restenosis and progression of atherosclerotic disease since atherosclerotic tissue is obtained. Athero-Express is an ongoing prospective study, initiated in 2002, with the objective to investigate the etiological value of plaque characteristics for long term outcome. Patients are included who undergo an endarterectomy of the carotid artery. At baseline blood is withdrawn, patients fill in an extensive questionnaire and diagnostic examinations are performed. Atherosclerotic plaques are freshly harvested, immunohistochemically stained and examined for the presence of macrophages, smooth muscle cells, collagen and fat. Parts of the atherosclerotic plaques are freshly frozen to study protease activity and protein and RNA expressions. Patients undergo a duplex follow up to assess procedural restenosis (primary endpoint) at 3 months, 1 year and 2 years. Secondary endpoints encompass major adverse cardiovascular events. In the future, the creation of this biobank with atherosclerotic specimen will allow the design of cross-sectional and follow up studies with the objective to investigate the expression of newly discovered genes and proteins and their interaction with patients and plaque characteristics in the progression of atherosclerotic disease. Objective is to include 1000-1200 patients in 5 years. In January 2004, 289 patients had been included. It is expected that 250 patients will be included yearly.

Retrospective surveys of patients with subarachnoid haemorrhage suggest that minor episodes with sudden headache (warning leaks) may precede rupture of an aneurysm, and that early recognition and surgery might lead to improved outcome. We studied 148 patients with sudden and severe headache (possible sentinel headache) seen by 252 general practitioners in a 5-year period in the Netherlands. Subarachnoid haemorrhage was the cause in 37 patients (25%) (proven aneurysm in 21, negative angiogram in 6, no angiogram done in 6, sudden headache followed by death in 4). 103 patients had headache as the only symptom, 12 of whom proved to have subarachnoid haemorrhage (6 with a ruptured aneurysm). Previous bouts of sudden headache had occurred in only 2. Other serious neurological conditions were diagnosed in 18. In the remaining 93, no underlying cause of headache was found; follow-up over 1 year showed no subsequent subarachnoid haemorrhage or sudden death. In this cohort, acute, severe headache in general practice indicated a serious neurological disorder in 37% (95% CI 29-45%), and subarachnoid haemorrhage in 25% (18-32%). 12% (5-18%) of those with headache as the only symptom. The notion of warning leaks as a less serious variant of subarachnoid haemorrhage is not supported by this study. Early recognition of subarachnoid haemorrhage is important but will probably have only limited impact on the outcome in the general population.

The clinical and electrophysiological features were prospectively studied of 75 patients (46 men and 29 women) with chronic polyneuropathy presenting in middle or old age in whom a diagnosis could not be made even after extensive evaluation and a follow up of six months. The mean age at the onset of symptoms was 56'5 years. The clinical features of chronic idiopathic polyneuropathy are heterogeneous. On clinical grounds 44 patients had a sensorimotor, 29 patients a sensory, and two patients a motor polyneuropathy. The overall clinical course in chronic idiopathic polyneuropathy was slowly progressive. None of the patients became severely disabled. Electrophysiological and nerve biopsy studies were compatible with an axonal polyneuropathy. Antibodies against myelin associated glycoprotein, gangliosides, and sulphatides were assessed in 70 patients and found to be negative.

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