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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.
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PMID:Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis. 140 40

We describe a pulsatile aneurysm in the skin of 16-year-old boy that was found to be a sign of a systemic vascular disease, that is, arterial fibromuscular dysplasia. The patient had aneurysms in the renal, cerebral, coronary, and other arteries; he developed renovascular hypertension and had a cerebrovascular accident and acute myocardial infarction at 17 years of age. This disease has not been previously reported in the dermatologic literature.
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PMID:Aneurysm in the skin: arterial fibromuscular dysplasia. 146 51

Nitroglycerin and the long-acting nitrates are widely used in all of the anginal syndromes and have proven effectiveness in relieving or preventing myocardial ischemia. Recent developments into nitrate mechanisms of action provide new insights as to the many anti-ischemic effects of these agents. Important concepts relating to coronary arterial endothelial function are germane to nitrate therapy. Endothelial-derived relaxing factor (EDRF) is presently believed to be nitric oxide (NO), which exerts vasodilatory and/or antiplatelet actions by increasing intracellular cyclic guanosine monophosphate as a result of activation of the enzyme guanylate cyclase. In the setting of coronary atherosclerosis, or even hyperlipidemia without histologic vascular disease, endothelial dysfunction may be present, promoting a vasoconstrictor/proplatelet aggregatory milieu. Nitroglycerin and the organic nitrates are NO donors; NO is the final product of nitrate metabolism, and in the vascular smooth muscle NO induces relaxation, resulting in vasodilation of arteries and veins. In the presence of inadequate EDRF production and/or release, it appears that nitroglycerin may partially replenish EDRF-like activity. Nitrates have long been known to have major peripheral circulatory actions resulting in a marked decrease in cardiac work. Venodilation and arterial relaxation result in a decrease in intracardiac chamber size and pressures, with a resultant decrease in myocardial oxygen consumption. In addition, a variety of direct coronary circulatory actions of the nitrates have been documented. These include not only epicardial coronary artery dilation, but the prevention of coronary vasoconstriction, enhanced collateral flow, and coronary stenosis enlargement. Recent work suggests that the nitrates may also act by preventing distal coronary artery or collateral vasoconstriction, which can reduce blood flow downstream from a total coronary obstruction. Thus, there are many anti-ischemic mechanisms of action by which nitroglycerin and the organic nitrates may be beneficial in both acute and chronic ischemic heart disease syndromes. The unique salutory effects of the nitrates in subjects with left ventricular dysfunction or congestive heart failure make these drugs particularly attractive for patients with abnormal systolic function and intermittent myocardial ischemia. Finally, the emergent role of intravenous nitroglycerin in acute myocardial infarction offers new prospects that nitrate therapy may prove to be beneficial in acute myocardial infarction as well as postmyocardial infarction for the reduction of left ventricular remodeling.
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PMID:Mechanisms of action of the organic nitrates in the treatment of myocardial ischemia. 152 24

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. In a further 24 patients with acute myocardial infarction elastase activity, inhibitory capacity and lipids during the course of the illness have also been investigated. Serum elastase-type activity was found to be significantly lower and inhibitory capacity significantly higher in the groups of patients than in the controls. HDL- and HDL2-cholesterol as well as apo A concentration showed significant negative correlation with elastase inhibitory capacity both in atherosclerotic and in control subjects. During the course of myocardial infarction a significant elevation of serum elastase-type activity could be observed at the end of the first week; serum triglyceride levels increased, HDL- and HDL2-concentrations decreased significantly in the first 3 weeks, than gradually approached the initial values. In the patients with an elevation of serum elastase-like activity by more than 30% in the first week, there was a significantly higher elevation of serum GOT and LDH1 and a greater occurrence of transmural (Q) infarction than in those with a smaller variation of elastase-like activity.
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PMID:Elastase-type enzymes and their relation to blood lipids in atherosclerotic patients. 159 1

Tissue plasminogen activator (t-PA) has been approved as thrombolytic therapy for the treatment of acute myocardial infarction, but this agent can cause serious bleeding complications including intracerebral hemorrhages. Mechanisms underlying the development of these hemorrhages have not been clarified. We report a patient who developed two intracerebral hemorrhages shortly after receiving t-PA for the treatment of an acute myocardial infarction, and who was found to have cerebral amyloid angiopathy at autopsy. Staining of cortical sections with Congo red and an antibody directed against beta amyloid protein (A4 peptide) disclosed specific involvement of most of the subarachnoid and superficial cortical vessels in the region of the two hemorrhages. Based on the findings in this patient and in 6 additional patients reported recently, it is likely that cerebral amyloid angiopathy plays a pathogenic role in some intracerebral hemorrhages associated with the administration of t-PA. The cautious use of t-PA with heparin in patients who are elderly or demented may be advisable.
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PMID:Intracerebral hemorrhage related to cerebral amyloid angiopathy and t-PA treatment. 191 Feb 76

Hemostatic disorders in coronary heart disease and cerebrovascular disease patients were examined by studying two groups of prothrombotic and prethrombotic markers. Sixty subjects (28 male, 32 female aged 64 +/- 6 years) were included in the study of which 30 suffered from coronary heart disease and 30 from cerebral vascular disease; the first group was subdivided into those subjects with quiescent preinfarction angina (21 cases) and those with acute myocardial infarction (9 cases), whereas the second group was subdivided into subjects with cerebral stroke (20 cases) and those with TIA (10 cases). Each subject underwent an assay to assess fasting blood levels of fibrinogen, factor VII, antithrombin III (using a chromogenic method), plasminogen tissue activator, beta-thromboglobulin and dimer-D (ELISA method) 24 hours after being admitted to hospital. From an analysis of results it was observed that of the four prothrombotic markers used, fibrinogen and factor VII showed a generic increase in comparison to coronary heart disease and cerebrovascular disease patients; this was paralleled by significant reduction of antithrombin III; differences were even more marked and significant in acute thrombo-occlusive (infarction, stroke) compared to functional forms (angina, TIA). In line with other studies, the Authors favour an irritative type endothelial response leading to a marked and surprising increase of tPA. The two prothrombotic markers (BTG, D-D) also showed a thrombotic development in the two groups of patients examined with more significant findings in the occlusive forms (infarction, stroke) in comparison to transitory forms. On the basis of these and other published results the Authors confirm the usefulness of monitoring prothrombotic markers (fibrinogen, factor VII, AT III) in apparently normal subjects with or without risk factors or with slight initial signs of arteriosclerotic disease; these call for longitudinal or cross-sectional studies of an epidemiology type, in addition to isolated assay for a generic assessment of the patient's biological status, even if it is not yet possible to elaborate a protocol for the certain and specific diagnosis of a thrombophilic condition. The value of prethrombotic markers is apparent in the acute occlusive stage of the disease as a form of prognostic and therapeutic monitoring, and in preinfarction and above all silent transitory forms where, together with the use of other techniques (Holter), it provides interesting openings for confirming the diagnosis of an in vivo microthrombotic genesis and the consequent introduction of antithrombotic drug therapy.
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PMID:[The thrombophilic status and ischemic cardiopathy]. 195 44

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. In further 24 patients with acute myocardial infarction dynamics of elastase activity, inhibitory capacity and of lipids during the course of the illness have also been investigated. Serum elastase-type activity was found to be significantly lower, inhibitory capacity significantly higher in the groups of patients than in the controls. HDL- and HDL2 cholesterol and apo-A concentrations showed significant negative correlations with elastase inhibitory capacity both in atherosclerotic and in control subjects. During the course of myocardial infarction a significant elevation of serum elastase-type activity could be observed at the end of the first week; serum triglyceride levels increased, HDL- and HDL2 concentrations decreased significantly in the first 3 weeks, then gradually approached the initial values. In the subgroup of patients with an elevation of serum elastase-like activity by more than 30% in the first week, there was a significantly higher elevation of serum GOT and LDH1 and a greater occurrence of transmural (Q) infarction than in those with a smaller variation of elastase-like activity.
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PMID:[Serum elastinolytic activity and blood lipids in various clinical forms of arteriosclerosis and in acute myocardial infarct]. 204 14

Aspirin inhibits thromboxane A2 and prostaglandin formation in platelets and prostaglandin I2 (prostacyclin) in vascular cells. It prevents platelet aggregation by irreversible acetylation of cyclooxygenase, a key enzyme in the arachidonic acid metabolism. Oral aspirin can be extensively hydrolyzed to inactive salicylate in the stomach and the liver (first-pass) before it enters the systemic circulation. Presystemic acetylation of platelets thus occurs during aspirin absorption, with a concomitant sparing of peripheral vascular cyclo-oxygenase, mainly exposed to salicylate. On the basis of its antiplatelet effect, aspirin has been assessed during the past two decades in patients with a history of myocardial infarction, stroke, transient ischemic attack or unstable angina. A meta-analysis of randomized controlled trials of long term aspirin treatment for secondary prevention of vascular disease indicated that aspirin (300-1500 mg daily) significantly reduced fatal and non-fatal vascular events. More recently aspirin (160 mg daily) produced a significant reduction in hospital vascular mortality and in non-fatal events in patients with suspected acute myocardial infarction. Combination of aspirin with streptokinase was significantly better than either drug alone. On the other hand two primary prevention trials of aspirin in healthy doctors did not show any modification of vascular mortality despite an overall reduction of non-fatal myocardial infarction. Resolution of some problems related to the mechanism of action of aspirin and to selection of trial populations will possibly increase the benefit/risk ratio of aspirin treatment for prevention of vascular disease.
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PMID:Aspirin as an antithrombotic drug: from the aggregometer to clinical trials. 215 Jul 36

A fatal intracerebral haemorrhage (ICH) associated with streptokinase (SK) treatment of an acute myocardial infarction is described. Autopsy examination showed a lobar ICH and severe cerebral amyloid angiopathy (CAA). The close temporal relationship between SK administration and intracranial haemorrhage, the absence of pretreatment risk factors for ICH, and the presence of CAA suggests that these are related phenomena. Accordingly: 1. There may be a synergistic relationship between CAA and intracranial haemorrhage induced by fibrinolytic agents; 2. Thrombolytic agents may induce more frequent than expected intracranial haemorrhage in conditions associated with a high incidence of CAA, notably old age and Alzheimer's disease; 3. A regional defect in haemostasis other than vessel fragility may contribute to the intracranial haemorrhagic predisposition of CAA; 4. Autopsy examination of cases of ICH is an essential part of the audit of clinical trials of fibrinolytic agents.
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PMID:Fatal streptokinase-induced intracerebral haemorrhage in cerebral amyloid angiopathy. 220 93

Early observations that the regular use of aspirin (acetylsalicylic acid, ASA), a nonsteroidal anti-inflammatory agent, seemed to protect against myocardial infarction and reduce platelet aggregation made this substance the most frequently used drug in large clinical trials. The objectives of these studies were to reduce thromboembolic complications in arterial cardiovascular diseases (prevention of myocardial infarction in unstable angina, secondary prevention of acute myocardial infarction, and increased patency of aortocoronary bypass grafts) and to reduce platelet deposition on artificial surfaces (artificial heart valves and hemodialysis shunts). Despite the recent synthesis of more selective inhibitors of arachidonic acid metabolism in blood platelets, and a multitude of questions concerning optimal dose, schedule, and mode of action that still remain open, ASA continues to be the most frequently used drug in arterial vascular disorders. Because of the frequent and potentially serious side effects of aspirin, mainly on the gastrointestinal tract, less toxic ways of inhibiting eicosanoid metabolism in blood platelets are attracting more and more interest. Among these, the alimentary substitution of omega-3 fatty acids for a competitive inhibition of the omega-6-arachidonic acid metabolism seems the most promising. Results with fish-oil diet raise the question of whether substitution of polyunsaturated lipid acids influence only platelet metabolism, or whether the action of "anti-platelet" drugs or diet in cardiovascular disorders is mediated primarily by leukocytes or monocytes. This new dietary principle, which possibly corrects only a poor alimentary habit of civilization, could open simple and adequate ways for even a primary prophylaxis of vascular disease by diet alone or, at least for therapeutic aims, in combination with drugs.
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PMID:Drugs or diet: do they protect against degenerative cardiovascular disease? 246 42


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