Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1972 and 1977, a permanent pacemaker has been implanted in 9 children for complete heart block, after repair of a congenital heart disease. Children's age ranged between 2 1/2 years and 13 years (mean age 8 years). The block had been caused by the operation in 8 children and was pre-existent in the last one. A permanent pacemaker was not implanted in another four children with postoperative complete heart block. In seven cases the pacemaker was implanted in the subclavear zone and connected to a transvenous electrode; in the remaining two cases the pacemaker was positioned subcutaneously in the abdomen and connected to an epicardial electrode. VVI-type pacemaker have always been used. Three children died after implantation because of chronic cardiac failure complicated, in one case, by surrhenalic insufficiency. In two cases the pacemaker was replaced because of battery exhaustion, as suggested by routine controls; in five cases, wire breakage occurred and it was replaced together with the pacemaker. In another case transvenous electrode displacement occurred; skin infection at pacemaker site occurred only once. No skin breakdown at pacemaker site has ever occurred, or any problem due to excessive pacemaker dimensions. Reappearance of normal synus rhythm was noted in one patient. No complication has been reported so far for the cases with postoperative complete heart block not treated with cardiac pacing.
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PMID:[Permanent pacemaker implantation in children after open heart cardiac surgery (author's transl)]. 75 59

After lobectomy a slight increase of pulmonary arterial pressure can already be observed in the state of rest. The resistance of the pulmonary vessels reveals a marked dependance on the date of operation, it increases moderately on strain, but more significantly in the state of rest. At the same time cardiac output is decreased due to the exhaustion of the myocard after straining. Cardiac insufficiency developing postoperatively is due to the reduction of pulmonary hypertension. The reduction of VC and a slight increase of resistance do not cause the arterial PO2 pressure to be lowered under conditions of strain or rest.
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PMID:[Haemodynamic and respiratory changes after lung resection (author's transl)]. 89 24

A system to improve analysis of the aortic pulsed Doppler velocity signal has been developed and used to study cardiac performance during a 4 min, 25 W incremental stage supine bicycle exercise to exhaustion. Twenty-two male subjects with stable chronic ischaemic heart disease were studied (15 with NYHA class II/III heart failure, and seven age-matched class I subjects). None had evidence of reversible ischaemia. Peak velocity (PV) from the intensity weighted mean velocity profile, early acceleration (eA) and stroke distance (SD) were all significantly lower at rest in class II/III compared to class I. For the change from rest to 50 W, PV did not alter, eAC increased significantly (P less than 0.05) and to a similar extent in both groups (18.6% class II/III vs 16.4% class I) and SD was reduced from 7.8 to 5.9 in class II/III (P less than 0.01) but did not change in class I (12.4 vs 11.8, ns). There was also a greater increase in heart rate (HR) in class II/III subjects (P less than 0.05). The duration of exercise was correlated with resting PV (r = 0.48, P less than 0.025) but was correlated best with the change in blood momentum (PV x Stroke volume x HR) between rest and peak exercise (r = 0.80, P less than 0.001). Thus Doppler velocimetry can give quantitative information on the response to exercise which discriminates between grades of ventricular dysfunction and is predictive of exercise capacity.
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PMID:Ascending aortic Doppler velocity and the prediction of exercise capacity in post-infarction left ventricular dysfunction. 159 22

The peptidergic, endogenous opioid system counteracts exogenous and endogenous stress factors. The system will be activated by stress, e.g., also in case of heart failure. The endogenous opioids endorphin, met-enkephalin, leu-enkephalin, dynorphin, casomorphin, and others split from precursor proteins (250-265 amino acids) by a specific proteolytic cleavage. In clinical and experimental heart failure the plasma levels of endorphin and lipotropin are changed as an evidence of the activated opioid system. In patients with chronic heart failure the plasma levels of endorphin and lipotropin are decreased, which is discussed as an exhaustion of the opioid system. In the case of experimentally induced right-heart failure in dogs the plasma levels of endorphin and lipotropin are increased. Morphine antagonists (naloxone hydrochloride) which penetrate into the cerebral system improve the disturbed hemodynamics in dogs with a right-heart failure. The improving effects results from central actions since opiate antagonists, which cannot penetrate the blood-brain-barrier (naloxone methobromide) have no effect. The actions of opioid peptides will be induced by inhibition of the depletion and the reabsorption of catecholamines in synaptic storages (isolated atria from guinea pig). In cultures from cardiac myocytes (chicken ventricle cells) enkephalins induced positive inotropic effects via receptor mediated mechanisms. The results showed modulating activities of endogenous opioids against the effect of activated sympathetic activity.
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PMID:[Role of endogenous opioids in heart failure]. 166 29

Forty-one men with documented myocardial infarction greater than 6 months previously were randomized to long-term (48 weeks) therapy with placebo or enalapril on a double-blind basis. All patients were receiving concurrent therapy with digitalis and a diuretic drug for symptomatic heart failure (functional class II or III). The mean age was 64 +/- 7.3 years and no patient suffered from exertional chest pain. Patients underwent maximal cardiopulmonary exertional chest pain. Patients underwent maximal cardiopulmonary exercise testing to exhaustion on an ergometer cycle nine times over the course of 48 weeks. Gas exchange data were collected on a breath by breath basis with use of a continuous ramp protocol. In the placebo group (n = 21), the mean (+/- SD) peak oxygen consumption (VO2) at baseline was 18.8 +/- 5.2 versus 18.5 +/- 5.5 ml/kg per min at 48 weeks (-1.4%, p = NS). In the enalapril group (n = 20), the corresponding values were 18.1 +/- 3.1 versus 18.3 +/- 2.6 ml/kg per min (+2.8%, p = NS). The mean VO2 at the anaerobic threshold for the placebo group at baseline study was 13.1 +/- 3.5 versus 12.8 +/- 2.1 ml/kg per min at 48 weeks (-2.2%, p = NS). The corresponding values for the enalapril group were 11.8 +/- 2.3 versus 11.8 +/- 2.4 ml/kg per min (+1.4%, p = NS). The mean total exercise duration in the placebo group at baseline study was 589 +/- 153 versus 620 +/- 181 s at 48 weeks (+5.4%, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of long-term enalapril therapy on cardiopulmonary exercise performance in men with mild heart failure and previous myocardial infarction. 185 29

The hemostatic alterations in two adult patients who were supported by left ventricular assist devices (LVADs) because of postcardiotomy heart failure were evaluated. In both patients, fibrinopeptide A and thrombin-antithrombin III complex increased markedly during the first several days, and thereafter decreased moderately but remained above normal over the entire procedure. Furthermore, fibrinopeptide B beta 15-42 and alpha 2 plasmin inhibitor-plasmin complex were also markedly increased over the entire course of LVAD treatment. These data show that the LVAD system strongly activates both the coagulation and the fibrinolytic system, even when thromboembolic or bleeding complications are not clinically evident. Furthermore, the decrease in physiological coagulation inhibitors, especially protein C, indicates that these factors are activated and consumed during LVAD treatment. Because protein C is important in regulating the coagulation cascade during LVAD treatment, exhaustion of this system might result in thromboembolic complications during LVAD treatment.
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PMID:Hemostatic alterations caused by ventricular assist devices for postcardiotomy heart failure. 199 93

Exposure of human body to high altitude environment initiate reaction which could be result whether of adaptation or of exhaustion. The purpose is to establish the human body environment which enables regeneration of own cells. Therefore, mechanism of reestablishment of prevention and recognition of symptoms and signs of insufficient adaptability on high altitude are of great interest for clinical and other medical investigators. Special position in research refers on cardiovascular system. Results show, according to effect of only one factor-catecholamines, that in course of physical training on high altitude, could be expected, cardiac muscle hypertrophy. It is proved, that under special circumstances catecholamines stimulate synthesis of proteins what enables faster regeneration of the cells. However, under conditions of myocardial ischemia, uncontrolled loading of these patients could lead to deterioration of heart function appearance of cardiac insufficiency.
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PMID:[Aspects of acclimatization of the human body to acute and chronic high-altitude hypoxia]. 209 85

Twenty-three patients with mild heart failure (I-II NYHA classes) on digitalis and diuretics were assigned to the following treatment in a random and double-blind fashion: ibopamine-captopril, ibopamine-placebo, captopril-placebo, and placebo-placebo. The doses of captopril and ibopamine were respectively 25 mg t.i.d. and 100 mg t.i.d. The incremental exercise time (until exhaustion) and the peak VO2 (oxygen consumption), the indexes of left ventricular function (by echo and nuclear stethoscope) and ventricular arrhythmias (evaluated by prolonged Holter monitoring) were assessed before randomization, at 45 days and at 3 months. Ejection fraction, exercise time, peak VO2, ventricular arrhythmias and heart rate (at rest and during exercise) appeared to be equally unaffected by each treatment. Our results show that ibopamine exerts no significant effects on either heart rate or ventricular arrhythmias and that indexes of left ventricular function are not modified by any treatment in mild congestive heart failure.
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PMID:Comparative effects of ibopamine and captopril in mild congestive heart failure. Focus on the long-term effects of inodilation on ventricular arrhythmias. 212 22

The current studies were undertaken to explore the relationship between enhanced sympathetic nervous activity and lymphocyte subset distribution in three settings: congestive heart failure, dynamic exercise, and beta-adrenergic agonist treatment. We compared the number and subset distribution of circulating lymphocytes in 36 patients with congestive heart failure and 31 age-matched control subjects. The number of circulating lymphocytes was lower in heart failure than in control. This was due to a reduction in Tsuppressor/cytotoxic and natural killer cells without significant alteration of Thelper cells. The extent of the alteration was similar in patients with idiopathic and ischemic heart failure, but the reduction was more pronounced in patients with New York Heart Association class III-IV than in class I-II. The plasma catecholamine elevation in heart failure was also independent of etiology but more pronounced in the more severely ill patients. We also assessed lymphocyte subsets after acute stimulation of sympathetic activity by dynamic exercise and after treatment with the beta-adrenergic agonist terbutaline. Dynamic exercise until exhaustion increased the number of circulating lymphocytes in healthy controls and heart failure patients in a subset-selective manner. By contrast, a 7-d treatment with terbutaline caused a reduction in the circulating number of lymphocytes in some subsets that was identical to that seen in heart failure patients. We conclude that prolonged sympathetic activity reduces the number of circulating lymphocytes by a beta-adrenergic mechanism. Such alterations might be involved in the pathophysiology of heart failure and other disease states involving increased activity of the sympathetic nervous system.
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PMID:Adrenergic control of circulating lymphocyte subpopulations. Effects of congestive heart failure, dynamic exercise, and terbutaline treatment. 215 6

Quantitative pathohistological investigations were performed on 300 samples of five different myocardial regions from 50 pigs with had suffered stress-related myocardial insufficiency on their transport to the slaughterhouse (transport exhaustion). The findings were compared to 1,200 myocardial samples from 200 clinically intact pigs for slaughter. Animals with transport-related damage exhibited with significance more and more severe inflammatory and degenerative myocardial alterations, such as round-cell infiltration, fiber necrosis, calcification, and fat infiltration. Many of these lesions had been manifest already prior to transport. Myocardially predamaged pigs were less capable than others of sustaining transport stress and were more predisposed to cardiac failure. Stress-related cardiovascular insufficiency, consequently, depended not only on direct stress but also on the general health condition of the myocardium. Causes and pathogenetic relevance of these alterations are discussed in some detail.
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PMID:[The pathomorphology and pathogenesis of acute cardiovascular failure in swine. 3. Histopathologic findings in the myocardium of swine with transport-related cardiovascular insufficiency]. 224 89


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