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 aim of this study was to evaluate the role of lipoprotein(a) in the carotid atherosclerosis and ischemic cerebrovascular disorders. Four groups of subjects were included: 49 patients with transient ischemic attacks, 61 with acute cerebral infarction, 48 with asymptomatic carotid atherosclerosis and a group of 50 healthy subjects. Lipoprotein(a) serum concentration and its correlation with various clinical parameters was analysed. The results revealed a significant difference between lipoprotein(a) serum levels in patients and healthy subjects and positive correlation between lipoprotein(a) serum levels and the degree of carotid atherosclerosis. Moreover, some other correlations are found and discussed. It was concluded that lipoprotein(a) is involved in the pathogenesis of carotid atherosclerosis, but it is not associated with the development of ischemic cerebrovascular disorders.
Atherosclerosis 1993 Jan 04
PMID:Lipoprotein(a) in patients with carotid atherosclerosis and ischemic cerebrovascular disorders. 845 51

In this study, the authors examined relations between coronary and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction. They ascertained the risk factors for carotid atherosclerosis and silent cerebral infarction complicating coronary heart disease (CHD) in 77 Japanese subjects. As coronary atherosclerosis progressed, the carotid ultrasonographic score and the brain computed tomographic score increased. Multivariate analyses showed that the significant and independent risk factors for carotid atherosclerosis in patients with CHD were age (p < 0.01) and apolipoprotein (apo) B (p < 0.05) and the factors for silent cerebral infarction were age (p < 0.05) and hypertension (p < 0.05). Their study confirms a positive relation between coronary atherosclerosis and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction in patients with CHD. Their data suggest that carotid atherosclerosis should be looked for in patients with CHD who are old and have a high value of apo B, and silent cerebral infarction should be looked for in those who are old and have hypertension, to prevent complicating symptomatic cerebral vascular disease (CVD). If severe carotid atherosclerosis or silent cerebral infarction are detected, antithrombotic medication should be given.
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PMID:Risk factors for carotid atherosclerosis and silent cerebral infarction in patients with coronary heart disease. 850 8

There have been few reports concerning the characteristics of cerebral infarction associated with migraine (CIAM), and especially about the subsequent fate of these patients. We studied 14 patients (9 female) with CIAM. In all these patients the onset of cerebral infarction was accompanied by a unilateral throbbing headache, in 8 also with a gradual build-up of neurological deficits. No other cause of cerebral infarction could be found in these patients. Twelve patients had had previous attacks of migraine, with auras in 6. The nature of the neurological deficit was similar to previous auras in only 3 of these patients. The 2 patients without a history of migraine both developed migraine attacks afterwards. During the same period we also studied 14 patients (8 female) with a cerebral infarct of unknown origin (CIUO). The infarct involved the occipital lobe in 11 of the 14 patients with CIAM, whereas this occurred in 4 patients with CIUO [relative risk (RR): 2.8; 95% confidence interval (CI): 1.2-6.6]. Patients with CIAM had risk factors for atherosclerosis significantly less often than patients with CIUO (RR: 0.1; 95% CI: 0.02-0.9). The functional outcome of patients with CIAM was better than in patients with CIUO: all 14 patients with CIAM were independent in their daily activities, compared with 9 patients with CIUO (RR: 1.6; 95% CI: 1.1-2.3). No patient in either group had a recurrent stroke during a median follow-up period of 5.8 years. In conclusion, CIAM is a stroke entity causing mostly infarcts in the occipital lobe; vascular risk factors are uncommon and prognosis is generally good.
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PMID:Cerebral infarcts associated with migraine: clinical features, risk factors and follow-up. 883 40

We used ultrasonography to evaluate atherosclerotic lesions in the common carotid arteries of 147 inpatients (82 men, 65 women; mean age, 72.2 years). We sought to determine the relation between these lesions and various risk factors for atherosclerosis, as well as the utility of ultrasonography in quantitative evaluation of atherosclerotic disease. A 7.5 MHz transducer was used and atherosclerotic lesions were evaluated on the basis of the thickness of their intimal-medial complex, which we term wall thickness. The relations between these measurements and age, sex, blood pressure, smoking history, lipid metabolism, diabetes mellitus, and atherosclerotic disease were studied. Wall thickness of the common carotid arteries correlated with age (men: r = 0.45; women: r = 0.38). Brinkman Index (r = 0.25), systolic blood pressure (r = 0.44), diastolic pressure (r = 0.18), and high-density lipoprotein cholesterol (HDL-C, r = -0.23). Multiple regression analysis with these risk factors as explanatory variables showed that age, Brinkman Index, systolic blood pressure, HDL-C, and diabetes mellitus contributed significantly to increased wall thickness. Wall thickness was significantly greater in patients with atherosclerotic disease such as cerebral infarction and ischemic heart diseases. These findings indicate that appropriate treatment for multiple atherosclerotic risk factors may be necessarily in the elderly.
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PMID:[Risk factors related to the wall thickness of the common carotid artery in elderly patients]. 899 3

To clarify the neuropathologic criteria for the diagnosis of vascular dementia principally caused by large-vessel cerebral infarction, we solicited autopsy cases of vascular dementia from 10 university neuropathology laboratories. We included only those cases with progressive dementia clinically diagnosed as Alzheimer's disease (AD) or multi-infarct dementia, in whom autopsy revealed only cerebral infarction, without significant neuropathologic features of AD or other neurodegenerative disorders. Only six cases, all men, met these criteria. Each of them had, for a year or longer, gradually increasing cognitive impairment sufficient to interfere with daily activities, without clear evidence of "stepwise" progression. The age of onset of dementia was 66 years or less in five of the six patients. The duration of dementia ranged from 2 to 14 years. Five of the six cases had a history of either cerebral ischemia or acute stroke with residual focal neurologic deficits. Only two were known to have hypertension. At autopsy severe atherosclerosis of the cerebral arteries was present in three cases; two of these had a thrombotic occlusion of one internal carotid artery and one had partial obstruction of other cerebral arteries. In five of six brains, gross infarctions were present involving the thalamus, caudate, putamen, or large portions of the frontal, parietal, and temporal lobes of one or both hemispheres. Vascular amyloid was absent in all but one of these five brains. In four cases, the dementia was clinically indistinguishable from AD except for a history of focal neurologic deficits. The difficulty encountered in finding large numbers of cases of VaD without coexisting neuropathologic evidence of AD suggests that "pure" vascular dementia is very uncommon.
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PMID:Clinical-neuropathologic findings in multi-infarct dementia: a report of six autopsied cases. 940 94

The predictive value of transesophageal echocardiography was investigated for the risk stratification of atherothrombotic or embolic cerebral infarction in patients with atrial fibrillation. Left atrial spontaneous echo contrast, peak flow velocity in the left atrial appendage and generalized atherosclerosis as estimated by the intima-media wall thickness of the thoracic aorta were assessed by transesophageal echocardiography in consecutive patients with paroxysmal (n = 25) or chronic (n = 60) atrial fibrillation (mean [+/-SD] age; 63 +/- 11 years). All patients underwent brain computed tomography or magnetic resonance imaging to evaluate the presence or absence of cerebral infarction. The location of cerebral infarction was divided into two territories, the cortical branch (cortical infarction) and deep perforators (perforating infarction), to evaluate embolic and atherothrombotic cerebral infarction, respectively. Cortical and perforating infarctions were found in 42% and 16% of all patients, respectively. The grade of spontaneous echo contrast was higher in patients with cortical infarction than in those without cortical infarction. Patients with perforating infarction showed thicker aortic wall compared with patients without perforating infarction. Other parameters had no predictive value to differentiate perforating from cortical infarctions. Multiple regression analysis revealed that spontaneous echo contrast and age were independent predictors of embolic cortical infarction, whereas intima-media wall thickness of the aorta and hypertension were useful in predicting the risk of atherothrombotic perforating infarction. Transesophageal echocardiography is useful for predicting embolic cortical infarction and atherothrombotic perforating infarction.
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PMID:[Transesophageal echocardiographic findings of cortical and perforating infarctions in patients with atrial fibrillation]. 921 Nov 2

The relationship between cerebrovascular disease and an insertion/deletion (I/D) polymorphism in intron 16 of the angiotensin-converting enzyme (ACE) gene is still being debated. We examined its role as a risk factor in patients with thrombotic brain infarction. The association between ACE polymorphism and ischemic stroke was examined in 181 patients with thrombotic brain infarction and 271 controls without strokes. The I/D polymorphism was examined using the polymerase chain reaction. Distributions of the ACE genotypes and alleles did not differ between the infarcted patients and the controls. Both distributions in patients with onset at age 60 years or younger were significantly higher than those in younger controls (genotype: chi 2 = 7.6, P = 0.02; allele: chi 2 = 5.6, P = 0.02). There were no significant differences in the distributions of ACE genotypes and alleles between the patients with lacunar infarcts and with cortical infarcts in all ages. There were also significant differences in the distribution of ACE genotypes and alleles between the younger and the elderly subgroup of patients with brain infarction (genotype: chi 2 = 12.9, P = 0.002; allele: chi 2 = 11.1, P = 0.0009). Furthermore, there was a significant decline in the frequency of the ACE D allele with increasing age in all patients with thrombotic brain infarction. These observations demonstrated a significant association between the ACE gene polymorphism and thrombotic brain infarction in patients age 60 years or younger in a Japanese population. Furthermore, there may be an association between the ACE D allele and mortality after cerebral infarction.
Atherosclerosis 1997 Jul 25
PMID:Polymorphism of the angiotensin-converting enzyme (ACE) gene in patients with thrombotic brain infarction. 924 59

To assess the prevalence of extracranial carotid artery atherosclerosis and its relation to principal cardiovascular risk factors in Chinese elderly patients, 100 cases aged from 54 to 94 were investigated with B-mode ultrasonography. Arterial intima-media thickening, plaque, mild stenosis (defined as a plaque that obstructed > 20% of the lumen diameter), and clinically significant stenosis (> 50% in cross-sectional area) were found in 79, 49, 40 and 3 patients, respectively. There was no significant correlation between carotid atherosclerosis and coronary heart disease, cerebral infarction, hypertension, hyperlipidemia or diabetes. In contrast, the prevalence of carotid atherosclerosis was increased with age (P < 0.05), so did the severity. Thus, age is a major risk factor for carotid atherosclerosis in the elderly.
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PMID:[The prevalence and risk factors of carotid atherosclerosis in elderly patients]. 927 42

A recent anatomical study has reported a relationship between the presence of ulcerated atheromatous plaque of the aortic arch and cerebral infarction. Several studies using transoesophageal echocardiography have established that atherothrombosis of the ascending and proximal is a potential source of systemic embolism. We have shown that aortic plaques > or = 4 mm in thickness increase the risk of cerebral infarction by 9. Several studies have shown that this localisation of atherosclerosis was also a powerful marker of general vascular risk. In the multicenter FAPS (French Study of Aortic Plaque in Stroke) trial, the authors followed up 331 patients who had suffered cerebral infarction, aged over 60 years, for a mean duration of 2.4 years. The occurrence rate of cerebral infarction and the incidence of cardiovascular complications (death, myocardial infarction, cerebral infarction, systemic embolism) was respectively 11.9% and 26% per year. The presence of plaques with thickness greater or equal to 4 mm was associated with an adjusted relative risk of 3.8 (95% confidence interval, 1.8 to 7.8) and 3.5 (95% confidence interval, 3.1 to 5.9) respectively. The influence of plaque morphology (thrombus, irregularity, absence of calcification), independently of its thickness, also seems to affect the prognosis. In this study, as in those reported by other groups, the influence of anti-thrombotic therapy was not specifically addressed. The definition of high risk plaques (thickness, irregularity, thrombus) could be useful in the evaluation of therapy which affects the atherosclerotic process (antiplatelet agents, anticoagulants, statins). We conclude that atherosclerosis of the ascending aorta and aortic arch is a potential source of systemic embolism and a powerful marker of overall vascular risk.
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PMID:[Evaluation of aortic atherosclerosis by transesophageal echocardiography. Prognostic implications]. 929 22

Hyperhomocysteinemia has been shown to constitute an independent risk factor for premature occlusive arterial disease. Moderate hyperhomocysteinemia is present in chronic uremic patients, who often develop premature atherosclerosis, but no direct evidence of an association between the occurrence of atherosclerotic cardiovascular accidents (CVAs) and hyperhomocysteinemia has yet been reported in such patients. We serially determined total plasma homocysteine (Hcy) levels in a cohort of 93 consecutive chronic renal failure, undialyzed patients (57 males, 36 females) with creatinine clearance (Ccr) < 50 ml/min.1.73 m2 and age > or = 50 years at start of follow-up, together with serial assessment of Ccr and blood lipid parameters. From January 1989 to December 1995, 24 patients (group 1) experienced myocardial infarction (18 cases, 13 males) or cerebral infarction (6 cases, 3 males) while the remaining 69 (group 2) remained free of CVAs. Patients in groups 1 and 2 did not differ with respect to age (66 +/- 1.8 vs. 65 +/- 1.1 years, mean +/- Se) or serum creatinine (227 +/- 24 vs. 251 +/- 36 mumol/l) at onset of a CVA (group 1) or at the end of follow-up (group 2). The mean Hcy level was significantly higher in group 1 (20.7 +/- 1.6 vs. 12.8 +/- 0.5 mumol/l, p < 0.0001), as was the proportion of patients with Hcy in excess of 14 mumol/l, the upper limit in healthy controls (83 vs. 30%, p < 0.0001). Logistic regression analysis identified Hcy as an independent risk factor for CVA, with an odds ratio of 11.4 (95% confidence interval 3.5-37.7), which remained significant after adjustment on other variables. We conclude that an elevated Hcy level is associated with a risk of occlusive arterial accidents in patients with chronic renal failure and that hyperhomocysteinemia contributes to the accelerated atherosclerosis complicating chronic uremia.
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PMID:Hyperhomocysteinemia is associated with atherosclerotic occlusive arterial accidents in predialysis chronic renal failure patients. 938 10


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