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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
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PMID:Etiology and pathogenesis of thromboembolism. 176 43

Epidemiological surveys show the clear association of hypertension with an increased risk of developing ischaemic heart disease. One method of quantifying atherosclerosis is to measure, at necropsy, the percentage of the intimal surface of the coronary arteries or aorta which is occupied by raised plaques. When this is done in a large number of subjects the amount of intimal involvement in any particular geographical population correlates directly with the frequency of ischaemic heart disease. In all these populations, whether at a high risk or low risk of developing ischaemic heart disease, hypertensive subjects have a greater intimal involvement by plaques than normotensive subjects. Thus, the increased risk in hypertension is, in part, mediated by possession of more plaques. Plaque growth is due to the accumulation of lipid from the plasma, the ingress of monocytes with their conversion to lipid filled foam cells and the formation of collagen by smooth muscle cells. Hypertension may act by altering endothelial function to potentiate all these processes. Mechanical stress on endothelial cells will evoke the formation of growth factors for smooth muscle cells. Plaque growth in man is also episodic due to the formation of thrombi; a proportion of these episodes are symptomatic producing acute myocardial ischaemia but the majority are silent leading to sudden plaque expansion. Thrombi over plaques are either due to endothelial denudation injury or more commonly due to the tearing of the cap of a plaque leading to deep intimal injury. Necropsy surveys of control populations show that subjects with hypertension have a greater frequency of recent plaque tears compared with normotensive subjects.
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PMID:Hypertension and atherosclerotic (ischaemic) heart disease. 194 81

Intermittent balloon occlusion of the coronary sinus was applied to 11 open chest dogs subjected to 3 hours of ligation of the left anterior descending coronary artery followed by 8 to 12 days of reperfusion. Anticoagulants were not given during the reperfusion period. Risk region was assessed by planimetry of autoradiographs made from ventricular slices. Infarct size was equivalent when assessed by planimetry of ventricular slices before and after staining with triphenyltetrazolium chloride. In the seven survivors, 30 +/- 8% of the risk region was infarcted. Seven of 11 control dogs survived (p = NS); 75 +/- 4% of the risk region was infarcted in the control animals (p less than 0.01 versus treated survivors). Light microscopic inspection of specimens stained with hematoxylin-eosin confirmed the border between necrotic and preserved myocardium. Thrombus was observed in the coronary sinus in all survivors in the treatment group. These findings confirm earlier short-term studies that demonstrated a potent anti-ischemic effect of intermittent coronary sinus occlusion. At the same time, coronary sinus thrombosis warrants caution in the application of this technique to myocardial ischemia in humans.
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PMID:Intermittent coronary sinus occlusion in dogs: reduction of infarct size 10 days after reperfusion. 357 46

To define the pathological features of Kawasaki disease (KD) in the healed stage (over 40 days of illness), 69 autopsied infants with clinically typical KD (25 in the healed stage and 38 in the acute stage) and atypical KD (four in the healed stage and two in the acute stage) were examined. In the medium-sized arteries with coronary aneurysm in KD, panvasculitis was evident in the acute stages, while scar formation was noted in the healed stage. Thrombi, marked intimal thickening, marked stenosis, and recanalization were seen in the coronary arteries. In KD without aneurysm, acute inflammation was localized in the intima and the perivascular area of the coronary arteries in the acute stages, but was absent in the healed stage. Although intimal thickening was noted, marked stenosis and thrombi were not evident in KD without aneurysm. In KD with and without aneurysm, acute angiitis in small arteries and micro-vessels and acute inflammation of various organs were noted in the acute stages, but disappeared in the healed stage. Fibrinoid necrosis of the artery was rare in the acute stages and was not noted in the healed stage. Atypical cases of KD showed the same pathological features as those in cases with clinically typical KD. The common cause of death in the healed stage was ischemic heart disease. Old myocardial infarction was noted in 80% of the cases, and acute myocardial infarction was seen in 35%. KD is an acute systemic inflammatory disease and KD without aneurysm is a disease with mild angiitis.
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PMID:Pathology of Kawasaki disease in the healed stage. Relationships between typical and atypical cases of Kawasaki disease. 376 34

In spite of major limitation in the application of computerized transmission tomography to the cardiovascular system, it has several unique advantages. The aim of this lecture is to give the recent advance and perspective of cardiac CT examination. The advantages include excellent spatial and contrast resolution and obtaining three dimensional images of the heart and the great vessels. Although CT scanning of the heart without contrast medium provides vague differentiation of the cardiac structures, with contrast medium injection it gives more precise information. Rapid sequential scanning with table movement may be useful to give tomographic images covering the whole heart. Since temporal resolution is improved with rapid sequential scanning at the fixed position, functional analysis of the cardiovascular system in a slice, for example patency of the aorto-coronary bypass graft, can be easily examined with excellent accuracy. ECG-gated scanning provides anatomical information with good temporal resolution, as well as functional values, such as left ventricular mass, left ventricular volume, left ventricular ejection fraction and cardiac output. These values obtained from cardiac CT showed a good correlation with the values from cine left ventriculography and a dye-dilution study. Thrombi or tumors in the cardiovascular lumen could be detected with CT examination. Attenuation of left ventricular wall motion, thinning of the ventricular wall and reduced regional myocardial thickness seemed to be major landmarks for computed tomographic diagnosis in ischemic heart disease. Cardiac CT examination may give the comparable information with echocardiography in this field. In the future, ultra-fast CT scanners will be developed to give the multiple section capacity for three dimensional imaging and to improve temporal resolution for cardiac functional analysis.
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PMID:[Application of computed tomography to cardiovascular system: present status and perspective]. 667 84

The thrombolytic and hemodynamic properties of intracoronary streptokinase (SK) application were studied in an in-vivo canine model with left circumflex coronary artery thrombosis, initiated by electrical stimulation (150 microA, DC for 6 h) of the artery's intima via an implanted silver wire. In pentobarbital-anesthetized, open-chest dogs acute myocardial ischemia was determined by a dehydrogenase-dependent staining of the coronary artery perfusion area. Thrombus weight was determined post-mortem. Saline-treated control animals developed coronary thrombosis after 3.1 +/- 0.4 h of stimulation. Thrombus weight was 64 +/- 3.1 mg. Acute infarct volume was 32 +/- 3.1% of total left ventricle, and 53 +/- 6.2% of the coronary artery risk region for infarction. At occlusive thrombosis, blood pressure, ventricular pressure and the LV dP/dtmax fell significantly, whereas heart rate and the end-diastolic filling pressure increased. Severe ST-segment elevation and loss of R wave voltage indicated myocardial ischemia. At 20 min into thrombotic vessel occlusion, 2,000 IU/min SK were infused by way of a Sones-catheter advanced to the thrombus. Coronary thrombosis consistently lysed after 12 +/- 0.7 min of SK infusion, and coronary blood flow as well as hemodynamics were restored. Only minor acute infarction was found indicating viability of ischemic jeopardized myocardium. In another group, the continuous SK-infusion (20 IU/kg/min) concomitant with electrical vessel stimulation prevented coronary thrombosis and acute ischemia, and no significant hemodynamic alterations were noted. These results indicate that intracoronary SK-infusion can lyse acute thrombosis as sequel of electrical stimulation. This prevents development of acute myocardial infarction. Continuous SK-infusion can completely prevent coronary thrombosis in response to intimal injury.
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PMID:Thrombolytic effects of intracoronary streptokinase on canine coronary artery thrombosis. 673 17

The relationship between thrombosis and atherosclerosis has been already suggested in the middle of the last century. More recently, in 1976 a hypothesis has been put forward which emphasize the leading role of chronic injury to endothelial cells followed by platelet attachment and the release of platelet derived growth factors in pathogenesis of atherosclerosis. There is also a growing body of evidence that cytokines, thrombin and the fibrinolytic system are involved in the initiation and progression of atherosclerotic lesions. Lipoprotein (a) is emerging as a link between atherogenic role of lipids and the haemostatic system. At the same time epidemiological data are pointing at the possible role of fibrinogen, factor VII and plasminogen activator inhibitor-1 as risk factors for ischemic heart disease. Thrombus formation is also responsible for the majority of acute coronary syndromes. On the other hand aspirin and other antiplatelet drugs seem to protect from vascular complications of atherosclerosis. Than the question which rather arises is: what is the best antithrombotic strategy in patients with cardiovascular diseases?
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PMID:[Should hemostatic factors be considered in the prevention of cardiovascular disease?]. 797 94

Thrombotic risk factors may be important in determining cardiovascular outcome in patients with symptomatic peripheral arterial disease. A cohort study with a 6-year follow-up period was established to determine the relationships between haemostatic and rheological factors and incident ischaemic heart disease (IHD) and stroke events in patients with peripheral arterial disease. A consecutive series of 607 patients with intermittent claudication was examined between 1989 and 1990 at the Peripheral Vascular Clinic, Royal Infirmary of Edinburgh. Main outcome measures were combined fatal and non-fatal stroke, non-fatal myocardial infarction (MI), coronary death and total coronary events. A total of 210 patients died during follow-up. 203 patients did not experience a vascular event or deterioration of limb ischaemia. Median levels of fibrinogen, von Willebrand factor (VWF), tissue plasminogen activator (t-PA) antigen, fibrin D-dimer and whole blood viscosity were significantly higher in those who experienced an event compared with those who did not. After adjusting for age and sex, fibrin D-dimer was significantly associated with risk of non-fatal myocardial infarction (RR 1.50, 95% CI 1.09-2.06, P < or = 0.01). Both fibrinogen and fibrin D-dimer were associated with risk of total coronary events (P < or = 0.05). The risk of stroke was related to baseline levels of t-PA antigen (RR 1.87, 95% CI 1.04-3.34, P < or = 0.05) and whole blood viscosity (RR 1.33, 95% CI 1.07-1.65, P < or = 0.01). All the relationships became weaker and statistically non-significant after further adjustment for cigarette smoking, systolic blood pressure, glucose and baseline IHD. The associations of these factors to IHD and stroke may therefore be partly related to cardiovascular risk factors, but are likely to be important in the pathogenesis of future atherothrombotic events in subjects with peripheral arterial disease.
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PMID:Haemostatic factors and prediction of ischaemic heart disease and stroke in claudicants. 953 45

Thrombus formation and vasospasm are involved in the initiation of acute ischemic events in the heart. Gender differences in persons with coronary artery disease and the incidence of myocardial ischemia have been clearly documented. In addition, it is well established that sex hormones influence the risk of developing coronary artery disease. Epidemiologic studies suggest that estrogen may exert a protective effect, yet the results of recently completed and ongoing prospective trials of estrogen and hormone (estrogen + progesterone) replacement suggest that these hormones can increase thrombotic events in postmenopausal women. This review focuses on sex (gender) differences in hemostasis and vascular reactivity and on the influence that sex hormones have on these physiologic systems. This review takes the novel approach of focusing on sex differences in hemostasis and vascular reactivity in healthy premenopausal women and men of a similar age. By comparing men and women in this age group, the confounding issues of age, pathology, or decline in sex hormone levels are avoided. Animal and in vitro investigations pertinent to examining potential cellular mechanism(s) of sex hormones in mediating these sex differences are discussed. We assume there is a relationship between the normal physiologic and pathologic effects of sex hormones; elucidating sex differences in normal cardiovascular function will help clarify the basis for sex differences in the incidence and manifestations of coronary heart disease and will aid in the future development of gender-specific therapies for cardiovascular disease.
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PMID:Sex differences and the effects of sex hormones on hemostasis and vascular reactivity. 1172 46

The evaluation of adolescents with chest pain, elevated cardiac enzymes, and abnormal electrocardiograms (ECGs) continues to pose diagnostic and management dilemmas. Myocardial infarction is an uncommon finding in this population and alternative diagnoses must be considered. Our database was retrospectively reviewed for adolescents age 16-18 years without prior cardiac history who underwent cardiac catheterization. Patients who presented with chest pain, elevated cardiac enzymes, normal ejection fraction, and abnormal ECGs were included. Management, diagnostic testing, and final diagnosis were reviewed. Nine adolescents (eight males and one female) without prior cardiac history were identified. The ECG findings in all patients were consistent with myocardial ischemia in a coronary distribution. Thrombotic coronary occlusion was not found in any patient. In adolescents without prior cardiac history of risk factors for myocardial infarction such as Kawasaki disease, familial hypercholesterolemia, or drug use who present with chest pain, multiple diagnoses must be considered even in the presence of focal ischemic ECG changes and elevated cardiac enzymes. Thrombolytic therapy or anticoagulation should be withheld until a definitive diagnosis of myocardial infarction has been made. Magnetic resonance imaging is the most useful tool to differentiate focal myocarditis from myocardial infarction.
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PMID:"Myocardial infarction" in adolescents: do we have the correct diagnosis? 1554 13


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