Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purposes of this study are to (1) demonstrate the association of elongations of the internal carotid artery (ICA), that is, kinking, coiling, tortuousity, and angulation, and the neurologic symptoms with high stroke risk; (2) compare the results of the surgical treatment versus the medical treatment alone; (3) contribute to the knowledge of the natural history of these anatomical particularities. From January 1992 to December 1994, 113 patients with ICA kinking, coiling, tortuousity, and angulation were randomized either to surgery (group I, n = 55) or not (group II, n = 58). Patients, who presented a carotid hemodynamically significant lesion (>60%) at the origin and associated distal elongation were excluded. The groups were comparable with regard to sex, age, risk factors for atherosclerosis, associated diseases, symptoms and anatomic feature of the contralateral ICA. Follow-up was obtained in all patients: it consisted of clinical evaluation and Duplex scan control at 3-month intervals during the follow-up period (6-36 months; average, 23). Histologic specimens were obtained in all surgically treated arteries. Early results were excellent: in group I, no patient died, no patient presented major or minor stroke. Only one patient had an immediate transient ischemic attack (TIA) which spontaneously recovered within 24 hours. All symptomatic patients examined the complete disappearance of clinical signs. There were no late deaths due to stroke and no late major or minor neurologic deficit occurred. All reconstructed ICAs were patent. In group II, three patients experienced a major stroke with hemiplegia due to ICA occlusion. Most of the symptomatic patients (37) of group II remained stable, while seven of them had worsening of symptoms and were referred for surgery. To conclude, all surgically treated patients had the complete relief of preoperative neurologic symptoms; none of the medically treated patients had an improvement. Although there was no statistically significant difference between the two groups with regard to stroke risk, three medically treated patients progressed to total occlusion. This suggests that kinking, coiling, tortuousity, and angulations of the ICA are not merely an anatomic curiosity but a potentially disabling, even fatal condition.
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PMID:The elongation of the internal carotid artery: early and long-term results of patients having surgery compared with unoperated controls. 918 65

The purpose of this study was to determine the prevalence and degree of carotid disease in patients with premature lower-extremity atherosclerosis. Seventy-six young men (mean age at onset of symptoms 42+/-0.5 years with premature lower extremity atherosclerosis who underwent complete carotid duplex scans were studied. The mean lowest ankle: brachial index was 0.49+/-0.02. Forty-seven patients (62%) required interventions to treat advanced leg symptoms, and 18 (24%) experienced disease progression during the study period. Carotid duplex scans showed internal carotid occlusions in eight (11%); advanced or critical plaque disease (60-99% diameter loss) in 14 (18%); moderate plaque disease (40-59% diameter loss) in 16 (21%); mild plaque disease (intimal thickening or 1-39% diameter loss) in 18 (24%); and normal carotid arteries in 20 (26%). Comparing the 20 subjects with normal carotid arteries to the S6 with any evidence of disease, there were no differences in age of onset, risk factors, coronary artery disease, mean ankle: brachial index, number of interventions, disease progression, amputation, or death. Fifteen (27%) of the patients with carotid atherosclerosis ultimately developed transient ischemic attack or stroke; 13 of these had advanced carotid stenoses or carotid occlusions. In conclusion, carotid plaque disease is prevalent among patients with premature atherosclerosis of the lower extremity. The presence of carotid atherosclerosis is not related to the degree of lower extremity atherosclerosis, nor to the rate of disease progression. Carotid duplex scans are indicated to screen these young patients for compelling lesions that might warrant prophylactic carotid endarterectomy.
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PMID:Utility of carotid duplex in young adults with lower extremity atherosclerosis: how aggressive should we be in screening young patients? 935 Jul 97

This study tested the hypothesis that stroke patients without a cardiac source of embolism suspected by clinical examination can be risk stratified by transesophageal echocardiography. Forty ischemic stroke patients without atrial fibrillation, prosthetic valves, ejection fraction < 20%, or recent myocardial infarction underwent multiplane transesophageal echocardiography: 24 (designated high risk) had > or = 1 of the following: left heart thrombus, vegetation, mass or spontaneous echo contrast, mobile ascending aortic or arch debris, patent foramen ovale, atrial septal defect or aneurysm, mitral annular calcification, mitral valve thickening, prolapse or mitral valve strands. End points were death, recurrent stroke, transient ischemic attack, myocardial infarction or peripheral embolism. Thirty-eight patients (95%) (23 high, 15 low risk) were followed for 14 +/- 8 months: 9 (24%) died of vascular causes including 4 who had a cardiac cause of death and 5 who had fatal strokes. Eight had recurrent strokes (4 nonfatal) and 1 nonfatal myocardial infarction occurred. Cardiovascular survival was predicted by transesophageal echocardiography: survival rates were 92% (low risk) and 63% (high risk) at 24 months (p = 0.036). Left atrial enlargement was independently associated with death from stroke (fatal stroke occurred in 25% of those with atrial enlargement compared to 8% of those with normal atrial dimension, p < or = 0.03), as was left atrial spontaneous echo contrast (50% died vs 9% without contrast, p < or = 0.03). Left ventricular hypertrophy and aortic atherosclerosis were both associated with the risk of recurrent stroke (30% of patients with ventricular hypertrophy had recurrent stroke compared to 10% with normal wall thickness (p < or = 0.05); 30% with aortic atherosclerosis had a recurrent stroke compared to none with a normal aorta (p < or = 0.05). Thus, transesophageal echocardiography clearly identifies patients at a high risk for cardiovascular mortality and morbidity after stroke despite an unsuspected source of embolism by clinical examination.
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PMID:Usefulness of transesophageal echocardiography in predicting mortality and morbidity in stroke patients without clinically known cardiac sources of embolus. 960 57

DNA polymorphisms in genes encoding apolipoproteins (apo) A-I, C-III, B and E and angiotensin-converting enzyme (ACE) have been proposed to be associated with the risk of coronary artery disease (CAD). We studied whether the same genetic markers would also be associated with the occurrence and extent of atherosclerosis in cervical arteries. DNA samples from 234 survivors of stroke or a transient ischaemic attack aged 60 years or less were examined. The presence of atherosclerosis was assessed using aortic arch angiograms. The SstI polymorphism of apoA-I/C-III gene locus, the XbaI polymorphism of apoB gene, common apoE phenotypes and the insertion/deletion polymorphism of the ACE gene were analysed. The allele frequencies of the apoA-I/C-III, apoB, apoE or ACE gene did not differ between the groups with (n = 148) or without (n = 85) cervical atherosclerosis. However, when patients with at least one apoE4 allele and one X2 allele of apoB were combined and compared with those without either of them (E2E3 or E3E3 and X1X1), a significant association with the presence of cervical atherosclerosis was found (P = 0.03). The patients having the E2E3 phenotype had a significantly elevated serum triglyceride level compared with those with the E3E3 phenotype (P = 0.03). Serum high-density lipoprotein (HDL) cholesterol was lower in the patients with the E2E3 phenotype than in those with the E3E3 and E3E4 (P = 0.01 and P = 0.06, respectively). The apoB or ACE genotypes were not significantly associated with serum lipid or lipoprotein levels. There was no association between the ACE gene polymorphism and the occurrence of hypertension. In conclusion, the interaction of common apoB and apoE alleles may increase the risk of atherosclerosis in cervical arteries.
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PMID:Genetic risk factors and ischaemic cerebrovascular disease: role of common variation of the genes encoding apolipoproteins and angiotensin-converting enzyme. 966 3

Inflammatory mediators secreted by activated leukocytes play a role in the pathogenesis of atherosclerosis. They may also affect the production of vasodilatory and platelet antiaggregatory factors such as nitric oxide (NO) and prostacyclin (PGI2) from the vascular endothelium. Production of NO and PGI2, the effecs of which are mediated by cyclic 3',5'-guanosine monophosphate (cGMP) and cyclic 3',5'-adenosine monophosphate (cAMP), respectively, is disturbed in atherosclerosis, whereas increased NO levels have been found in acute cerebral ischemia. To investigate leukocyte activation and its possible influence upon endothelial function in cerebral ischemia we measured plasma neutrophil gelatinase-associated lipocalin (NGAL) and soluble tumor necrosis factor receptor protein-1 (sTNFR-1) by ELISA, and intraplatelet cAMP and cGMP by radioimmunoassay in 59 patients with acute ischemic stroke or transient ischemic attack (mean age 71 years, 27 males) and after a 1-year follow-up in 57/59 (97%) patients. NGAL (152 +/- 58 vs. 126 +/- 48 microgram/l), sTNFR-1 (3.50 +/- 2.2 vs. 2.59 +/- 1.31 microgram/l), and cAMP (5.12 +/- 1.71 vs. 4.06 +/- 0.92 pmol/10(9) platelets) were higher (p < 0.001) after follow-up than in acute cerebral ischemia. At follow-up sTNFR-1 and cGMP partially correlated (r = 0.31; p < 0.05), controlling for age and platelet count. In conclusion, plasma NGAL and sTNFR-1 and intraplatelet AMP increase after acute cerebral ischemia, indicating chronic inflammatory activity and endothelial activation. Plasma sTNFR-1 levels are related to intraplatelet cGMP levels.
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PMID:Increasing levels of leukocyte-derived inflammatory mediators in plasma and cAMP in platelets during follow-up after acute cerebral ischemia. 977 47

Nine patients (group A) were found on magnetic resonance angiography (MRA) to have excessive carotid artery, vertebral artery, and vertebrobasilar junction tortuosity. A control group (group B) were age- and sex-matched to group A patients, were selected randomly from our MRA or stroke data banks, and had not undergone MRA for evaluation of migraine, "carotidynia," or pulsatile tinnitus. Factors more prevalent in group A patients included migraine, chronic daily headache, carotidynia, pulsatile tinnitus, and a positive family history of headache. Factors more prevalent in group B patients included a positive family history of stroke, large-vessel atherosclerosis, and scan evidence of ischemic infarctions; many group B patients had undergone MRA for stroke or transient ischemic attack evaluation. Men were slightly underrepresented at 44%, and were younger than women (34 +/- 6 years vs. 43 +/- 3 years; p = 0.01). Relationships in this preliminary study between arterial tortuosity and migraine seem evident.
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PMID:Tortuosity of carotid and vertebral arteries: a magnetic resonance angiographic study. 978 Aug 56

Carotid endarterectomy (CEA) is one of the most commonly used surgical methods in the treatment of cerebral stroke with both therapeutic and also prophylactic implications. CEA has been used in surgical practice for 40 years. At the beginning it was very popular and was widely used. Later, the opposite extreme was reached, and its therapeutic efficacy was denied unjustifiably. However, at the beginning of the ninetieth three large controlled studies were completed (North American Symptomatic Carotid Endarterectomy Trial, European Carotid Surgery Trial and Veterans Administrations Symptomatic Trial) and the results of these trials were the basis for establishing the solid criteria for the surgical procedure in some groups of symptomatic patients with stenosis of the internal carotid artery. Thus, CEA was in again. In accordance with the attitudes of the American Association Ad Hoc Committee (1995), evidenced indications for CEA in patients with symptomatic stenosis of the internal carotid artery (in the group with surgical risk less than 6%) include (a) single or recurrent episodes of TIA in the last 6 months, "crescendo" TIA combined with carotid stenosis > 70% with or without plaque ulceration, with or without antiplatelet therapy, and (b) mild stroke in last 6 months with carotid stenosis > 70% with or without plaque ulceration, with or without antiplatelet therapy. The authors report their experience and results of a six-month pilot study of 301 patients, of whom 248 were operated on for symptomatic carotid stenosis with low combined perioperative morbidity and mortality (0.6%). Also, indications for surgical reconstruction of carotid and coronary arteries in patients with marked signs of atherosclerosis in both arterial systems are discussed.
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PMID:[Indications for carotid endarterectomy in patients with symptoms: when, where?]. 986 92

Release of inflammatory mediators from leukocytes and endothelial release of vasoactive factors are both important in the pathogenesis of atherosclerosis. To evaluate the concentrations of a specific marker for macrophage activation, neopterin, and the potent endothelial derived vasoconstrictive peptide endothelin-1 (ET-1), during the acute and chronic stages of cerebral ischemia, plasma concentrations of neopterin and ET-1 were measured in 59 patients with acute cerebral infarction or transient ischemic attack (median age 73 years, range 43-93, 27 men) and after a 1-year follow-up in 57/59 (97%) of patients. Plasma neopterin was higher at follow-up (6.3 nmol/L [3.7-21.6] vs 5.6 nmol/L [3.5-17.2]; p < 0.05) than at the acute stage, whereas the plasma ET-1 concentration was unchanged. Plasma concentrations of both neopterin and ET-1 correlated directly with age both in the acute stage (r = 0.42 and r = 0.35, respectively; p < 0.01) and after follow-up (r = 0.34; p < 0.05 and r = 0.27; p = 0.05, respectively). In conclusion, plasma neopterin increased after acute cerebral ischemia, indicating chronic inflammatory activity and continuous macrophage activation in ischemic cerebrovascular diseases.
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PMID:Increasing plasma neopterin and persistent plasma endothelin during follow-up after acute cerebral ischemia. 992 83

Moderately elevated plasma homocysteine levels have been established as an independent risk factor for atherosclerosis and its complications, including cerebrovascular disease. A common mutation (C677T) in the gene encoding for the enzyme methylenetetrahydrofolate reductase (MTHFR) has been linked to increased plasma homocysteine levels in homozygous carriers, particularly in the presence of low folate levels. However, the results of most of the previous studies suggest that the C677T MTHFR mutation is not a significant risk factor for arterial disease. This discrepancy might, at least partly, be due to the fact that plasma homocysteine levels are influenced by several other factors, including age, gender, renal function, and vitamin status. We investigated the relation between plasma homocysteine levels, the C677T MTHFR mutation, and these other factors in a population of 96 patients with transient ischemic attacks or minor strokes and in 96 age- and sex-matched healthy control subjects. We further tested the value of a multivariate model for the prediction of plasma homocysteine levels under particular consideration of the MTHFR mutation status. In the patients, plasma homocysteine levels were significantly higher than in the healthy control subjects. With regard to the MTHFR mutation, the distribution of the C/C, C/T, and T/T genotypes was not significantly different between patients and healthy control subjects. Univariate (linear regression) analysis revealed significant (positive) correlations between plasma homocysteine levels on the one hand and age and creatinine on the other, the latter particularly in subjects with creatinine levels in the upper quartile. Significant (negative) correlations were found between plasma homocysteine levels, vitamin B12, and folate levels. However, these relations could much better be expressed by means of a multiplicative regression model. T/T subjects exhibited slightly higher homocysteine levels than C/C and C/T subjects; however, the differences between the 3 genotypes were not significant. Multivariate (stepwise regression) analysis revealed age, vitamin B12 levels, folate levels, and creatinine levels as significant independent variables influencing plasma homocysteine levels, whereas the MTHFR mutation status and gender were removed from the model. Considering all 192 subjects, only 28.8% of the variance of plasma homocysteine levels could be accounted for by the model. However, in homozygous carriers of the MTHFR mutation, the predictive power of the model is very high, explaining 76.1% of the variance of plasma homocysteine levels. According to our results, the C677T mutation does not constitute a major risk factor for transient ischemic attack or minor stroke, even under consideration of other possibly confounding factors that are known to affect plasma homocysteine levels. However, it is possible to predict plasma homocysteine levels in homozygous carriers of the mutation with high accuracy. The knowledge of the MTHFR mutation status may therefore help to identify subjects at high risk for hyperhomocysteinemia.
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PMID:Genetic and nongenetic factors influencing plasma homocysteine levels in patients with ischemic cerebrovascular disease and in healthy control subjects. 1036 Jun 32

Ischemic stroke, myocardial infarction and peripheral arterial disease are different clinical manifestations commonly due to the same underlying disease, i.e. atherosclerosis with subsequent thrombosis/embolism (atherothrombosis). Many clinical trials of secondary prevention after stroke or TIA have evaluated the benefit of long-term use of antiplatelet drugs in reducing the risk of subsequent vascular events. Aspirin and triclopidine have been shown to be effective in placebo-controlled studies for the composite outcome of stroke, myocardial infarction, or vascular death. Contrasting with these benefits, there were potentially serious, though rare, adverse effects. These considerations certainly justify the development of new antiplatelet agents. Clopidogrel is a new ADP-receptor antagonist, with a greater activity in animal models of thrombosis. CAPRIE (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events) was a randomized, blinded, international trial designed to assess the relative efficacy of clopidogrel and aspirin in reducing the risk of the outcome cluster of ischemic stroke, myocardial infarction, or vascular death, as well as to assess their relative safety. 19,185 patients were recruited. The intention-to-treat analysis showed that the relative risk reduction was 8.7% (95% CI 0.3-16.5, p = 0.043) in favor of clopidogrel from an overall annual event rate of ischemic stroke, myocardial infarction, or vascular death, ranging from 5.83% in the aspirin group to 5.33% in the clopidogrel group. The percentage of adverse events reported was higher in the aspirin group for all categories except rash, diarrhea, and abnormal liver function. It seems likely that clopidogrel will replace ticlopidine for stroke prevention, because of its better safety profile, and comparable efficacy. Clopidogrel probably will not replace aspirin as the first line therapy for many clinicians because of its higher cost and lack of widespread experience. However, other clinicians have already decided that they will use clopidogrel as first choice, because of the significant advantage over aspirin demonstrated in the CAPRIE study.
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PMID:Clopidogrel for cerebrovascular prevention. 1047 7


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