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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma fibrinogen is a major determinant of platelet aggregation and blood viscosity. The decrease in plasma fibrinogen by bezafibrate is associated with a decrease in the risk of reinfarctions. To strengthen the predictive value of plasma fibrinogen with respect to cardiovascular risk, we performed a meta-analysis of studies conducted between 1984 and 1998. Emphasis has been put on the relationship between high levels of plasma fibrinogen and fatal and/or nonfatal cardiovascular events in both the general population and in patients with previous cardiovascular events. Twenty-two studies (13 prospective, 5 cross-sectional, and 4 case-control) addressing the association between fibrinogen plasma concentrations and cardiovascular disease were analyzed. The overall estimate of risk of cardiovascular event in subjects with plasma fibrinogen levels in the higher tertile, was twice as high as that of subjects in the lower one (odds ratio, 1.99; 95% confidence interval, 1.85 to 2.13). High plasma fibrinogen levels were associated with an increased risk of cardiovascular disease in healthy as much as in high-risk individuals. A metaregression showed no confounding effects attributable to selected characteristics of retrieved studies. A subgroup analysis (study design, follow up, mean fibrinogen levels, percentage of smokers, and mean age) allowed us to conclude that fibrinogen is an independent risk factor for cardiovascular disease; that it interacts with major determinants of myocardial and cerebrovascular ischemia; and that, in secondary prevention studies, it enhances by 8% the prediction of future events by established risk factors. Thus, fibrinogen measurements should be encouraged to refine the overall risk profiles of individuals and to better tailor preventive interventions.
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PMID:Measuring plasma fibrinogen to predict stroke and myocardial infarction: an update. 1036 66

Hypertension is a significant and prevalent risk factor for the development of cardiovascular disease and target organ damage. The urgency of treatment of high blood pressure depends on the level of blood pressure elevation and the presence of coexistent risk factors for cardiovascular disease. Likewise, the level to which blood pressure is reduced is not restricted to the definition of high blood pressure but instead depends on the underlying disease. Diabetes and renal insufficiency, for example, require blood pressure goals below those that are traditionally defined. In the absence of contraindications, beta-blockers and diuretics are still recommended as first-line agents for treatment of uncomplicated hypertension. Calcium channel antagonists also may reduce mortality. In patients with diabetes, ACE inhibitors are effective first-line agents in type 1 and type 2 diabetic patients who are hypertensive or have microalbuminuria. ACE inhibitors may be beneficial in patients with nondiabetic renal insufficiency as well. Calcium channel antagonists may have some effect in retarding progression of diabetic nephropathy although a recent trial found a higher incidence of death as a secondary endpoint in hypertensive diabetic patients who were treated with calcium channel antagonists. Beta-blockers seem to be safe and well tolerated in patients with mild to moderate intermittent claudication, although patients with rest pain or limb ischemia have not been studied. Beta-blockers should not be used in patients with asthma. Dihydropyridine calcium channel antagonists are the preferred treatment of hypertension in patients with Raynaud's but should be avoided in patients with severe gastroesophageal reflux disease. NSAIDs, particularly piroxicam and indomethacin, raise mean blood pressure by approximately 5 mm Hg, enough to consider a change of either NSAID or antihypertensive to one that is not as affected by NSAIDs. Cyclosporine A can induce hypertension by its vasoconstrictive effects, particularly on the kidney. Calcium channel antagonists may antagonize this vasoconstriction while allowing the clinician to reduce the dose of cyclosporine A required to achieve its immunosuppressive effect.
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PMID:Evaluation and treatment of hypertension. 1046 27

Depression represents a major public health problem. It is estimated that 13-20% of the population has some depressive symptoms at any given time and about 5% of the population is assumed to suffer from major depression. Known pathological processes include ischemia, neoplasia, necrosis, apoptosis, infection, and inflammation. Of those, inflammation is the most compatible with the waxing and waning course of depression, and could explain the biology of this disorder that has a fluctuating course with severe episodes that can be followed by partial or complete remission. Over the years a body of evidence has been accumulated suggesting that major depression is associated with dysfunction of inflammatory mediators. Major depression commonly co-occurs with ischemic heart disease and decreased bone mineral density. Depressive symptoms are known to have a negative impact on cardiovascular prognosis, increasing the mortality rate of coronary artery disease. Several lines of evidence indicate that brain cytokines, principally interleukin-1beta (IL-1beta) and IL-1 receptor antagonist may have a role in the biology of major depression, and that they might additionally be involved in the pathophysiology and somatic consequences of depression as well as in the effects of antidepressant treatment. A particularly unique and novel aspect of the studies and views discussed here is their potential to lead to interventions which may reduce the morbidity and mortality risks for osteoporosis, cardiovascular disease, and behavioral symptoms in patients with major depression. We also discuss the emerging concept of peripheral and central cytokine compartments: their integration and differential regulation is a key element for the optimal functioning of the immune and nervous systems.
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PMID:The role of inflammatory mediators in the biology of major depression: central nervous system cytokines modulate the biological substrate of depressive symptoms, regulate stress-responsive systems, and contribute to neurotoxicity and neuroprotection. 1048 47

Endothelial cell function in all segments (arterioles, capillaries, and venules) of the microvasculature is compromised in tissues exposed to ischemia and reperfusion (I/R). This endothelial cell dysfunction is manifested as an impaired ability of arterioles to vasodilate, enhanced fluid filtration and leukocyte plugging in capillaries, and leukocyte-endothelial cell adhesion and increased protein extravasation in venules. An imbalance in the production of reactive oxygen species and nitric oxide contributes to most of these responses. The risk factors for cardiovascular disease, hypercholesterolemia, diabetes, and hypertension all appear to exacerbate the microvascular responses to I/R. A common feature of the deleterious effects of these risk factors is the enhanced oxidant stress experienced by endothelial cells, which appears to promote leukocyte-endothelial cell adhesion via transcription-independent (early response) and dependent (late response) processes. The exaggerated endothelial barrier dysfunction elicited by I/R in hypercholesterolemic animals is linked to the enhanced leukocyte recruitment, while the enhanced protein extravasation in postischemic venules of diabetic animals occurs independently of leukocyte recruitment.
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PMID:Ischemia-reperfusion: mechanisms of microvascular dysfunction and the influence of risk factors for cardiovascular disease. 1050 Oct 90

Peripheral vascular disease is characterized by progressive atherosclerotic deterioration of peripheral arteries and coronary and cerebral vascular complications. Antiplatelet treatment retards the progression of peripheral atherosclerosis but it is still unclear if this is associated with a reduced risk of amputation. Vasodilator prostaglandins have been administered in critical ischemia but the results have been disappointing. An alternative approach to enhance peripheral vasodilation is to increase nitric oxide production, which is reduced in peripheral vascular disease, particularly in the case of severe ischemia. Critical ischemia secondary to thromboembolism has been treated with thrombolysis within 7 days of the acute episode, but this approach is no more effective than vascular surgery in reducing amputation; earlier treatment should be planned to further investigate its clinical efficacy. The effect of antiplatelet treatment in preventing cardiovascular events was investigated in three randomized trials with negative results. A post-hoc analysis of the CAPRIE study demonstrated that clopidogrel is superior to aspirin in preventing cardiovascular disease. This suggests that antiplatelet treatment may be efficacious in this setting; future study should assess if its combination with other drugs, such as statins, that retard coronary atherosclerotic progression, could further reduce cardiovascular complications in peripheral vascular disease.
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PMID:[The future prospects of antithrombotic therapy in peripheral vasculopathy]. 1056 84

BACKGROUND: The introduction of the drug sildenafil (Viagra; Pfizer, New York, NY) into the armamentarium for treatment of erectile dysfunction is a major advance. Many of the patients who will benefit from its use have cardiovascular disease. Erectile dysfunction and cardiovascular disease share common risk factors. Although the metabolic demands of sexual activity are modest and the associated risk for coronary events is low, the clinician caring for cardiac patients needs to be aware of the pharmacology and hemodynamic profile of sildenafil in those with heart disease who use cardioactive drugs. METHODS AND RESULTS: We reviewed the current literature relating to the pharmacology, hemodynamic profile, efficacy, safety, and clinical application of sildenafil in patients with cardiovascular disease. Sildenafil is highly effective in the treatment of erectile dysfunction. The overall incidence of cardiovascular adverse events is low and similar to placebo. Current postmarketing data do not suggest an increase in cardiovascular death in sildenafil users. The drug is contraindicated in those taking organic nitrates. It should be used with caution and on an individual basis in patients who have active coronary ischemia and heart failure with tenous blood pressure and volume status. CONCLUSIONS: When used with discretion, sildenafil is safe, effective, and has the potential to greatly enhance quality of life in the relatively large proportion of the population with heart disease.
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PMID:Viagra and Cardiovascular Disease. 1068 47

Injury to the cardiovascular system causes an elevated expression of endothelin-1 (ET-1) and activation of several important signaling pathways including the mitogen-activated kinase (MAPK) cascade. The activation of these pathways has been implicated in the pathogenesis of cardiovascular disease caused by hypoxia, infections, and ischemia /reperfusion injury, cardiomyopathy and restenosis after balloon angioplasty. Important downstream targets of the MAPK and ET-1 pathways are the cell cycle regulatory molecules (cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors). Regulation of these molecules contributes to remodeling throughout the cardiovascular system. In addition, cell cycle molecules are important in the regulation of angiogenesis. These new data have led to the development of potential therapeutic modalities targeting these regulatory molecules in order to ameliorate various cardiovascular disease states.
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PMID:Cell cycle molecules and diseases of the cardiovascular system. 1076 98

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.
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PMID:Review: Biology and relevance of C-reactive protein in cardiovascular and renal disease. 1080 56

A spectrum of distinctive clinical presentations and electrocardiographic patterns have been recognized in neonates with ventricular arrhythmias. These may range from an incidental finding on a routine physical to cardiovascular collapse due to ventricular fibrillation. It has become increasingly important that the clinician considers ventricular tachycardia in the neonate with tachycardia when the QRS normal does not appear normal. In general, isolated premature ventricular depolarizations, couplets and non-sustained ventricular tachycardia in the absence of heart disease are associated with a favorable prognosis. Most of these arrhythmias tend to resolve during the first month of life. Conversely, sustained ventricular arrhythmias associated with ischemia, myocarditis or ventricular tumors are associated with a guarded prognosis. Treatment is based on the definition of associated cardiovascular disease, support of hemodynamic status and the judicious use of antiarrhythmic agents. Finally, there has been an increased recognition of idiopathic forms of ventricular tachycardia in the neonate which are associated with a favorable prognosis and may not require pharmacologic treatment. This review will discuss these arrhythmias in neonates, associated forms of cardiovascular disease, current treatment options and long-term prognosis.
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PMID:Ventricular arrhythmias. 1082 88

Cardiovascular disease is the major cause of morbidity and mortality in patients with diabetes. Diabetic individuals have a 200% to 400% greater risk for vascular disease than nondiabetics, with a disproportionately greater burden of disease complications in non-white minorities. Although the atherosclerotic plaques in the two groups are similar, diabetics have more severe and more diffuse disease than nondiabetics. Recent advances in the treatment of coronary disease have improved survival for diabetics and nondiabetics, but diabetics still have double the case fatality rate as nondiabetics, and diabetic women have particularly poor outcomes. Diabetic individuals also have an increased frequency of silent ischemia, systolic and diastolic left ventricular dysfunction, and cardiac autonomic neuropathy. The high frequency of modifiable risk factors provides great opportunities for prevention, the cornerstones of therapy being glycemic control, aggressive risk factor modification, and ongoing patient surveillance and monitoring to facilitate early disease detection and prompt intervention. In patients with coronary disease who require revascularization, both mechanical coronary interventions and bypass surgery are effective therapies. Patients with multivessel coronary disease have better results following bypass surgery with arterial grafts than following coronary interventions. However, diabetic patients are at increased risk for poor long-term outcome following either revascularization modality, with high rates of restenosis following mechanical interventions and the development of atherosclerosis in conduits following bypass surgery.
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PMID:Cardiovascular disease in patients with diabetes: clinical considerations. 1082 4


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