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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Information obtained during the past decade suggests that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering coronary thrombosis is supported by finding that (1) the frequencies of the onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations, with similar increases in the period from 6 AM to noon; (2) the frequency of transient myocardial ischemia shows a similar increase in the morning, and episodes are often preceded by mental or physical triggers; (3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi; (4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state, or coronary vasoconstriction, are accentuated in the morning; and (5) aspirin and beta-adrenergic blocking agents that affect certain of these processes have been shown to prevent disease onset. The hypothesis presented is that occlusive coronary thrombosis occurs when (1) an atherosclerotic plaque becomes vulnerable to rupture; (2) mental or physical stress causes the plaque to rupture; and (3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of the onset of acute disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.
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PMID:Triggering and hourly variation of onset of arterial thrombosis. 134 90

The importance of the thrombotic component of coronary heart disease is increasingly recognised, and in particular the role of the coagulation system in this process. The Northwick Park Heart study was the first major prospective study to identify both fibrinogen and factor VIIc as risk factors, as powerful as total cholesterol in predicting ischaemic events. Since then, a number of epidemiological studies have confirmed the importance of fibrinogen, not just in CHD but in stroke as well. A variety of environmental factors are known to influence levels of factor VII and fibrinogen and therefore support their role in the development of coronary thrombosis. Both are known to increase with age and body weight and are relatively elevated in diabetes. Fibrinogen is strongly related to smoking habit and a substantial proportion of the IHD risk associated with smoking is mediated through this relationship. There is a dose response effect between number of cigarettes smoked and level of fibrinogen and an inverse relationship with time since cessation of the habit. Factor VII is known to correlate with total cholesterol level, and there is a relationship between dietary variability of fat intake and factor VII, which is likely to play an important role in the risk of CHD. The case for using either anticoagulation or anti platelet agents in secondary prevention of myocardial infarction is now clear, but there are still uncertainties in primary prevention which relate to the ideal dose intensity of either aspirin or anti-coagulation and the type of patient most likely to benefit. The ongoing Thrombosis Prevention Trial identifies middle-aged males at high risk of a myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma fibrinogen and factor VII as risk factors for cardiovascular disease. 150 57

A wide array of clinical trials over the past two decades has established that aspirin is indicated to prevent myocardial infarction in patients with clinically evident coronary artery disease, and to prevent stroke in patients with a history of stroke or TIAs. The most likely mechanism by which aspirin decreases the incidence of myocardial infarction is by preventing coronary thrombosis in patients with obstructive coronary artery disease. This protective effect of aspirin should occur in patients with both clinically silent and clinically evident coronary artery disease. For this reason, it has been recommended that patients with risk factors for coronary artery disease also should be treated with prophylactic aspirin. Advanced age is one of the strongest risk factors for coronary artery disease, and the mortality of myocardial infarction rises steeply with increased age. A prospective randomized study of US male physicians without a history of myocardial infarction demonstrated a 44% reduction in myocardial infarction in those treated with 325 mg aspirin every other day. The treatment effect occurred only in those aged 50 or older. A prospective study of US nurses aged 34 to 65, without a history of diagnosed coronary artery disease, demonstrated a 32% decrease in those who took one to six aspirin per week. Again, the treatment effect was seen only in those aged 50 or older. Given these findings, the authors believe that prophylactic aspirin is indicated in men and women aged 50 or older who do not have contraindications to its use. The authors recommend a dose of 325 mg of aspirin every other day, a dose with minimal side effects.
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PMID:Prophylactic aspirin and the elderly population. 157 70

An animal model of coronary artery spasm-coronary thrombosis-acute myocardial infarction (CAS-CATH-AMI) was obtained by injecting ergonovine(0.22 mg/kg) directly into the left coronary artery (LCA) of 17 dogs under general anesthesia. Various parameters of the experimental group were compared with those of the control group consisting of 5 dogs. The following changes were observed: increased average arterial blood pressure (MAP), pulmonary capillary wedge pressure (PCWP), stroke volume (SV, P less than 0.05), PAP (P less than 0.01) transient decreased cardiac output (CO); elevated ST-T in EKG; ventricular arrhythmia in 60% of animals; transient spasm of 50%-75% of LCA in the LCA angiographs; enhancement of platelet aggregation and TXB2 (P less than 0.01) and decline of 6 Keto-PGF1 alpha, SAO2 (P less than 0.05), indicating acute hypoxia and high coagulating pathophysiological changes after CAS. Pathological examination one hour after CAS induction revealed CATH(53%) in addition to CAS induced morphological changes of the CA and myocardium, as well as necrosis of the corresponding sites in its early stage. This study provides a reproducible animal model of CAS-CATH-AMI for research of coronary heart disease and pathomorphological criteria for the diagnosis of CAS. It also shows that CAS may lead to CATH-AMI, therefore, prevention of CATH and AMI is possible.
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PMID:Animal model of coronary artery spasm-coronary thrombosis-acute myocardial infarction. A study on hemodynamics, EKG, coronary angiography, biochemistry and pathology. 211 65

Bay U 3405 [(3R)-3-(4-fluorophenylsulfonamido)-1,2,3,4-tetrahydro-9- carbazolepropanoic acid] potently inhibits platelet aggregation, thromboxane A2-induced contraction of smooth muscles, and coronary artery thrombosis. We have previously demonstrated inhibition of arachidonic acid-induced sudden death by Bay U 3405. The purpose of this study was to investigate the effects of Bay U 3405 on thromboembolism provoked by collagen. Collagen fibrils dissolved in an isotonic glucose solution were injected into a marginal ear vein of anesthetized rabbits. Sudden death occurred within a few minutes due to elevated thromboxane A2 levels causing intravascular platelet aggregation and myocardial ischemia. In the vehicle-treated group, 100% of the animals died. One of the most prominent parameters was the massive fall in blood pressure. All animals pretreated with 10 mg/kg orally Bay U 3405 survived, showing only a transient hypotensive effect. Tracings of the electrocardiogram and heart rate were unchanged. Bay U 3405 will therefore be useful to elucidate the role of thromboxane A2 in various cardiovascular and respiratory diseases.
Stroke 1990 Dec
PMID:Effect of Bay U 3405, a new thromboxane antagonist, on collagen-induced thromboembolism in rabbits. 226 Jan 39

Recognition that myocardial infarction is caused by coronary thrombosis has stimulated a search for a safe, rapidly acting, and effective thrombolytic regimen. Tissue plasminogen activator (t-PA) can provide relatively clot-selective thrombolysis, but one quarter of patients fail to achieve reperfusion, lysis speed is not optimal, and higher doses have been associated with an increased incidence of hemorrhagic stroke. We report the results of a multicenter study of pro-urokinase, a second naturally occurring plasminogen activator that has structural similarities to t-PA but has a different mechanism of action. Pro-urokinase was administered 3.9 +/- 1.1 hours after the onset of chest pain to 40 patients with acute myocardial infarction with angiographically confirmed complete coronary occlusion (TIMI grade 0). After a 90-minute intravenous infusion of pro-urokinase (4.7-9 million units, 36-69 mg) 51% (20 of 39) of the patients demonstrated reperfusion (TIMI grade 2 or 3) occurring 64.8 +/- 22.3 minutes after initiation of therapy. Fibrinogen levels fell only 10 +/- 17% from baseline, confirming the fibrin specificity of pro-urokinase. As with t-PA, however, this specificity was only relative. alpha 2-Antiplasmin decreased to 39% and plasminogen decreased to 64% of initial values. Fibrinogen degradation products increased 63% and the fibrin-specific D-dimer increased 8.7-fold. Thus, pro-urokinase produces relatively clot-selective coronary thrombolysis similar to that produced by t-PA, but the use of either pro-urokinase or t-PA alone in higher doses would be likely to produce more nonspecific effects.
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PMID:Clot-selective coronary thrombolysis with pro-urokinase. 249 4

During the past 5 years it has been clearly established that there is a prominent morning increase in the frequency of onset of acute myocardial infarction. Similar increases have also been observed for the related conditions of sudden cardiac death, stroke and episodes of transient myocardial ischemia. The period from 6 a.m. to noon is also a time when a number of physiologic processes that could contribute to the onset of coronary thrombosis are intensified. Arterial pressure, which could lead to plaque rupture, rises; coronary tone increases; and platelet aggregability, which could contribute to a hypercoagulable state, increases. The immediate significance of these observations is the emphasis that should be placed on pharmacologic protection of patients during the morning hours. The primary longer-term significance of the recognition of the morning increase of onset of acute cardiovascular disease is the contribution it makes to the concept that onset of coronary thrombosis at any time of the day is frequently triggered by the activities of the patient. Investigation of this possibility may yield more information about the mechanism of disease onset and facilitate design of more effective preventive therapy.
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PMID:Morning increase of onset of myocardial infarction. Implications concerning triggering events. 256 81

Information obtained during the past decade suggests the need to reexamine the possibility that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering onset of coronary thrombosis is supported by the findings that 1) the frequencies of onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations with parallel increases in the period from 6:00 AM to noon, 2) transient myocardial ischemia shows a similar morning increase, and episodes are often preceded by mental or physical triggers, 3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi, 4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state or coronary vasoconstriction, are accentuated in the morning, and 5) aspirin and beta-adrenergic blocking agents, which block certain of these processes, have been shown to prevent disease onset. The hypothesis is presented that occlusive coronary thrombosis occurs when 1) an atherosclerotic plaque becomes vulnerable to rupture, 2) mental or physical stress causes the plaque to rupture, and 3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of onset of acute disease suggests the need for pharmacologic protection of patients during vulnerable periods, and provides clues to mechanism, the investigations of which may lead to improved methods of prevention.
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PMID:Circadian variation and triggers of onset of acute cardiovascular disease. 229 45

This review has discussed some metabolic and endocrine changes that can be associated with a stress type of metabolism, diabetes, obesity, hypertension, smoking and the consumption of diets rich in fat and refined sugar, or poor in ascorbate. These are some of the risk factors associated with premature atherosclerosis, coronary thrombosis and stroke. It has been proposed that an increased control of metabolism by the 'stress' or counter-regulatory hormones, relative to insulin, is a common feature of these risk factors. Particular emphasis was placed upon the action of the glucocorticoids which can produce insulin insensitivity, leading to hyperglycaemia, hypertriglyceridaemia, hypercholesterolaemia and hyperinsulinaemia. Furthermore, glucocorticoids can decrease energy expenditure and, together with insulin, promote energy deposition. These observations provide a partial explanation for the metabolic changes that can accompany the risk factors and clarify why they interact in promoting atherosclerosis.
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PMID:Possible connections between stress, diabetes, obesity, hypertension and altered lipoprotein metabolism that may result in atherosclerosis. 268 77

There are 2 striking differences in the practice of medicine in the US and in the UK: 1) in the former, there is a great emphasis on private medicine, and 2) in the US there is a much higher incidence of litigation, whereas in the UK, family planning services are free, and litigation in this area is almost unknown. British medical opinion agrees with the US on the following oral contraceptive contraindications: 1) cancer of the breast, ovary, uterus, vagina, or cervix; 2) coronary thrombosis, pulmonary embolism, deep vein thrombosis, angina pectoris, or stroke; and 3) unusual or unexplained vaginal bleeding. Both countries agree that it is inadvisable to give the combined pill over the age of 45, and over the age of 35 in smokers. The UK agrees with 75% of the routines adopted by US doctors on a patient's 1st visit for oral contraceptives. However, a patient who becomes amenorrheic while taking the pill is not regarded as lightly in the UK as she would be in the US; she is closely monitored. If 1 of 4 risk factors (age 35 or over, hypertension, obesity, or smoking) is evident, a patient in the UK is closely supervised while taking the pill. If more than 2 risk factors are present, a UK doctor may advise against the pill. Since the 1960s the media have both praisd and condemned the pill. There is no doubt that, in the field of contraceptive advice, the US and the UK lead the way, and a closer liaison between the 2 medical professions is essential to reassure patients.
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PMID:Contraceptive advice: how the English differ from the Americans. 309 Feb 54


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