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)

This investigation is designed to study the circadian rhythm (CR) of blood pressure (BP) and heart rate (HR) in heart transplanted patients (HTP). The research was performed on 10 heart failure patients (HFP), IV NYHA class, who underwent heart transplantation (HT) because of a primary congestive cardiomyopathy. The 24-h BP and HR monitorings were performed by means of a non-invasive method in pre-operative stage, over the 4 post-operative days, 6 and 12 months after surgery. ANOVA and Cosinor method validated the occurrence of a statistically significant CR in HFP. Over the 4 days after HT, the Serial Section Analysis did not show a 24-h periodicity of BP and HR: 6 months after HT, the BP and HR CR was not validated as well. One year after HT, the BP and HR CR was statistically detected. A significant difference between HTP and the clinically healthy subjects was validated only for the mean value of HR. In our opinion, the consolidation of the BP and HR CR 1 year after HT might be regarded as a clinical feature of a reacquired matching of cardiac function with vascular activity.
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PMID:[Circadian rhythm of arterial blood pressure and heart rate in patients with heart transplantation: a longitudinal study before and after transplantation]. 179 88

The natriuretic, diuretic, and hypotensive responses to infused atrial natriuretic peptide (ANP) were measured in rats 4 weeks after myocardial infarction induced by coronary artery ligation. Rat [1-28]-ANP was infused intravenously in doses of 0.1, 0.3, and 1.0 microgram/kg/min for 30 min each under pentobarbital anesthesia. There was a marked natriuresis, diuresis, and fall in blood pressure in rats with infarction but each response was significantly attenuated when compared with sham-operated controls (ANOVA: p less than 0.01, p less than 0.05, and p less than 0.01, respectively). Urinary cyclic guanosine monophosphate (cGMP) excretion in rats with infarction was higher than that of controls but rose to the same absolute level in both groups in response to ANP infusion (0.3 microgram/kg/min). Reduced ANP responsiveness may result from impaired postreceptor mechanisms or from physiological antagonism by angiotensin II. Reduced ANP responsiveness may partly explain impaired salt handling in heart failure.
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PMID:Atrial natriuretic peptide infusion in chronic heart failure in the rat. 247 48

In a preliminary double-blind study in African patients with heart failure, enalapril tended to increase treadmill exercise duration relative to placebo (95% confidence interval--11.5 to 144.3 s). This was associated with a significant improvement in NYHA functional class and subjective well being (P less than 0.05 ANOVA) with a concomitant reduction in body weight (P less than 0.05 ANOVA). It significantly increased pulse pressure during forearm isometric exercise (P less than 0.05 ANOVA), but the Valsalva's manoeuvre and the orthostatic response were unchanged.
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PMID:Enalapril in African patients with congestive cardiac failure. 254 54

Clinical data on the contributory role of heart failure to thromboembolic risk does not differentiate between systolic and diastolic left ventricular dysfunction. We therefore conducted a population-controlled cross-sectional study to determine levels of plasma fibrinogen (associated with thromboembolism), fibrin D-dimer (a marker of fibrin turnover) and von Willebrand factor (a marker of endothelial dysfunction) in patients with ischaemic heart disease (a common cause of diastolic dysfunction) in whom left ventricular diastolic function was defined by echocardiography. We studied 106 patients: those with normal left ventricular function (n = 42, Group 1); those with left ventricular dysfunction but without aneurysms (n = 34, Group 2); and those with left ventricular aneurysm formation (n = 30, Group 3). Each of these groups was subdivided into those with (a) and without (b) diastolic dysfunction. Diastolic dysfunction was present in over 60% of patients, irrespective of left ventricular systolic impairment. There were no significant differences in median levels of plasma fibrinogen, fibrin D-dimer or von Willebrand factor in each group of patients with ischaemic heart disease, whether or not left ventricular diastolic dysfunction was present (Mann-Whitney test; P = N.S.). Systolic (rather than diastolic) dysfunction was the main correlate of these (analysis of variance, general linear model--ANOVA-GLM--P < 0.05) and the greatest abnormalities of fibrinogen, endothelial dysfunction and intravascular fibrin turnover were seen in patients with left ventricular aneurysms whether or not diastolic dysfunction was present. This study demonstrates that there is no evidence of a significant additional contribution to thrombotic risk (as assessed by plasma fibrinogen, von Willebrand factor and fibrin D-dimer) for patients with left ventricular diastolic dysfunction. A relationship is noted between some prothrombotic factors and Doppler indices of flow, which suggests a possible association between cardiac haemodynamics and thrombogenesis.
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PMID:Is diastolic dysfunction associated with thrombogenesis? A study of circulating markers of a prothrombotic state in patients with coronary artery disease. 755 62

Angiotensin converting enzyme (ACE) inhibitors are of proven value in patients with severe chronic heart failure (CHF). Studies of the effects of ACE inhibitors on exercise capacity and quality of life in mild CHF have produced conflicting results. We have studied the effects of quinapril, a new ACE inhibitor with a relatively short plasma half-life, in mild CHF. Once daily (o.d.) dosing was compared with twice daily (b.i.d.) dosing in a three-way cross-over, double-blind, placebo-controlled trial. Thirty-two patients (two female), mean age 59 (range 32-76) years were enrolled in three cardiology centres in the U.K. in 29 patients, and non-ischaemic in three. The mean (range) radionuclide ejection fraction was 20.4% (8%-47%). Following full familiarization with the protocol, the treadmill exercise time (modified Bruce protocol) was determined for each patient during a placebo run-in phase, and at the end of each of three 8-week double-blind treatment phases with quinapril o.d., quinapril b.i.d. (maximal total daily dose 20 mg) and placebo. Three patients were withdrawn due to adverse events while receiving quinapril (unstable angina, exacerbation of CHF and arrhythmia); there were no deaths and no patient was withdrawn due to hypotension. Mean exercise time (the primary end-point) was 65 s and 53 s longer in patients receiving quinapril o.d. and b.i.d. respectively compared to placebo (both P < 0.01, ANOVA). There was no significant period effect during the trial and no significant difference between the two quinapril dosing regimens. Quinapril had no significant effect on secondary end-points including ejection fraction, functional class and quality of life.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A multicentre, double-blind, placebo-controlled trial of quinapril in mild, chronic heart failure. 845 62

We evaluated the analytical characteristics and clinical usefulness of a commercially available IRMA kit for measuring plasma concentrations of atrial natriuretic peptide (ANP) in healthy subjects and in patients with heart failure. The method uses two monoclonal antibodies prepared against sterically remote epitopes of the ANP molecule; the first antibody is coated on the solid-phase beads, and the second is radiolabeled with 125I. Fifty-nine healthy subjects and 77 patients with heart failure were studied. After subjects had rested 20 min in a recumbent position, blood samples were collected from a brachial vein into ice-chilled disposable polypropylene tubes containing aprotinin and EDTA. Plasma samples were immediately separated by centrifugation and stored at -20 degrees C until assay. The working range (CV <15%) was 10-2000 ng/L. The detection limit (2.13 +/- 0.91 ng/L) was similar to those reported for other IRMAs but was much better than those of RIAs. For healthy subjects, the results of this method (18.0 +/- 10.6 ng/L, range 4.7-63 ng/L, median 16.7 ng/L, n = 59) were similar to those generally reported for the most accurate methods, i.e., those using preliminary extraction and chromatographic purification of plasma samples. Measured plasma ANP was significantly associated with the severity of clinical symptoms, i.e., NYHA class (ANOVA, P <0.0001), and with the left ventricular ejection fraction (n = 62, r = 0.618, P <0.0001). Patients with severe heart failure showed greatly increased values (NYHA III-IV: 257.4 +/- 196.6 ng/L, n = 23).
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PMID:Analytical performance and clinical usefulness of a commercially available IRMA kit for measuring atrial natriuretic peptide in patients with heart failure. 885 46

We tested the hypothesis that concurrent inhibition of the renin angiotensin system by enalapril (5 mg) and the sympathetic nervous system by alpha 1 adrenergic blockade (prazosin 1 mg) will be superior to enalapril alone in 17 patients with heart failure on standard therapy, in a single blind, placebo-controlled, randomized parallel group study for 4 weeks. Enalapril alone induced a significant increase in exercise time from 499 +/- 412 s to 707 +/- 608 s (P < 0.05, ANOVA), but the increase induced by the enalapril + prazosin combination was significantly greater (P < 0.025, MANOVA) from 214 +/- 271 to 1007 +/- 784 s as was the increase in creatinine clearance (P < 0.05).
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PMID:Concurrent alpha 1 adrenergic blockade and angiotensin converting enzyme inhibition in the treatment of congestive heart failure. 901 70

Nitric oxide (NO) is a free radical gas and a short-lived messenger which has many paracrine functions. Direct assessment of NO production is very difficult in vivo. However, the paranasal cavities generate a high amount of NO which diffuses in the nasal cavity where it can be easily measured. Several studies have suggested alterations of the NO production in heart failure. Thus, we assessed nasal NO concentration in normal subjects and in heart failure patients. The nasal NO concentration averaged 227 +/- 10 ppb in the control group (n = 20), and 210 +/- 10, 198 +/- 20 and 159 +/- 54 ppb in New York Heart Association (NYHA) class II (n = 30), III (n = 28) and IV (n = 7) patients, respectively (mean +/- standard error [SE], not significant using analysis of variance [ANOVA]). Nasal NO level was not influenced by age, sex or etiology of the heart failure or by treatment with frusemide, angiotensin-converting enzyme inhibitor or digoxin. However, treatment with NO-releasing drugs (nitrates or molsidomine) significantly decreased the nasal NO level in heart failure patients. A two-way ANOVA revealed that treatment with a NO-releasing drug influenced nasal NO concentration (P = 0.0005), whereas NYHA class did not (P = 0.23), with a trend towards an interaction between the two parameters (P = 0.09): the inhibitory effect of NO-releasing drug on nasal NO concentration was more pronounced in severe heart failure. In an additional group of 12 patients (NYHA class II or III), the nasal NO concentration was 174 +/- 19 ppb during NO-releasing drug treatment and increased to 231 +/- 27 ppb 3 days after withdrawal of the nitrates (P = 0.0007 using paired t-test). Conversely, the nasal NO concentration in another group of seven patients (NYHA class II or III) was 219 +/- 32 ppb without nitrate treatment and decreased to 188 +/- 28 ppb 7 days after nitrate addition (P = 0.02 using paired t-test). In contrast, the nasal NO concentration in another group of ten ischemic patients without heart failure was 203 +/- 25 ppb without nitrate treatment and was similar (207 +/- 28 ppb) 7 days after nitrate addition (not significant using paired t-test). In conclusion, nasal NO production is normal in heart failure, except in patients receiving NO-releasing drugs. Nasal NO concentration could be useful for investigating the mechanism(s) by which exogenous NO donors decrease endogenous NO production.
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PMID:Nasal nitric oxide concentration is decreased in heart failure patients receiving nitrates. 952 91

Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels increase in patients with heart failure with the progression of clinical symptoms and with the deterioration of hemodynamics; consequently, assay methods for these peptides may be useful in the follow-up of cardiac patients. Non-competitive immunoradiometric assay (IRMA) methods for ANP or BNP do not generally require preliminary extraction and/or purification of the plasma sample, and so may be more suitable than competitive immunoradiometric assay (RIA) methods for the routine assay of plasma peptide concentrations. We evaluated the analytical characteristics and clinical usefulness of two IRMAs for plasma ANP and BNP, to verify whether these methods may be considered suitable for the follow-up of patients with heart failure. Both methods are based on the solid-phase sandwich IRMA system, which uses two monoclonal antibodies prepared against two sterically remote epitopes of peptide molecule; the first antibody was coated on the beads solid-phase and the second was radiolabeled with 125I. Blood samples were collected from a brachial vein in ice-chilled disposable polypropylene tubes containing aprotinin and EDTA after the patient had rested for at least 20 min in the recumbent position. Plasma samples were immediately separated by centrifugation and stored at -20 C until assay. The IRMA methods showed a better sensitivity and a wider working range sensitivity (about 2 ng/l) than those of RIA methods. Moreover, the normal range found with these methods (ANP = 16.1 +/- 8.6 ng/l, 5.2 +/- 2.8 pmol/l, BNP = 8.6 +/- 8.2 ng/l, 2.5 +/- 2.4 pmol/l) was similar to that generally reported using the most accurate methods, such as the other IRMAs or RIAs, using a preliminary extraction and purification of plasma samples with chromatographic procedures. Our results obtained in patients with different degrees of heart failure indicate that plasma ANP and BNP increase with the progression of clinical symptoms (NYHA class) (ANOVA p < 0.0001). Indeed, circulating levels of ANP (R = -0.701, no. = 86) and BNP (R = -0.745, no. = 55) were significantly (p < 0.0001) and negatively correlated with the left ventricular ejection fraction values. Furthermore, a close curvilinear regression (R = 0.960, no. = 215) was found between ANP and BNP values, because plasma BNP progressively increases more than plasma ANP in patients with different stages of heart failure. In conclusion, IRMA methods are preferable for the measurement of plasma ANP and BNP for experimental studies and routine assay because they are more practicable, sensitive and accurate than RIA procedures. Finally, BNP assay appears to be better than ANP for discriminating between normal subjects and patients with different degrees of heart failure.
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PMID:Circulating levels of cardiac natriuretic peptides (ANP and BNP) measured by highly sensitive and specific immunoradiometric assays in normal subjects and in patients with different degrees of heart failure. 959 Dec 13

Myocardial tumor necrosis factor-alpha (TNF-alpha) is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischemia-reperfusion injury (I/R), sepsis, chronic heart failure, and cardiac allograft rejection. Cardiac resident macrophages and cardiomyocytes themselves produce TNF-alpha. In this regard, adenosine (ADO) has been reported to reduce macrophage TNF-alpha production. Our purposes were to determine whether (1) I/R induces rat myocardial TNF-alpha production; (2) ADO decreases ischemia-induced rat myocardial TNF-alpha production; (3) ADO functionally protects human myocardium against I/R; and (4) TNF-alpha-binding protein (TNFBP; p55) confers similar protection when substituted for ADO pretreatment. To study this, human atrial trabeculae were obtained during cardiac surgery and suspended in organ baths, paced at 1 Hz, and force development was recorded during I/R (45/120 min) with or without ADO pretreatment (125 microM x 10 min), or TNFBP (1 microgram/ml) during I/R. Isolated rat hearts were perfused using the Langendorff method undergoing I/R (20/40 min) with or without ADO pretreatment (125 microM x 2 min) and rat myocardial expression of TNF-alpha was assessed by ELISA. Results demonstrated that I/R increased rat myocardial TNF-alpha levels from 324 +/- 36 to 902 +/- 77 pg/g (P < 0.05; ANOVA and Bonferroni/Dunn) and decreased human myocardial developed force (DF) to 18 +/- 2% of baseline (%BDF; P < 0.05). ADO pretreatment decreased ischemia-induced rat myocardial TNF-alpha production (356 +/- 107 pg/g; P < 0.05) and increased postischemic DF of human myocardium to 39 +/- 3% BDF (P < 0.05. Further substantiating the link between ischemia-induced TNF-alpha production and injury, TNFBP administration similarly improved post-I/R function of human myocardium (55 +/- 5% BDF; P < 0.05 vs. I/R alone). We conclude that (1) I/R induces rat myocardial TNF-alpha production; (2) ADO pretreatment decreases I/R-induced rat myocardial TNF-alpha production; (3) ADO improves human myocardial function; (4) TNFBP confers similar protection; and (5) inhibition/neutralization of TNF-alpha represents a novel strategy for protecting human myocardium against ischemia and reperfusion injury.
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PMID:Adenosine reduces cardiac TNF-alpha production and human myocardial injury following ischemia-reperfusion. 969 10


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