Vascular risk factors

Kumar V, Anand R, Messina J, et al An efficacy and safety analysis of Exelon in Alzheimer s disease with concurrent vascular risk factors. Eur J Neurol 7 159-169, 2000... 

Breteler MM. Vascular risk factors for Alzheimer s disease An epidemiologic perspective. Neurobiol Aging 2000 21(2) 153-160. 

Baggio G, Donazzan S, Monti D, et al. Lipoprotein(a) and lipoprotein profile in healthy centenarians A reappraisal of vascular risk factors. FASE J 1998 12 433 137. 

Clifford RM, Davis WA, Batty KT, et al. 2005. Effect of a pharmaceutical care program on vascular risk factors in type 2 diabetes The Fremantle diabetes study. Diabetes Care 28 771—6. 

Inzitari D, Diaz F, Fox A, Hachinski VC, Steingart A, Lau C, Donald A, Wade J, Mulic H, Merskey H (1987) Vascular risk factors and leuko-araiosis. Arch Neurol 44 42-47... 

Schulz UG, Rothwell PM (2003). Differences in vascular risk factors between aetiological subtypes of ischemic stroke in population-based incidence studies. Stroke 34 2050-2059... 

Schulz UG, Flossman E, Rothwell PM (2004). Heritability of ischemic stroke in relation to age, vascular risk factors and subtypes of... 

Psychogenic attacks are usually situational, for instance occurring in open spaces. Suggestive features include age less than 50 years, lack of vascular risk factors, symptoms affecting the non-dominant side (Rothwell 1994), hyperventilation, other medically unexplained symptoms or non-organic motor or sensory signs. 

Non-stroke vascular disease or vascular risk factors... 

Vascular risk factors (Ch. 2) and diseases should be sought. It is unusual for an ischemic stroke or TIA to occur in someone with no vascular risk factors, unless they are very old, or are young with some unusual cause of stroke (Ch. 6). A history of heart disease may be relevant and cardiac symptoms should be specifically inquired about. 

Fig. 10.7. Use of T2-weighted and diffusion-weighted (DWI) MRI. (a) A patient without vascular risk factors presented with a history of transient left arm and facial weakness 10 days earlier. The T2-weighted image (left) is normal but DWI (right) shows an acute right parietal infarction (arrow), (b) A patient presented with a history of transient right arm and facial weakness and sensory loss nine days before presentation. The T2-weighted image (left) is normal but the DWI (right) shows an acute left thalamic infarction (arrow).

From these studies, it appears that the medium- and long-term prognosis after TIA is more dependent on underlying vascular risk factors than characteristics of the event itself. 

Aortic arch atheroma is now increasingly diagnosed by transesophageal echocardiography in patients with TIAs or ischemic stroke, but so far there are no surgical, or indeed medical, treatment options over and above controlling vascular risk factors and antiplatelet drugs. One trial of medical treatment has been started, the Aortic Arch Related Cerebral Hazard (ARCH) trial (MacLeod et al. 2004). 

Vascular risk factors previous stroke, hypertension, diabetes, contralateral internal cerebral artery occlusion, peripheral vascular disease... 

Luchsinger JA, Reitz C, Honig LS, Tang MX, Shea S, Mayeux R (2005) Aggregation of vascular risk factors and risk of incident Alzheimer disease. Neurology 65 545-551 Mark RJ, Lovell MA, Markesbery WR, Uchida K, Mattson MP (1997) A role for 4-hydroxynonenal, an aldehydic product of hpid peroxidation, in disruption of ion homeostasis and neuronal death induced by amyloid beta-peptide. J Neurochem 68 255-264 Markesbery WR (1997) Oxidative stress hypothesis in Alzheimer s disease. Free Radic Biol Med 23 134-147... 

In addition to age, other factor s are associated with an inareased risk of AD. In developed countries, AD appears to be more common in v omen. Lack of education is a risk factor for senile dementia in China and Europe (Zhang et al., 1990 Schmand et al., 1997). Head daunra is also a risk factor for both sporadic (Mortimer et al., 1991) and familial AD (Guo et al., 2000). Silent myocardial infarcts and coronary stenosis triple the risk for AD (Aronson etal., 1990 Sparks etal., 1990), suggesting the importance of vascular risk factors. Other potential risk factors being studied include diabetes and hypertension (Ott et al., 1999 Peila et al., 2002 Qiu etal., 2005). As discussed below, a large number of genetic mutations are now associated with either early-onset AD or with increased risk of late-onset AD. 

Upregulation of adhesion molecules has been documented in human stroke patients [7]. It was demonstrated that leukocytes from patients suffering an ischemic stroke or transient ischemic attack showed increased CDl la expression within 72 hours of the onset of symptoms [123]. Increased ICAM-1 expression on the surface of vessels fi om cerebral cortical infarcts was detected in four patients [124]. In some studies, soluble isoforms of adhesion molecules shed fi om the surfaces of activated cells were quantified in serum. Serum endothelial-leukocyte adhesion molecule-1 (ELAM-1, E-selectin) levels increased up to 24 hours after stroke. Similar increases were observed in serum vascular cell adhesion molecule-1 (VCAM-1) levels and these increases were sustained up to 5 days [125]. In contrast, serum ICAM-1 levels in acute ischemic stroke patients have been found to be lower than or the same as those of asymptomatic control subjects matched for age, sex, and vascular risk factors [125,126]. The reason not to detect an increase in serum levels of adhesion molecules might be due to the late enrolling of patients. Once adhesion molecules bind to leukocytes and endothelial cells, they can no longer be detected in serum [7]. 

Several cases of intravenous immunoglobulin-related thrombosis have been reported (78,79). It can be either venous or arterial (80). It has been suggested that thrombosis can be caused by platelet activation and increased plasma viscosity (79). In patients with vascular risk factors, such as old age, hypertension, and a history of stroke or coronary artery disease, complications, such as myocardial infarction, pulmonary embolism, stroke, and acute spinal cord events, have been described (80). Intravenous immunoglobulin enhances platelet aggregation and the release of adenosine triphosphate in human platelets in vitro. In addition, there is a dose-related increase in plasma viscosity with increasing plasma immunoglobulin concentration (79,80). 

Kivipelto M, Helkala EL, Laasko MP, et al. Midlife vascular risk factors and Alzheimer s disease in later life Longimdinal population based study. BMJ 2001 322 1447-1451. 

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