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Query: UMLS:C0007222 (cardiovascular disease)
 65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because cardiovascular disease (CVD) is the most important cause of death in women in the United States, it is imperative that the main risk factors for CVD in women be identified and modified. The risk factors that have the strongest impact on the incidence of CVD in women are not necessarily the same as those for men. The risk for women increases at menopause, most likely because of the decrease in levels of circulating estrogen. The classic risk factor for CVD is altered lipid levels. In middle-aged women, elevated low-density lipoprotein cholesterol levels are somewhat less important relative to lowered levels of high-density lipoprotein cholesterol and elevated triglyceride levels as independent risk factors. The metabolic syndrome, which encompasses a range of conditions known to be CVD risk factors, also has a greater impact on the incidence of CVD in women than in men. Various emerging risk factors appear to be important indicators for vascular disease in women, including C-reactive protein, homocysteine, and lipoprotein(a) levels. Many of these risk factors are affected by hormone replacement therapy, which may diminish CVD risk in postmenopausal women. Because of the complex origin of CVD, it is important to target the full array of risk factors for modification, rather than focusing on a single factor or treatment to the exclusion of other important markers.
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PMID:Risk factors for coronary artery disease in women. 1208 1

There is increasing evidence that certain microbial agents may have an etiopathogenic role in the development of atherothrombosis. Helicobacter pylori, a bacterium that causes peptic ulcer disease, has been suggested as one of the microbes involved in the development of atherothrombosis. This hypothesis is based on the following observations: a) a higher prevalence of Helicobacter pylori infection in patients with coronary artery disease, myocardial infarction, or cerebrovascular disease; b) the coincidence of Helicobacter pylori infection and cardiovascular risk factors, such as serum cholesterol and triglyceride concentrations and plasma fibrinogen; c) Helicobacter pylori seropositivity correlates with acute-phase proteins associated with higher risk of coronary disease, such as C-reactive protein, and d) controversial PCR studies indicating the presence of Helicobacter pylori in atheromas. Analysis of the scientific evidence suggests that Helicobacter pylori infection could indirectly contribute to the development and severity of atherothrombosis and cardiovascular disease.
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PMID:[Helicobacter pylori: a new cardiovascular risk factor?]. 1211 24

Cardiovascular pathology is the major cause of death in uraemia. There is evidence that a chronic inflammation with activation of C-reactive protein, interleukin-6, tumour necrosis factor-alpha and other cytokines is associated with vascular pathology, both in the general population and in dialysis patients. The cardiovascular system, and particularly the vascular wall, is the main target of the inflammatory process. Inflammation of the coronary arteries could be involved in the development of atherosclerosis and its related clinical syndromes. In the uraemic state, an increased production of pro-inflammatory cytokines may trigger the onset and progression of atherosclerosis and favour the subsequent complications, such as plaque fissuration and rupture. However, inflammatory cytokines also have a depressant action on the myocardium, thus inducing myocardial dysfunction. Together, these conditions may ultimately enhance the risk of myocardial infarction and death. From this standpoint, cardiovascular disease should also be investigated with the traditional biochemical inflammation markers and the evaluation of the circulating cytokine level, although new reliable markers could provide further diagnostic help. New therapeutic approaches should also be considered.
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PMID:Cardiac effects of chronic inflammation in dialysis patients. 1214 71

Inflammation is thought to play a central role in the aetiology and outcome of atherosclerosis. C-reactive protein (CRP) is a prominent product of the inflammatory response syndrome and a marker of overall and cardiovascular death in the general population and in dialysis patients. CRP is 5- to 10-fold higher in haemodialysis patients than in healthy controls and clearly is multifactorial in origin. A number of endogenous factors have been identified in vitro [angiotensin II, lipopolysacharide, modified low-density lipoprotein (LDL), advanced glycation end-products, homocysteine, viral infections] which all are able to trigger a nuclear factor (NF)-kappaB-mediated inflammatory, interleukin-6-driven, response via the generation of oxygen free radicals (oxidative stress). In addition, exogenous factors (dialysate endotoxin, vascular access, cuprophane dialyser material) have been identified in clinical studies which are also responsible, at least in part, for high serum CRP levels. Some of these factors function by themselves as non-traditional cardiovascular risk factors. Whether CRP is simply a marker of cardiovascular disease and mortality or whether it is in the causal pathway of the disease remains an open question. Recent data are in favour of a direct involvement in the pathogenesis of disease, since binding of CRP to degraded LDL enhances complement activation and induces the expression of tissue factor.
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PMID:C-reactive protein a marker for all-cause and cardiovascular mortality in haemodialysis patients. 1254 10

Recent epidemiological data have documented associations between C-reactive protein (CRP), the prototypical acute phase response protein, and cardiovascular disease in general population. Given the lipoprotein binding and complement activation of CRP and its localization in atherosclerotic vessels, there is a strong likelihood that CRP may be involved in the atherosclerotic process. Statin therapy seems to have action anti-atherosclerosis by inhibiting vascular atherosclerotic inflammation: clinical trials are needed. This review would be an update on the topic.
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PMID:C-reactive protein, atherosclerosis and cardiovascular disease. An update. 1214 63

The primary prevention of acute coronary syndromes is an open question. The scientific progress has discovered new biochemical markers of cardiovascular disease risk that may be useful for primary prevention. They are plasmatic markers of inflammation (serum amyloid A, C-reactive protein, phospholipase A2) and of infection (seropositivity to Chlamydia pneumoniae, cytomegalovirus). They are plasmatic markers of endothelial activation (adhesion molecules such as ICAM-1, VCAM-1) immunological markers (autoantibodies against oxydized LDL, hemostatic markers (TFPI, PAI-1) and metabolic indices (Lpa, homocystein). A gap is evident between the scientific progress in the knowledge of the epidemiology of cardiovascular pathology and its application in clinical practice. The priority should become the population approach to primary prevention: the rapidly changing and complex global context presents new challenges for public health practitioners struggling to implement preventive policies and programmes. New risk factors of cardiovascular disease have been pointed out by research. This study shows the situation on the topic with critique and updated analysis.
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PMID:[Cardiovascular prevention: new biochemical plasmatic markers of risk]. 1220 97

Elevated ferritin levels have been reported as a risk factor for coronary heart disease in Finnish and Italian studies. Studies in other populations have found no association between ferritin and cardiovascular disease raising the possibility of confounding with other cardiovascular risk factors. We determined ferritin levels, metabolic cardiovascular risk factors, C-reactive protein (CRP), anthropometric measurements and blood pressure in 815 men and women aged 26 years. In women serum ferritin correlated with CRP, waist measurement, body mass index (BMI), and triglycerides. In multiple regression analysis CRP alone was independently associated with serum ferritin. Serum ferritin in men correlated with waist measurement, BMI, triglycerides and high-density lipoprotein (HDL) cholesterol. After adjustment for the other variables, waist measurement was the only independent predictor of ferritin. Ferritin levels in young men and women are associated with obesity and serum triglycerides, HDL cholesterol in men and inflammation in women. Confounding may contribute to reports of associations between ferritin and cardiovascular disease.
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PMID:Relationship of serum ferritin with cardiovascular risk factors and inflammation in young men and women. 1261 82

Inflammatory responses are associated with cardiovascular disease and may be associated with dementing disease. We evaluated the long-term prospective association between dementia and high-sensitivity C-reactive protein, a nonspecific marker of inflammation. Data are from the cohort of Japanese American men who were seen in the second examination of the Honolulu Heart Program (1968-1970) and subsequently were reexamined 25 years later for dementia in the Honolulu-Asia Aging Study (1991-1996). In a random subsample of 1,050 Honolulu-Asia Aging Study cases and noncases, high-sensitivity C-reactive protein concentrations were measured from serum taken at the second examination; dementia was assessed in a clinical examination that included neuroimaging and neuropsychological testing and was evaluated using international criteria. Compared with men in the lowest quartile (<0.34mg/L) of high-sensitivity C-reactive protein, men in the upper three quartiles had a 3-fold significantly increased risk for all dementias combined, Alzheimer's disease, and vascular dementia. For vascular dementia, the risk increased with increasing quartile. These relations were independent of cardiovascular risk factors and disease. These data support the view that inflammatory markers may reflect not only peripheral disease, but also cerebral disease mechanisms related to dementia, and that these processes are measurable long before clinical symptoms appear.
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PMID:Early inflammation and dementia: a 25-year follow-up of the Honolulu-Asia Aging Study. 1221 Jul 86

Coronary heart disease (CHD) is the leading cause of death in the industrialized world. Recent laboratory and clinical studies have shown that inflammation plays a pivotal role in the inception, progression, and destabilization of atheromas. The acute-phase reactant C-reactive protein (CRP) has been shown to reflect systemic and, perhaps, vascular inflammation and to predict future cardiovascular events in asymptomatic individuals. The relative risk associated with CRP is independent of other cardiovascular disease risk factors. High-sensitivity assays (hs-CRP) are needed for the measurement of CRP concentration for the purpose of predicting the risk of future coronary events. Available assays must be standardized because patients' results will be interpreted using population-based cutpoints. An algorithm for risk stratification incorporating hs-CRP and total cholesterol to high-density lipoprotein cholesterol ratio has been developed. Statin class drugs and aspirin appear to modulate CHD risk in those with increased hs-CRP concentration. Several prospective studies are now underway to specifically develop novel clinical utilities and therapeutic strategies for hs-CRP.
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PMID:C-reactive protein and coronary heart disease: diagnostic and therapeutic implications for primary prevention. 1221 88

Rheumatoid arthritis (RA) patients experience a markedly increased frequency of cardiovascular disease. We evaluated cardiovascular risk profiles in 79 RA patients and in 39 age-matched and sex-matched osteoarthritis (OA) patients. Laboratory tests comprised ultrasensitive C-reactive protein (CRP) and fasting lipids. Insulin sensitivity (IS) was determined by the Quantitative Insulin Sensitivity Check Index (QUICKI) in all OA patients and in 39 of the RA patients. Ten RA patients were on glucocorticoids. RA patients exercised more frequently than OA patients (chi2 = 3.9, P < 0.05). Nine RA patients and one OA patient had diabetes (chi2 = 4.5, P < 0.05). The median CRP, the mean QUICKI and the mean high-density lipoprotein (HDL) cholesterol were 9 mg/l (range, 0.5-395 mg/l), 0.344 (95% confidence interval [CI], 0.332-0.355) and 1.40 mmol/l (95% CI, 1.30-1.49 mmol/l) in RA patients, respectively, as compared with 2.7 mg/l (range, 0.3-15.9 mg/l), 0.369 (95% CI, 0.356-0.383) and 1.68 mmol/l (95% CI, 1.50-1.85 mmol/l) in OA patients. Each of these differences was significant (P < 0.05). After controlling for the CRP, the QUICKI was similar in RA and OA patients (P = 0.07), while the differences in HDL cholesterol were attenuated but still significant (P = 0.03). The CRP correlated with IS, while IS was associated with high HDL cholesterol and low triglycerides in RA patients and not in OA patients. A high CRP (>/= 8 mg/l) was associated with hypertension (chi2 = 7.4, P < 0.05) in RA patients. RA glucocorticoid and nonglucocorticoid users did not differ in IS and lipids (P > 0.05). Excess cardiovascular risk in RA patients as compared with OA patients includes the presence of decreased IS and HDL cholesterol in RA patients. The latter is only partially attributable to the acute phase response. The CRP, IS, HDL cholesterol, triglycerides and hypertension are inter-related in RA patients, whereas none of these relationships were found in OA patients.
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PMID:Cardiovascular risk in rheumatoid arthritis versus osteoarthritis: acute phase response related decreased insulin sensitivity and high-density lipoprotein cholesterol as well as clustering of metabolic syndrome features in rheumatoid arthritis. 1222 8


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