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

We investigated whether peak filling rate (PFR) obtained from ECG gated radionuclide ventriculography (RNV) reflects left ventricular (LV) relaxation rate or not. Five patients with angina pectoris, 5 patients with old myocardial infarction and 6 controls were studied by simultaneous acquisition of RNV and LV pressure. RNV was performed in modified left anterior oblique position before and during angiotensin II (A II) infusion to elevate their blood pressure about 25 mmHg (A-1) and 50 mmHg (A-2). The data were acquired in a list mode and LV volume curves were reconstructed by forward and backward gating from the R wave of ECG. Actual PFR and corrected PFR by stroke volume (/SV), by end diastolic volume (/EDV), by instantaneous volume (/IV) were calculated from LV volume curve and its first differential curve. LV pressure was simultaneously measured by the catheter-tip micromanometer, and the time constant (T) of assumed exponential decline in LV pressure was calculated as index of LV relaxation rate. Although there was no correlation between actual PFR and T, corrected PFR (/EDV) and PFR (/IV) correlated with T. PFR (/EDV) decreased and T increased during A-1 and A-2. Decrease of PFR (/EDV) corresponded with increase of T. Thus, corrected PFR (/EDV) obtained from RNV reflects the rate of LV relaxation, and was considered to be an useful index to evaluate LV diastolic function.
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PMID:[An examination of left ventricular peak filling rate and ventricular relaxation rate by simultaneous acquisition of radionuclide ventriculography and left ventricular pressure]. 262 80

A study was performed to assess the natural history, prognostic factors, and lipid and apolipoprotein abnormalities of idiopathic ischemic childhood stroke. A case series of 42 children, retrospectively identified with idiopathic ischemic strokes, were reassessed an average of 7.4 years (range, 1 to 19 years) after presentation. Patients were interviewed and examined, and fasting serum was obtained for lipid and apolipoprotein analysis. Poor outcome was defined as moderate to severe hemiparesis, special educational needs, epilepsy, recurrent stroke, or stroke-related death. Eighteen (43%) of the patients had a poor outcome. Among them were moderate to severe hemiparesis in 14 (78%), recurrent strokes in seven (39%), and one death. Poor outcome was evident early in their clinical course. Independent of outcome, lipid abnormalities including an elevated triglyceride and low-density lipoprotein cholesterol, and a depressed high-density lipoprotein cholesterol were seen in one third of all patients. A depressed ratio of apolipoprotein A-1 to apolipoprotein B (using adult normative values) was seen in half of the entire cohort. Clinical features of children with unexplained ischemic strokes at presentation and their subsequent course are described. Significant risk factors for a poor outcome include (1) persistence of hemiparesis 1 month after the stroke, (2) cortical as opposed to subcortical location, and (3) bilateral occlusive disease with telangiectasia on cerebral angiography. Previously described risk factors for an unfavorable prognosis, including occurrence during infancy and presentation with seizures, were not substantiated. Lipid abnormalities occur at an increased frequency in children after unexplained ischemic strokes. Prospective assessment of lipoprotein profiles are needed to further assess clinical significance. Assessing apolipoproteins may provide further insight than lipid values alone.
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PMID:Natural history, prognosis, and lipid abnormalities of idiopathic ischemic childhood stroke. 880 16

Despite dramatic improvement in treatments for reducing risk for coronary heart disease (CHD), it is still the leading cause of mortality in the developed world. In the past decade, a major improvement in reducing low-density lipoprotein (LDL) cholesterol has been achieved with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins). This approach has been shown to be beneficial in both primary and secondary prevention of CHD. On the other hand, while a reduced high-density lipoprotein (HDL) cholesterol level is an independent CHD risk factor, no HDL cholesterol goal has yet been established. The Helsinki Heart Study and the Veterans Affairs High-density Lipoprotein Intervention Trial documented that increasing HDL cholesterol with gemfibrozil significantly decreases coronary events or stroke in CHD patients either with elevated non-HDL cholesterol or normal LDL cholesterol levels plus low HDL cholesterol. Investigations with statins have focused on their efficacy not only in significantly decreasing total cholesterol, LDL cholesterol, and triglyceride levels but also in increasing HDL cholesterol concentrations. The two different classes of drugs (statins and fibrates) have different effects on the various HDL subspecies. As new members of these drug classes and other novel drugs are emerging, there is interest in clarifying whether HDL is only a bystander (an indicator for other CHD risk factors) or it has an active role in the development of CHD. If HDL has an active role, there is a need to determine if any HDL subspecies are protective. It is now clear that HDL plays a pivotal role in cellular cholesterol efflux via the interaction of apolipoprotein A-I with the ATP binding cassette transporter A-1. Thereafter the cholesterol is esterified by lecithin:cholesterol acyltransferase; HDL is remodeled by cholesterol ester transfer protein (CETP) and hepatic lipase. The cholesterol in HDL can either be transferred to apolipoprotein B-containing particles via CETP or delivered directly to the liver with the help of scavenger receptor B1.
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PMID:HDL in atherosclerosis: actor or bystander? 1271 34

Systemic Lupus Erythematosus (SLE) is an autoimmune disorder affecting multiple organ systems. Treatment of the disease has contributed dramatically in the long-term survival of the patients and now SLE has become a chronic inflammatory disorder. Present data suggest 5, 10 and 20-year survival rates of 93%, 85% and 68% respectively. Accelerated atherosclerosis and early coronary artery disease have become important causes of death and hospitalisation in SLE patients. Many cardiovascular risk factors can be considered: disease activity (particularly kidney involvement), sedentary life (in nearly 70% of the patients), hyperlipidemia, antiphospholipid antibodies, serum homocysteine and many others. Although traditional risk factors are operative in patients with SLE, the risk for myocardial infarction was increased 8.3 folds after controlling these factors in a study, suggesting that SLE itself was the strongest risk factor for cardiovascular disease. Lipid abnormalities may play a major role in increasing cardiovascular risk in SLE patients who are characterized by elevated triglycerides, very low-density lipoprotein cholesterol (VLDL-C), reduced levels of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (Apo) A-1. Anticardioli-pin antibodies may influence lipid levels in SLE; in particular SLE patients with IgG anticardiolipin antibodies had significantly lower HDL-C compared with patients with no anticardiolipin antibodies. Elevation of serum homocysteine is observed in 15% of SLE patients and is significantly associated with the development of stroke and arterial thrombotic events. The antiphospholipid syndrome (APS) is an acquired thrombotic disorder characterised by recurrent venous or arterial thrombosis or recurrent miscarriages, or both, associated with the presence in the serum of IgG or IgM anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LAC). APS may occur as a primary disorder (PAPS) or associated with connective tissue diseases, mainly systemic lupus erythematosus (secondary APS). Primary and secondary APS are both associated with a significant increase of cardiovascular risk.
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PMID:[Cardiovascular risk factors in systemic lupus erythematosus and in antiphospholipid syndrome]. 1285 54

Whole-blood viscosity appears to be an independent predictor of stroke, carotid intima-media thickening, and carotid atherosclerosis. The purpose of this study was to examine for relationships between whole-blood viscosity and blood lipids in young healthy subjects over a range of shear rates. Twenty-seven healthy men and women aged 10 to 25 years having a range of low-density lipoprotein (LDL) cholesterol values 88 to 258 mg/dL and body mass index z scores -1.18 to 2.64 SDs were studied. Whole-blood viscosity at shear rates from 1 to 1000 per second was measured using an automated capillary viscometer. Blood lipids were measured using standard techniques. Triglyceride-rich lipoproteins were isolated by ultracentrifugation at density of <1.020 g/mL, and a high ratio of cholesterol to triglyceride was used as an indicator of lipoprotein remnants. Whole-blood viscosity at shear rates of 100 to 1000 per second showed significant negative correlations with apolipoprotein A-1, but not with high-density lipoprotein cholesterol. Whole-blood viscosity at a shear rate of 1000 per second correlated with LDL cholesterol and inversely with LDL size. On stepwise multivariate analysis, apolipoprotein A-1 accounted for 14.7% of the variation in whole-blood viscosity at a shear rate of 150 per second. This study points to the importance of high-density lipoprotein particle number on whole-blood viscosity at physiological shear rates. The physiological significance of the relationships between whole-blood viscosity and LDL cholesterol and LDL particle size at a very high shear rate remains to be determined.
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PMID:The influence of lipoproteins on whole-blood viscosity at multiple shear rates. 1593 11

Cardiovascular diseases are major causes of mortality and disease in the Indian subcontinent, causing more than 25% of deaths. It has been predicted that these diseases will increase rapidly in India and this country will be host to more than half the cases of heart disease in the world within the next 15 years. Coronary heart disease and stroke have increased in both urban and rural areas. Case-control studies indicate that tobacco use, obesity with high waist:hip ratio, high blood pressure, high LDL cholesterol, low HDL cholesterol, abnormal apolipoprotein A-1:B ratio, diabetes, low consumption of fruits and vegetables, sedentary lifestyles and psychosocial stress are important determinants of cardiovascular diseases in India. These risk factors have increased substantially over the past 50 years and to control further escalation it is important to prevent them. National interventions such as increasing tobacco taxes, labelling unhealthy foods and trans fats, reduction of salt in processed foods and better urban design to promote physical activity may have a wide short-term impact.
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PMID:Epidemiology and causation of coronary heart disease and stroke in India. 1808 49

ApoA-1 (apolipoprotein A-1) is the main component of HDL (high-density lipoprotein) and stabilizes PON-1 (paraoxonase-1), which prevents lipid peroxidation and oxLDL (oxidized low-density lipoprotein) formation. Autoantibodies against apoA-1 [anti-(apoA-1) IgG] have been found in antiphospholipid syndrome and systemic lupus erythematosous, two diseases with an increased risk of thrombotic events, as well as in ACS (acute coronary syndrome). OxLDL levels are also elevated in these diseases. Whether anti-(apoA-1) IgGs exist in other prothrombotic conditions, such as APE (acute pulmonary embolism) and stroke, has not been studied and their potential association with oxLDL and PON-1 activity is not known. In the present study, we determined prospectively the prevalence of anti-(apoA-1) IgG in patients with ACS (n=127), APE (n=58) and stroke (n=34), and, when present, we tested their association with oxLDL levels. The prevalance of anti-(apoA-1) IgG was 11% in the ACS group, 2% in the control group and 0% in the APE and stroke groups. The ACS group had significantly higher median anti-(apoA-1) IgG titres than the other groups of patients. Patients with ACS positive for anti-(apoA-1) IgG had significantly higher median oxLDL values than those who tested negative (226.5 compared with 47.7 units/l; P<0.00001) and controls. The Spearman ranked test revealed a significant correlation between anti-(apoA-1) IgG titres and serum oxLDL levels (r=0.28, P<0.05). No association was found between PON-1 activity and oxLDL or anti-(apoA-1) IgG levels. In conclusion, anti-(apoA-1) IgG levels are positive in ACS, but not in stroke or APE. In ACS, their presence is associated with higher levels of oxLDL and is directly proportional to the serum concentration of oxLDL. These results emphasize the role of humoral autoimmunity as a mediator of inflammation and coronary atherogenesis.
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PMID:Anti-(apolipoprotein A-1) IgGs are associated with high levels of oxidized low-density lipoprotein in acute coronary syndrome. 1808 36

Many mechanisms contribute to the complex pathophysiology of sickle cell disease (SCD), with dysfunction of the vascular endothelium as a unifying theme. Specifically, hemolysis-associated low arginine and nitric oxide (NO) bioavailability, amplified by NO synthase uncoupling, elevated arginase activity, superoxide production, oxidative stress, accumulation of arginine analogs such as asymmetric dimethylarginine, ischemia-reperfusion injury, inflammation, apolipoprotein A-1 depletion, and a hypercoagulable state are significant mechanisms contributing to endothelial dysfunction. Genetic polymorphisms also influence disease severity. Clearly the variable spectrum of disease is the consequence of multiple events and genetic susceptibility that go beyond the occurrence of a single amino acid substitution in the beta globin chain of hemoglobin. Recent studies begin to demonstrate overlap among these seemingly unrelated processes. Impaired NO bioavailability represents the central feature of endothelial dysfunction, and is a common denominator in the pathogenesis of vasculopathy in SCD. The consequences of decreased NO bioavailability include endothelial cell activation, upregulation of the potent vasoconstrictor endothelin-1, vasoconstriction, platelet activation, increased tissue factor, and activation of coagulation, all of which ultimately translate into the clinical manifestations of SCD. Evidence supporting vasculopathy subphenotypes in SCD, including pulmonary hypertension, priapism, cutaneous leg ulceration, and stroke, will be reviewed and relevance to other hemolytic disorders including the thalassemia syndromes will be considered.
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PMID:Mechanisms of vasculopathy in sickle cell disease and thalassemia. 1907 78

We aimed at challenging the prognostic accuracies of myeloperoxidase (MPO) and antibodies anti-apolipoprotein A-1 (anti-apoA-1 IgG), alone or in combination, for major adverse cardiovascular events (MACE) prediction, one year after carotid endarterectomy (CEA). In this prospective single centre study, 178 patients undergoing elective CEA were included. Serum anti-apoA-1 IgG and MPO were assessed by enzyme-linked immunosorbent assay prior to the surgery. Post-hoc determination of the MPO cut-off was performed by receiver operating characteristics (ROC) analyses. MACE was defined by the occurrence of fatal or non-fatal acute coronary syndromes or stroke during one year follow-up. Prognostic accuracy of anti-apoA-1 IgG was assessed by ROC curve analyses, survival analyses and reclassification statistics. During follow-up, 5% (9/178) of patients presented a MACE, and 29% (52/178) were positive for anti-apoA-1 IgG. Patients with MACE had higher median MPO and anti-apoA-1 IgG levels at admission (p=0.01), but no difference for the 10-year global Framingham risk score (FRS) was observed (p=0.22). ROC analyses indicated that both MPO and anti-apoA-1 IgG were significant predictors of subsequent MACE (area under the curve [AUC]: 0.75, 95% confidence interval [95%CI]: 0.61-0.89, p=0.01; and 0.74, 95%CI: 0.59-90; p=0.01), but combining anti-apoA-1 IgG positivity and MPO>857 ng/ml displayed the best predictive accuracy (AUC: 0.78, 95%CI: 0.65-0.91; p=0.007). It was associated with a poorer MACE-free survival (98.2% vs. 57.1%; p<0.001, LogRank), with a positive likelihood ratio of 13.67, and provided incremental predictive ability over FRS. In conclusion, combining the assessment of anti-apoA-1 IgG and MPO appears as a promising risk stratification tool in patients with severe carotid stenosis.
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PMID:Serum levels of anti-apolipoprotein A-1 auto-antibodies and myeloperoxidase as predictors of major adverse cardiovascular events after carotid endarterectomy. 2336 7

We investigated the activation and pathophysiological roles of indoleamine 2,3-dioxygenase (IDO) and kynurenine aminotransferase (KAT) in patients with ischemic stroke. Patients were recruited from the acute stroke unit of a general hospital within 24 hours post-stroke. The immune transmission turbidity method was used to determine the concentration of serum high-sensitivity C-reactive protein (hsCRP), apolipoprotein A-1 and apolipoprotein B. The concentrations of triglyceride, cholesterol, high density lipoprotein (HDL), low density lipoprotein and non-esterified fatty acids were determined using an enzymatic method. Tryptophan (TRP), kynurenine (KYN) and kynurenine acid (KYNA) concentrations were determined by high performance liquid chromatography. The National Institutes of Health Stroke Scale (NIHSS) was used to assess the neurological deficits at admission and 3 weeks post-stroke. The IDO and KAT activity ratio were calculated by KYN/TRP and KYNA/KYN, respectively. The correlation between hsCRP and IDO, KAT and NIHSS score was also analyzed. A total of 81 patients with ischemic stroke and 35 normal controls were recruited. Lower TRP, KYNA, HDL and KAT activity ratio were found in the stroke group compared to the control group (p<0.05). The levels of hsCRP and IDO activity ratio were much higher in the stroke group than the control group (p<0.01). The IDO activity in patients with ischemic stroke showed a positive correlation with hsCRP (r=0.425, p=0.027). In addition, hsCRP and IDO levels were positively associated with the NIHSS score both at admission and 3 weeks post-stroke. These data suggest an inflammatory response characterized by up-regulated IDO activation in ischemic stroke, which might be closely relevant to its pathophysiology.
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PMID:Serum indoleamine 2,3-dioxygenase and kynurenine aminotransferase enzyme activity in patients with ischemic stroke. 2441 93


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