Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac adaptation due to sport activity are usually interpreted as physiological process induced by cardiac overload during vigorous and continued muscle activity. The aim of this work was to evaluate long term cardiac effects of competitive sport activity performed in youth, after retirement. In particular we investigated: 1) whether cardiac adaptations to exercise are reversible and 2) whether or not previous competitive activity affects the cardiac ageing process or modifies ventricular function. We studied 23 professional retired athletes (PRA): 16 football players and 7 boxers, aged 40-60, who had been active in their sports for 16 years mean and who completely interrupted training and competition for at least 10 years. Our evaluation consisted of a questionnaire, a clinical assessment, an electro- and echocardiographic examination at rest. Data obtained in PRA were compared with those of twenty subjects matched for sex, age and weight who had never been athletes (control group = C) (Tab. I). We found: left ventricular hypertrophy in 5 cases (according to the "Point Score System" electrocardiographic evaluation): tall T waves in the precordial leads in 4 and conduction defects in other 4 cases. One subject had evidence of ischemic heart disease. Eleven cases were normal (Tab. II). Echocardiographic data demonstrated concentric heart hypertrophy and depressed ventricular function in PRA. Cardiac mass calculations were significantly higher in PRA with respect to C, more so for wall thickening than for cavitary enlargement. We concluded that: 1) cardiac adaptation due to physical exercise are not completely reversible and 2) systolic ventricular work, evaluated by means echocardiographic indices (EF, CSF and CSR) is depressed in PRA.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Long-term effects of competitive sport activity on the heart of professional ex-athletes]. 295 85

Systemic and coronary hemodynamic effects of acebutolol (10 mg i.v.), a cardioselective beta-adrenoceptor blocking agent were investigated in 11 patients with coronary artery disease and significant arterial obstructive lesions. Efficacy was assessed by simultaneous left and right heart catheterization and with an inlaying Webster thermodilution catheter in the coronary sinus. The data were compared with data from 7 other patients who received 2 mg i.v. of propranolol, a non-cardioselective beta-blocker. With acebutolol, (1) the heart rate was reduced significantly (p less than 0.001), (2) no significant changes were observed in the LVSP, LVEDP, mean PWP, LVmax dp/dt/p, LV negative dp/dt/p, CI, SWI and SPI, (3) CSF and MVO2 decreased significantly (p less than 0.01) 5 min after injection and (4) the CVR showed a significant elevation (p less than 0.05) after 5 min. With propranolol, (1) the heart rate decreased significantly (p less than 0.05), (2) there were no significant changes in LVSP and LVEDP, (3) the mean PWP increased significantly (p less than 0.05), (4) the LVmax dp/dt/p, CI and SWI decreased significantly (p less than 0.05), (5) the CSF and MVO2 decreased markedly (p less than 0.01) and (6) the CVR increased markedly (p less than 0.01). As compared to the effects of 2 mg i.v. of propranolol, those produced by acebutolol (10 mg i.v.) were characterized by a predominant negative chronotropic action with minimal negative inotropic action, combined with a reduction in CSF and MVO2. The findings suggest that the efficacy of acebutolol in pump failure caused by myocardial ischemia during effort angina is mediated by improvement of the myocardial oxygen demand-supply imbalance.
 ...
PMID:Systemic and coronary hemodynamic effects of beta-adrenoceptor blocking agents in coronary artery disease. 343 Jul 29

AR-L 115 has been shown to improve left ventricular (LV) pump function in patients with advanced congestive cardiomyopathy by the intravenous and oral routes. Since AR-L 115 effects on myocardial oxygen consumption (MVO2) and coronary blood flow (CSF) are unknown, the hemodynamic, myocardial metabolic, and ECG responses to AR-L 115 (2 mg/kg bolus) were monitored at 9-, 14-, and 9-minute intervals in seven patients with coronary disease, exhibiting ischemia during pacing stress only. Maximal responses occurred at the fourteenth minute after AR-L 115. There were (average) increases in cardiac index by 30%, heart rate by 19%, CSF by 39%, MVO2 by 34%, and LV dp/dt max by 27%. There were (average) decreases in peak LV systolic pressure by 13%, LV end-diastolic pressure by 42%, systemic vascular resistance by 34%, and in coronary vascular resistance by 37%. All changes were significant (p less than 0.05). Myocardial lactate extraction, stroke work index, and stroke index remained unchanged (p greater than 0.05). The modest increase in MVO2 is possibly explained by the increase in contractility being partially offset by reductions in LV preload and afterload. AR-L 115-improved LV pump function was accompanied by moderate increases in MVO2 and CSF but without evidence of myocardial ischemia.
 ...
PMID:Hemodynamic and myocardial energetic changes induced by the new cardiotonic agent, AR-L 115, in patients with coronary artery disease. 714 47

AR-L115 has been shown to substantially improve myocardial pump function in patients (pts) with advanced congestive cardiomyopathy by i.v. and by p.o.-route. Since AR-L115 effects on myocardial oxygen consumption (MVO2) and coronary blood flow (CSF) are unknown, the hemodynamic myocardial metabolic and ECG-responses to AR-L115 (2 mg/kg BW bolus) were monitored at the 9, 14 and 19-min interval in 7 patients coronary 3-vessel disease, exhibiting ischemia during pacing stress only. Maximal responses occurred at the 14th min after AR-L115. THere were (average) increases in cardiac index by 30%, in heart rate by 19%, in CSF by 39%, in MVO2 by 34%, and in dp/dt max by 27%. There were (average) decreases in peak systolic pressure by 13%, in PCW by 30%, in LVEDP by 42%, in systemic vascular resistance by 34%, and in coronary vascular resistance by 37%. All changes were significant (p less than 0.05). Unchanged (p greater than 0.05) remained myocardial lactate extraction, stroke work index, and stroke-index. The only moderate increase in MVO2 is possibly explained in that the increase in contractility was a least partially offset by the reductions in pre- and after load. The AR-L115-induced improved pump function was accompanied by moderate increases in MVO2 and CSF, but without evidence of myocardial ischemia.
 ...
PMID:[Hemodynamics and metabolic-energetic expenses of the influence of AR-L115 in patients with coronary artery disease (author's transl)]. 726 26

Recent studies have suggested that cytokines such as macrophage colony-stimulating factor (M-CSF) might be involved in the pathogenesis of ischaemic heart disease. Macrophage colony-stimulating factor, granulocyte-colony stimulating factor (G-CSF), granulocyte-macrophage-colony stimulating factor (GM-CSF), stem cell factor (SCF), interleukin-3 (IL-3) and interleukin-7 (IL-7) are potent cytokines belonging to the same structual class that may affect function, growth and apoptosis both in the heart and other organs. The aims of the present study were to characterize a post-infarction model in the mouse and to examine mRNA expression of M-CSF, GM-CSF, SCF, IL-3 and IL-7 during the development of heart failure. Myocardial infarction (MI) was induced in mice by ligation of the left coronary artery. Average infarct size was 40% and the mice developed myocardial hypertrophy and pulmonary oedema. Ribonuclease (RNAase) protection assays showed abundant cardiac expression of M-CSF and SCF. After MI, we measured down-regulation of cytokine mRNA expression in the heart (M-CSF, SCF), lung (M-CSF), liver (M-CSF) and spleen (M-CSF) compared with sham. Cardiac G-CSF, GM-CSF and IL-7 mRNAs were not detected. In conclusion, abundant cardiac gene expression of M-CSF and SCF was found. In our mouse model of MI, M-CSF and SCF were down-regulated in the heart and several other organs suggesting specific roles for these cytokines during development of ischaemic heart failure.
 ...
PMID:Gene expression of colony-stimulating factors and stem cell factor after myocardial infarction in the mouse. 1210 Mar 56

Mobilization of bone marrow stem cells by granulocyte-colony-stimulating factor (G-CSF) is considered to be an alternative to invasive transplantation of autologous myoblasts or stem cells directly into injured cardiac tissue. We have started a 24 week randomized open study in order to elucidate effects of G-CSF (filgrastim) on clinical, hemodynamic and neurohumoral status of patients with NYHA class II-IV chronic heart failure due to ischemic heart disease with zones of nonviable myocardium and left ventricular ejection fraction <40% as well as to assess safety of addition of G-CSF to standard therapy with ACE inhibitors and beta-blockers. It is planned to include 20 patients into each filgrastim (5 mg/kg/day) and control (0.9% NaCl) groups. Methods to be used: dobutamine stress echocardiography for detection of myocardial viability, magnetic resonance tomography, 6-minute walk test, quality of life questionnaire. By the present time 5 patients were included (4 in filgrastim and 1 in control group) and passed 3-6 months points. A control patient died suddenly on 11th week. All patients in filgrastim group are alive (1 experienced obvious improvement, 2 remained stable, and 1 deteriorated and required urgent hospitalization). None of the patients had signs of appearance of 'regenerated' myocardial zones. The patient with positive clinical dynamics was characterized by young age (48 years), moderately severe heart failure (NYHA class II) and pronounced leukocyte reaction to filgrastim (12 fold increase in white blood cell count with appearance of myelocytes and myeloblasts ). In contrast patients without improvement were older than 60 years, had NYHA class III heart failure and experienced just 6-8 fold increases in leukocyte count. These factors are suggested to be predictors of clinical efficacy of G-CSF in patients with heart failure.
 ...
PMID:[Mobilization of bone marrow stem cells in the management of patients with heart failure. Protocol and first results of ROT FRONT trial]. 1289 Dec 52

Mobilization of stem cells into the peripheral circulation for myocardial regeneration using subcutaneous injections of granulocyte-colony-stimulating factor (G-CSF) has been tested in both patients with acute myocardial infarction (AMI) and patients with chronic myocardial ischaemia. G-CSF treatment seems to be safe and unblinded trials in patients with AMI were encouraging. However, larger double-blind placebo-controlled trials have not been able to demonstrate effect of G-CSF treatment. In patients with chronic myocardial ischaemia, small-unblinded G-CSF trials did not show effect on myocardial perfusion and function. In both patient populations, G-CSF did mobilize stem cells of known importance to myocardial regeneration, but there seemed to be a general lack of homing of the stem cells into the ischaemic myocardium. In AMI, factors of importance to homing of stem cells, stem cell derived factor-1, are maximally elevated in plasma 3 weeks after infarction, suggesting that this time point could be the optimal time for stem cell mobilization treatment. The known complex interaction of stem cells and cytokines for induction of vasculogenesis should be implemented in future clinical trials, to elucidate whether G-CSF mobilization of stem cells might be useful as a new regenerative treatment in patients with ischaemic heart disease.
 ...
PMID:Myocardial regeneration induced by granulocyte-colony-stimulating factor mobilization of stem cells in patients with acute or chronic ischaemic heart disease: a non-invasive alternative for clinical stem cell therapy? 1706 71

Macrophage colony-stimulating factor (M-CSF), known as a hematopoietic growth factor, induces vascular endothelial growth factor (VEGF) production from skeletal muscles. However, the effects of M-CSF on cardiomyocytes have not been reported. Here, we show M-CSF increases VEGF production from cardiomyocytes, protects cardiomyocytes and myotubes from cell death, and improves cardiac function after ischemic injury. In mice, M-CSF increased VEGF production in hearts and in freshly isolated cardiomyocytes, which showed M-CSF receptor expression. In rat cell line H9c2 cardiomyocytes and myotubes, M-CSF induced VEGF production via the Akt signaling pathway, and M-CSF pretreatment protected these cells from H(2)O(2)-induced cell death. M-CSF activated Akt and extracellular signal-regulated kinase signaling pathways and up-regulated downstream anti-apoptotic Bcl-xL expression in these cells. Using goats as a large animal model of myocardial infarction, we found that M-CSF treatment after the onset of myocardial infarction by permanent coronary artery ligation promoted angiogenesis in ischemic hearts but did not reduce the infarct area. M-CSF pretreatment of the goat myocardial infarction model by coronary artery occlusion-reperfusion improved cardiac function, as assessed by hemodynamic parameters and echocardiography. These results suggest M-CSF might be a novel therapeutic agent for ischemic heart disease.
 ...
PMID:Macrophage colony-stimulating factor improves cardiac function after ischemic injury by inducing vascular endothelial growth factor production and survival of cardiomyocytes. 1771 42

Arsenicosis is a multisystem disorder, with virtually no system spared from its vicious claw; though its predominant manifestations are linked to cutaneous involvement. Cutaneous effects take the form of pigmentary changes, hyperkeratosis, and skin cancers (Bowen's disease, squamous cell carcinoma, and basal cell epithelioma). Peripheral vascular disease (blackfoot disease), hypertension, ischemic heart disease, noncirrhotic portal hypertension, hepatomegaly, peripheral neuropathy, respiratory and renal involvement, bad obstetrical outcome, hematological disturbances, and diabetes mellitus are among the other clinical features linked to arsenic toxicity. The effects are mediated principally by the trivalent form of arsenic (arsenite), which by its ability to bind with sulfhydryl groups present in various essential compounds leads to inactivation and derangement of body function. Though the toxicities are mostly linked to the trivalent state, arsenic is consumed mainly in its pentavalent form (arsenate), and reduction of arsenate to arsenite is mediated through glutathione. Body attempts to detoxify the agent via repeated oxidative methylation and reduction reaction, leading to the generation of methylated metabolites, which are excreted in the urine. Understandably the detoxification/bio-inactivation process is not a complete defense against the vicious metalloid, and it can cause chromosomal aberration, impairment of DNA repair process, alteration in the activity of tumor suppressor gene, etc., leading to genotoxicity and carcinogenicity. Arsenic causes apoptosis via free radical generation, and the cutaneous toxicity is linked to its effect on various cytokines (e.g., IL-8, TGF-beta, TNF-alpha, GM-CSF), growth factors, and transcription factors. Increased expression of cytokeratins, keratin-16 (marker for hyperproliferation) and keratin-8 and -18 (marker for less differentiated epithelial cells), can be related to the histopathological findings of hyperkeratosis and dysplastic cells in the arsenicosis skin lesion.
 ...
PMID:Pathogenesis, clinical features and pathology of chronic arsenicosis. 1917 78

After acute myocardial infarction (AMI), reopening of a totally occluded infarct-related artery (IRA) at a subacute stage is still controversial in symptom-free patients. However, in patients with persistent ischemic symptoms and inadequate collaterals to the infarct area, recanalization is thought to provide beneficial effects. In addition to augmenting myocardial perfusion, we hypothesized that the benefit of recanalization involves the manipulation of circulating stem cell-mobilizing cytokines. This study included 30 patients with a totally occluded IRA and ongoing ischemic symptoms (the study group) and 30 patients with a partially occluded IRA (the control group). All patients underwent successful angioplasty and/or stenting. Before and immediately after the coronary intervention, blood granulocyte-colony-stimulating factor (G-CSF), stem-cell factor (SCF), vascular endothelial growth factor (VEGF), and stroma-derived factor-1 (SDF-1alpha) were measured. After recanalization, G-CSF levels significantly increased in the study group compared to the control group (P=0.03). SDF-1alpha levels in the study group decreased relative to the controls (P=0.02). However, no significant changes in VEGF or SCF levels between the two groups were found. In the multivariate analysis, reopening of a totally occluded IRA was independently and significantly associated with changes in G-CSF and SDF-1alpha levels after recanalization. In conclusion, our data suggest that the benefits of late reperfusion of a totally occluded IRA in patients with ongoing myocardial ischemia may involve mechanisms associated with stem cell-mobilizing and plaque-stabilizing cytokines. This study provides the rationale to investigate serial changes in cytokines and the numbers of circulating progenitors after reperfusion in the future.
 ...
PMID:Late reperfusion of a totally occluded infarct-related artery increases granulocyte-colony stimulation factor and reduces stroma-derived factor-1alpha blood levels in patients with ongoing ischemia after acute myocardial infarction. 1960 48


1 2 Next >>