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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, acute phase reactants have been reevaluated as not merely biochemical markers of inflammation but also as active modulators of the inflammatory response. C-reactive protein - which is normally present in serum in only trace amounts, but whose concentration may rise markedly with inflammatory stimuli - was the first human acute phase protein discovered. It is now clear that cytokines are the major mediators of acute phase protein induction: interleukin-6 currently is felt to be the principal cytokine influencing C-reactive protein acute changes. Several studies have provided convincing evidence that among normal men, base-line serum levels of C-reactive protein are predictive of future myocardial infarction and ischemic stroke. The relevance of acute phase reactants in morbidity and mortality of haemodialysis patients has not been fully elucidated until now: in fact a few studies have implicated C-reactive protein in malnutrition, EPO-resistance, as a cardiovascular risk factor and as a marker of chronic stimulation in haemodialysis. The authors suggest the hypothesis of the occurrence of long-term complications in patients exposed to contaminated dialysate and suggest that back-filtration may induce a chronic, slowly developing inflammatory state that may be abrogated by avoiding backfiltration of contaminated dialysate.
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PMID:Plasma C-reactive protein in haemodialysis. 1044 72

Hypertension is a cardiovascular risk factor classically attributed to a reduction in the calibre and/or number of small arteries and arterioles resulting in increased peripheral vascular resistance. The definition of blood pressure as a product of total peripheral resistance (TPR) and cardiac output, however, does not take into account the fluctuation of blood pressure and flow during the cardiac cycle, with systolic and diastolic blood pressure representing the extremes of pulse pressure fluctuations. Diastolic blood pressure is closer to mean blood pressure (and therefore to TPR) than systolic blood pressure, and as such has been used as a marker for the diagnosis of hypertension. However, this approach has no rational basis and was challenged by the Framingham Heart Study which demonstrated that systolic rather than diastolic blood pressure is a better risk marker for stroke and coronary artery disease in subjects aged 45 years and older. This view has subsequently been confirmed by several epidemiological and interventional studies. Systolic blood pressure is closely associated with pulse pressure and is determined by the pattern of left ventricular ejection, arterial stiffness and timing of arterial wave reflections, i.e. the geometrical and viscoelastic properties of large conduit arteries. In humans, with ageing and hypertension, the arteries stiffen as a result of progressive degeneration of the arterial media, increased collagen and calcium content, and dilation and hypertrophy of large arteries and the aorta. Thus, the increase in systolic blood pressure (as a result of arterial damage) increases the fatigue of arterial walls and accelerates arterial damage, producing a self-perpetuating cycle.
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PMID:Influence of arterial pulse and reflective waves on systolic blood pressure and cardiac function. 1046 60

Homocystinuria, an inherited disease in which plasma levels of homocysteine are high, was discovered in the sixties and it soon became clear that the affected patients had striking features of generalized atherosclerosis. The most common causes of death were arterial and venous thrombosis, stroke, or myocardial infarction. Observations in this human model of hyperhomocysteinemia led to studies in the general population whose findings suggest - though not conclusively- that homocysteine is a cardiovascular risk factor. The same is true for patients with chronic renal failure who almost always have moderate to severe high blood homocysteine levels. Homocysteine accumulates in relation to the concentration of its precursor, S-adenosylhomocysteine, a powerful competitive transmethylation inhibitor. Inhibition of a methyltransferase required to repair damaged proteins has actually been detected in uremic patients' red blood cells. However, in view of the multiple, widespread metabolic roles of S-adenosylmethionine-dependent methyltransferases, in many organs and tissues including the vascular endothelium, hypomethylation is currently interpreted as one of homocysteine's most important mechanisms of action. Various biological compounds, including small molecules and nucleic acids, as well as proteins, which are involved in the pathophysiology of thrombosis and atherosclerosis, are all potential targets of hypomethylation. Epidemiological studies and experimental models tend to confirm that homocysteine is both a cardiovascular risk factor and a uremic toxin, acting through different mechanisms.
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PMID:Homocysteine, a new cardiovascular risk factor, is also a powerful uremic toxin. 1049 66

HYPERHOMOCYSTEINEMIA: There are experimental data arguing for a role of homocysteine in several processes involved in atherosclerosis. Multiple retrospective and prospective studies performed in populations with high cardiovascular risk have shown that high homocysteine levels are associated with increased risk of coronary artery disease, stroke and peripheral vascular disease. In populations free of cardiovascular disease, prospective studies have demonstrated that homocysteine is a risk factor for cardiovascular disease while in other publications, no such prognostic value is found for high serum levels of homocysteine. PERSPECTIVE AND PREVENTION: There are highly promising perspectives for prevention due to the fact that serum homocysteine levels fall off systematically after simple dietary supplementation with vitamin B. Nevertheless, there is no formal proof to date from therapeutic trials suggesting that such a supplementation would reduce the risk of cardiovascular disease. FURTHER INFORMATION REQUIRED: In terms of epidemiology and clinical expression, further research into homocysteine as a cardiovascular risk factor should not be based on case-control studies which can be expected to provide information of limited usefulness, but rather on interventional trials to determine the primary or secondary preventive effect on cardiovascular disease. A large-scale pragmatic study using diet supplementation in a wide population might provide answers to still open questions.
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PMID:[Homocysteine and cardiovascular disease: what is the connection?]. 1055 15

A family history of cardiovascular disease predicts cardiovascular risk in the next generation, which is either the result of inherited traits or certain living habits in some families. The aim of our study was to evaluate both variables and particularly the role of one of the possible genetic risk factors--angiotensin-converting enzyme (ACE) gene polymorphism. History and anthropometric and biochemical parameters, ACE gene polymorphism and carotid wall thickness--intima media thickness (IMT) were studied in two groups of children: in children whose parents had a stroke before the age of 45 years and in children without a positive family history. The preliminary results of the present study failed to confirm our hypothesis that ACE gene polymorphism is a cardiovascular risk factor in children of parents with premature stroke.
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PMID:Angiotensin-converting enzyme gene polymorphism as a cardiovascular risk factor in children. 1065 33

The Framingham Study established hypertension as a major cardiovascular risk factor and quantified its atherogenic cardiovascular disease potential. An historical perspective is presented on the epidemiological insights about hypertension derived from 50 years of Framingham Study research into the prevalence, incidence, determinants and hazards of hypertension. Existing misconceptions about the presence of critical levels of blood pressure, the impact of the systolic and diastolic components of blood pressure, the hazard 'mild' hypertension, the impact in advanced age and the hazard of left ventricular hypertrophy. The importance of isolated systolic hypertension and the pulse pressure were demonstrated. It has been demonstrated that hypertension seldom occurs in isolation of other atherogenic risk factors, with which it tends to cluster. This clustering with other metabolically linked risk factors has been shown to reflect insulin resistance promoted by weight gain and abdominal obesity. Obesity was shown to be one of the major determinants of hypertension in the general population. Left ventricular hypertrophy was shown to be an ominous harbinger of cardiovascular disease rather than an incidental compensatory phenomenon. Multivariate risk profiles for coronary disease, stroke, peripheral artery disease and heart failure have been devised to facilitate incorporation of elevated blood pressure in a global, multivariate cardiovascular risk assessment.
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PMID:Fifty years of Framingham Study contributions to understanding hypertension. 1072 12

Hypertension is one of the main risk factors for cerebrovascular disease (stroke), coronary artery disease (acute myocardial infarction), congestive heart failure (both systolic and diastolic dysfunction), and renal dysfunction. The risk is related to blood pressure level and to the presence of target organ damage. Together with hypertension, other cardiovascular risk factors, such as hyperlipidemia and/or diabetes, also contribute to the chain of events leading to atherosclerosis, vascular complications and death. Three-quarters of middle-aged, urban population show at least one cardiovascular risk factor and 91.3% of all hypertensives show at least one cardiovascular risk factor in addition to hypertension itself. In most populations, the risk of cardiovascular disease rises steeply with age. This powerful effect of age on disease risk has important consequences for the risk of cardiovascular disease related to blood pressure and other risk factors. At most ages the risk for cardiovascular diseases is higher in men than in women, although this difference declines with increasing age and is greater for coronary heart disease than for stroke; in the United States from age 34 to 74 the risk of death from coronary heart disease is 2- to 3-fold greater in men; the risk of death from stroke is 30% higher in men than in women; after age 75 the risk of death from stroke and from coronary heart disease is similar in men and women. Postmenopausal women share the same risk with men for cardiovascular disease. For many years the study and treatment of hypertension has been largely directed toward diastolic blood pressure; the importance of elevated systolic blood pressure in the management of cardiovascular disease is being largely underrecognized. Convincing evidence is presently available indicating that elevated systolic blood pressure is even a stronger predictor than diastolic blood pressure for progression of cardiovascular disease and adverse outcomes. The clinical and laboratory evaluation and drug treatment of the hypertension is related to age. The elderly benefit from treatment of elevated systolic blood pressure as much or even more than middle-aged hypertensive subjects. Two large clinical trials on treatment of isolated systolic hypertension, the Systolic Hypertension in the Elderly Program (SHEP) and the Systolic Hypertension in Europe Study (Syst-Eur), have demonstrated that antihypertensive drug therapy in elderly patients with isolated systolic hypertension effectively reduces the risk of stroke and other major cardiovascular events.
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PMID:[Hypertension as a function of age]. 1090 25

Despite the growing evidence that plasma homocysteine is a cardiovascular risk factor, the mechanism behind the vascular injuries is still unknown. Studies are difficult as a result of the fact that little is known about the formation of different homocysteine species in vivo. Since extracellular glutathione and cysteine may influence the formation of different homocysteine species, we have in the present study investigated the different fractions of homocysteine and their relation to the different fractions of glutathione and cysteine in stroke patients and control subjects. We found a ratio of about 32-33% between reduced and total plasma glutathione concentrations and 2.6 3.0% between reduced and total plasma cysteine concentrations both in patients and in healthy control subjects. We noted an elevated concentration of total plasma homocysteine in stroke patients, but no difference in the ratio between reduced and total plasma homocysteine concentrations in patients and control subjects (mean value 1.20 and 1.10%, respectively). However, in a subgroup of patients with higher concentrations of total plasma homocysteine, we observed a significantly lower ratio of reduced to total plasma homocysteine compared to a subgroup of patients with lower concentration of total plasma homocysteine. A low reduced/total ratio of plasma homocysteine in combination with elevated plasma homocysteine concentrations might reflect an increased pro-oxidant activity in plasma from these patients. Thus, increased pro-oxidant activity in plasma might be one factor, besides genetic and nutritional factors, that could explain hyperhomocysteinemia. Since substantial evidence indicates that progression of atherosclerosis is related to enhanced pro-oxidant activity, the premature vascular disease associated with increased plasma homocysteine concentration might be as a result of increased pro-oxidant activity and the elevated plasma homocysteine concentration may only reflect the increased oxidative stress.
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PMID:Redox status of plasma homocysteine and other plasma thiols in stroke patients. 1092 31

Heart valve calcifications are rarely recognized as a potential source for cerebral embolism. Previous studies have identified mitral, but not aortic, valve calcifications to be risk factors for stroke. Based on these studies, heart surgery is unlikely to be indicated in patients who present with a stroke and an 'incidental' aortic valve calcification. We report a case of a 46-year-old man presenting with acute onset of left-sided weakness and numbness. A previous smoking history was the only cardiovascular risk factor found. Head CT scan revealed a right middle cerebral artery territory infarct and an adjacent high-density lesion. CT angiography demonstrated the presence of calcific embolic material in the middle cerebral artery. A search for embolic sources revealed a calcific aortic stenosis (CAS). Initially placed on coumadin, the patient developed silent myocardial infarction 2 months later, presumed to be also embolic in origin from the CAS. After aortic valve replacement, the patient has been symptom-free during a 2-year follow-up. In conclusion, CT angiography may be the method of choice for detecting calcific cerebral emboli, and demonstration of a causal relationship between CAS and an embolic stroke by CT angiography may be an important adjunct in surgical decision-making.
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PMID:Stroke as the first manifestation of calcific aortic stenosis. 1097 Oct 29

Cardiovascular disease is the major cause of death in patients with end-stage renal disease (ESRD). ESRD patients are almost invariably hypertensive. They all have acquired combined hyperlipidemia and increased Lp(a), hyperhomocysteinemia, decreased physical activity, psychosocial stress, insulin resistance, procoagulant factors, left ventricular hypertrophy, and increased oxidative stress. Diabetes mellitus, a major risk factor for both cardiovascular disease and ESRD, has become the commonest cause of ESRD. If ESRD patients choose to smoke, the additive risk is profound. Moreover, ESRD patients are becoming older and are often menopausal if female. Finally, ESRD patients have a dramatic tendency for vascular and cardiac calcification, probably related to hyperphosphatemia and hyperparathyroidism. Cardiovascular disease is also a major risk in patients with decreased renal function of nearly any degree. Data from the HDFP study showed that patients with a serum creatinine concentration > 1.5 mg/dl had a profoundly higher risk of cardiovascular disease than patients with creatinine values below this value. These data were recently corroborated in the HOPE study. Microalbuminuria (MAU), with or without diabetes mellitus, indicates increased cardiovascular disease risk even without decreases in glomerular filtration rate. We found earlier that nondiabetic hypertensive patients with MAU had much higher rates of myocardial infarction, stroke, and peripheral vascular disease, than similar hypertensive patients without MAU. In conclusion, the presence of decreased renal function or MAU is a major cardiovascular risk factor. ESRD can be regarded as a catastrophic risk factor. Prophylactic measures known to be effective in reducing the risk from cardiovascular disease are grossly underused. Unfortunately, they are less effective in patients with renal disease, and new strategies are needed.
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PMID:Renal disease as a risk factor for cardiovascular disease. 1119 57


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