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

1. This study examined whether brain and atrial natriuretic peptides (BNP, ANP) are secreted together through the coronary sinus from the heart, and whether plasma concentrations of BNP and ANP were affected by ergometric exercise in patients with essential hypertension. The effects of temocapril, a potent angiotensin-converting enzyme (ACE) inhibitor, on plasma concentrations of these peptides was also examined. 2. The plasma concentrations of immunoreactive (ir) BNP and ir-ANP in the coronary sinus in seven patients with ischaemic heart disease during cardiac catheterization were far greater than values with plasma obtained at the same time from the femoral artery. 3. The plasma concentrations of ir-BNP and ir-ANP increased with exercise and were correlated with each other. Temocapril reduced the blood pressure and slightly (but significantly) decreased the levels of both peptides at rest and during exercise. 4. The results suggest that BNP and ANP were secreted together through the coronary sinus from the heart. The secretion was increased by exercise and suppressed by acute ACE inhibition. The increase in these peptides during exercise may reflect a compensatory mechanism against further elevation of blood pressure.
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PMID:Atrial and brain natriuretic peptides: secretion during exercise in patients with essential hypertension and modulation by acute angiotensin-converting enzyme inhibition. 138 38

1. The response of venous plasma natriuretic peptides (atrial natriuretic peptide, ANP, and brain natriuretic peptide, BNP) plasma cyclic guanosine monophosphate (cGMP) and vasoactive hormones to dynamic exercise has been studied in 16 subjects undergoing diagnostic exercise tolerance for ischaemic heart disease (IHD), and in five healthy control subjects. 2. In patients with IHD, plasma ANP increased 3-fold (mean 16 +/- 2.5 pmol/L pre-exercise, 51 +/- 11 pmol/L after exercise, P < 0.01). Increase in plasma BNP (10.5 +/- 1.6 pmol/L pre-exercise, 13 +/- 2 pmol/L after exercise, P < 0.01) was proportionately much less than ANP but more sustained. In exercising normal subjects, plasma ANP levels doubled (P < 0.01) but there was no significant change in plasma BNP levels. 3. In patients with IHD, there was a significant correlation between levels of plasma ANP and BNP before exercise (r = 0.97, P < 0.001) as well as during exercise (r = 0.79, P < 0.001). 4. Hormone responses in patients with positive exercise tests did not differ significantly from those with negative tests. 5. Although resting levels of plasma ANP and BNP in IHD are correlated, the findings indicate different mechanisms of secretion. The low BNP/ANP ratio in response to acute dynamic exercise presumably reflects the predominance of ANP in pre-secretory atrial stores.
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PMID:Atrial and brain natriuretic peptide response to exercise in patients with ischaemic heart disease. 840 35

A specific and sensitive radioimmunoassay (RIA) for the N-terminal fragment of proatrial natriuretic peptide (NproANP) was developed. Antiserum raised in rabbits against a mixture enriched with prohormone was 100% cross-reactive with human proANP(1-30). Plasma concentrations of proANP(1-30) and ANP immunoreactivities (ir-) were simultaneously measured in healthy subjects and patients with congestive heart failure (CHF; 26 dilated cardiomyopathy and 5 ischemic heart disease). High plasma levels of both ir-proANP(1-30) and ir-ANP were detected in CHF patients. Circulating ir-ANP levels were elevated in New York Heart Association functional Classes II and III patients but not in Class I patients. However, plasma levels of ir-proANP(1-30) were higher in asymptomatic patients than in healthy subjects, and markedly increased in patients of Classes II and III. Analysis of ir-proANP(1-30) by gel filtration chromatography or reverse-phase high pressure liquid chromatography revealed a 10 kDa peptide circulating as a distinct entity. These findings indicate that: (i) the most probable form of NproANP in human plasma is a 10 kDa peptide and (ii) in CHF patients the rise in plasma ir-proANP(1-30) levels is more pronounced than the variation in plasma ir-ANP. Thus, NproANP plasma levels may prove to be a more sensitive marker of left ventricular dysfunction than ANP.
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PMID:Plasma levels and molecular forms of proatrial natriuretic peptides in healthy subjects and in patients with congestive heart failure. 856 71

The objective of the study was the evaluation of natriuretic peptides in ischemic heart disease. Atrial and brain peptides (ANP, BNP) were elevated in patients with ischemic heart failure, as compared with patients with angina without over failure, and controls (p < 0.01). BNP/ANP ratio was higher in NYHA class IV than in class III patients (2.67 +/- 0.87 vs. 1.52 +/- 0.59, respectively). Patients in the angina group, in whom elevated BNP or ANP was found, had subclinical systolic or diastolic dysfunction. There was inverse correlation between BNP, ANP and the left-ventricular ejection fraction (each r = 0.78, p < 0.001). We conclude that BNP is elevated as a result of myocardial dysfunction, but not of ischemia and seems to be a better index of disease stage and prognosis than ANP.
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PMID:Brain and atrial natriuretic peptides in patients with ischemic heart disease with and without heart failure. 863 Oct 38

This study was performed to determine effects of atrial and brain natriuretic peptides (ANP, BNP) on neutrophils-induced endothelial injury which is known to play a role in the pathophysiology of ischemia/reperfusion myocardial injury and to examine whether the effects of ANP and BNP on neutrophils are modulated by neutral endopeptidase 24.11 (NEP) in neutrophils themselves. The incubation of human neutrophils with ANP and BNP inhibited the neutrophils-induced detachment of cultured human endothelial cells (HEC). The inhibitory effect of ANP and BNP was associated with the suppressions of the neutrophils adhesiveness to HEC, CD18 expression on the neutrophils and elastase release from the neutrophils. Coincubation with UK73967 or phosphoramidon, inhibitors of NEP, potentiated all of the effects of ANP and BNP on the neutrophil functions, and the NEP inhibitors protected degradation of ANP and BNP by the neutrophils. NEP enzymatic activity in the particulate fractions and immunoreactive NEP expression were found to increase in the neutrophils from patients with early phase of acute myocardial infarction (AMI) by 5.2- and by 4.2-fold of the neutrophils from patients with late phase of AMI, respectively. In an in vivo canine model of myocardial ischemia/reperfusion, the intravenous administration of UK73967 suppressed the neutrophil adherence to endothelium and the neutrophil accumulation in the ischemic/reperfused myocardium. The results indicate that ANP and BNP, which are known to increase in AMI, modulate the neutrophil functions and exert protective effects against the neutrophils-induced endothelial cytotoxity. But the effects are suppressed due to their degradation by the neutrophil own NEP. Thus, neutrophil NEP, which also increases in AMI, may play a role in the pathophysiology of neutrophils-mediated ischemia/reperfusion endothelial and myocardial injury.
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PMID:Neutral endopeptidase 24.11 in neutrophils modulates protective effects of natriuretic peptides against neutrophils-induced endothelial cytotoxity. 863 98

To elucidate the predictors of the mortality rate in the elderly with chronic heart failure (HF), 120 consecutive patients (mean age, 75.2 +/- 7.8 years) with heart failure (NYHA I-II) were analyzed prospectively for 5 years. [Methods] Left ventricular ejection fraction (EF), left ventricular diastolic and systolic dimension (LVDD and LVDS) and wall thickness (WT) were measured by echocardiogram. Venipuncture for measurement of ANP and norepinephrine (NE) was done in supine position after 30 minute rest. [Results] 1) HF was associated with hypertension (47.5%), ischemic heart disease (34%), valvular disease (15%) and atrial fibrillation (AF, 23%). 2) 15 and 11 patients died for cardiac and non-cardiac events, respectively. 3) There was no difference in mean ages, gender, blood pressure, plasma-NE, EF, LVDD, LVDS, WT and AF between cardiac death and control groups. However, plasma ANP was higher in cardiac death group (173 pg/ml) than in control group (76 pg/ml) (p < 0.01). 4) Cox proportional hazard regression model revealed that ANP was an independent predictor for cardiac death (p < 0.005). We conclude that only plasma ANP level predicts long-term prognosis of chronic heart failure in the elderly.
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PMID:[Long-term prognosis of chronic heart failure in the elderly]. 874 62

Regular physical activity can have a favourable impact on other risk factors of ischaemic heart disease (IHD) and associated diabetes (DM), such as obesity, hypertension, dyslipidaemia, insulin resistance and others. This important part of treatment of diabetes is frequently difficult to implement because of the lack of willingness ("adherence") of type 2 diabetics to practice regular exercise, and unequivocal data are lacking on the intensity of exercise which will influence effectively these risk factors and be at the same time safe, readily available and psychologically acceptable. The objective of the work was to find out whether walking, i.e. locomotor activity with a low to medium intensity can effectively influence parameters of aerobic capacity and blood lipids. The authors submit the results of two groups of type 2 diabetics. The experimental group B (n = 10, age 57 +/- 7 years, BMI 31 +/- 3, duration of DM 8 +/- 5 years) participated in a 12-week training programme of walking; at the beginning and at the end of this period indicators of aerobic capacity at the level of the anaerobic threshold (VO2ANP) were evaluated as well as at the level of the symptom limited maximum (VO2SL, TepO2SL), and the blood lipid levels. In the control group A (n = 6, age 58 +/- 7 years, BMI 32 +/- 4) indicators of aerobic capacity and blood lipids were assessed after a 12-week period of the usual habitual physical activity. In group B the 12-week walking training led to significant improvement of parameters of aerobic capacity at the level of the anaerobic threshold (ANP), oxygen pulse at the level of the symptom limits maximum (SL) and a significant reduction of total and LDL cholesterol. In the control group no significant changes occurred in aerobic capacity nor blood lipid values. The training programme where walking was selected as physical activity with a low to medium intensity can be considered suitable for everyday life of motivated patients with type 2 diabetics, preferably in the form of a domestic training programme. The prerequisite of success is its regular and frequent evaluation by health professionals.
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PMID:[The effect of walking exercise on aerobic capacity and serum lipids in type 2 diabetics]. 1272 89

Angiogenic gene therapy in angina pectoris has been disappointing so far. Reasons might be that the administered genes already are overexpressed in ischemic myocardium, or that atrial and brain natriuretic peptides (ANP and BNP) are overexpressed, as they have anti-angiogenic effects. Five stable angina pectoris patients without heart failure were studied. Left ventricular biopsies were taken during coronary by-pass surgery from a region with stress-inducible ischemia and from a normal region. Both ANP and BNP but not vascular endothelial growth factor (VEGF) and VEGF-receptor 1 and 2 were overexpressed in ischemic regions compared to non-ischemic regions as measured by real-time PCR. The expression of 15 other angiogenic genes measured by oligonucleotide arrays was not consistently increased in ischemic regions. The overexpression of ANP and BNP suggests an anti-angiogenic effect in ischemic heart disease. The lack of overexpression of angiogenic genes supports the concept of therapeutic overexpression of these genes.
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PMID:ANP and BNP but not VEGF are regionally overexpressed in ischemic human myocardium. 1531 4

The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery (n = 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls (n = 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 +/- 101 to 1,268 +/- 334 pg/ml (P < 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM (P < 0.01). The cardiac ANP secretion was significantly correlated with changes in LER (r = -0.57, P < 0.01) and tau (r = 0.73, P < 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.
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PMID:Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy. 1617 69

The myocardium represents a major source of several families of peptide hormones under normal physiological conditions and the plasma concentrations of many of these "cardiac peptides" (or related pro-peptide fragments) are substantially augmented in many cardiac disease states. In addition to well-characterised endocrine functions of several of the cardiac peptides, pleiotropic functions within the myocardium and the coronary vasculature represent a significant aspect of their actions in health and disease. Here, we focus specifically on the cardioprotective roles of four major peptide families in myocardial ischemia and reperfusion: adrenomedullin, kinins, natriuretic peptides and the urocortins. The patterns of early release of all these peptides are consistent with roles as autacoid cardioprotective mediators. Clinical and experimental research indicates the early release and upregulation of many of these peptides by acute ischemia and there is a convincing body of evidence showing that exogenously administered adrenomedullin, bradykinin, ANP, BNP, CNP and urocortins are all markedly protective against experimental myocardial ischemia-reperfusion injury through a conserved series of cytoprotective signal transduction pathways. Intriguingly, all the peptides examined so far have the potential to salvage against infarction when administered specifically during early reperfusion. Thus, the myocardial secretion of peptide hormones likely represents an early protective response to ischemia. Further work is required to explore the potential therapeutic manipulation of these peptides in acute coronary syndromes and their promise as biomarkers of acute myocardial ischemia.
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PMID:Cardioprotective actions of peptide hormones in myocardial ischemia. 1751 66


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