Background and Purpose —The goal of the present study was to examine a series of putative risk factors of poststroke dementia (PSD), especially those factors usually associated with cerebrovascular disease and degenerative dementia, in a series of 251 consecutive unselected stroke patients. Methods —A standard protocol was prospectively applied at admission and 3 months after stroke; this protocol included clinical, functional, and cognitive assessments, hemogram and serum biochemistry, ECG and CT exams, apolipoprotein E and angiotensin-converting enzyme genotype, and neuropsychological examination. After a neuropsychological examination and an interview with a relative, the following diagnostic criteria were used: the Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV for dementia after stroke, DSM-III-R for previous dementia and dementia stage, and Association Internationale pour la Recherche et l’Enseignement en Neurologie (NINDS-AIREN) for vascular dementia. Results —Seventy-five cases (30%) demonstrated dementia at 3-month follow up; 25 of them (10%) had demonstrated dementia before the stroke. Dementia was unrelated to type (ischemic/hemorrhagic) or location of stroke, vascular factors (hypertension, diabetes, ischemic heart disease, or hypercholesterolemia), apolipoprotein E or angiotensin-converting enzyme genotype, and serum homocysteine. Age (odds ratio [OR] 1.1, 95% CI 1.03 to 1.2), previous nephropathy (OR 6.1, 95% CI 1.5 to 24.3), atrial fibrillation (OR 4.4, 95% CI 1.4 to 13.9), low Canadian Neurological Scale score at discharge (OR 0.5, 95% CI 0.4 to 0.6), and previous mental decline assessed by the shortened Spanish version of the Informant Questionnaire on Cognitive Decline in the Elderly (SS-IQCODE; OR 1.2, 95% CI 1.1 to 1.4) were the correlates of dementia in logistic regression analyses. The same risks factors were found when cases with previous dementia and with hemorrhagic stroke were excluded. Conclusions —Dementia is frequent after ischemic or hemorrhagic stroke. Age, nephropathy, atrial fibrillation, previous mental decline, and stroke severity independently contribute to the risk.

Poststroke dementia : clinical features and risk factors

Stroke is a major cause of death in the elderly, and risk of dementia increases after stroke. Poststroke dementia （PSD） covers all types of dementia after stroke, and is an important cause of disability in the elderly. The prevalence of PSD varies from 31.4% to 21.5% in 3 months to 4 years after the stroke. Its incidence increases with time after the stroke. Stroke and dementia share a number of risk factors. Stroke can be the direct cause of dementia and may also produce dementia by precipitating the onset of degenerative disease.

Key words: 
stroke ;  dementia ;  Alzheimer＇s disease ; risk factor

Poststroke Dementia

Advanced glycation end products (AGEs) are produced through the non enzymatic glycation and oxidation of proteins, lipids and nucleic acids. Enhanced formation of AGEs occurs particularly in conditions associated with hyperglycaemia such as diabetes mellitus (DM). AGEs are believed to have a key role in the development and progression of cardiovascular disease in patients with DM through the modification of the structure, function and mechanical properties of tissues through crosslinking intracellular as well as extracellular matrix proteins and through modulating cellular processes through binding to cell surface receptors [receptor for AGEs (RAGE)]. A number of studies have shown a correlation between serum AGE levels and the development and severity of heart failure (HF). Moreover, some studies have suggested that therapies targeted against AGEs may have therapeutic potential in patients with HF. The purpose of this review is to discuss the role of AGEs in cardiovascular disease and in particular in heart failure, focussing on both cellular mechanisms of action as well as highlighting how targeting AGEs may represent a novel therapeutic strategy in the treatment of HF.

/pdf/role-of-advanced-glycation-end-products-in-cardiovascular-59nfj22gal.pdf

Role of advanced glycation end products in cardiovascular disease

C-reactive protein (CRP) is a member of the pentraxin family of proteins, which are characterised by a cyclic pentameric structure and radial symmetry. The five identical 24-kDa protomers consist of 206 amino acids, and are noncovalently linked. CRP binds to a range of substances such as phosphocholine, fibronectin, chromatin, histones, and ribonucleoprotein in a calcium-dependent manner. It is a ligand for specific receptors on phagocytic leukocytes, mediates activation reactions on monocytes and macrophages, and activates complement. Plasma CRP is the classical acute-phase protein, increasing 1,000-fold in response to infection, ischemia, trauma, burns, and inflammatory conditions. A growing number of studies suggest that CRP is an independent risk factor for atherosclerotic vascular disease. Plasma CRP concentrations in the highest quartile are associated, depending on the subject group, with 1.5- to 7-fold increases in relative risk. In the high-risk endstage renal failure population, a raised CRP is associated with up to 5.5-fold increased relative risk of CVD and 4.6-fold increased relative risk of death. This review examines the relationships between CRP, cardiovascular disease, and mortality, with special reference to renal disease.

Review: Biology and relevance of C-reactive protein in cardiovascular and renal disease.

The history of dialysis and diet can be viewed as a series of battles waged against potential threats to patients' lives. In the early years of dialysis, potassium was identified as "the killer", and the lists patients were given of forbidden foods included most plant-derived nourishment. As soon as dialysis became more efficient and survival increased, hyperphosphatemia, was identified as the enemy, generating an even longer list of banned aliments. Conversely, the "third era" finds us combating protein-energy wasting. This review discusses four questions and four paradoxes, regarding the diet-dialysis dyad: are the "magic numbers" of nutritional requirements (calories: 30-35 kcal/kg; proteins > 1.2 g/kg) still valid? Are the guidelines based on the metabolic needs of patients on "conventional" thrice-weekly bicarbonate dialysis applicable to different dialysis schedules, including daily dialysis or haemodiafiltration? The quantity of phosphate and potassium contained in processed and preserved foods may be significantly different from those in untreated foods: what are we eating? Is malnutrition one condition or a combination of conditions? The paradoxes: obesity is associated with higher survival in dialysis, losing weight is associated with mortality, but high BMI is a contraindication for kidney transplantation; it is difficult to limit phosphate intake when a patient is on a high-protein diet, such as the ones usually prescribed on dialysis; low serum albumin is associated with low dialysis efficiency and reduced survival, but on haemodiafiltration, high efficiency is coupled with albumin losses; banning plant derived food may limit consumption of "vascular healthy" food in a vulnerable population. Tailored approaches and agreed practices are needed so that we can identify attainable goals and pursue them in our fragile haemodialysis populations.

/pdf/the-diet-and-haemodialysis-dyad-three-eras-four-open-4o0jishl5f.pdf

The Diet and Haemodialysis Dyad: Three Eras, Four Open Questions and Four Paradoxes. A Narrative Review, Towards a Personalized, Patient-Centered Approach

Atherosclerotic cardiovascular disease is a significant cause of morbidity and mortality in patients with chronic renal failure. It is unclear, however, if atherosclerosis in fact occurs at a higher incidence compared with the nonuremic population matched for age, hypertension, and diabetes mellitus or if it occurs at an accelerated rate following the onset of end-stage renal disease. The extent of true atherosclerotic lesions, versus clinically diagnosed "atherosclerosis," in patients with chronic renal failure is equally unclear. Potentially, the uremic state per se, the dialysis treatment, and factors unrelated to renal failure may participate in atherogenesis. The relative contribution of each of these factors is unknown. In this review, we discuss the pathology of "atherosclerotic" lesions in patients with chronic renal failure and the putative factors involved in atherogenesis in this population and describe the results of available studies examining the issue of accelerated atherosclerosis in uremia.

Atherosclerosis in chronic renal failure

Spurious hypophosphatemia in a patient with multiple myeloma

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Atherosclerosis in chronic renal failure

Spurious hypophosphatemia in a patient with multiple myeloma