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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

Autologous fat injection for soft tissue augmentation in the face is claimed to be a safe procedure. However, there are several case reports in the literature where patients have suffered from acute visual loss and cerebral infarction following fat injections into the face. Acute visual loss after injection of various substances into the face is a well-known complication of such interventions. We report two further patients who suffered from ocular and cerebral embolism after fat injections into the face. For the intravasation of fat particles there are three preconditions: well-vascularized tissue, fragmentation of parenchyma, and, especially, a local increase in pressure in the affected tissue. Fat injections into the face lead to an acute local increase in pressure in highly vascularized tissue. We assume that fragments of fatty tissue reach ocular and cerebral arteries by reversed flow through branches of the carotid arteries after they are introduced into facial vessels. The manifestation of fat embolism appears either immediately after the fat injection or after a latency period. Fat embolism can remain subclinical and may not be recognized, or the clinical features may be misinterpreted. To minimize the risk of such a major complication, fat injections should be performed slowly, with the lowest possible force. One should avoid fat injections into pretraumatized soft tissue, for example, after rhytidectomy, because the risk of intravasation of fat particles may be higher. Metabolic disturbances such as hyperlipidemia may also contribute to the clinical manifestation of fat embolism Routine funduscopic examinations after fat injections into the face could help to provide data for future estimation of the patient's general risk.
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PMID:Autologous fat injection for soft tissue augmentation in the face: a safe procedure? 961 80

We attempted to clarify the temporal profile and the predisposing factors for progressing neurological disorders in the patients with acute cerebral infarction in the territory of the deep perforators of the carotid system. The subjects were 19 patients with mild hemiparesis admitted to our hospital within 24 hours of stoke onset, and their mean age was 59.9 +/- 9.1. Six of those patients (about 32%) had gradual neurological deterioration after admission (progressive cases), and they had poor outcome compared with non-progressing patients. The mean progressing period was 3.7 +/- 1.0 days. Our examination suggest that both the changes in systemic hemodynamics and the risk factors for cerebrovascular disease (hypertension, diabetes mellitus, hyperlipidemia) do not always provide a correlation with the development of progressing stroke. However, we speculate that the impairment of the microcirculation plays a major role in progressing stroke in the territory of penetrating arteries because of the result that the mean infarct size of progressive patients had a tendency to be larger than that of non-progressive patients in the chronic stage.
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PMID:[Clinical course of acute deep infarcts in carotid system--pathogenesis of progressing stroke]. 1065 39

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

We reported a 68-year-old man with anti-phospholipid antibody syndrome who presented slowly progressive pure motor monoparesis(PMM) in left upper extremity as a sign of cerebral infarction. He had history of hypertension and hyperlipidemia. He first noticed clumsiness in left fingers, then weakness of left fingers with drop hand developing gradually in 2 to 6 weeks. He began to feel difficulty in raising left upper arm in 8 weeks and was admitted to our hospital. On admission, he exhibited severe weakness in distal portion and moderate weakness in proximal portion of left upper extremity. Deep tendon reflexes were slightly hyperactive in left side. Muscle strength of right upper extremity and bilateral lower extremities were normal. There was no sensory and autonomic abnormality. Laboratory examination revealed high titer of anti-cardiolipin IgM antibody. Brain MRI demonstrated a small cortical infarction in the right precentral gyrus. Cerebral angiography revealed severe stenosis in right common carotid artery. Other examinations including EMG were unremarkable. PMM in left upper extremity was considered to be caused by the ischemic lesion in the precentral motor cortex. Slowly progressive course might be explained by the hypovolemic factor due to the marked stenosis in right common carotid artery, poor collateral circulation, and abnormal coagulation caused by anti-phospholipid antibody syndrome.
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PMID:[A case of antiphospholipid antibody syndrome with cerebral infarction showing slowly progressive pure motor monoparesis in unilateral upper extremity]. 1121 63

Obesity causes many undesirable health disorders such as diabetes mellitus, hyperlipidemia, hypertension and so on. Recently, those life style-affecting diseases is increasing, especially the increment of diabetes mellitus is prominent. In 2000, Japan obesity society issued the new standard of the evaluation of obesity and new diagnostic criteria of obesity as a disease for Japanese. According to this issue, obesity was evaluated by body mass index(BMI). And, 18.5 < BMI < 25 is normal, 25 < BMI < 30 is obese 1, 30 < BMI < 35 is obese 2, 35 < BMI < 40 is obese 3, and 40 < is obese 4. Obesity as a disease is defined by two cases. The first category is composed of two items; one is BMI > 25, and the other is having one disease worsen by obesity, such as diabetes mellitus, hyperlipidemia, hypertension, hyperuricemia, coronary heart disease, cerebral infarction, sleep apnea syndrome, fatty liver, deformative arthritis. The second category is the visceral type of obesity with BMI > 25, which was diagnosed by west size, over 85 cm for men, and over 90 cm for women, and by visceral fat area over 100 cm2 in abdominal CT.
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PMID:[Evaluation of obesity and diagnostic criteria of obesity as a disease for Japanese]. 1126 12

To clarify the influence of elevated serum lipoprotein (a) (Lp(a)) concentration on ischemic heart disease (IHD) and the perforating artery occlusion type of cerebral infarction (CI) in elderly patients with type 2 diabetes, we measured the serum levels of Lp(a) of type 2 diabetic patients (n = 158, 81 men and 77 women). The group was followed up prospectively for 4 years and the incidence of IHD or CI was monitored. The diagnosis of CI was confirmed by computed tomography and that of IHD, which includes myocardial infarction and angina pectoris, was diagnosed by electrocardiogram and blood chemistry examination, Lp(a) concentrations of 20 mg/dl or more were identified as elevated Lp(a) levels and Lp(a) concentrations of less than 20 mg/dl were identified as normal Lp(a) levels. A Kaplan-Meier survival analysis (log-rank test) assessed the time to event rate stratified by an Lp(a) cutoff point of 20 mg/dl. The predictive value for CI or IHD events was assessed by multiple logistic regression analysis. The probability of IHD events was significantly higher in the elevated Lp(a) group than in the normal Lp(a) group without a history of IHD but was similar in the two groups for those patients with a history of IHD. There was no significant difference between the elevated Lp(a) group and the normal Lp(a) group with regard to CI events in patients without a history of CI and with a history of CI. On multiple logistic regression analysis, Lp(a), hyperlipidemia and a history of IHD were significant predictors of IHD and hypertension, hyperlipidemia and a history of CI were significant predictors of CI. These results show that elevated serum Lp(a) concentrations is an independent risk factor for IHD, but not for the perforating artery occlusion type of CI in type 2 elderly diabetic patients.
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PMID:[A four-year prospective study on the influence of serum elevated lipoprotein (a) concentration on ischemic heart disease and cerebral infarction in elderly patients with type 2 diabetes]. 1152 63

We report two patients who survived childhood acute lymphoblastic leukaemia (ALL) following treatment with chemotherapy, total body irradiation (TBI) and bone marrow transplantation (BMT). The first case presented with an acute cerebral infarction at 23 years of age and was found to have non-ketotic diabetes and gross mixed hyperlipidaemia; the second presented with non-ketotic diabetes, hypertension, proteinuria and dyslipidaemia at age 16 years. The association of glucose intolerance with other vascular risk factors in young adult survivors of BMT was recently highlighted in a follow-up study of 23 survivors of BMT [1], but none presented with such gross mixed hyperlipidaemia. The improving survival rates of childhood malignancy over the last two decades will present adult physicians with patients who have accelerated vascular risk at a young age who will require early treatment to modify it.
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PMID:Adverse metabolic and cardiovascular risk following treatment of acute lymphoblastic leukaemia in childhood; two case reports and a literature review. 1167 78

The recent advance of the carotid artery echotomography indicates the intima media thickness(IMT) of the carotid artery as one of surrogate endpoints of atherosclerosis in subjects with multiple risk factors, such as hypertension, hyperlipidemia, and diabetes mellitus. IMT is shown to be increased in subjects with hyperlipidemia, type 1 and 2 diabetes mellitus, and other several diseases. Also, increase in IMT is related with the prevalence of cerebral infarction and coronary artery diseases. The carotid artery plaques including soft or calcified plaques were shown to predict appearance of strokes. Several drugs, such as anti-diabetogenic drugs(insulin-sensitizer, biguanides, and alfa-glucosidase inhibitor), hypotensive drugs(ACEI, Ca-blocker), and anti-platelet drugs were shown to attenuate the progression of IMT. Recently, we have shown that an anti-platelet drug arrested the progression of IMT and significantly reduced appearance of asymptomatic cerebral infarction in subjects with type 2 diabetes. These data clearly indicate the usefulness of the carotid artery echography in subjects with atherosclerosis and IMT could evaluate the effects of treatment for atherosclerosis.
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PMID:[Evaluation of carotid artery lesion by echography]. 1473 40

Obesity is widely recognized as a risk factor for coronary artery disease, but opinion is divided regarding whether it is an independent risk factor for cerebrovascular disease; even now there is no common view. In this study, the review sought to focus on a prospective study, but since obesity and non-obesity basically cannot be randomly assigned, randomized controlled trials (RCT) are nonexistent. Accordingly, a cohort study (a method of clinical study in which the obesity group is actively followed up for comparison with the non-obesity group in regard to cerebrovascular disease) was mainly conducted. For reference, retrospective case-control studies are also shown. As a result, most epidemiological surveys on the relation between simple obesity and cerebrovascular disease denied any relation. That is, obesity alone, determined only on the basis of height and weight as shown by BMI (body mass index), etc., cannot be an independent risk factor for cerebrovascular disease; obesity can become a risk factor only when accompanied by hypertension, hyperlipidemia, impaired glucose tolerance, etc. Recently, however, most papers conclude that abdominal obesity is a risk factor for cerebral infarction, provided that there are no data confirming that obesity is a risk factor for hemorrhagic cerebrovascular disease (cerebral hemorrhage and subarachnoid hemorrhage).
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PMID:Obesity as a risk factor for cerebrovascular disease. 1509 22


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