Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.
 ...
PMID:Sleep disordered breathing and risk factors for cardiovascular disease. 1239 60

Acute coronary syndromes, stroke, and sudden death are common complications of a disrupted atherosclerotic plaque. Unstable plaque is a result of multiple factors but is commonly characterized by an infiltrate of inflammatory cells. Medical research strongly supports a role for inflammation in the pathogenesis, progression, and disruption of atherosclerotic plaque. Medical science also has improved our understanding of the complex interactions between our environment and our immune, coagulation, and cardiovascular systems. Clinical studies have demonstrated systemic markers of inflammation to be strong predictors of clinical events, and specific treatments of atherosclerosis and its risk factors have been associated with reductions in inflammatory markers. The authors review the current understanding of the role of inflammation in the pathogenesis of atherosclerosis, the common inflammatory markers, and potential anti-inflammatory therapy. Among several potential circulating markers of vascular inflammation, high sensitivity C-reactive protein is best validated and standardized as a marker for cardiovascular risk assessment. Nevertheless, there remain many uncertainties in utilizing C-reactive protein in clinical practice. Here, the authors describe the central role of C-reactive protein in atherosclerosis, review the studies demonstrating predictive value of C-reactive protein, describe the factors requiring consideration when utilizing C-reactive protein, discuss clinical scenarios in which measurement of C-reactive protein may be helpful, and suggest ways to interpret and treat elevated C-reactive protein levels. Finally, the authors summarize future expectations for assessing and modulating the vascular inflammation to inhibit initiation and progression of the atherosclerotic process.
 ...
PMID:Role of inflammation in cardiovascular disease: how to use C-reactive protein in clinical practice. 1241 33

A 27-year-old woman was admitted to our hospital because of headache, fever and right neck pain. Neurological examination revealed mild meningeal signs, and hyper-reflexia in all extremities. In the laboratory tests, white-cell count was 13,000/mm3, rheumatoid factor(RF) and C-reactive protein(CRP) were positive. The cerebro-spinal fluid showed pleocytosis (56/mm3, neutorophils and lymphocytes were 26 and 28, respectively). Thus, she was diagnosed as aseptic meningitis. A few days later, she had weakness and dysesthesia of the right face and the left extremities. Pulse therapy with intravenous methylprednisolone was started. A magnetic resonance imaging (MRI) of the brain showed a hemorrhagic infarction in the right parietal lobe. In hemostatic markers, thrombin-antithrombin III complex(TAT; 106 ng/dl), D-dimer 1234 ng/dl, prothrombin fragment 1 + 2(F1 + 2; 2.36 nmol/L), beta-thromboglobulin (beta TG; 4,300 ng/dl) and platelet factor 4 (PF-4; 1,770 ng/dl) were extremely elevated. On duplex ultrasonography, a low echo lucent plaque was observed at the right internal carotid artery and the mean blood flow velocity in the right carotid artery was decreased. She was placed on oral prednisolone and warfarin for suspected stroke due to hypercoagulability associated with vasculitis. Afterwards, she discharged from our hospital. Two months later, she was readmitted to our hospital because of irregular menses and vaginal bleeding. Endometrial uterus biopsy was conducted, which revealed a grade I endometrioid adenocarcinoma. She was under total uterectomy without tumor recurrence. After the radical operation, white-cell count, RF, CRP, TAT, D-dimer, F1 + 2, and beta TG were normalized, and the mean flow velocity of the right common carotid artery was increased. Thereafter, she did not experience stroke recurrence. Therefore, we speculated that she had stroke due to hypercoagulability in association with malignancy, that is Trousseau's syndrome. We also assumed that aseptic meningitis, brainstem encephalitis associated with vasculitis in this patient are other clinical variants of paraneoplastic syndrome through immunological mechanisms associated with malignancy. We emphasize that patients with Trousseau's syndrome can be associated with other paraneoplastic manifestations such as vasculitis as seen in this patient.
 ...
PMID:[A young patient with endometrioid adenocarcinoma who suffered Trousseau's syndrome associated with vasculitis]. 1247 93

The higher rates of coronary heart disease (CHD), stroke, and venous thrombosis among women taking estrogen and progesterone (E+P) compared with placebo in the Women's Health Initiative clinical trial have important implications for women's health. Previous studies in both men and women have shown that estrogen therapy lowers low-density lipoprotein cholesterol and raises high-density lipoprotein cholesterol. The changes in these lipoproteins should be associated with at least a 30% decline in CHD risk. Estrogens increased very-low-density lipoprotein (VLDL) triglyceride levels and C-reactive protein. There is evidence that estrogens increase thrombin generation and fibrinolysis. The increase in VLDL triglycerides may enhance thrombotic risk as well as higher levels of atherogenic lipoproteins, such as dense low-density lipoprotein. Genetic variations in estrogen receptors and thrombosis or fibrinolysis may also be important in risks associated with E+P therapy. The increased risk of CHD and stroke with E+P therapy may be attributable to rise in VLDL triglycerides and thrombosis.
 ...
PMID:Hormone replacement therapy and risk of cardiovascular disease: implications of the results of the Women's Health Initiative. 1252 19

This study investigated how fibrinogen and C-reactive protein (CRP) levels change in response to neural damage occurring after ischaemia, and the relationship between the distribution of the arterial lesion, the disease prognosis and the levels of these substances. Fibrinogen and CRP levels were measured in blood samples obtained from 83 patients admitted to hospital within 72 h of a first ischaemic stroke. The patients were evaluated clinically with the Glasgow Outcome Scale (GOS), and results were compared with 43 age-matched controls. The fibrinogen and CRP levels in unconscious patients with hemiparesis or hemiplegia were higher than those in conscious hemiplegic patients. Also, the difference in GOS values between the unconscious patients with hemiparesis or hemiplegia and conscious patients with hemiparesis or hemiplegia was statistically significant. Patients with large infarcts in the median cerebral artery and anterior cerebral artery had higher fibrinogen and CRP concentrations than the control group. In conclusion, fibrinogen and CRP may be important measures for determining the prognosis and outcome in patients following ischaemic stroke.
 ...
PMID:Plasma concentrations of C-reactive protein and fibrinogen in ischaemic stroke. 1252 86

Statins reduce cholesterol levels through competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the key enzyme that regulates cholesterol synthesis. The cholesterol-lowering effect of statins is also due to an increase in the uptake of cholesterol by cells as a result of intracellular cholesterol depletion and enhanced expression of low-density lipoprotein (LDL) receptors. The use of statins as lipid-lowering agents has lead to remarkable changes in the treatment and prevention of ischemic heart disease. Results of large clinical trials of patients with ischemic heart disease have demonstrated that statins reduce inflammatory markers such as C-reactive protein, an independent risk factor in the disease. Statins exhibit properties that are beyond their lipid-lowering effects. These non-lipid-lowering properties involve the inhibition of the isoprenoid pathway through decreased synthesis of many nonsteroidal isoprenoid compounds. The focus on the immunomodulatory effect of statins is the result of the positive outcome of pravastatin treatment in cardiac transplantation patients, as well as angiographic regression studies showing insignificant changes in the degree of coronary stenosis despite a large reduction in cardiac events. Statin treatment reduces the risk of ischemic stroke despite the fact that LDL cholesterol is not directly associated with the risk of stroke. This observation lead to the investigation of the role of statins in inflammation and the immune system. Recent research data demonstrated that statins inhibit the induction of the major histocompatibility (MHC) class II expression by interferon-gamma (IFN-gamma), leading to repression of MHC II-mediated T-cell activation. Furthermore, statins inhibit the expression of specific cell surface receptors on monocytes, adhesion molecules and also integrin-dependent leucocyte adhesion. While statins may stimulate the secretion of caspase-1, IL-1beta and IL-18 in peripheral mononuclear cells in response to Mycobacterium tuberculosis, they exhibit additional effects on inflammation by decreasing IL-6 synthesis in human vascular smooth muscle cells (VSMC) in vitro. The focus of this monograph is to highlight the role of statins in the modulation of the immune system and inflammatory processes.
 ...
PMID:Modulation of the inflammatory process by statins. 1269 8

Coronary instability has been associated with multifocal plaque activation in the coronary circulation and in remote vascular districts, suggesting a systemic cause of instability, possibly inflammation. Magnetic resonance imaging offers a great potential for the detection of plaque inflammation. We describe the case of a 73-year-old female admitted for unstable angina, elevated levels of C-reactive protein and three-vessel disease, in whom carotid ultrasound examination revealed an atherosclerotic plaque of the left proximal internal carotid artery with an irregular profile and a heterogeneous echographic texture, determining a 50% stenosis. Magnetic resonance imaging of the plaque before and after contrast enhancement by gadolinium-DTPA showed the following signs of inflammation: an increased vessel wall thickness, an increased triple inversion recovery-fast spin-echo signal intensity indicative of tissue edema, and a homogeneous plaque contrast enhancement indicative of an increased capillary permeability and neovasculature. As the carotid stenosis was < 70% and did not give rise to any symptom, the patient was submitted to coronary bypass surgery without concomitant carotid endarterectomy. Two days later she developed an ischemic stroke with right brachiocrural hemiplegia. In the present case report, the simultaneous presence of coronary instability and a carotid plaque with magnetic resonance features suggestive of inflammation, which was probably responsible for the stroke complicating cardiac surgery, may indicate a multifocal plaque instability.
 ...
PMID:Carotid plaque inflammation in a patient with unstable angina. 1276 76

Peripheral arterial disease, which is caused by atherosclerotic stenosis or occlusion of the leg arteries, is an important manifestation of systemic atherosclerosis. The age-adjusted prevalence of symptomatic and asymptomatic peripheral arterial disease is approximately 12% in the general population. The overall prevalence and incidence of the disease is likely to increase with the aging of the population. Peripheral arterial disease is a relatively benign condition in terms of local disease. Five years after the diagnosis, 75% of the patients remain clinically stable. On the contrary, life expectancy, even in the absence of any history of myocardial infarction or ischemic stroke, has decreased by 10 years. These patients have approximately the same relative risk of death from cardiovascular causes as do patients with history of coronary or cerebrovascular disease. Moreover, the severity of peripheral arterial disease is closely associated with the risk of myocardial infarction and death from vascular disease. The lower the ankle-brachial index, the greater the risk of cardiovascular events. Furthermore, peripheral arterial disease is a significant independent predictor for cardiovascular mortality also in coronary patients. The risk factors associated with peripheral arterial disease are essentially the same as for coronary heart disease: older age, cigarette smoking, diabetes mellitus, hypertension, and hyperlipidemia. The excess morbidity and mortality for cardiovascular disease in these patients has not been fully explained. Patients with peripheral arterial disease show a systemic endothelial dysfunction and an increase in the serum concentration of activated white blood cells, endothelin, and C-reactive protein that may trigger acute coronary syndromes. In peripheral arterial disease the functional status is often severely impaired. Peak exercise performance has decreased to about 50% of that of age-matched controls, equivalent to moderate-severe heart failure. Epidemiological studies support the concept that patients affected by peripheral arterial disease, without established coronary heart disease, have a coronary heart disease high risk equivalent. In spite of this, peripheral arterial disease remains an underdiagnosed and undertreated disease. As the role of cardiologists is expanding, the purpose of this review was to awaken the clinician to the significance of lower limb atherosclerotic occlusive diseases.
 ...
PMID:[Why are cardiologists to be concerned about obliterating arterial disease of the lower leg?]. 1278 66

Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to identify (1) the extent to which a peripheral inflammatory response is activated in patients following acute stroke, and (2) whether there was evidence for preexisting peripheral inflammation. Thirty-six patients with ischaemic stroke within 12 h of onset of symptoms had serial blood samples taken up to 12 months for analysis of markers of inflammation. Thirty-six control subjects, individually matched for age, sex and degree of atherosclerosis, were also studied. Median C-reactive protein (CRP) was elevated, relative to controls (2.08 mg/l), from admission (4.31 mg/l) (p</=0.001) until 3 months (2.90 mg/l) (p</=0.01), the greatest elevation occurring at 5-7 days (17.67 mg/l) (p</=0.001). Elevations were also seen in erythrocyte sedimentation rate (ESR) and white blood cell (WBC) count until 3 months. Median plasma IL-6 was also elevated, relative to controls (9 pg/ml), by 24 h after onset of symptoms (22 pg/ml) (p</=0.01), and remained elevated at 5-7 days (23 pg/ml) (p</=0.01), but not at 3 months. Less marked elevations in these markers were seen in patients without evidence of infection except for IL-6, which was not increased in the absence of infection. These data provide evidence of an early and sustained peripheral inflammatory response to acute ischaemic stroke in patients with or without evidence of infection. The very early increase in concentrations of inflammatory markers after stroke may either be induced by stroke itself, or may indicate a preexisting inflammatory condition in stroke patients which may contribute to the development of stroke.
 ...
PMID:An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis. 1279 26

The recent focus on emerging cardiovascular risk factors, such as C-reactive protein, homocysteine, and small, dense low-density lipoprotein (LDL), may give the false impression that the current approach to the assessment of cardiovascular disease risk fails to identify a large section of the high-risk population. On the contrary, the new guidelines of the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) propose classifying an enormous number of individuals, including people with any form of atherosclerotic disease, diabetes, and a combination of major risk factors, into the category of high risk (>20% likelihood of a major coronary event or stroke in 10 years). Considering the widespread prevalence of the metabolic syndrome-a high-risk condition characterized by mild hypertension, mild dyslipidemia, hyperglycemia, and visceral obesity-we may be faced with the challenge of implementing aggressive risk reduction therapies in as much as 30% of the adult US population. From the point of view of risk assessment, a practical approach is to follow the NCEP guidelines (ie, place patients with diabetes and those with atherosclerotic complications in the highest risk category), apply the Framingham calculation to determine risk in people with common risk factors, and initiate early intervention in people who have familial hypercholesterolemia (LDL cholesterol >200 mg/dL) or a family history of early cardiovascular disease. The emerging risk factors may be useful for further stratifying risk in individuals with intermediate risk and the presence of risk factors not included in the Framingham calculation.
 ...
PMID:A practical approach to risk assessment to prevent coronary artery disease and its complications. 1286 51


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>