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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk factors for acute cerebral ischemia in geriatrics were assessed in two groups of 100 patients by comparing anamnestic data (based on a personal questionnaire) to laboratory data. The first group included patients affected by ischemic ictus not more than 45 days prior to the start of the study; the second group comprised geriatric subjects whose clinical characteristics were considered "normal for their age". The study took into account both the quality and quantity of findings. It was observed that risk factors play a more important role in women. Arterial hypertension, cardiopathies, cerebrovascular symptomatology, drug therapy, hyperfibrinogenemia and the number of red blood cells were the most important risk factors, followed by hematocrit, hemoglobin, total cholesterol and ATS ratio. The importance of the familiar factor for women and the lack of a role for HDL cholesterol in men were underlined.
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PMID:[Risk factors of acute cerebral ischemia in geriatrics. Personal observations]. 204 17

The Canadian Erythropoietin Study Group conducted a randomized, placebo-controlled trial to examine the effect of human recombinant erythropoietin on the treatment of anemia in 118 hemodialysis patients. The effectiveness of therapy on hemoglobin concentration and quality of life has been reported elsewhere. Herein is reported the effect of erythropoietin therapy on blood pressure. Patients receiving erythropoietin had a significant increase in diastolic blood pressure (DBP; p = 0.001) and required increased antihypertensive medication. There was no difference in the incidence of severe hypertension (DBP greater than 110 mm Hg or hypertension-related seizure) between placebo-treated patients (13%) and those receiving erythropoietin (14%). The development of severe hypertension in erythropoietin-treated patients was associated with a history of receiving antihypertensive medication or having native kidneys in situ. In the first 5 weeks of the study, there was a correlation between the change in hemoglobin concentration and the change in DBP (r = 0.42, p less than 0.001). Although erythropoietin therapy was associated with a significant increase in DBP, there was no difference between placebo- and erythropoietin-treated patients with respect to severe hypertension or hypertension-related seizures.
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PMID:Effect of recombinant human erythropoietin therapy on blood pressure in hemodialysis patients. Canadian Erythropoietin Study Group. 204 74

Cardiovascular disease is a frequent complication of insulin-dependent diabetes mellitus (IDDM), but the prevalence, interrelations, and risk factors of its principal components (coronary, cerebrovascular, and lower-extremity arterial disease) and of medial arterial wall calcification are not well understood. To address these issues, data from the Epidemiology of Diabetes Complications Study (n = 657) baseline examination were examined. The term coronary heart disease (CHD) was applied to those with myocardial infarction or angina, whereas lower-extremity arterial disease (LEAD) was applied to those who had undergone amputation of a lower limb or who had an ankle to arm blood pressure ratio less than 0.8 at rest or after exercise. Calcification of the lower-extremity arteries was considered to be present if ankle pressure was more than 100 mm Hg higher than brachial pressure. Although the prevalence of CHD was low, LEAD was significantly more common in women than in men (p less than 0.01), whereas calcification was more frequent in men than in women (p less than 0.01). Ten percent of those with LEAD also had CHD, and 8% with LEAD had calcification. Modeling of potential risk factors (e.g., diabetes duration and glycosylated hemoglobin) revealed that duration, female gender, fibrinogen, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and high density lipoprotein cholesterol to apolipoprotein A-I ratio were independent predictors of LEAD, whereas for CHD only, diabetes duration and hypertension contributed to CHD. Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. The results suggest that although LEAD, CHD, and calcification often coexist, their risk factor profiles differ.
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PMID:Cardiovascular disease and arterial calcification in insulin-dependent diabetes mellitus: interrelations and risk factor profiles. Pittsburgh Epidemiology of Diabetes Complications Study-V. 206 46

In a retrospective study, we analyzed the prevalence of diabetes-associated late complications in 549 type 1 (insulin-dependent) diabetic patients who have been treated at the University Hospital of Ulm between 1980 and 1987. Retinopathy, proteinuria and neuropathy depended on the duration of the disease, whereas age was the major determinant of large vessel disease. After 20 years of diabetes, 85% of the patients showed retinopathy, half of them proliferative retinopathy, 52% had persistent proteinuria (greater than 500 mg/day), 20% of them were under dialysis. 74% of the patients showed signs of peripheral and/or autonomic neuropathy, 19% had manifestations of large vessel disease. There was no consistent correlation between the levels of glycosylated hemoglobin and the occurrence of diabetic late complications. However, hypertension was closely associated with both small and large vessel disease.
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PMID:[Prevalence of secondary complications in patients with type I diabetes mellitus. Results of a retrospective analysis of 549 type I diabetic patients of the Ulm University clinic]. 208 8

The cerebral white matter is highly susceptible to ischemic damage because of its location in the end-fields of penetrating arteries. Our studies have shown that hypertension, short-term variability of blood pressure, decreased oxygen dissociation of hemoglobin, and increased resistance of cerebral arterioles play important roles in the pathogenesis of Binswanger type dementia. While hypoperfusion was most remarkable in the frontal area and dopamine metabolism in the cerebrospinal fluid was impaired in Binswanger type dementia, cerebral blood flow decreased most conspicuously in the parietal area and there was an impairment of noradrenaline metabolism in the cerebrospinal fluid in senile dementia of Alzheimer type. Previous anatomical studies have indicated that the ascending dopaminergic system predominantly innervates the frontal cortex, while the noradrenergic system projects all cortical areas, including the parietal cortex. Our findings suggest frontally-dominant dysfunctions in Binswanger type dementia.
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PMID:[Pathogenesis and pathophysiology of ischemic leukoencephalopathy]. 209 78

Thrombotic thrombocytopenic purpura (TTP) is a syndrome that occurs mainly in adults with multiorgan microvascular thrombosis consisting of thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal involvement, and fever. The female to male ratio is 3:2, and peak incidence occurs in the 3rd decade of life. Clinical signs are the consequence of hyaline thrombosis and occlusion of capillaries and arterioles. Renal ailment manifests itself in hematuria and proteinuria with azotemia and even overt renal failure. In severe disease, azotemia is typical of hemolytic uremic syndrome (HUS). TTP was first described in 1925 by Moschcowitz. The clinical picture of TTP consists of a prodromal phase, a viruslike disease occurring in up to 40% of patients. 60% have neurologic disturbances, 90% have purpura initially, and fever occurs in all. Anemia is often severe with hemoglobin values of 7-9 gm/dl, renal involvement in 90%, and renal failure in 40-80% of patients. Clinical variants include the acute and fulminant variety mortality, the chronic form, and the relapsing form. Predisposing factors and triggering agents are autosomal recessive inherited traits in acute idiopathic TTP, systemic diseases, tumor antigens, pregnancy and puerperium, viruses (endotoxins for HUS), and possibly oral contraceptives and hypertension. Therapy includes corticosteroids (prednisone 100-400 mg/day); heparin for postpartum HUS; and antiplatelet agents (Dextran 70, aspirin, and dipyridamole in high doses). The infusion of PGI2 is controversial; splenectomy is also questionable; and vincristine, azathioprine, and cyclophosphamide have unproven efficacy. Fresh-frozen plasma exchange is the method of choice as it produces survival in 90%. Others are iv immunoglobulins, vitamin E, and dialysis and renal transplant. Platelet transfusions are contraindicated because of sudden death and decreased survival.
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PMID:Thrombotic thrombocytopenic purpura and related disorders. 210 74

A method of ICP management is presented based upon maintenance of cerebral perfusion pressure ( CPP = SABP - ICP) at 70-88 mm Hg or in some cases greater. To do this, we have employed volume expansion, nursed patients in the flat position, and actively used catecholamine infusions to maintain the SABP side of the CPP equation at levels necessary to obtain the target CPP. CSF drainage and mannitol have freely been used to maintain the ICP portion of the equation. Thirty-four consecutive patients with GCS less than or equal to 7 were admitted to the Neurosurgical Intensive Care Unit (GCS = 5.1 +/- 1.4) and managed with this protocol. CPP was maintained at 84 +/- 11 mm Hg, ICP was 23 +/- 9.8 mm Hg, and SABP averaged 106 +/- 11 mm Hg. CVP was 8.0 +/- 3.7 mm Hg and average fluid intake was approximately 5.4 +/- 3.9 liters/d. Output averaged 5.0 +/- 4.0 liters/d; additionally, albumin (25%) (33 +/- 44 gm/d) and PRBCs were used for vascular expansion and hemoglobin was maintained (11.5 +/- 1.4 gm/dl). Three patients died of uncontrolled ICP (all protocol errors). Four other patients succumbed, none secondary to ICP and all secondary to potentially avoidable complications. Morbidity (GOS = 4.2 +/- 0.87) appeared to be as good or superior to previous methods of therapy. Overall, mortality was 21% and that from uncontrollable ICP was 8%. This approach to the management of intracranial hypertension proved safe, rational, and greatly enhanced the therapeutic options available. It was also consistent with optimal care of other organ systems. The results bring into question many of the standard tenets of neurosurgical ICP management and suggest new avenues of investigation.
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PMID:Cerebral perfusion pressure management in head injury. 211 69

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
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PMID:Myocardial protection: what the anesthesiologist does. 213 51

The premise of this article is that morphologic changes observed in cerebral arteries after subarachnoid hemorrhage play an important role in the pathogenesis of associated ischemic deficits observed in this disorder. Secondly, the arteriopathic response of cerebral arteries to subarachnoid blood is similar in many respects to that observed in systemic vessels under various pathologic conditions, and common pathogenic mechanisms may exist. The data supporting these premises may be summarized as follows: 1. Morphologic changes in human and animal cerebral arteries after subarachnoid hemorrhage are temporally associated with angiographic and clinically significant vasospasm. 2. Profound morphologic changes in cerebral arteries after subarachnoid hemorrhage do not contribute to structural narrowing of the lumen through increases in vessel wall mass. Nevertheless, structural changes may act in concert with contractile mechanisms to alter normal physiologic responses and maintain a narrowed lumen. 3. The agent responsible for arterial narrowing and morphologic changes in cerebral arteries after subarachnoid hemorrhage is contained in the erythrocyte component of whole blood and is most likely hemoglobin. 4. The volume and duration of exposure of subarachnoid blood to the artery appears to be significant in the development of the angiopathic response. 5. Ultrastructural abnormalities in systemic vessels associated with hypertension, atherogenesis, and endothelial damage are similar in many respects to those seen after subarachnoid hemorrhage.
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PMID:Morphologic changes in cerebral arteries after subarachnoid hemorrhage. 213 52

The prevalence of microalbuminuria and persistent proteinuria was studied in a population of 801 diabetic patients (535 with type II and 266 with type I diabetes). Urinary albumin excretion rate (AER) was measured on morning samples by laser nephelometry. Normoalbuminuria, as defined, in the absence of contaminated urine, by an albumin: creatinine (A/C) ratio below 2, was found in 551 patients, microalbuminuria (NC greater than or equal to 2 with AER below 200 mg/l) in 190 patients and persistent proteinuria (AER greater than or equal to 200 mg/l) in 60 patients. Microalbuminuria was present in 48 (18 p. 100) IDDM patients and 142 NIDDM patients. In IDDM patients, AER increased with the duration of the disease with no apparent influence of age at the onset. The prevalence of hypertension was 25 p. 100 and 61 p. 100 in IDDM patients with microalbuminuria and macroproteinuria respectively versus 10 p. 100 in patients with normoalbuminuria. This prevalence increased in NIDDM patients from 39.3 p. 100 with normoalbuminuria to 40.8 p. 100 and 76.2 p. 100 with microalbuminuria or macroproteinuria respectively. Proliferative retinopathy in type I and type II patients with normal AER was 7.4 p. 100 and 1.2 p. 100 respectively increasing to 15.2 p. 100 and 8.9 p. 100 with microalbuminuria and 27.8 p. 100 and 23.1 p. 100 with macroproteinuria. The prevalence of coronary disease increased from 4 to 10.4 p. 100 in patients with type I diabetes and microalbuminuria. The prevalence of cardiac failure increased from 1.5 to 2.1 p. 100 in type I diabetics and from 3.2 to 7.8 p. 100 in type II diabetics in the presence of microalbuminuria. Patients with microalbuminuria had increased levels of glycosylated hemoglobin A 1C but statistical difference was only obtained for patients with type II diabetes. Routine analysis of AER in diabetics allows early detection of diabetic nephropathy and emphasizes the need for tight metabolic and blood pressure control. Hypertension can be detrimental to nephropathy but might also initiate renal lesions in NIDDM patients.
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PMID:[Microalbuminuria and diabetic nephropathy. Detection and correlation with other degenerative complications]. 214 8


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