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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apoprotein-AI concentrations were measured in whole blood in 13 male mountaineers before, during and after a strenuous climb of 8 weeks' duration. The AI concentration almost doubled in 3 weeks and remained elevated at that level for the full period of the climb. This study demonstrates the rapid rate at which high density lipoproteins can rise and the very high levels (148 +/- 29 mg/dl in whole blood) that can be reached. The rise can be attributed at least in part to exercise though other factors such as exposure to cold, hypoxia and mental stress might also have contributed.
Atherosclerosis 1979 Oct
PMID:Marked increase in high density lipoproteins in mountaineers. 22 72

Episodes of ST depression are closely related to transient decreases in regional myocardial perfusion during physical or mental stress. At the onset of these events, there is transient constriction of atherosclerotic stenoses, with an increase in myocardial demand as reflected by increases in heart rate and blood pressure. Recent research has shown that normal epicardial coronary arteries respond to these provocations and to increasing blood flow with progressive vasodilation. In contrast, atherosclerotic vessels lose this ability to dilate and may show paradoxical constriction. This abnormal constriction parallels the response of the arteries to acetylcholine, which can be used to assess the ability of the coronary endothelium to regulate vasodilation. The loss of endothelium-dependent vasodilation appears to be an important functional manifestation of coronary atherosclerosis and a potential triggering mechanism for transient ischemia. Dysfunctional endothelium may also result in a procoagulant surface, with cell adherence and local thrombus formation. Restoration of normal endothelial function is likely to emerge as an important therapeutic objective in the management of myocardial ischemia and coronary atherosclerosis.
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PMID:New insights into the management of myocardial ischemia. 144 5

Platelet function can be assessed by various techniques in vitro or in vivo, but methodological problems in the field are considerable. By use of the conventional in vitro technique (Born aggregometry), it has been shown that sympathoadrenal activation in vivo (e.g., mental stress, epinephrine infusions, exercise, and surgical stress) may result in either enhanced or reduced platelet aggregability in vitro. In vivo measures of platelet function (platelet counts, size distribution, and aggregability, as reflected by filtragometry ex vivo) more consistently indicate platelet activation during stress. Platelet-specific proteins in plasma are less readily affected by stress. Elevations of circulating epinephrine do not seem to explain proaggregatory effects of stress. Aggregatory responses to epinephrine may be enhanced by propranolol in vitro, because of unopposed alpha 2-stimulation (beta 2-stimulation attenuates aggregation). Other in vitro effects of beta-blockade seem to be related to nonspecific effects at very high concentrations. Studies of the effects of beta-blockade in vivo have yielded conflicting data. Some studies suggest that beta 2-blockade may reduce platelet cAMP and enhance aggregability in vitro; other studies show that propranolol attenuates platelet aggregability, particularly in patients with ischemic heart disease. There is, however, a need for well-conducted studies assessing platelet function in vivo during beta-blockade to evaluate whether platelet responses contribute to favorable effects of beta-blockade in unstable angina, for example, or after myocardial infarction. Methodological developments are needed to better understand platelet function in vivo in humans. Available data suggest that stress enhances and beta-blockade reduces platelet function. This may influence thrombus formation in the short term and atherosclerosis in the long term.
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PMID:Effects of stress and beta-blockade on platelet function. 168 10

Although there has been extensive research attempting to identify psychophysiologic mechanisms linking psychological events and behavior patterns with risk for coronary heart disease, these are important potential mechanisms that remain largely unexplored. One of these mechanisms is thrombosis, which is widely recognized as the precipitant of acute coronary events (myocardial infarction and sudden ischemic death). A major element in arterial thrombosis is the platelet, and platelet inhibition has been shown to be effective in preventing coronary events. In the present paper, platelet physiology and pathophysiology are reviewed. Platelet function testing and the clinical role of platelet activation in atherosclerosis and acute coronary events are also discussed. Because epinephrine and possibly shear stress are clinically important activators of platelets, it is proposed that platelet reactivity to psychological stress may be a major mechanism in coronary events. The literature to date supports the hypothesis that platelet activity is increased by emotional stress. Suggestions are made for future research in this area.
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PMID:Platelets and coronary heart disease: potential psychophysiologic mechanisms. 175 49

Platelet aggregability was studied in 18 healthy volunteers during mental stress (a colour word test; CWT) and low- and high-dose adrenaline infusions using an ex vivo technique (filtragometry) and conventional in vitro aggregometry. CWT and high-dose adrenaline (3.4 nmol l-1 in plasma) shortened filtragometry readings, suggesting increased platelet aggregability in vivo. Low-dose adrenaline had no effect despite higher adrenaline levels in plasma (0.9 nmol l-1) than during CWT (0.4 nmol l-1). Platelet sensitivity to ADP in vitro was reduced following CWT and further reduced following adrenaline infusions. In vitro, adrenaline (50 nmol l-1) had little effect on platelet aggregation per se, but enhanced aggregability evoked by ADP (at ED50). Adrenaline potentiation of ADP-induced aggregation was enhanced after CWT, but was not related to filtragometry responsiveness to stress in vivo. Serum LDL-cholesterol levels were inversely correlated to filtragometry readings at rest, suggesting an adverse influence on platelet aggregability in vivo. HDL-cholesterol levels were inversely correlated to platelet sensitivity to ADP in vitro, suggesting a positive influence. Thus, sympatho-adrenal activation enhances platelet aggregability in vivo (as assessed by ex vivo filtragometry), but adrenaline alone cannot explain the pro-aggregatory effect of mental stress. Serum lipoprotein alterations associated with increased risk for atherosclerosis seem to enhance platelet aggregability. The conventional in vitro technique may poorly reflect platelet aggregability in vivo.
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PMID:Platelet aggregability in humans: contrasting in vivo and in vitro findings during sympatho-adrenal activation and relationship to serum lipids. 212 99

Although mental stress as well as hypercholesterolaemia have been individually linked with atherosclerosis, the relationship between mental stress and hypercholesterolaemia is poorly understood. Serum lipid profile was studied in eight male medical student volunteers before, near and after examinations. Identical observations were also made on seven well-matched control volunteers. As compared to pre-exam levels, total serum cholesterol (T-C) increased significantly (P less than 0.05) near exams, and so did low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C). The HDL-C/T-C and HDL-C/LDL-C ratios remained essentially constant throughout the study. Control subjects did not show any significant change in serum lipid profile. Further serial measurement in five of the subjects revealed that examination-related changes were transient. Moreover, a second examination after about 40 days did not evoke any change in the lipid profile. The response to examination stress may be related to the enhanced utilisation of cholesterol in the adrenal cortex for steroidogenesis.
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PMID:Relationship of examination stress to serum lipid profile. 381 30

The effect of standardized mental stress on the hemostatic system was studied in 160 patients with coronary heart disease. The diagnosis of coronary atherosclerosis was documented by selective coronary angiographic findings. Emotional tension was modelled using the method of counting with interswitching in conditions of time deficit, irritating light and sound signals, as well as critical remarks about the work performed. According to the protective-adaptive activation of the anti-clotting system, the patients were divided into two groups: 1 with activation of heparin activity of the blood and fibrinolysis, 2 with depressed fibrinolysis and lowered blood heparin. Prior to the onset of the study the patients of both groups exhibited hypercoagulation as compared with the control group. The maximum degree of hypercoagulation was observed in the second group patients. Hypercoagulative changes both at rest and under stress were shown to depend on the degree of coronary artery damage.
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PMID:[Changes in the hemostatic system and the progression of arteriosclerosis in ischemic heart disease patients]. 652 Dec 50

Mental stress often causes myocardial ischemia in patients with coronary artery disease (CAD). There is increasing evidence that the coronary microcirculation of patients with atherosclerosis may be dysfunctional, with the potential of contributing to myocardial ischemia. This study investigated sympathetically mediated coronary microcirculatory and regional noradrenergic effects of mental stress. We measured left anterior descending coronary artery blood flow and norepinephrine kinetics at rest and during a 10-minute video game in 10 CAD patients with nonsignificant atherosclerosis of this artery and in 5 patients with normal coronary angiograms (NCA). The 2 groups did not differ in their responses of systemic and cardiac norepinephrine spillovers, heart rate, and blood pressure during mental stress. Patients with NCA had microvascular dilation during mental stress (26 +/- 9% [mean +/- SD] decline in coronary vascular resistance from baseline, p < 0.01), whereas patients with CAD did not (9 +/- 20% decline, p = 0.11). Six patients with CAD then received intracoronary phentolamine (1.7 micrograms/kg/min for 5 minutes, followed by 0.17 micrograms/kg/min) and played the video game again. In contrast to nonsignificant changes in coronary resistance during the initial video game (6 +/- 15% decline, p = 0.20), coronary vascular resistance decreased significantly during the repeat video game (25 +/- 19% decline, p = 0.02). Vasomotor responses of epicardial coronary artery segments did not differ between the 2 video game studies. Five other patients (4 with CAD, 1 with NCA) repeated the video game during intracoronary administration of 5% dextrose, with systemic and coronary hemodynamic and noradrenergic responses unchanged from those during the initial video game.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetically mediated effects of mental stress on the cardiac microcirculation of patients with coronary artery disease. 761 Nov 45

The role of mental stress in ischemic heart disease is two-fold: as a risk factor of coronary artery disease and as a trigger of acute ischemic attacks in patients with established coronary atherosclerosis. The role of stress as a risk factor is still controversial. Data regarding the relationship between occupational factors and development of coronary atherosclerosis have not been confirmed. A type personality, above all when anger and hostility traits are present, seems to be a predisposing factor for the development of coronary artery disease. These data however, were not confirmed in study groups including patients with a higher prevalence of other, more important, risk factors. Stress can have an important role as a trigger of acute ischemic attacks. This is indirectly shown by the circadian distribution of the main manifestations of ischemic heart disease (sudden death, myocardial infarct, ST segment depression). In fact, their incidence is significantly higher in the morning hours, after awakening, when mental stress is higher. In the laboratory setting, mental stress can induce myocardial ischemia in a variable percentage of patients (0 to 80%). Prevalence of mental stress-induced myocardial ischemia varies depending on the stressor used, the patients group and, above all, the diagnostic tool. Ischemic episodes induced by mental stress, in fact, are generally silent and less severe and extensive than those elicited by exercise stress testing. It is therefore often necessary to use methods, such as myocardial scintigraphy, with higher sensitivity for the detection of myocardial ischemia in comparison with ECG. Patients with mental stress-induced myocardial ischemia tend to present higher scores on measures of aggressivity, anger and hostility. These psychological features are related to a hightened cardiovascular reactivity with a brisk and greater increase in heart rate and blood pressure after exposure to stress. It would be therefore useful to identify patients with such a behaviour by psychological assessment and/or analysis of sympatho-vagal balance by analysis of heart rate variability. The mechanism by which mental stress can induce myocardial ischemia is represented by an increase in myocardial oxygen demand, through the increased heart rate and blood pressure, probably associated with an increase in coronary vascular resistance. This last phenomenon is likely caused by small coronary vessel constriction mediated by alpha-adrenergic activation and by a reduced EDRF release by the damaged endothelium.
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PMID:[Stress and ischemic heart disease]. 802 44

The vascular endothelium is the site of formation of several powerful mediators. One of these is NO, a chemically unstable radical formed by enzymatic conversion of L-arginine in the presence of molecular oxygen. NO elicits relaxation of VSMC by activating cytosolic guanylate cyclase. NO also counteracts platelet adhesion and aggregation. The biological actions of NO make it a key substance in the endogenous defense against vascular occlusion and thrombosis. The basal formation of NO maintains a moderate but significant vasodilation in the systemic resistance vessels and counteracts platelet activity. When blood flow in conduit arteries is increased there is an augmented endothelial formation of NO, eliciting flow-dependent vasodilation. Beside this, several vasodilators (acetylcholine, bradykinin, histamine, substance P) operate by stimulating endothelial NO formation. On the other hand, drugs like nitroglycerin and papaverine operate independently of the vascular endothelium. Vasodilator mechanisms, physiological as well as pharmacological, may therefore be characterized as endothelium-dependent (i.e. NO-mediated), or endothelium-independent (i.e. not mediated by NO). Physiologically, mixed mechanisms occur. Failure of the vascular endothelium to elicit NO-mediated vasodilatation may be due to decreased formation, increased degradation, decreased sensitivity to the NO formed, or a mixture of these factors. Irrespective of the mechanism behind, this is referred to as endothelial dysfunction. Endothelial dysfunction occurs in several cardiovascular settings, like atherosclerosis, hypercholesterolaemia, diabetes, and essential hypertension. Endothelial dysfunction leads to an impaired tissue perfusion, increased local vascular resistance, decreased defense against thrombus formation, and possibly also decreased defense against hypertrophy of the VSMC in the vessel wall media. In patients with CHD, endothelial dysfunction leads to an impaired coronary flow response to physical and mental stress, and to promotion of platelet adherence and aggregability. Endothelial dysfunction is thereby a probable aggravating factor in the atherosclerotic process, adding a functional component on top of the structural lesions characterizing this disease. A particular form of endothelial dysfunction, limited to the arterial resistance vessels, may explain the symptoms and clinical characteristics of microvascular angina. In patients with essential hypertension, endothelial dysfunction prevails, adding a functional component to the structural factors also in this disease. Hitherto, the only therapeutic tools available to restore endothelial dysfunction appear to be restriction of the dietary intake of lipids, possibly reinforced with intake of antioxidants like fish oil and vitamin E. However, large clinical trials to confirm the efficacy of such therapy in reversing endothelial dysfunction have not been conducted. In the future, more directly acting therapeutic regimens, aimed at supporting or substituting the endogenous formation of NO, are likely to appear as well.
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PMID:Endothelial nitric oxide and cardiovascular disease. 815 Dec 63


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