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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dynamics of decompensatory changes in the heart (in cardiomyocytes, connective tissue stroma of the myocardium, neural structures, microcirculatory bed) has been followed under conditions of developing stenosis of the pulmonary trunk. The data have been obtained by means of various investigational methods: histological - injection of vessels with Indian ink - gelatin, impregnation of the neural structures after Bielschowsky - Gros; histochemical - to reveal functional activity of parasympathetic and sympathetic neural structures after Koelle - Gomori and Falck - Hillarp - Govyrin, and electronmicroscopically. At the beginning of the experiment destructive processes predominate. By the first month, compensatory-adaptive processes develop in the heart. By the first year, persisting hypoxia and quick exhaustion of all cardiac structures result in development of the heart failure.
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PMID:[Changes in heart structure in intrapericardial stenosis of the pulmonary trunk]. 732 14

Thalassaemia major determines an impaired effort tolerance because of a condition of severe anaemia, progressive left ventricular dysfunction, pulmonary circulation compromise. The aim of our study is to evaluate haemodynamic response to exercise in thalassaemic patients without clinical features of heart failure. We have selected 13 patients affected by thalassaemia major (Thal+; 10-18 years). Each patient was transfused when haemoglobin values were < 9-9.5 g/dl and was treated with desferrioxamine (40 mg/kg sc) when serum ferritin values were > 2,000 ng/ml. Thal+ patients were compared with normal subjects (Thal- 10-16 years). No patient assumed hypotensive therapy, no had familiar history of hypertension. Both groups have undergone an ergometric stress test at the cycloergometer, with increase of 25 W every 2 min, up to the reaching of the maximum age-related heart rate, or up to muscle exhaustion or unbearable dyspnea, followed by a 10 min recovery phase. The following parameters were taken in consideration: systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), the product of the heart rate by the systolic blood pressure (DP), at rest, at the maximum common work (MCW), at maximum stress and in the recovery phases. At rest, only DP showed significant differences between the two groups: in Thal+ patients higher than in Thal- (p = 0.045). At the MCW, Thal+ patients had SBP (p = 0.019), DBP (p = 0.01), HR (p = 0.035) and DP (p = 0.003) higher than Thal- patients. At maximum stress only DBP showed significant differences in Thal+ patients (p = 0.019), although Thal+ patients achieved lower levels of workload (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiovascular adaptation to the stress test in subjects with Cooley's disease]. 780 70

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

The paper describes the sequence of events typical in the pathogenesis of germinal layer hemorrhage (GLH): An initial, often prenatal, severe asphyxic event, leading to abolishment of autoregulation of cerebral perfusion, and, most likely, to hypoxic-ischemic lesions in the endothelium of the large capillaries of the germinal matrix. The hypoxia is accompanied by exhaustion of myocardial energy reserves with circulatory failure, hypotension and aggravation of cerebral ischemia. In the period immediately after birth, circulation failure proceeds with cardiac insufficiency, hypotension, cerebral ischemia, and possibly venous hypertension. Following resuscitation, arterial blood pressure gradually increases (type 3) with increased strain on the damaged germinal matrix capillary walls in the absence of autoregulation. This effect is further aggravated by arterial blood pressure increments of type 1 and 2 leading to GLH, possibly with increments of venous pressure as a contributing factor.
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PMID:On the pathogenesis of germinal layer hemorrhage in the neonate. 831 97

Maximal treadmill exercise responses were compared with light forearm isometric exercise responses in patients with chronic, stable heart failure (n = 14), and normal sedentary controls (n = 11). Isometric exercise was performed to exhaustion with 25% of maximal voluntary contraction. Gas-exchange analysis was used to determine oxygen consumption (VO2), carbon dioxide production (VCO2), and minute ventilation (VE) during exercise. Significant correlations were observed in normal controls, but not in patients with heart failure, between peak isotonic exercise and peak isometric exercise for VO2 (r = 0.75, p = 0.001) and VCO2 (r = 0.67, p <0.03), and between submaximal isotonic exercise (50% of peak) and peak isometric exercise for VO2 (r = 0.75, p = 0.007), VCO2 (r = 0.67, p = 0.02), and VE (r = 0.71, p = 0.01). At 90 seconds after isometric exercise in both groups, significant correlations (p <0.05) were observed with peak isotonic exercise for VE (r = 0.62 normals, and r = 0.63 heart failure). Plasma norepinephrine increased significantly (p <0.01) after both isotonic and isometric exercise in patients with heart failure, although peak values were greater with isotonic than with isometric exercise (p = 0.01). Plasma atrial natriuretic peptide and renin activity did not change with either isotonic or isometric exercise. In conclusion, maximal isotonic exercise responses are not predictive of peak isometric VO2 or VCO2 in patients with heart failure. However, VE during maximal isotonic exercise predicts postisometric exercise ventilation in both normals and patients with heart failure; this may determine the extent of dyspnea that patients with heart failure experience with isometric activities of daily living.
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PMID:Comparison of metabolic, ventilatory, and neurohumoral responses during light forearm isometric exercise and isotonic exercise in congestive heart failure. 860 69

Patients with chronic heart failure have an increased ventilation/carbon dioxide production ratio (VE/VCO2) during exercise. Recently it was discussed whether the cause of this increase was a ventilatory stimulus driven other than by CO2. Dyspnoea during exercise is thought to be related to impaired respiratory function. However, clinical confirmation is scarce. Ninety-two patients (age 51 +/- 9 years) with heart failure due to idiopathic dilated cardiomyopathy exercised on a bicycle ergometer to exhaustion, and measurement of ventilatory gases and Swan-Ganz catheterization were performed. The maximal oxygen consumption corrected for body weight (VO2max. kg-1) was 16.6 +/- 5.5 ml x min-1 x kg-1. The increase in (VE/VCO2) during exercise was related to an increase in respiratory rate (r = 0.43; P < 0.00001) but not to an increase in cardiac index or capillary wedge pressure. Nineteen patients stopped exercising because of dyspnoea. Their maximal tidal volume and VO2max . kg-1 were lower than the 67 patients who stopped exercise because of fatigue (P < 0.001 and P < 0.00001 respectively). Other variables showed no significant difference. In conclusion, the increase in VE/VCO2 during exercise may reflect a non-CO2 driven ventilatory stimulus as it cannot be attributed to increased pulmonary vascular pressures or an insufficient increase in cardiac output leading to a ventilation-perfusion mismatch. Low oxygen uptake is a prominent finding in patients with chronic heart failure who experienced dyspnoea during exercise, and dyspnoea is in part related to impaired respiratory function.
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PMID:Ventilation and dyspnoea during exercise in patients with heart failure. 868 22

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

Diminished body cell mass in heart failure patients contributes to poor prognosis and decreased quality of life. The level of daily energy intake needed to maintain body cell mass and optimal physiological function in heart failure patients is unknown. Thus, we examined daily energy expenditure in free-living heart failure patients to estimate daily energy requirements. Daily energy expenditure (doubly labeled water) and its components (resting and physical activity energy expenditures) were measured in 26 heart failure patients (25 men and one woman aged 69 +/- 7 years) and 50 healthy controls (48 men and two women aged 69 +/- 6 years). Resting energy expenditure was measured by indirect calorimetry; physical activity energy expenditure from the difference between daily and resting energy expenditure; body composition by dual-energy x-ray absorptiometry; leisure time physical activity from a questionnaire; and peak oxygen consumption ([peak VO2] n = 16 heart failure patients) from a treadmill test to exhaustion. Plasma markers of nutritional status were also considered. Daily energy expenditure was 17% lower (2,110 +/- 500 v 2,543 +/- 449 kcal/d) and physical activity energy expenditure 54% lower (333 +/- 345 v 728 +/- 374 kcal/d) in heart failure patients compared with healthy controls. Daily energy expenditure was related to physical activity energy expenditure (r = .79, P < .01), resting energy expenditure (r = .63, P < .01), leisure time physical activity (r = .63, P < .01), and peak VO2 (r = .58, P < .01) in heart failure patients. Stepwise regression analysis showed that daily energy requirements in heart failure patients were best estimated by a combination of resting energy expenditure and reported leisure time physical activity (total R2 = 61%; standard error of the estimate, +/- 333 kcal/d). Daily energy requirements predicted from equations derived in healthy elderly were inaccurate when applied to heart failure patients, deviating -10% to +30% from measured daily energy expenditure. We conclude that despite low levels of activity, markers of physical activity predicted daily energy needs in heart failure patients. We provide a new equation to estimate energy needs in free-living heart failure patients based on measurements of daily energy expenditure.
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PMID:Daily energy requirements in heart failure patients. 936 88

In this study, insomnia in 80-year-olds was related to medical, psychological and social factors. The data were based on examinations every year in people aged between 80 and 89 years. Of 333 people living in the city of Lund and born in 1908, 67% participated. Increased severity of insomnia was significantly associated with use of diuretics, other cardiovascular drugs, hypnotics and laxatives, and with nervousness, difficulty relaxing, anorexia, nausea, constipation, backache, feeling cold, sweating, loss of weight, dizziness, depression, general fatigue, exhaustion, angina pectoris, cardiac insufficiency, worsened objective and subjective health, presence of negative T-waves on ECG, anxiety, total life satisfaction, neuroticism, disbelief in a just world, feeling lonely and lower survival rates. Thus insomnia has widespread associations with different aspects of life in 80-year-olds.
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PMID:Insomnia in an 80-year-old population: relationship to medical, psychological and social factors. 978 73

The aim of the present study was to evaluate the relationship between exercise capacity and ventilatory response in patients with stable old myocardial infarction. We performed cardiopulmonary exercise test in 61 patients with stable old myocardial infarction and in 30 healthy men. Each subject exercised on a bicycle ergometer until exhaustion. Patients who had anginal pain or electrocardiographic ischemic changes during exercise were excluded. The patients were classified into three groups according to peakVO2 achieved during exercise, using Weber's method: group A, peakVO2 > or = 21 ml/min/kg (n = 4); group B, 14 < or = peakVO2 < 21 ml/min/kg (n = 45); and group C, peakVO2 < 14 ml/min/kg (n = 12). With progressive increases in VCO2, VE increased linearly below the anaerobic threshold (AT) level. The slope of the linear regression line between VCO2 and VE (SLOPE) was calculated in each subject. The mean SLOPE of the healthy men (group N) and groups A, B and C were 25.8 +/- 0.5, 25.1 +/- 0.5, 28.9 +/- 0.8 and 37.1 +/- 1.7 (x 10(-3), respectively. Thus, the SLOPE was steeper in patients with lower peakVO2. It is difficult to perform a maximal exercise tolerance test on patients with chronic heart failure to evaluate their exercise capacity. We can assess exercise capacity by the slope of the linear regression line between VCO2 and VE (SLOPE) at the lower exercise level.
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PMID:Relationship between exercise capacity and ventilatory equivalent for carbon dioxide in patients with stable old myocardial infarction. 1042 Aug 74


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