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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several epidemiological studies have produced longitudinal data identifying fibrinogen as a major cardiovascular risk factor. Cross-sectional results show strong associations between fibrinogen and a variety of demographic variables, cardiovascular risk factors, or diseases. Clinical cohort studies demonstrate that fibrinogen might also be a risk factor for the sequelae of cardiovascular disease. Knowledge about the determinants of the plasma level of fibrinogen in health and disease is as yet incomplete. Understanding of the mechanisms leading to the atherothrombogenic action of fibrinogen is also fragmentary. Fibrinogen strongly affects blood coagulation, blood rheology and platelet aggregation; in addition fibrinogen and its metabolites have direct effects on the vascular wall. Finally, fibrinogen is a prominent acute phase protein. All of these phenomena might provide some insight into the pathophysiological mechanisms involved. It is concluded that fibrinogen represents a major, independent risk factor that should now be included into the cardiovascular risk profile.
Atherosclerosis 1993 Apr
PMID:The role of fibrinogen as a cardiovascular risk factor. 831 54

Numerous epidemiologic studies have clearly shown that high plasma fibrinogen levels are strongly correlated with the frequency of myocardial infarction, stroke, and peripheral atherosclerosis. These data indicate that measurements of fibrinogen should be included in cardiovascular risk factor profiles. Since thrombosis is recognized as the central mechanism of these atherosclerotic complications, it seems advisable to accept the predictive value of this protein. Fibrinogen is involved in platelet aggregation, blood rheology, and endothelial cell injury, which are thought to play a key role in thrombogenesis. Fibrinogen may predict bypass occlusion but appears to have no significant influence on restenosis following successful coronary angioplasty. Furthermore, fibrinogen represents an acute-phase protein, being of no specificity. Its level varies genetically, as well as circadian and seasonal variations, and is influenced by a number of circumstances and drugs. Plasma levels of fibrinogen decrease by life-style changes, smoking cessation, and different medications such as fibrates, but the risk-lowering effect is not proven yet.
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PMID:Fibrinogen: its role in the hemostatic regulation in atherosclerosis. 835 54

Hypertension is an important cardiovascular risk factor. High blood pressure per se is not a disease but a hemodynamic alteration associated with vascular disease. Two classes of drugs are especially effective in lowering blood pressure and preventing cardiovascular complications, angiotensin converting enzyme (ACE) inhibitors and calcium antagonists. The hemodynamic effects of ACE inhibitors and calcium antagonists are complementary. While ACE inhibitors inhibit the renin-angiotensin system and reduce sympathetic outflow, calcium antagonists dilate large conduit and resistance arteries. Certain calcium antagonists, such as verapamil, lower heart rate. In the blood vessel wall, the local vascular effects of ACE inhibitors and calcium antagonists are also complementary. While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide. Calcium antagonists reduce smooth muscle cell proliferation and atherosclerosis. In hypertensive animals, verapamil and trandolapril normalize endothelial dysfunction. In large angiographic trials, nifedipine and nicardipine reduced the development of new atherosclerotic plaques. After myocardial infarction, verapamil reduces mortality and cardiac events in patients without heart failure. In contrast, ACE inhibitors are effective after myocardial infarction in patients with impaired left ventricular function. Urinary albumin excretion rate decreases during ACE inhibitor therapy or with a calcium antagonist such as verapamil; combination of the two drugs has an additive effect. In resistance arteries, hypertension is associated with an increased media/lumen ratio. ACE inhibitors, but not beta-blockers, markedly improve these structural changes. In summary, ACE inhibitors and calcium antagonists have a complementary profile, both in their hemodynamic and local vascular action. Hence, combination therapy with these two classes of drugs appears particularly useful in patients with hypertension, not only to lower blood pressure, but hopefully to achieve improved cardiovascular protection.
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PMID:Vascular protective effects of ACE inhibitors and calcium antagonists: theoretical basis for a combination therapy in hypertension and other cardiovascular diseases. 856 68

Vascular cell membranes from patients with essential hypertension (EH) and animals with genetic forms of hypertension have been found to have alterations in the content of free cholesterol and negatively charged phospholipids that may modify their function. Since membrane and lipoprotein lipids exchange freely, the lipid composition of lipoproteins may be an indirect measure of the content of vascular and other cells. To determine whether abnormalities are present in the lipid and phospholipid composition of lipoproteins from patients with EH, 30 EH (11 women; 19 men) and 20 normotensive control subjects were studied. Since significant gender differences were present in a number of parameters of lipoprotein composition, male and female data were examined separately. The EH group of both sexes tended to have higher plasma TG and VLDL + LDL and HDL2 lipid levels than their respective controls. Not only were the calcium-binding phospholipids phosphatidylinositol (PI) + phosphatidylserine (PS), and the membrane fluidizer phosphatidylethanolamine (PE) were significantly reduced in their VLDL + LDL, but all phospholipids (L, sphingomyelin (SPH), PI + PS, and PE) were significantly reduced in their neutral lipid content in both the HDL2 and HDL3 subfractions. These directional changes in lipoprotein FC and phospholipid in the EH women significantly increased the EH FC/PC (mol/mol) ratio in their plasma, a new cardiovascular risk factor, (EH 1.08 +/- 0.22 vs. control 0.86 +/0 0.08; P < 0.01) and lowered the SPH/PC ratio HDL2 and HDL3 in EH patients of both sexes. These findings showed that lipoproteins in normolipidemic EH women are relatively enriched in FC and in EH patients of both sexes depleted in certain phospholipids lacking in lipoproteins, their functional properties could be altered and vascular tone increased.
Atherosclerosis 1995 Oct
PMID:Abnormal lipoprotein phospholipid composition in patients with essential hypertension. 880 66

In 17 patients with primary mixed hyperlipidemia we studied levels and composition of lipoproteins in fasting plasma, lipoprotein-modifying enzymes, and postprandial lipoprotein metabolism after an oral fat-tolerance test supplemented with vitamin A before, and 12 weeks after treatment with etophylline clofibrate. With treatment, fasting plasma cholesterol, triglycerides, and the levels of very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), and low density lipoproteins (LDL) decreased significantly; high density lipoprotein (HDL) cholesterol increased significantly. Treatment caused also an increase in the protein content of IDL, a decrease in the triglyceride content of LDL, and an increase in the size of LDL as assessed by gradient gel electrophoresis. Concentrations of triglycerides, chylomicrons, and chylomicron remnants after an oral fat load supplemented with vitamin A decreased by 33%, 30% and 6%, respectively (P < 0.005; P < 0.01; and P < 0.05). The activity of lipoprotein lipase and hepatic lipase in postheparin plasma increased by 51% and 45%, respectively (P < 0.01; P < 0.05). We found a decrease in the mass concentration of cholesteryl ester transfer protein (P < 0.05). Stepwise multiple regression analysis showed that the triglyceride content of LDL is determined primarily by fasting triglycerides (r = + 0.53, P < 0.05;baseline) and cholesteryl ester transfer protein (r = + 0.49, P < 0.05; 12 weeks); in contrast, the triglyceride content of HDL3 is determined exclusively by accumulation of postprandial triglycerides (r = + 0.67; P < 0.05; baseline) and postprandial chylomicrons (r = +0.87; P < 0.005; 12 weeks). We conclude that hypolipidemic treatment with etophylline clofibrate favorably affects the cardiovascular risk factor profile in primary mixed hyperlipidemia.
Atherosclerosis 1995 Oct
PMID:Treatment of primary mixed hyperlipidemia with etophylline clofibrate: effects on lipoprotein-modifying enzymes, postprandial lipoprotein metabolism, and lipoprotein distribution and composition. 880 71

The longitudinal and exhaustive data accumulated in morbidity registers make them high performance tools to develop specific surveys for clinical assessment. Coronary heart disease morbidity registers provide examples of structure able to collect and analyse useful information for decision making in the field of public health and medicine. There are three registers in France. Because of their geographic distribution in areas with contrasting levels of health status (Lille, Strasbourg, Toulouse), comparative data generally is applicable to France in general with regional variety. Data on medical care are already available. The measurement of cardiovascular risk factor levels, a full part of the longitudinal survey, offers the opportunity to develop a competence in the field of population-based study organisation. Several specific clinical assessment studies on medical care distribution, or on the short- or middle-term effect of screening and prevention atherosclerosis centres, should be proposed. Contacts between persons in charge of decision and register co-ordinators are necessary to fit questions to answers. These registers are able to provide high quality information whose conclusions can be generalised. For the last ten years, ischaemic heart disease registers have developed a high quality level in epidemiology and consistent national and international networks that can be considered as convenient structure providing helpful information for decision.
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PMID:[Use of registries for specific evaluation studies: example of ischemic cardiopathies]. 893 66

Lipoprotein (a) [Lp(a)] has been known for more than 20 years as a peculiar "variant" of low-density lipoproteins (LDL), the recent interest for which mostly derives from its epidemiological and maybe pathogenetic link with coronary artery disease and atherosclerosis. The protein moiety of Lp(a)-apo(a)-is a glycoprotein produced by the liver, with evident structural analogies with plasminogen. A large variety of apo(a) isoforms have been described, with large variability in molecular weight, encoded by alleles located on chromosome 6. Plasma concentrations of Lp(a) are largely genetically determined, but variations on these levels are induced by changes in hepatic synthesis due to changes in control factors (for example in proteinuric syndromes). Many-but not univocal-epidemiological pieces of evidence indicate that high plasma concentrations of Lp(a) are associated with atherosclerosis and its cardiac, cerebral and peripheral manifestations, thereby potentially identifying a new cardiovascular risk factor, independent from plasma concentrations of LDL. This review will discuss such evidence and the mechanisms potentially linking Lp(a) and atherosclerosis. Proposed mechanisms include, among others, the susceptibility of Lp(a) to oxidation, the interference with mechanisms of fibrinolysis and the induction of endothelial activation.
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PMID:[Lipoprotein(a) as an athero-thrombotic risk factor: epidemiologic evidence and possible pathogenetic mechanisms]. 900 65

Cardiovascular disease is the major cause of death in patients with end-stage renal disease, and the incidence of atherosclerosis-related complications is significantly higher in dialysis patients than in nonuremic controls. This study aimed at evaluating atherosclerotic involvement of carotid vessels in hemodialysis patients and in a group of subjects with a similar cardiovascular risk factor pattern using echo color Doppler ultrasonography. Carotid lesions have been evaluated, taking into account plaque characters (surface, echogenicity), the most severe luminal narrowing, and the number of vessels involved. A large number of vascular plaques has been observed in uremic patients: 73.8% versus 44% in the control group (chi square test = 10.98; P < 0.01). A high prevalence of carotid lesions has been found in both patients and controls with clinical evidence of cardiovascular complications. Finally, we have considered the presence of carotid lesions with a topographic evaluation. The presence of atheromatous lesions in hemodialysis patients compared with control subjects was statistically significant different in all the vessels except common carotid (internal carotid: chi-square test = 8.59, P < 0.01; external carotid; chi-square test = 13.46, P < 0.01; bulb chi-square test = 7.90; P < 0.01). Our data clearly show that the hemodialysis population suffers from a higher degree of atherosclerosis than age- and sex-matched controls with similar cardiovascular risk patterns, suggesting that the uremic state in conservative and substitutive treatment per se may contribute to "advanced" atherosclerosis. However, this does not enable us to state that hemodialysis accelerates atherosclerosis. In fact, the progression of atherosclerosis might be related to atherogenic factors operative before regular dialysis.
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PMID:Echo color Doppler imaging of carotid vessels in hemodialysis patients: evidence of high levels of atherosclerotic lesions. 915 9

Family history of atherosclerosis has been recognised as an nonmodifiable cardiovascular risk factor. Lipid levels, together with hypertension and diabetes, appear to have an inheritable component. The aim of the study was to ascertain whether lipoprotein abnormalities of 169 adult patients with non-coronary atherosclerosis were associated with a family history of atherosclerosis. Besides intermediate density lipopoprotein composition and Lp(a) levels, we focused on apo(a) and apo E phenotypes, LDL cholesterol/apo B ratio, VLDL triglyceride/HDL cholesterol ratio, and environmental factors. We found that patients with a family history of atherosclerosis had a higher prevalence of VLDL triglyceride/HDL cholesterol ratio above 1.8 (51.3% vs 34.7%) than patients without. Similarly, there was a significant inverse correlation between both considered ratios (r = -0.24, p < 0.05). The odds ratio of the presence of both abnormal ratios (4.60, 95% CI, 1.41-15.00) and low molecular weight apo(a) isoforms (3.30, 95% CI, 1.05-10.30 and family history of atherosclerosis was independent of smoking and hypertension. Apo(a) isoform size seems to be more important than Lp(a) concentrations in the family history of atherosclerosis risk determination. Subsequent analysis showed that patients with a family history of atherosclerosis had a greater-than-fourfold increased risk of having one or both abnormal ratios reflecting metabolic disturbances which probably constitute a combined trait. Family history of atherosclerosis may constitute a specific lipoprotein-related marker of atherosclerosis. Such a marker often precedes the onset of overt disease and may contribute to identifying patients with an atherogenic lipoprotein profile even in the absence of classical lipid risk factors.
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PMID:Interaction of family history of atherosclerosis with atherogenic lipid traits in men with non-coronary atherosclerosis. 929 77

Congenital homocysteinuria is a rare inherited metabolic disorder with early onset atherosclerosis and arterial and venous trombosis. Moderate hyperhomocysteinemia is more frequently encountered and is recognized as an independent cardiovascular risk factor. Several case-control studies demonstrate an association between venous thromboembolism and moderate hyperhomocysteinemia. A patient with moderate hyperhomocysteinemia has a 2-3 relative risk of developing an episode of venous thromboembolism. The occurrence of mild hyperhomocysteinemia in heterozygotes for the mutation of Leiden factor V involves a 10-fold increase in the risk of venous thromboembolism. The biochemical mechanism by which homocysteine may promote thrombosis is not fully recognized. Homocysteine inhibits the expression of thrombomodulin, the thrombin cofactor responsible for protein C activation, and inhibits antithrombin-III binding. Treatment with folic acid reduces the plasma level of homocysteinemia, but no study has demonstrated its efficacy in reducing the incidence of venous thromboembolism or atherosclerosis. Hyperhomocysteinemia should be included in the screening of abnormalities of hemostasis and thrombosis in patients with idiopathic thromboembolism, and mild hyperhomocysteinemia may justify a trial of folic acid.
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PMID:[Homocysteine and venous thromboembolism]. 930 44


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