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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis of the incidence of thromboembolism and heart ruptures with reference to different causative factors was conducted on the basis of 585 patients dying of myocardial infarction during the recent 30 years (autopsy data) and 1417 patients with myocardial infarction (298 mortality cases among them) hospitalized during the recent 10 years. A reduction of the incidence of thromboembolism and an increase of the incidence of heart ruptures in the recent years were revealed. Thromboembolism and heart ruptures play an important role among the causes of mortality in myocardial infarction. The development of thromboembolism in myocardial infarction is favoured by the macro-focal nature of the heart lesion, repeated necroses of the myocardium, localization of infarction in the posterior and posteriolateral zones, old age of the patients (over 60), presence of diabetes mellitus and acute cardiac aneurysm. Thromboembolism occurs with the same incidence rate within the initial 7 days, and later during the acute phase. Thrombi are most often found in the cardiac cavities, pulmonary, renal and splenic vessels, in the cerebral, mesenteric and other vessels. Heart ruptures are favoured by the macro-focal nature of the cardiac lesion, localization of the infarction in the anterior and anteriolateral zones, old age (over 60), presence of acute cardiac aneurysm. Most frequently the ruptures are observed in primary myocardial infarction within the initial 5--7 days of the disease. The use of anticoagulants in myocardial infarction decreases the incidence of thromboembolic complications and heart ruptures.
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PMID:[Thormboembolisms and heart ruptures in myocardial infarct]. 75 50

Thrombotic events may occur in patients who present with severe uncontrolled diabetes or with diabetic coma. As a possible explanation for this, platelet function was investigated at presentation with diabetic ketoacidosis and during treatment in 10 patients. Concentrations of the platelet-specific proteins, platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) were elevated and fell towards normal with treatment. Despite evidence of increased aggregation in vivo, platelets from subjects with ketoacidosis were insensitive to adenosine 5'-diphosphate (ADP), sensitivity increasing with correction of ketoacidosis. Platelets from ketoacidotic diabetics were initially insensitive to the anti-aggregatory action of prostacyclin (PGI2) and became normal with treatment. Initial blood glucose concentrations correlated with log10 ADP concentrations (r = 0.72, p less than 0.01) and with log10 PGI2 ID50 (the PGI2 concentration required to half-inhibit ADP-induced aggregation) (r = 0.66, p less than 0.025). Glucose concentrations throughout the 2-week study period correlated with all log10 ADP concentrations (r = 0.32, p less than 0.005) and all log10 PGI2 ID50 concentrations (r = 0.51, p less than 0.001). The decrease in ADP sensitivity in ketoacidosis, paradoxical in view of the evidence of increased in vivo platelet aggregation, may result from an acquired platelet storage pool deficiency.
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PMID:Paradoxical platelet behaviour in diabetic ketoacidosis. 295 Nov 59

Changes in the choroidal artery were examined at autopsy in 16 Japanese patients with hypertension and insulin-dependent diabetes mellitus. These changes could be divided into 1) arteriosclerotic ones consisting of intimal thickening due to migration of smooth muscle cells, 2) hyaline deposits in the subendothelium, 3) extensive degeneration (moth-eaten atrophy and necrosis) of medial smooth muscle cells, and 4) changes resulting from fibrinoplatelet thrombi and their organization (recanalization and obstruction). The intimal thickening and medial damage correlated with aging, were accelerated by hypertension, and were remarkable in arterioles less than 60 micron in diameter. Diabetes mellitus apparently did not enhance these vascular changes. Thrombotic occlusion or narrowing of the choroidal artery was frequently observed in the arterioles of patients with hypertension and diabetes mellitus who had chronic azotemia or renal insufficiency. Subendothelial hyaline deposits were increased in patients with diabetes. The narrowing or obstructive changes in the choroidal artery were extensive in the intraocular blood vessels. These changes may be secondary and induce damage to other intraocular blood vessels and tissues, including the retina.
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PMID:Clinical choroidal thrombosis, hypertension, and diabetes mellitus: an electron microscopic study. 333 93

Although lipids have received most attention in relation to atherosclerosis, vessel injury also has a role in the development of atherosclerotic lesions. Thrombi that form at sites of injury can be incorporated into the wall, causing thickening, and platelets that adhere to damaged vessel walls release a growth factor (PDGF) that stimulates smooth muscle cell proliferation. The early lesions of atherosclerosis are focal and develop around vessel orifices and branches in relation to the patterns of blood flow and areas of increased permeability and endothelial cell damage. Platelets also contribute to the complications of advanced atherosclerosis caused by occlusive thrombi, thromboembolism, and spasm. The causes of vessel wall injury are not established, although there is evidence pointing to disturbed blood flow, hypertension, antigen--antibody complexes, complement, materials originating from platelets and white blood cells, bacteria, endotoxin, viruses, smoking, dietary lipids, homocystinemia, diabetes, other metabolic disorders, and stress. Platelets do not adhere to intact endothelium, but they adhere to the constituents of the subendothelium, release the contents of their granules (including PDGF), and form thromboxanes. If blood flow is disturbed, platelet--fibrin thrombi can form at sites of injury. Platelet adherence to a damaged wall does not require von Willebrand factor except under conditions of high wall shear. Repeated injury of a vessel wall leads to the development of lipid-rich atherosclerotic lesions, even in normocholesterolemic animals, but these lesions do not form if the experimental animals are made thrombocytopenic before injury is induced. Measurable changes in platelets that are associated with the clinical complications of atherosclerosis include shortened survival, release of granule contents (platelet factor 4, beta-thromboglobulin, thrombospondin), formation of thromboxanes, and decreased buoyant density. "Antiplatelet drugs" such as aspirin are proving to be beneficial in selected groups of patients, such as those with unstable angina. Thromboxane synthetase inhibitors and agents that block the thromboxane receptor on platelets are under investigation. Long term administration of "antiplatelet drugs" to affect the rate of development of atherosclerosis seems neither feasible nor desirable. Modification of dietary and smoking habits and control of hypertension are more likely to be beneficial for most individuals.
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PMID:The role of platelets in the development and complications of atherosclerosis. 351 36

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Rupture of atherosclerotic plaque resulting in intravascular thrombosis and myocardial infarction (MI), while a common sequelae of de novo atherosclerotic lesions, is an uncommon consequence of restenosis. We hypothesize that the rarity of MI associated with restenotic lesions is a result of cellular and biochemical modifications induced by the local response to mechanical injury rendering the site resistant to rupture. Clinical and angiographic features of patients presenting with symptomatic primary (n = 24) or restenotic coronary lesions (n = 12) who underwent directional atherectomy were compared. Histologic analysis and immunostaining for 92-kDa gelatinase were performed on each atherectomy specimen. There was no significant difference between the 2 groups regarding age, gender, incidence of diabetes, smoking, hypertension, hypercholesterolemia, or previous MI. Lesion length, extent, and distribution of disease and percent stenosis were not significantly different between groups. However, 8% of primary lesions were hypercellular compared with 75% of restenotic specimens (p = 0.0001). Hypercellularity in restenotic specimens was shown by adjacent section staining to be composed of smooth muscle cells. Ninety-two kDa gelatinase was expressed in 79% of primary lesions versus 0% of restenotic specimens (p = 0.0001). Thrombus was identified in 54% of primary lesions versus 22% of restenotic lesions (p <0.05). These findings suggest that, independent of clinical or angiographic influences, balloon injury induces increased lesion cellularity and reduced expression of 92-kDa gelatinase, possibly resulting in a reduced propensity for plaque rupture and thrombosis.
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PMID:Differential expression of 92-kDa gelatinase in primary atherosclerotic versus restenotic coronary lesions. 910 98

Platelet aggregation and spontaneous thrombolytic activity were assessed in patients with non-insulin dependent diabetes and stroke using a shear-induced and agonist-induced platelet aggregation test. The Thrombotic Status Analyser (TSA), induces platelet-rich thrombus formation solely by shear forces, while whole blood platelet aggregometry measures platelet reactivity to different agonists. These tests were employed in the present study because in earlier studies they both demonstrated that platelet aggregability in healthy volunteers was unchanged with age. On the other hand, it is known that thrombolytic activity decreases with age in males, but not in females. In diabetic patients shear-induced platelet aggregability varied according to the stage of nephropathy but platelet aggregation to collagen was suppressed at all stages. Platelet reaction to shear stress was enhanced in stroke patients with haemorrhagic episodes but not in patients with lacunar infarction. In contrast, platelet reactivity to collagen was suppressed and changes in ADP-induced platelet aggregability were inconsistent. Suppressed thrombolysis was observed only in diabetes with minor renal defect. Fibrinogen was increased in diabetes with stage III and IV nephropathy. Fibrinopeptide A (FPA) and D-dimer were increased in stroke. Thus, the observed increase in fibrinogen, FPA and D-dimer is inconsistent with changes in platelet aggregability. Our present findings suggest that a shear-induced platelet aggregation test is superior to other tests such as agonist-induced platelet aggregation and thrombotic markers such as fibrinogen, FPA and D-dimer in detecting a prothrombotic state. It is concluded that elderly males may have a prothrombotic state not because of platelet hyper-aggregability but because of suppressed thrombolytic activity. On the other hand, a prothrombotic state in patients with non-insulin dependent diabetes and after stroke may be due to changes in age-independent platelet aggregability.
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PMID:A global platelet test of thrombosis and thrombolysis detects a prothrombotic state in some patients with non-insulin dependent diabetes and in some patients with stroke. 1117 45

Thrombotic disease is rare in neonates. The main risk factors at this age are perinatal asphyxia, maternal diabetes, sepsis, polycythemia, dehydration, a low cardiac output, and in primis the catheterization of central lines. Another important risk factor is inherited thrombophilia. Arterial thrombosis is even more rare than venous thrombosis and less related to most of the risk factors listed above; it occurs more frequently in the iliac, femoral, and cerebral arteries but very rarely in the aorta. Most of the described cases of aortic thrombosis are associated with the catheterization of an umbilical artery and involve the descending tract and the renal arteries; very few relate to the ascending tract and the aortic arch. The possible role of virus-induced primary vascular endothelium damage in the etiopathogenesis of neonatal arterial thrombosis has been previously hypothesized. Herpesviruses, particularly human cytomegalovirus (HCMV), can infect endothelial cells and directly damage intact vascular endothelium, altering its thromboresistant surface as a result of procoagulant activity mediated by specific viral surface phospholipids, necessary for the coagulation enzyme complex assembly that leads to thrombin generation. We describe a case of congenital aortic arch thrombosis. The clinical, laboratory, and virologic pictures; the anatomopathologic findings (fully compatible with viral infection); the detection of HCMV in various tissues (including the aorta); and the absence of other causes of aortic thrombosis make it possible to attribute the case to a severe congenital HCMV infection with multiple organ involvement, after the primary infection of the mother. The hemostatic system disorders and hemodynamic disturbances related to viral cardiac damage explain the clinical features of the case and indicate that congenital HCMV infection should be included among the causes of neonatal aortic thrombosis.
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PMID:Neonatal aortic arch thrombosis as a result of congenital cytomegalovirus infection. 1173 41

Atrial fibrillation (AF) is the most common cardiac arrhythmia. AF is paroxysmal or persistent and becomes permanent when it does not convert to sinus rhythm spontaneously or when attempted cardioversion fails. The prevalence of AF is 0.4% in the general population and increases with age up to 6-8% in octogenarians. In men, the age-adjusted prevalence is generally higher than in women. During AF, synchronous mechanical atrial activity is disturbed, resulting in haemodynamic impairment. This can give rise to thrombus formation and embolism to the systemic circulation. Thrombus associated with AF arises most frequently in the left atrial appendage. Cerebrovascular emboli in AF patients most often manifest as transient ischaemic attacks or ischaemic strokes. The overall rate of ischaemic stroke among patients with nonrheumatic AF averages 5% per year, but the rate increases with age. Patients with AF are at higher risk of cerebrovascular events from all causes. Of all strokes, one in every six occurs in patients with AF. Including transient ischaemic attacks and silent strokes detected radiographically, the overall rate of all cerebrovascular events in AF patients rises to more than 7% per year, although approximately one third of these are due to causes that are only secondarily or incidentally associated with AF or related anticoagulant therapy. Antiarrhythmic therapy is useful to improve cardiac rate and function in AF. However, to reduce first or recurrent emboli, antithrombotic therapy is of paramount importance. Results from several randomized clinical trials of antithrombotic therapies have shown that adjusted-dose warfarin reduces first or recurrent stroke by about 60% compared with placebo. When patients with nonvalvular AF are anticoagulated, the odds against ischaemic stroke and intracranial bleeding favour an INR between 2.0 and 3.0. Acetylsalicylic acid is less efficacious than warfarin in AF patients, reducing the risk of stroke by about 20%. Therefore, this antiplatelet agent should be used only for AF patients at low risk. Anticoagulation is the current treatment modality in AF patients at high or intermediate risk, i.e. patients with history of transient ischaemic attack or stroke, those aged >65 years, those with a history of hypertension, diabetes, heart failure or structural heart disease, valvular disease or significant systolic dysfunction. The benefit of dual antiplatelet regimens in AF patients is unknown, and combining antiplatelet agents with different mechanisms of action is an important topic for future investigation.
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PMID:Long-term outcome after stroke due to atrial fibrillation. 1269 12

Atrial fibrillation (AF) is an independent risk factor for ischemic stroke. In patients with AF, cardioembolias present about 10% of ischemic strokes. Transesophageal echocardiography is an ideal instrument for diagnostics of intracardiac thrombi. An aim of the study was to find the high risk markers for stroke in patients with AF of non-valvular origin. The patients have been divided into 2 groups with and without stroke in anamnesis. To search for stroke dependence of clinical and echocardiographic high risk markers, the data were analyzed using Poly Analyst Power statistical package. In the group of the patients with stroke in the anamnesis, echocardiographic markers for high risk of thromboembolia occurred significantly more frequently. Thrombi in the left atrial or its appendage were registered in 12.5% patients without stroke in anamnesis and in 31% of those, who survived stroke. The independent risk factors for stroke were age, AF duration, left ventricular ejection fraction, diabetes mellitus and arterial hypertension.
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PMID:[Risk and prevention of atrial fibrillation of non-valvular origin]. 1528 30


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