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

The role of digoxin in treatment of cats with dilated cardiomyopathy and other forms of myocardial failure is unclear. We evaluated the chronotropic and inotropic effects of digoxin by comparing baseline, noninvasive indices of cardiac performance with those obtained after 9 +/- 1.3 (mean +/- SEM) days of digoxin treatment in 6 cats with heart failure attributable to dilated cardiomyopathy. Two-dimensionally directed, M-mode echocardiography and electrocardiography were used to determine left ventricular shortening fraction, preejection period (PEP), ejection time (LVET), PEP to LVET ratio, velocity of circumferential fiber shortening, electromechanical systole, heart rate, and PR interval. Treatment consisted of administration of furosemide (mean dosage, 2.4 mg/kg of body weight/day), digoxin in tablet form (approximately 0.01 mg/kg, q 48 h), aspirin (80 mg, q 48 h), and a commercial low-salt diet. In addition, 2 cats were administered short-term, low-dose fluids IV, and 2 were given taurine supplementation at rates of 500 and 1,000 mg/day. Other off-loading or inotropic agents were not administered. Therapeutic or toxic serum digoxin concentration was achieved in all cats. Significant (P less than 0.05) improvement was detected in mean values for shortening fraction, PEP, PEP to LVET ratio, and velocity of circumferential fiber shortening. Mean electromechanical systole and LVET did not change significantly. Improvement, as assessed by indices of cardiac function, was documented in 4 of the 6 cats treated with digoxin, including the 2 cats given taurine supplementation. In the cats given taurine, positive inotropic effect was observed prior to the time when taurine-induced improvement in ventricular function is detectable.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Efficacy of digoxin for treatment of cats with dilated cardiomyopathy. 234 18

PURPOSE OF INVESTIGATION - Bioimpedance cardiography has been suggested as a non-invasive means to monitor cardiac function but has not been tested in cases of severe ventricular dysfunction. This study compared thermodilution stroke volume, ventriculographic left ventricular ejection fraction, bioimpedance stroke volume, and the maximum first derivative of the bioimpedance signal dZ/dtmax, during the development of experimental congestive heart failure. DESIGN - Simultaneous thermodilution stroke volume, ventriculography, and bioimpedance measurements were serially measured in pigs following acute pacing, and after 1, 2, and 3 weeks of tachycardia. Thermodilution stroke volume measurements were obtained by positioning a thermistor tipped catheter into the pulmonary artery and integrating the thermodilution curve with respect to heart rate. Left ventricular stroke volume and ejection fractions were measured from single plane ventriculograms using the area-length method. Using a series of electrodes positioned on the thoracic segment and a low level current (2.5 ma), the bioimpedance waveform was recorded and stroke volume and dZ/dtmax computed. SUBJECTS - The subjects were eight pigs (23-30 kg) with developing ventricular dysfunction due to chronic rapid atrial pacing (240 beats.min-1) and four controls. MEASUREMENTS AND MAIN RESULTS - Left ventricular ejection fraction decreased significantly from acutely paced values following 7 d tachycardia [60(SEM 1)% v 41(3)% respectively, p less than 0.01] and continued to decline with longer durations of tachycardia. A significant correlation was observed between ejection fraction and dZ/dtmax (r = 0.74, n = 32). Thermodilution and bioimpedance stroke volumes fell significantly from acutely paced values after week 2 of tachycardia [thermodilution: 13.8(0.9) v 8.5(1.4) ml; bioimpedance: 13.6(1.1) v 11.2(1.5) ml respectively, p less than 0.05] and were highly correlated throughout the study period (r = 0.90, n = 32). However, bioimpedance overestimated thermodilution values at week 2 (p less than 0.05) and at week 3 of tachycardia [thermodilution: 8.4(0.8) ml v bioimpedance: 9.6(1.0) ml, NS]. CONCLUSION - In a tachycardia induced model of heart failure, bioimpedance was significantly correlated with thermodilution stroke volume. The peak first derivative of the bioimpedance signal dZ/dtmax may provide a non-invasive index of ventricular pump performance. While these results are promising, further studies are required to evaluate the diagnostic value of bioimpedance cardiography in the clinical setting.
 ...
PMID:Relationship between bioimpedance, thermodilution, and ventriculographic measurements in experimental congestive heart failure. 237 97

Evaluation of new drugs for the treatment of patients with heart failure requires assessment of the inotropic effects of these agents. Use of traditional indexes of contractility has been limited by the confounding effects of load on these measures of contractile function, although they have yielded meaningful conclusions in some studies. Recently, the end-systolic pressure volume relation (ESPVR) has emerged as a relatively load-independent measure of contractility. Because it is difficult to construct the relation in the clinical setting, several approximations have been introduced, some of which have significant limitations. We have applied the ESPVR to the assessment of the inotropic effect of the new dihydropyridine calcium channel blocker, nicardipine, in 15 patients with heart failure caused by systolic dysfunction. We constructed left ventricular pressure-volume loops from micromanometer pressure and radionuclide volume and manipulated afterload with nitroprusside. In response to intravenous nicardipine, mean arterial pressure fell from 91 +/- 4 (mean +/- SEM) to 72 +/- 2 mm Hg, left ventricular end-diastolic pressure fell from 27 +/- 2 to 23 +/- 3 mm Hg, cardiac index increased from 1.7 +/- 0.1 to 2.4 +/- 0.1 L/min/m2, and left ventricular ejection fraction increased from 0.15 +/- 0.01 to 0.19 +/- 0.01 (all p less than 0.05). Heart rate did not change. A rightward shift of the ESPVR, indicating a negative inotropic effect of nicardipine, was observed in 12 of 14 patients (p less than 0.05). We conclude that nicardipine improves left ventricular pump performance despite its negative inotropic effect in patients with severe heart failure. The improvement in pump performance can be attributed to afterload reduction.
 ...
PMID:Techniques for assessing inotropic effects of drugs in patients with heart failure: application to the evaluation of nicardipine. 240 15

We studied the hemodynamic effects of four doses of milrinone, administered by intravenous (i.v.) infusion alone and after autonomic blockade with prazosin, propranolol, atropine, and clonidine. Plasma concentrations of milrinone (50-600 ng/ml) were similar to those used for the treatment of cardiac failure and were unaltered by autonomic blockade. When given alone, milrinone induced dose-dependent increases in heart rate (maximum increase 21 +/- 4, SEM, beats/min) and cardiac output (CO) (maximum 44 +/- 9%) and reduced systemic vascular resistance (SVR) by a maximum of 32 +/- 5%. After autonomic blockade, milrinone caused a similar fall in SVR and a smaller but significant (7 +/- 2 beats/min) rise in heart rate, but no change in CO. The increase in CO produced in normal humans by acute i.v. infusions of milrinone depends on intact cardiovascular reflexes.
 ...
PMID:Effect of autonomic blockade on the hemodynamic responses of normal human subjects to acute intravenous milrinone. 243 30

Felodipine is a potent arteriolar vasodilator. Its possible myocardial effects were studied by placing dogs anaesthetized with chloralose on cardiopulmonary bypass. A balloon was then inserted into the left ventricular cavity with a vent alongside it. Isovolumic contractions (developed pressure or maximal rate of rise of pressure) were studied as the intraventricular balloon was inflated to various levels. Total coronary venous return was collected to measure coronary blood flow and felodipine concentrations. In seven vagotomized and beta-blocked preparations, a small positive inotropic effect was found [32 +/- 11 (SEM)%, p less than 0.05]; the maximum effect was reached at arterial plasma felodipine concentrations of between 7 and 20 nM and was accompanied by appreciable coronary vasodilatation. In five dogs, infusion of the solvent vehicle (5% polyethylene glycol) alone had no effect. In three more dogs, an infusion of nitroprusside caused coronary vasodilatation, but no positive inotropic effect. The results show that at low concentrations, felodipine has a positive inotropic effect in vivo. These findings suggest that the properties of myocardial calcium agonist and vascular smooth muscle antagonist properties may coexist in the same dihydropyridine molecule. The favorable effects of this drug in the treatment of heart failure can be explained not only by reduction of peripheral resistance, but also by a moderate positive inotropic effect.
 ...
PMID:The positive inotropic effect of felodipine in isovolumically beating dog heart. 244 2

Atrial natriuretic peptides (ANP) exert vasodilating and natriuretic actions. The present study was undertaken to test the effect of low dose infusions of synthetic ANP on hemodynamic and humoral variables of patients with severe heart failure. Eight patients, aged 26 to 71 years, with severe congestive heart failure due to ischemic heart disease or idiopathic dilated cardiomyopathy were included in the study. Synthetic human (3-28) ANP was infused at doses ranging from 0.5 to 2 micrograms/min for up to 3 h. Pulmonary capillary wedge pressure fell from 24 +/- 1 to 16 +/- 2 mm Hg (mean +/- SEM) (p less than 0.01) and cardiac index tended to rise from 2 +/- 0.2 to 2.3 +/- 0.2 L/min/m2 (NS), while blood pressure and heart rate did not change. One patient experienced a marked drop in pulmonary capillary wedge and arterial blood pressure that necessitated the administration of saline. ANP infusion did not alter plasma renin activity or plasma aldosterone, norepinephrine, or vasopressin levels. It decreased plasma epinephrine levels from 0.472 +/- 0.077 to 0.267 +/- 0.024 nmol/L (p less than 0.05). Plasma ANP levels were markedly elevated in all patients before initiating the infusion. They had no predictive value for the hemodynamic response to exogenous ANP. No correlation was observed between the hemodynamic effects of ANP and those induced by the subsequently administered converting enzyme inhibitor captopril, which seemed to improve cardiac function more consistently.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Infusion of atrial natriuretic peptide to patients with congestive heart failure. 246 56

To evaluate the relationship between plasma atrial natriuretic polypeptide (ANP), hemodynamic parameters, and plasma catecholamines and, in addition, to determine whether circulating ANP is metabolized in the pulmonary circulation, plasma concentrations of ANP were determined in 40 patients with chronic left-sided heart failure. After at least 30 minutes of bed rest with the patient in the supine position, blood samples were drawn simultaneously from both the main pulmonary artery (mPA) and the ascending aorta (Ao) before administration of contrast medium. The plasma ANP concentrations significantly decreased from the mPA to the Ao (135.3 +/- 18.1 pg/ml vs 127.4 +/- 19.4 pg/ml; mean +/- SEM, p less than 0.05). The plasma ANP level in the mPA correlated with the plasma norepinephrine level in the Ao (r = 0.71, p less than 0.01), right atrial pressure (r = 0.34, p less than 0.05), mean pulmonary capillary wedge pressure (r = 0.829, p less than 0.001), and left ventricular end-diastolic pressure (LVEDP) (r = 0.88, p less than 0.001). Of the various hemodynamic parameters and plasma catecholamine concentrations in the Ao, only LVEDP was found to be an independent and significant predictor of plasma ANP levels in the mPA. These results indicate that ANP released from the heart is regulated mainly by preload (LVEDP) in cases of left-sided heart failure and that circulating ANP is metabolized in the pulmonary circulation. In conclusion, the plasma ANP concentration may be a useful noninvasive index of LVEDP in patients with chronic left-sided heart failure.
 ...
PMID:Plasma atrial natriuretic polypeptide as an index of left ventricular end-diastolic pressure in patients with chronic left-sided heart failure. 252 73

Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase.
 ...
PMID:Plasma atrial natriuretic peptide in patients with acute myocardial infarction: effects of streptokinase. 252 82

The nature of plasma cardiodilatin, the amino-terminal product of the human pro-atrial natriuretic peptide, was investigated by two separate radioimmunoassays directed against the N-terminal and the putative C-terminal of the cardiodilatin molecule: ANP-[Asn1-Lys16] and ANP-[Lys87-Arg98], respectively. Serial dilutions of normal and cardiac failure plasma exhibited parallelism with the synthetic peptide standard curves in both assays. The concentrations of N- and C-terminal cardiodilatin-immunoreactivity equivalents (-IE) were significantly higher in cardiac failure patients. N-terminal-IE: 912 +/- 87, normal subjects 129 +/- 13 (mean +/- SEM); C-terminal-IE: 7979 +/- 1784, normal subjects 895 +/- 213 (both p less than 0.001). Although the concentrations determined by the two assays were not identical, significant correlations were found between them in both normal subjects (r = .69, p less than 0.001) and cardiac failure patients (r = .72, p less than 0.01). Characterisation by gel permeation and fast protein liquid chromatography demonstrated coelution of the N- and C-terminal cardiodilatin immunoreactivities in a single chromatographic peak. These results suggest that the circulating cardiodilatin in normal subjects and patients with cardiac failure contains the entire prohormone amino-terminal sequence ANP-[Asn1-Arg98].
 ...
PMID:Pro-atrial natriuretic peptide (1-98): the circulating cardiodilatin in man. 252 25

In order to determine the relationships between allograft function and the recipient's plasma concentrations of atrial natriuretic factor (ANF), plasma ANF was measured by radioimmunoassay for 14 days after cadaveric renal transplantation in 9 patients aged 19-64 years. All received immunosuppression with prednisolone, azathioprine, and cyclosporine. No patient was in heart failure. During the study period, six grafts functioned, and three were nonfunctioning--two due to rejection and one to acute tubular necrosis. Plasma ANF concentration at the time of transplantation was 48 +/- 16 pmol/L (mean +/- SEM) range 15-145 pmol/L. In the six patients with functioning grafts, ANF declined in parallel with the fall in serum creatinine (658 +/- 35 to 210 +/- 34 mumol/L). In the three with nonfunctioning grafts, serum creatinine and plasma ANF concentration both increased. There was overall a significant linear relation between serum creatinine and plasma ANF (r = 0.527, P less than 0.001). The changes in plasma ANF after renal transplantation bore no relationship to changes in body weight or blood pressure. However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). We conclude that elevated plasma ANF concentrations in end-stage renal disease are restored to normal by successful renal transplantation, implying that renal function is a determinant of plasma ANF concentration. Circulating plasma ANF may also have a direct effect on allograft sodium excretion.
 ...
PMID:Plasma atrial natriuretic factor and graft function in renal transplant recipients. 253 Jun 66


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>