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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intravascular adhesion and aggregation of platelets initiate hemostasis and arterial thrombosis. In vitro, platelet aggregation is induced by many different agents; which of these is responsible for aggregation in vivo is now under investigation. For this purpose, we have developed novel techniques for the reproducible determination of bleeding times in mesenteric arterioles of rats and rabbits. Local infusions of enzyme systems which remove adenosine diphosphate (ADP) greatly increase the bleeding time at arterial injuries distal to the site of infusion. These observations establish the involvement of ADP in the activation of platelets for primary hemostasis. Direct measurement of free adenosine triphosphate (ATP), as an indicator of ADP, at such injury sites indicates that enough ADP for activating platelets is released very rapidly from damaged vessel walls and much later from the platelets themselves. This bleeding-time technique has also shown that hemostatic platelet aggregation is delayed less by the inhibition of the production of thromboxane A2 than by that of ADP. These observations provide an explanation for the ineffectiveness of any simple platelet-inhibiting drug (including aspirin) by itself, whenever arterial (e.g., coronary or cerebral) thrombosis is initiated by hemorrhages into atheromatous plaques. On the other hand, aspirin is significantly effective when myocardial infarction follows unstable angina and when strokes follow transient episodes of cerebral ischemia. This partial effectiveness can be explained by an action of aspirin on platelets, assuming that, in such cases, their thromboembolic aggregation is initiated by hemodynamic effects of atheromatous lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelets and blood vessels. 608 14

The case is described of a 32-year-old female patient who has suffered since puberty from acute migraine attacks and Raynaud syndrome of both hands. In June 1981 acute posterior cerebral ischemia occurred. 11/2 years later the patient was hospitalized for acute myocardial infarction with normal and patent coronary arteries. Thereafter, the patient was treated with nifedipin and anticoagulation, and no other vascular complications have since occurred. The authors suggest that the patient is suffering from a diffuse vasospastic disorder leading to migraine attacks, Raynaud syndrome, cerebrovascular ischemia and myocardial infarction, in view of the fact that the patient has no other known risk factors for early vascular complications.
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PMID:[Vasospastic syndrome in a young women with migraine, Raynaud's disease, cerebral ischemia and myocardial infarction]. 650 63

Hyaluronidase has been shown clinically and experimentally to reduce the effects of tissue ischemia in myocardial infarction and hemorrhagic shock. Dimethyl sulfoxide (DMSO) has been shown to reverse the effects of cerebral ischemia in the primate model. A caudally based dorsal skin flap in the rat was used to study the effects of these two drugs in physiological doses on skin flaps, and to investigate their mechanisms of action. This study demonstrates that both hyaluronidase and DMSO, which are nontoxic in physiological doses, can increase the surviving length of an experimental skin flap. It is hypothesized that these substances exert their effect by decreasing tissue edema and by aiding in the transport of nutritive substances to the flap during its acute phase.
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PMID:The effect of hyaluronidase and dimethyl sulfoxide (DMSO) on experimental skin flap survival. 663 21

One-hundred-forty patients with atrial fibrillation (AF) due to non-rheumatic, non-valvular heart disease (NVHD) who suffered a cerebral infarct were identified. Fifty-three (38%) died of the initial stroke. The surviving patients were followed up to 9 years without anticoagulant therapy. In the 59 patients available for follow-up, the risk of recurrent cerebral ischemia remained at approximately 20% per year throughout the 9 year observation period. The recurrence rate was the same regardless of age, sex, previous myocardial infarction, or whether chronic AF or intermittent AF were present. Only 7 (12%) died from a second stroke, however. The high annual rate of recurrence and lack of controlled therapeutic trials in this population of patients warrant a prospective study to define the benefits and relative risks of anticoagulant therapy in AF due to NVHD.
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PMID:Risk of recurrent stroke in patients with atrial fibrillation and non-valvular heart disease. 665 28

We reviewed a series of 181 patients who were treated with therapeutic plasma exchange ( TPE ) a total of 1,389 times. Complications were associated with 22 (1.6%) of the procedures and involved 20 (11%) of the patients. Six of the complications were of a technical nature and did not affect the medical conditions of the patients. 8 patients developed the following serious medical problems: unexplained death during the post- TPE period, myocardial infarction, pulmonary embolus, loss of consciousness, myocardial ischemia, cerebral ischemia and chest pain. Although these problems were temporally associated with TPE none of them could be attributed to the TPE with certainty. The remaining eight medical complications were of a less serious nature.
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PMID:The complications of therapeutic plasma exchange. 673 Apr 24

Systematic blood coagulation analyses were conducted in 32 severely hypertensive patients treated with the angiotensin converting enzyme inhibitor captopril. Two hours after the first captopril dose, fibrin monomer complexes had already increased. This rise was even more distinct after 26 h and 1 week. Tests after 6 and 12 months of therapy showed a regression of fibrin monomer complexes to pretreatment values. In several patients with a marked increase in fibrin monomer complexes, the partial thromboplastin time (PTT) became shorter and antiplasmin activity increased. The most pronounced increase in fibrin monomer complexes was seen in patients with a rapid and excessive blood pressure reduction. The concentration of fibrin monomer complexes also rose in 15 healthy normotensive subjects, after a single oral dose of captopril (25 mg). Additionally, the PTT was shortened and antiplasmin significantly rose. An inhibition of fibrinolysis by captopril could be demonstrated by the effect on fibrin plates and thrombus weight after streptokinase. Out of 58 patients with severe hypertension and atherosclerosis treated with captopril, 7 patients suffered vascular complications during antihypertensive therapy: myocardial infarction (n = 2), coronary insufficiency (1), cerebral ischemia (1), renal insufficiency (3). These ischemic lesions may be partly explained by the alterations of coagulation and fibrinolysis under captopril therapy.
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PMID:Effects of the converting enzyme inhibitor captopril on blood coagulation and fibrinolysis in man. 675 Feb 21

Four antiplatelet drugs have been evaluated in cerebrovascular disease and in coronary heart disease--dipyridamole, clofibrate, sulfinpyrazone, and aspirin. There is no evidence that dipyridamole or clofibrate is beneficial in patients with stroke or myocardial infarction. Aspirin is effective in reducing stroke and death in patients with transient cerebral ischemia. Although aspirin has not been reported to significantly (statistically) reduce mortality or frequency of ischemic events in patients with acute myocardial infarction, five of six randomized trials showed a similar favorable trend. Sulfinpyrazone seems to be ineffective in the treatment of transient cerebral ischemia, but there is evidence that it decreases the incidence of sudden death in patients with myocardial infarction. In patients with prosthetic heart valves, the combined use of aspirin or dipyridamole with an oral anticoagulant is more effective in preventing systemic embolism than an oral anticoagulant alone.
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PMID:Selection and results of antiplatelet therapy in the prevention of stroke and myocardial infarction. 700 33

The state of blood coagulation was examined in 244 patients with acute cerebral ischemia from the data of thromboelastography performed with the use of the image recognition methods. Eight variants of the hemocoagulation system response grouped into 3 leading hemocoagulation syndromes, such as hypercoagulation, hypocoagulation and mixed (hyper-hypocoagulation) ones, were differentiated. Rapid determination of the hemocoagulation response type (with the aid of discriminant analysis, without using a computer) in any patient with cerebral ischemia makes it possible to conduct (on respective clinical indications) individualized differentiated treatment with anticoagulants, desaggregants, or their combination. The method may be of use in treating other pathological conditions (thromboembolic disease, myocardial infarction, obliterations of lower extremity vessels, etc.) with these means.
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PMID:[Use of mathematical methods of pattern recognition to evaluate the status of blood coagulation in acute cerebral ischemia]. 716 78

Transient ischaemic attacks (TIA) are defined by the focal and sudden loss of a cerebral function or the vision of one eye, resolving without sequelae within 24 hours and related to a vascular cause, thromboembolic much more frequently than haemodynamic. TIA represent between 9% and 25% of all cerebrovascular accident (CVA) with a variable global incidence from one study to another, between 0.2 and 3.3/1,000/year. The natural history of TIA is characterized by an excess mortality and an increased risk of cerebral infarction and myocardial infarction. It is therefore essential to recognize these events in order to prescribe effective preventive treatment. The clinical picture is characterized by a usually brief focal deficit (2 to 30 min, on average) and a normal clinical examination. The diagnosis is therefore exclusively based on the clinical interview. Complementary investigations have a dual objective: 1) to eliminate other diseases likely to cause transient neurological manifestations, and 2) to detect the mechanism and cause of cerebral ischaemia; the commonest causes are atheromatous stenosis and emboligenic heart disease. In addition to the routine laboratory examinations, basic complementary investigations consist of cerebral CT scan, cervical ultrasound and echocardiography. Conventional angiography is performed less and less frequently due to the progress in ultrasound and vascular imaging (helicoidal CT scan and magnetic resonance angiography). The treatment of TIA is designed to prevent cerebral and myocardial infarction, and to decrease the cardiovascular mortality [2]. In the short-term, it is essentially based on heparin, while waiting for the results of the aetiological assessment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transient cerebral ischemic complications. The neurologist's point of view]. 763 3

The case of a persistent primitive hypoglossal artery (PHA) in a 72-year-old man dead from myocardial infarction is presented. The autopsy showed the presence of a semicircular marginal infarct on the surface of the left cerebral hemisphere. The PHA anastomized the basilar artery origin with the left internal carotid artery, running through the left hypoglossal canal together with the hypoglossal nerve. The vertebral and posterior communicating arteries were hypoplastic. The PHA represented the morphological base on which the cerebral vascular insufficiency acted, following the generalized circulatory insufficiency due to the myocardial infarct, causing the cerebral infarct. Based on the embryology of the cranial arteries and on the morphological findings we suggest that the persistence of the hypoglossal artery: 1) precedes the vertebral and posterior communicating arteries hypoplasia causing it by competition for the territory of distribution; 2) gives rise to an almost complete dependence of the cerebral circulation from the carotid system with predictable ischemic consequences in the case of a critical reduction of the carotid blood flow; 3) may be associated with an anomalous structure of the vessel wall and exposes the basilar trunk to an unusual haemodynamic stress, predisposing to the onset of aneurysms.
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PMID:The persistent primitive hypoglossal artery: a rare anatomic variation with frequent clinical implications. 774 Dec 81


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