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 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbits kept on a routine diet and subjected, under conditions of free behavior, to long-term chronic (for a period of 4 months) stimulation of hypothalamic zones which give rise to negative emotions had marked stable endogenic hyperlipidemia (hypercholesterolemia, hypertriglyceridemia), a decrease in the blood heparin content, shortening of blood coagulation time, and mild (by 11%) but significant increase of arterial pressure. The extent of these changes differed with the animals. The dynamics of the increase in the blood cholesterol and triglyceride levels differed both in the degree of the increase as compared to the initial levels (by 44 and 74%, respectively) and in the latent period of attaining maximum deviations. There was a definite connection between the changes in the levels of triglycerides and heparin in blood. When rabbits were given small doses of methylthiouracil and stimulation was continued on that background, the blood cholesterol level grew still more (up to 110% of the initial level). The data obtained attest to the role of prolonged emotional stress in the genesis of stable metabolic and vasomotor disorders which may promote the development of preconditions for the origin of such cardiovascular diseases as atherosclerosis, hypertensive disease, and coronary thrombosis.
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PMID:[Effect of the chronic stimulation hypothalamic negative emotiogenic zones on a change in blood lipid and heparin content and on arterial pressure]. 67 10

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
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PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42

The epidemiology and etiology, pathophysiology, diagnosis, clinical presentation, complications, and treatment of acute myocardial infarction (AMI) are reviewed. Major risk factors for AMI include age, sex (men greater than women), family history, race, hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus, and diet. AMI occurs when there is a prolonged decrease in oxygen supply to the myocardium caused by coronary thrombosis or coronary vascular spasm. Traditional drug treatment of uncomplicated AMI includes oxygen, laxatives, and analgesics. For analgesia, narcotic agonists are generally preferred, although intravenous nitroglycerin is of value for both reducing infarct size and relieving pain. Fibrinolytic therapy is also indicated in these patients. Low-dose heparin should be initiated on admission to the hospital. Beta-adrenergic blocking agents have proven useful in reducing the incidence of ventricular fibrillation and sudden death. Antiplatelet agents may also be used to decrease long-term mortality. Recent studies have focused on reduction of infarct size using agents such as beta blockers, calcium-channel blockers, nitroglycerin, and thrombolytics. Revascularization procedures are required in some patients to re-establish adequate coronary perfusion. Most patients who survive AMI initially have a relatively uncomplicated clinical course. An increasing number of therapeutic interventions are available for acute and chronic treatment of AMI.
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PMID:Current concepts in clinical therapeutics: acute myocardial infarction. 352 26

2 young, menstruating females without any of the major risk factors (hypertension, diabetes mellitus, hyperlipidemia) developed acute myocaridal infarctions while taking oral contraceptives; their clinical histories and laboratory and arteriographic studies are presented. In the first patient (aged 29) who took Ortho-Novum 2 mg. for 11 months prior to infarction and who had an abnormal glucose tolerance test, selective coronary angiography revealed a segmental occlusion of the proximal left anterior descending coronary artery. In the second patient (aged 38) who took Enovid for several years prior to infarction, selective coronary angiography showed slight irregularity of the left anterior descending coronary artery; no evidence of akinesis or dyskinesis of the ventricular wall was noted. Although incidence of coronary artery disease in young, menstruating women has always been very low, recently there have been scattered case reports of women with acute myocardial infarction in absence of major risk factors; all cases shared the common features of oral contraceptive use prior to infarction, and unusual distribution and peculiar appearance of lesions in coronary arteries. Such reports, although rare, in young females taking synthetic estrogen do suggest that a relationship may exist between oral contraceptive agents and thromboembolic phenomena, especially coronary thrombosis. Mechanisms by which oral contraceptives might precipitate thrombosis are discussed. It is suggested that coronary artery disease should be suspected in young oral contraceptors suffering chest pain even though they are still menstruating and are free of major risk factors.
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PMID:Coronary thrombosis in young women on oral contraceptives: report of two cases and review of the literature. 470 63

This report describes the simultaneous manifestation of ischemic heart disease and nephrotic syndrome in a 37-year-old woman presenting with acute anterior myocardial infarction. Symptoms of nephrotic syndrome, such as facial and peripheral edema accompanied by proteinuria and hyperlipidemia, and onset of severe retrosternal pain developed within 24 h. Coronary angiography revealed a complete thrombotic occlusion of the proximal portion of the left anterior descending artery with no evidence of arteriosclerotic lesions. Histologic examination of renal biopsy, including electron microscopy, revealed evidence of minimal change glomerulonephritis. Ultrastructural studies demonstrated widespread effacement of epithelial foot processes. Elevated levels of circulating fibrinogen appeared to be an important factor for the hypercoagulable state in this patient, suggesting a causative relationship between coronary thrombosis and nephrotic syndrome.
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PMID:Simultaneous manifestation of acute myocardial infarction and nephrotic syndrome. 966 62

We studied both the time course and risk factors for adverse clinical events after percutaneous coronary intervention (PCI). Such information is critical to clinical decision-making, but scant quantitative data exist to describe the time course of these adverse outcomes. Patients enrolled in the Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis-II (IMPACT-II) trial were analyzed. Patients undergoing elective, urgent, or emergency PCI (n = 4,010) were randomized to receive either placebo or 1 of 2 eptifibatide regimens during intervention. We evaluated the time to the primary end point of the trial, the 30-day composite of death, myocardial infarction, repeat nonelective PCI, nonelective bypass surgery, or stenting for abrupt closure. Adverse events occurred in 407 patients (10.1%). Because the risk of events declined substantially between 6 and 9 hours (66% occurred within 6 hours), events were classified as occurring before or after 6 hours. Independent predictors of "early" events included dissection, pre- and postprocedural coronary blood flow, side-branch occlusion, procedural thrombolytic use, previous bypass, presentation with unstable angina, absence of diabetes, and hyperlipidemia. The predictors of "late" events included lower weight, increased baseline heart rate, coronary dissection, and procedural thrombolytic use. The risk of ischemic events were greatest immediately after PCI and rapidly declined, so that by 9 hours the hazard function plot was flat; 66% of events occurred within 6 hours of PCI. Knowledge of the risk factors for early and late events help risk-stratify patients before and after intervention for myocardial ischemic events.
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PMID:Timing of and risk factors for myocardial ischemic events after percutaneous coronary intervention (IMPACT-II). Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis. 1072 45

We describe the case of a young HIV-positive patient undergoing three-drug antiretroviral therapy that included a protease inhibitor for 9 months, who was admitted to the hospital with an acute myocardial infarction. A coronary angiogram revealed occlusion caused by a thrombus in the proximal third of the anterior descending artery. Complete recanalization was obtained after an angioplasty was performed. At the time of the infarction, only the triglyceride levels were found to be high. Metabolic alterations associated with the prolonged use of protease inhibitors have been described such as an increase in the triglyceride and cholesterol serum levels, diabetes, resistance to insulin, lipodystrophy, and pancreatitis. The consequences of chronic hyperlipidemia are well known in the medical literature, especially premature coronary artery disease. No family history of coronary artery disease was identified in this patient. Whether the genesis of this localized coronary thrombosis was due to a change in the metabolism of the vascular endothelium caused by the protease inhibitors, or by related dyslipidemia, is still to be determined. In this case, the data suggest a strong link between coronary insufficiency and prolonged use of the protease inhibitor.
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PMID:Acute Myocardial Infarction in a 34-Year-Old HIV-Positive Female Patient While Undergoing Active Antiretroviral Therapy Containing a Protease Inhibitor. 1108 68

Stearic acid has been claimed to be prothrombotic. Elevated plasma factor VII coagulant activity (FVIIc) may raise the risk of coronary thrombosis in the event of plaque rupture. Fibrinogen, an acute-phase protein, is necessary for normal blood clotting; however, elevated levels of fibrinogen increase the risk of coronary heart disease (CHD). Here I report the results of three controlled, human dietary intervention studies, which used a randomized crossover design to investigate the hemostatic effects of stearic acid-rich test diets in healthy young men. A diet high in stearic acid (shea butter) resulted in a 13% lower fasting plasma FVIIc than a high palmitic acid diet, and was 18% lower than a diet high in myristic and lauric acids (P = 0.001) after 3 wk of intervention. The stearic acid-rich test fat increased plasma fibrinogen concentrations slightly compared with the myristic-lauric acid diet (P < 0.01). When investigating the acute effects of fatty meals, those high in stearic acid (synthesized test fat) resulted in a smaller postprandial increase in FVII than those high in trans and oleic FA, indicating a smaller increase in activated FVII after ingesting stearic acid compared with fats high in monounsaturated FA, probably caused by lower postprandial lipemia. Thus, the present investigations did not find dietary stearic acid to be more thrombogenic, in either fasting effects compared with other long-chain FA, or in acute effects compared with dietary unsaturated FA, including trans monounsaturated FA. The slightly increased effect on fasting plasma fibrinogen may be biologically insignificant, but it should be investigated further.
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PMID:Influence of stearic acid on hemostatic risk factors in humans. 1647 7

Little is known about the management of coronary thrombosis in myeloproliferative disease. The occurrence of myocardial infarction in myeloproliferative disease is mostly attributed to coronary thrombosis due to hyperviscosity and thrombocytosis. We presented three cases of acute myocardial infarction associated with polycythemia vera in one patient (male, age 33 years) and essential thrombocytosis in two patients (male, ages 36 and 46 years). None of the patients had diabetes mellitus, hypertension, hyperlipidemia, or a positive family history. One patient with early presentation received thrombolytic therapy, and all the patients were treated with aspirin, beta-blocker, angiotensin 2 receptor blocker, statin, low-molecular-weight heparin, parenteral nitrate, and clopidogrel for acute coronary syndrome, and hydroxyurea for essential thrombocytosis. Control angiographies showed patent coronary arteries in all the cases.
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PMID:[Development of acute coronary syndrome in three patients with essential thrombocythemia or polycythemia vera]. 1845 85

A 41-year-old woman presented with acute angina in the emergency unit. Additionally, she reported pain in both legs and a weight loss of 5 kilograms within the last 10 days. ECG revealed an acute anterior myocardial infarction. However, immediate coronary angiography showed open arteries with minimal arteriosclerosis. A characteristic rise of cardiac enzymes together with an akinesis of the anterior wall and an adjacent mural thrombus was highly suggestive of a transient coronary thrombosis. Further investigations showed occlusion of multiple arteries in both legs and a splenic infarct. Although there was a typical risk profile including smoking, hyperlipidemia and regular estrogen medication, a further work-up was started. Urin analysis was decisive for the presence of proteinuria and a severe nephrotic syndrome. The definite diagnosis was made by direct biopsy of the kidney that revealed the characteristic findings of a minimal change glomerulopathy. Rapid remission could be induced by high-dose oral steroids. During routine work-up of coronary syndromes, especially in those with normal coronaries, rare but treatable causes of myocardial infarction and coagulopathy have to be thought of and should carefully be excluded.
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PMID:[41-year-old female patient with ST-elevation myocardial infarction and multiple arterial emboli]. 2043 64


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