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)

The plasma alpha-atrial natriuretic polypeptide (alpha-ANP) concentration in the peripheral veins of children with congenital heart diseases was measured by radioimmunoassay and compared with cardiac catheterization data. Every patient with heart failure had a higher alpha-ANP concentration (132.1 to 858.7 pg/mL) than the upper limit of the normal range (11.7 to 98.7 pg/mL), whereas more than half of the patients without heart failure had a normal alpha-ANP concentration. Although none of the 13 children with atrial septal defect had heart failure, their mean (+/- SD) plasma alpha-ANP concentration (99.4 +/- 40.7 pg/mL) was significantly higher than that in control children (44.6 +/- 22.3 pg/mL). The plasma alpha-ANP concentration was significantly correlated with the pulmonary blood flow/systemic blood flow (Qp/Qs) ratio in the children with atrial septal defect. In the 34 children with ventricular septal defect the plasma alpha-ANP concentration increased in relation to increasing size of the defect. The plasma alpha-ANP concentration was significantly correlated with the Qp/Qs ratio, pulmonary artery pressure, and left atrial pressure, estimated from mean pulmonary artery wedge pressure, in the children with ventricular septal defect. In the children with tetralogy of Fallot, the mean plasma alpha-ANP concentration was normal, and mean right and left atrial pressures were not increased. The elevated alpha-ANP concentration in the three patients with heart failure decreased after their conditions improved with various treatments. Thus the measurement of alpha-ANP concentration may be valuable in evaluating the presence or absence of heart failure and the response to treatment in children with congenital heart diseases. Distention of the right and left atrial might induce the release of alpha-ANP in patients with atrial and ventricular septal defects, respectively.
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PMID:Relationship between plasma atrial natriuretic polypeptide concentration and hemodynamic measurements in children with congenital heart diseases. 295 77

To investigate the atrial natriuretic polypeptide (ANP) levels in congenital heart diseases, we measured plasma immunoreactive ANP (ir-ANP) in 29 patients with left-to-right shunt, and right auricle ir-ANP in 25 patients who underwent operation. The levels of ir-ANP in the pulmonary artery correlated with that in the femoral vein (r = 0.95, P less than 0.001), mean pulmonary arterial pressure (r = 0.74, P less than 0.001) and right atrial pressure (r = 0.53, P less than 0.01). The right auricle ir-ANP level was high in patients with heart failure combined with pressure or volume overload of the right atrium, as observed in tricuspid atresia, complete endocardial cushion defect, and total anomalous pulmonary venous drainage. These results suggest that the production of ANP in the atrium increases as a compensatory or secondary response to persistent release of ANP into the circulation in cardiac diseases.
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PMID:Plasma and right auricle concentrations of atrial natriuretic polypeptide in children with cardiac diseases. 297 Mar 89

To examine the interrelationship between human atrial natriuretic polypeptide (hANP) and cyclic 3'5'-guanosine monophosphate (cyclic GMP), plasma concentrations of these compounds were determined in 61 disease-free humans, as controls, and in 35 patients with congestive heart failure. Levels of plasma hANP (199.6 +/- 53.7 pg/ml) and cyclic GMP (12.6 +/- 1.7 pmol/ml) in patients with congestive heart failure were significantly higher than in the control subjects (hANP 57.1 +/- 2.8 pg/ml, cyclic GMP 5.2 +/- 0.3 pmol/ml). Although plasma hANP concentrations in the patients with congestive heart failure tended to increase with the severity of cardiac dysfunction, there was no significant correlation between the levels of plasma hANP and the grade of heart failure, classified according to the New York Heart Association. However, a significant correlation was found between plasma hANP and cyclic GMP concentrations in both the healthy subjects and the patients with congestive heart failure, and a weak positive correlation between plasma hANP and cyclic 3'5'-adenosine monophosphate (cyclic AMP) concentration in the patients with congestive heart failure. Thus, changes in plasma cyclic GMP concentration depend to some extent on the plasma concentrations of hANP.
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PMID:Relationship between atrial natriuretic polypeptide and cyclic 3'5'-guanosine monophosphate in human plasma. 303 37

Although early experiments in animals and humans suggested that digitalis glycosides increased cardiac output only in the failing heart, later studies showed that these cardiotonic agents increase intraventricular systolic pressure and decrease relaxation time in the normal animal. The controversy concerning the peripheral vascular or direct cardiac effects of digitalis was finally resolved when new methods were applied to the study of the effects of this drug on intraventricular pressures and cardiac contractile force. Other positive inotropic agents, such as the adrenergic agonists, have also been tested for the treatment of heart failure. However, during long-term oral or intravenous therapy, the effectiveness of these drugs appears to diminish. Clinical studies of glucagon, a polypeptide with positive inotropic and chronotropic effects, have revealed its potential for causing side effects and its reduced activity in patients with chronic heart failure. With the discovery of several new types of inotropic agents, i.e., the bipyridines and the imidazole and benzimidazole derivatives, interest in revising our therapeutic approach to congestive heart failure has increased. This review discusses recent developments in this area.
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PMID:Historical perspectives on inotropic agents. 351 Jul 79

Cardiac phenotypic modulation and remodeling appear to be involved in the pathophysiology of cardiac hypertrophy and heart failure. We undertook this study to examine whether angiotensin II (Ang II) in vivo, independent of blood pressure, contributes to cardiac phenotypic modulation and remodeling. A low dose (200 ng/kg per minute) of Ang II was continuously infused into rats by osmotic minipump for 24 hours or 3 or 7 days to examine the effects on the expression of cardiac phenotype-related or fibrosis-related genes. This Ang II dose caused a small and gradual increase in blood pressure over 7 days. Left ventricular mRNAs for skeletal alpha-actin, beta-myosin heavy chain, atrial natriuretic polypeptide, and fibronectin were already increased by 6.9-, 1.8-, 4.8-, and 1.5-fold, respectively, after 24 hours of Ang II infusion and by 6.9-, 3.3-, 7.5-, and 2.5-fold, respectively, after 3 days, whereas ventricular alpha-myosin heavy chain and smooth muscle alpha-actin mRNAs were not significantly altered by Ang II infusion. Ventricular transforming growth factor-beta 1 and types I and III collagen mRNA levels did not increase at 24 hours and began to increase by 1.4-, 2.8-, and 2.1-fold, respectively, at 3 days. An increase in left ventricular weight occurred 3 days after Ang II infusion. Treatment with TCV-116 (3 mg/kg per day), a nonpeptide selective angiotensin type 1 receptor antagonist, completely inhibited the above-mentioned Ang II-induced increases in ventricular gene expressions and weight. Hydralazine (10 mg/kg per day), which completely normalized blood pressure, did not block cardiac hypertrophy or increased cardiac gene expressions by Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin II induces cardiac phenotypic modulation and remodeling in vivo in rats. 776 70

Coronary resistance arteriolar diameter importantly regulates myocardial blood flow, and is influenced by circulating neurohumoral agents. Angiotensin II (A-II) is a circulating polypeptide that is chronically elevated in heart failure and serves as a potent peripheral vasoconstrictor agent. However, its effects on isolated coronary resistance arterioles is relatively unknown. We compared the vasomotor effects of A-II on coronary epicardial and resistance arterioles in vitro from both the canine and porcine heart in order to determine the effects of A-II in different vascular beds and species. Epicardial rings were studied under isometric recording conditions, while resistance arterioles (50-150 microns) were studied in vitro using a video imaging system to record diameter. A-II, whether applied to passively distended or preconstricted porcine resistance arterioles, did not cause vasoconstriction when applied as a bolus or as cumulative doses. In preconstricted canine resistance arterioles, A-II elicited dose-dependent vasodilation (EC50 = 0.2 nM). In passively distended canine arterioles, high concentrations of A-II (0.1 microM) applied as a bolus elicited transient vasoconstriction in 28% of the vessels studied. In large epicardial rings, A-II was a weak vasoconstrictor, with greater potency in canine arteries compared to porcine arteries. In canine arteries, vasoconstriction to A-II was augmented after incubation with indomethacin. In contrast to the findings in canine arteries, the A-II vasoconstrictor response in porcine coronary arteries was decreased after incubation with indomethacin or removal of the endothelium. Thus, A-II elicits the release of a vasodilator prostanoid in epicardial canine coronary arteries and a vasoconstrictor prostanoid in porcine vessels which modulate the vasomotor action of A-II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of angiotensin II on canine and porcine coronary epicardial and resistance arteries. 798 58

It has been proposed that angiotensin converting enzyme (ACE) may play a role in the metabolism of the vasodilator peptide vasoactive intestinal polypeptide (VIP). Reduced metabolism following treatment with ACE inhibitors may cause accumulation of VIP which in turn may mediate some of the beneficial haemodynamic effects of ACE inhibition observed in patients with heart failure. This study has shown that inhibition of local vascular ACE does not interfere with the vascular effects of VIP on forearm resistance vessels when this peptide is infused into the brachial artery of normal volunteers. These results suggest that endothelial ACE plays little part in the metabolism of intravascular VIP.
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PMID:Lack of effect of enalaprilat on the action of vasoactive intestinal polypeptide in the human forearm. 839 Feb 78

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system and its beneficial modification with the use of angiotensin-converting enzyme inhibin after inferior wall myocardial infarction (MI) was evaluated. Fifty patients with acute inferior MI were randomly assigned to receive 5 mg per day of either enalapril or placebo after admission. Blood tests for neurohormone levels and echocardiograms were performed at initial examination and 4 weeks later. Baseline characteristics were similar in the two groups. Four weeks after randomization, patients treated with enalapril had lower end-diastolic volume (146 +/- 29 vs 167 +/- 15 ml; p = 0.04), end-systolic volume (56 +/- 18 vs 107 +/- 17 ml; p = 0.03), serum norepinephrine levels (320 +/- 93 vs 465 +/- 77 pg/ml; p < 0.01), angiotensin II levels (18 +/- 6 vs 54 +/- 11 pg/ml; p < 0.01), and atrial natriuretic polypeptide levels (106 +/- 9 vs 122 +/- 17 pg/ml; p = 0.05) than patients given placebo. The incidence of heart failure after MI was also lower in this group (4% vs 16%; p = 0.009). Results show that there is early neurohumoral activation in the course of acute inferior wall MI. Enalapril reduces neurohumoral levels and preserves ventricular volumes. These effects were associated with a reduction in the incidence of heart failure 4 weeks after MI in these patients.
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PMID:Effects of enalapril on ventricular volumes and neurohumoral status after inferior wall myocardial infarction. 847 46

The effects of cilazapril on exercise tolerance and neurohumoral factors were investigated in old myocardial infarction (OMI) patients with asymptomatic heart failure and reduced left ventricular ejection fraction. Cilazapril (0.5 mg) was administered once daily to OMI patients (n = 20) [NYHA class I, sinus rhythm, ejection fraction by radionuclide scanning < 50% (36.8 +/- 9.1%, mean +/- SD)]. Two weeks later, five patients were excluded from the study because of cough or hypotension, and 15 patients received 1.0 mg cilazapril once daily for the next 6 weeks. Exercise tolerance, neurohumoral factors and ejection fraction were measured in OMI patients before and after administration of cilazapril. Seven age-matched healthy adults served as the controls. OMI patients had latent heart failure because their exercise tolerance values and aldosterone levels were lower and alpha-atrial natriuretic polypeptide levels were higher than those in healthy subjects. In OMI patients, 8 weeks after cilazapril administration, exercise duration increased from 545 +/- 59 to 590 +/- 74 sec (p < 0.05), anaerobic threshold from 17.5 +/- 3.2 to 20.1 +/- 2.8 ml/min/kg (p < 0.05), peak-VO2 from 23.5 +/- 4.7 to 27.1 +/- 4.4 ml/min/kg (p < 0.05), plasma renin activity from 1.34 +/- 1.13 to 5.82 +/- 5.47 ng/ml/hr (p < 0.01) and alpha-atrial natriuretic polypeptide decreased from 100.7 +/- 44.3 to 80.5 +/- 28.0 pg/ml (p < 0.05). In patients with asymptomatic left ventricular dysfunction after myocardial infarction, 8 week's cilazapril administration improved exercise tolerance and neurohumoral conditions.
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PMID:[Effect of cilazapril on exercise tolerance and neurohumoral factors in patients with asymptomatic chronic heart failure after myocardial infarction]. 852 61

N-terminal parts of proatrial natriuretic polypeptide have been proposed to be sensitive and specific markers of congestive heart failure (CHF). A prerequisite for use of a clinical marker is knowledge of day-to-day variation and dependence on age and sex. Immunoreactive N-terminal proatrial natriuretic polypeptide (31-67) (ir-N-ANP(31-67)) was measured in a clinically relevant population of healthy individuals. A total of 21 females (mean age 52 years, range 42-76) and 26 males (mean age 54 years, range 42-73), without cardiovascular disease, were included in the study. No correlation was found between ir-N-ANP(31-67) and sex. A statistically significant positive linear correlation (ir-N-ANP pmol 1(-1) = 182+ (8.2 x age in years) (p = 0.004) was found between age and ir-N-ANP(31-67). For the youngest subjects (42 years) the expected mean ir-N-ANP(31-67) was 530 pmol 1(-1), and for the oldest subjects (76 years) it was 800 pmol 1(-1). For all the subjects, the median ir-N-ANP(31-67) was found to be 626 pmol 1(-1) (range 300-1151). The day-to-day variation was studied and no significant difference was found in the plasma concentration of two samples taken 2-5 days apart. Of the individual day-to-day variation, 95% would be expected to be in the interval from -244 to 188 pmol 1(-1) (mean +/- 2 x SD). We conclude that ir-N-ANP(31-67) rises with age. The age-dependent rise in ir-N-ANP(31-67) is modest, but should be taken into consideration in order to use ir-N-ANP(31-67) as a diagnostic marker of CHF. The day-to-day variation is found to be rather high and cannot be neglected if N-ANP(31-67) is to be used as a marker of asymptomatic heart failure.
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PMID:Proatrial natriuretic polypeptide (31-67) in healthy individuals: day-to-day variation and influence of sex and age. 854 4


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