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

Several studies have shown that bus driving is a high risk occupation for ischaemic heart disease (IHD). In order to study contributing factors in the job, all full-time bus drivers in the three major cities in Denmark were followed for ten years. It was hypothesized that bus drivers who reported job strain and job dissatisfaction would have an excess risk of subsequent death due to IHD. Of 2465 bus drivers, 2045 (83%) responded to a questionnaire distributed in 1978 on psychosocial well-being and work conditions. The men had their mortality recorded during the years 1978-1988. Information on causes of death was obtained from the Danish Register of Causes of Death. Some 212 respondents died during the follow-up period, 59 from IHD Relative risk (RR) for death due to IHD and all other causes of death was calculated. As expected, we found a significantly increased risk of death due to IHD in bus drivers working in high traffic intensity areas, RR = 1.6. In contrast to what was expected, men who reported never experiencing mental exhaustion after work, that their job was very varied, that their job was something special, and those who reported that they would choose the same job again, had an excess risk. Death due to other causes was positively associated with marital status only. We suggest that inconsistencies in the literature on self-assessed job strain and risk of IHD may be partly explained by the fact that studies in general have focused on absence or presence of the psychosocial factor in question. A more differentiated assessment of exposure might prove more useful.
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PMID:[Self-evaluated job satisfaction and ischemic heart disease. A 10-year follow-up study of bus drivers in a big city]. 794 Oct 50

In the progression from myocardial hypertrophy to heart failure, abnormalities in the interstitial space of the heart seem to play a critical role. The formation of an extracellular oedema and the alterations in coronary subendocardial perfusion are associated with the development of interstitial fibrosis. Cardiac experimental studies documented the presence of augmented interstitial fluid volume and pressure and a subsequent remodelling of the fibrillar network of the extracellular space of the myocardium during the phases of the cardiovascular response to a sudden overload. Variations of the Starling's forces balance caused by enhanced endothelial permeability or due to an impairment of cardiac lymphatic drainage may contribute to the development of an acute heart failure. During stable hyperfunction, the organization of a chronic oedema should account for interstitial changes in the hypertrophic myocardium. Reactive fibrosis seems to be under hormonal control. The activation of the renin-angiotensin-aldosterone system is responsible for interfascicular and intercellular accumulation of fibrillar collagen within the cardiac interstitium. Perivascular fibrosis in the subendocardium may impair intramyocardial distribution of coronary flow. When an inadequate hypertrophy occurs, because of an elevation in ventricular wall stress, myocardial oxygen consumption rises and this may lead to the exhaustion of coronary blood flow reserve in the subendocardial layers. This underperfusion may be responsible for the development of myocardial ischemia. Coronary hemodynamic changes in the microcirculation as those prompted by interstitial alterations may contribute to the onset of myocyte necrosis and to the formation of restorative fibrosis. The progressive mechanical overload of the spared hypertrophied myocytes could explain the initiation of a positive feedback mechanism which perpetuates endomyocardial perfusion impairment, interstitial oedema and remodelling, finally, causing myocyte deaths and fibrous tissue proliferation. These structural alterations and their pathophysiological counterparts appear to be closely related to the evolution from compensatory hypertrophy to chronic myocardial failure in hypertrophic heart disease.
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PMID:[From myocardial hypertrophy to heart failure: role of the interstitium]. 802 50

To separate the independent effects of age and silent myocardial ischemia on the left ventricular response to aerobic exercise, maximal upright cycle ergometry was performed in three groups: 8 clinically healthy older men [76 +/- 3 (SE) yr] with ischemic electrocardiogram (ECG) and Tl scan responses to prior maximal treadmill exercise (old silent ischemic subjects), 16 age-matched men with normal ECG and Tl scan responses (old controls), and 21 healthy young (33 +/- 1 yr) men (young controls). Although the left ventricular ejection fraction, end-diastolic volume index, and end-systolic volume index were similar in the three groups at rest, with increasing work loads there was a progressive increase in the end-diastolic volume index and a blunted decline in end-systolic volume index in the two older groups, which was most apparent in the old silent ischemic subjects. Thus, at peak effort, end-diastolic volume index was largest in old silent ischemic subjects (101 +/- 6 ml/m2), intermediate in old controls (85 +/- 6 ml/m2), and smallest in young controls (67 +/- 3 ml/m2) (P < 0.002); conversely, left ventricular ejection fraction was highest in young controls (85 +/- 2), intermediate in old controls (76 +/- 3), and lowest in the old silent ischemic group (66 +/- 2) (P < 0.001). At exhaustion the peak systolic pressure-end-systolic volume index was significantly lower in the silent ischemic group than in young controls (6 +/- 1 vs. 25 +/- 4 mmHg.ml-1 x m-2, respectively; P < 0.001) with the old controls in between (16 +/- 5 mmHg.ml-1 x m-2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Additive effects of age and silent myocardial ischemia on the left ventricular response to upright cycle exercise. 822 45

Several studies have shown that bus driving is a high-risk occupation for ischaemic heart disease (IHD). In order to study contributing factors in the job, all male full-time bus drivers in the three major cities in Denmark were followed for 10 years. It was hypothesized that bus drivers who reported job strain and job dissatisfaction would have an excess risk of subsequent death due to IHD. Of 2465 bus drivers, 2045 (83%) responded to a questionnaire distributed in 1978 on psychosocial well-being and work conditions. The men had their mortality recorded during the years 1978-1988. Information on causes of death was obtained from the Danish Register of Causes of Death. Some 212 respondents died during the follow-up period, 59 from IHD. Relative risk (RR) for death due to IHD and all other causes of death was calculated. As expected, we found a significantly increased risk of IHD in bus drivers working in a high traffic intensity area, RR = 1.6. In contrast to what was expected, men who reported a high degree of job satisfaction had increased risk of IHD. Those who did not look for another job had a highly significant sixfold increased risk of future death from IHD. Also those who reported never experiencing mental exhaustion after work, that their job was very varied, that their job was something special, and those who reported that they would choose the same job again, had an excess risk. Death due to other causes was positively associated with marital status only. We suggest that inconsistencies in the literature on self-assessed job strain and risk of IHD may be partly explained by the fact that studies in general have focused on absence or presence of the psychosocial factor in question. A more differentiated assessment of exposure might prove more useful.
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PMID:Self-assessed job satisfaction and ischaemic heart disease mortality: a 10-year follow-up of urban bus drivers. 844 47

Nitrates have been periodically controversial since their introduction in 1867 as a treatment for angina pectoris. The goal of this synopsis is to delineate the special and unchanged high ranking of nitrates in the treatment of angina pectoris with particular consideration to the dosage and dosage intervals. The anti-anginal/anti-ischemic effect of nitrates originates predominantly from the preload reduction induced by venous dilation; additionally, an accompanying coronary dilation can be of assistance. The special role of the preload reduction differentiates nitrates from beta blockers and calcium antagonists. But the initial positive anti-anginal/anti-ischemic effect can be lost under long-term treatment due to nitrate tolerance. This development of tolerance has been demonstrated for oral, intravenous and transdermal administration. Various mechanisms have been held accountable for this complex occurrence: exhaustion of the thiol pool, neurohumoral counter-regulation, and recently, an overproduction of free radicals. Nitrate tolerance has mean-while been recognized as a relevant clinical problem. The key to avoidance of nitrate tolerance lies in the interval therapy recommended by Stewart as early as 1905: it concludes that continual, 24-hour protection by nitrates alone is impossible. The ideal compromise between avoiding the development of tolerance and an optimal anti-ischemic protection, the duration of which should be as long as possible, demonstrates that approximately 12 hours of protection are clinically possible. As we showed in 1983, the administration of a single, high dose of slow-release ISDN effects this compromise. Asymmetric dosage intervals that guarantee the maintenance of anti-anginal/anti-ischemic nitrate effect may be alternatively used. A 12-hour patch-free interval is generally recommended for treatment with nitrate patches. Similarly, a 12-hour infusion-free period has been recommended for intravenous nitrate administration in patients with stable angina pectoris. In patients with unstable angina pectoris, the situation is more complex-probably due to the anti-platelet effect of nitrates. As has been the practice in the past, nitrates are to be the basic treatment of angina pectoris; as opposed to nifedipine, nitrates lead to a decrease in end-diastolic volume primarily through preload reduction. Nitrates have been documented to be highly effective in treating angina pectoris and myocardial ischemia; they demonstrate a high rate of "responders". Nitrates are the physiological substitute treatment of atherosclerotic vessels with EDRF-deficiency; they improve hemodynamics in the presence of congestive heart failure. Nitrates inhibit platelets in vivo and are standard medication for PTCA as well as other coronary interventions. They demonstrate only few untoward effects and are inexpensive.
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PMID:[Characteristics of angina pectoris therapy with nitrates]. 876 20

The basis of the scientific method is the development of intellectual models, the predictions of which are then subjected to scientific evaluation. The more robust test of any such model is one that aims to refute or falsify its predictions. Successful refutation forces revision of the model: the revised model persists as the "truth" until its predictions are, in turn, refuted. Thus, any scientific model should persist only as long as it resists refutation. An unusual feature of the exercise sciences is that certain core beliefs are based on an historical physiological model that, it will be argued, has somehow escaped modern, disinterested intellectual scrutiny. This particular model holds that the cardiovascular system has a limited capacity to supply oxygen to the active muscles, especially during maximal exercise. As a result, skeletal muscle oxygen demand outstrips supply causing the development of skeletal muscle hypoxia or even anaerobiosis during vigorous exercise. This hypoxia stimulates the onset of lactate production at the "anaerobic," "lactate," or ventilation thresholds and initiates biochemical processes that terminate maximal exercise. The model further predicts that the important effect of training is to increase oxygen delivery to and oxygen utilization by the active muscles during exercise. Thus, adaptations that reduce skeletal muscle anaerobiosis during exercise explain all the physiological, biochemical, and functional changes that develop with training. The historical basis for this model is the original research of Nobel Laureate A. V. Hill which was interpreted as evidence that oxygen consumption "plateaus" during progressive exercise to exhaustion, indicating the development of skeletal muscle anaerobiosis. This review confirms that Hill's research failed to establish the existence of the "plateau phenomenon" during exercise and argues that this core component of the historical model remains unproven. Furthermore, definitive evidence that skeletal muscle anaerobiosis develops during submaximal exercise at the anaerobic threshold initiating lactate production by muscle and its accumulation in blood is not currently available. The finding that exercise performance can improve and metabolism alter before there are measurable skeletal muscle mitochondrial adaptations could indicate that variables unrelated to oxygen use by muscle might explain some, if not all, training-induced changes. To accommodate these uncertainties, an alternate physiological model is proposed in which skeletal muscle contractile activity is regulated by a series of central, predominantly neural, and peripheral, predominantly chemical, regulators that act to prevent the development of organ damage or even death during exercise in both health and disease and under demanding environmental conditions. During maximal exercise, the peripheral regulation of skeletal muscle function and hence of oxygen use by skeletal muscle, perhaps by variables related to blood flow, would prevent the development of muscle rigor, especially in persons with an impaired capacity to produce ATP by mitochondrial or glycolytic pathways. Regulation of skeletal muscle contractile function by central mechanisms would prevent the development of hypotension and myocardial ischemia during exercise in persons with heart failure, of hyperthermia during exercise in the heat, and of cerebral hypoxia during exercise at extreme altitude. The challenge for future generations of exercise physiologists is to identify how the body anticipates the possibility of organ damage and evokes the appropriate control mechanism(s) at the appropriate instant.
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PMID:1996 J.B. Wolffe Memorial Lecture. Challenging beliefs: ex Africa semper aliquid novi. 1064 33

Children who underwent arterial switch operation for simple transposition of the great arteries in the neonatal period are now reaching an age when exercise testing becomes feasible. This study was conducted to assess exercise tolerance and electrocardiographic response to exercise stress in 50 asymptomatic children, aged 4 to 9 years, using the Bruce walking treadmill protocol to voluntary exhaustion. Heart rate and blood pressure response to exercise stress, endurance time, and electrocardiographic changes were analyzed and compared with those of age-matched normal children. Forty-seven patients had normal exercise capacity and parameters. One patient, whose coronary angiogram showed occlusion of the left main coronary artery, developed electrocardiographic signs of myocardial ischemia during exercise. In 1 patient with a single right coronary artery ostium and in another, who underwent a neonatal internal mammary bypass graft for obstruction of the right coronary artery, the resting electrocardiogram showed ventricular premature complexes and exercise stress-induced salvos of ventricular tachycardia. We conclude that most of the children who underwent the neonatal arterial switch operation for simple transposition of the great arteries have a normal exercise capacity. Exercise testing appears to be useful in detecting ischemic damage or exercise-induced arrhythmias possibly secondary to reduced coronary flow reserve.
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PMID:Results of the Bruce treadmill test in children after arterial switch operation for simple transposition of the great arteries. 946 7

The common aspect in pathogenetic mechanism of occurrence of myocardial infarction with presence or absence of pathologic Q-wave on electrocardiogram, is associated with systemic inflammatory process with involvement of activated neutrophils and monocytes, whose increased oxygen radical production may lead to damage of endothelial cells and cardiomyocyte lipid membranes. For neutrophils and monocytes redox regulation study, 58 myocardial infarction patients were examined by means of chemiluminescenne and nitroblue tetrasolium test. Significant increase of phagocyte functional activity in all patients was observed. Substantially higher parameters of neutrophil hydrogen peroxide and hypochloric acid production were revealed in Q-wave myocardial infarction patients. This assumes the prevalence of irreversible lipid peroxidation in cardiomyocytes destruction process because of neutrophil redox metabolism activation. The absence of significant difference in neutrophil superoxide production and plasma superoxide dismutase in both types of myocardial infarction suggests not only the sufficient functional reserve of their membrane NADPH-oxidase, but the presence of an additional source of active oxygen forms, probably associated with xantinoxidase reaction with activated neutrophil protease participation. The evaluated more expressed chemiluminescence activation index in Q-wave myocardial infarction patients reflects the exhaustion of plasma "antiradical potential", associated with the decrease of antioxidant reserve, and creating conditions for uncontrollable lipid peroxidation intensification. Thus, the heterogeneity of redox metabolism of neutrophils and monocytes in non-Q-myocardial infarction and Q-myocardial infarction patients reflects the difference in cardiomyocyte damage mechanisms in both types of ischemic heart disease aggravation.
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PMID:Redox Regulation of Neutrophils and Monocytes in Different Types of Myocardial Infarction. 1268 97

The immune system plays a role in the progression of coronary artery diseases and its clinical manifestations as acute coronary syndromes. It is well established that psychological factors can act as risk factors for acute coronary syndromes. This review describes psychoneuroimmunological pathways involved in coronary disease progression and documents that the stage of coronary disease is a major determinant of pathophysiological mechanisms accounting for the association between psychological risk factors, immune system parameters, and acute coronary syndromes. Chronic psychological risk factors (e.g., hostility and low socioeconomic status) are important at early disease stages, episodic factors (e.g., depression and exhaustion) are involved in the transition from stable to unstable atherosclerotic plaques, and acute psychological triggers (e.g., mental stress and anger) can promote myocardial ischemia and plaque rupture. The psychoneuroimmunological pathways are described for each of these three types of psychological risk factors for acute coronary syndromes.
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PMID:The integration of cardiovascular behavioral medicine and psychoneuroimmunology: new developments based on converging research fields. 1283 24

Changes of blood insulin content were studied in patients with ischemic heart disease with various functional classes of acute and chronic heart failure and at different disease stages. It was established that latent hyperinsulinemia which became evident at induced myocardial ischemia was present on all stages of development of ischemic heart disease. In acute heart failure due to developed myocardial infarction hyperinsulinemia manifested in 58.3% of patients. Amount of insulin in blood increased almost 3 times. During progression of chronic heart failure insulin content significantly decreased, probably because of exhaustion of insulin producing function and development of its relative or absolute deficit. At terminal stage of congestive heart failure insulin level was < or = 1 microU/ml. The authors believe that severity of clinical signs of acute and chronic heart failure are determined by sensitivity of myocardium to insulin, content of insulin in blood, and also depends on compensatory possibilities of insulin producing function at each stage of development of the disease.
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PMID:[Possible role of hyperinsulinemia in pathogenesis of acute and chronic cardiac failure in patients with ischemic heart disease (data of clinical studies)]. 1688 22


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