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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pharmacokinetics of dihydroquinidine were studied in 8 patients with congestive heart failure following a 22 min intravenous infusion of a quinidine preparation that contained 5.9% dihydroquinidine as an impurity. Using a thin layer chromatography-fluorometric assay procedure for dihydroquinidine, the post-infusion plasma dihydroquinidine concentrations declined biexponentially. The half-life of the fast and slow dispositional processes was 4.42 +/- 1.81 min and 6.52 +/- 2.40 h, respectively. The central compartment volume for dihydroquinidine in these patients was 0.44 +/- 0.11 l/kg with an overall apparent volume of distribution of 1.14 +/- 0.38 l/kg. The computed values of total body plasma clearance of dihydroquinidine ranged from 1.29 to 2.69 ml/min/kg with a mean value of 1.94 +/- 0.60 ml/min/kg. In these patients, approximately 16% of the administered dihydroquinidine dose was excreted intact into the urine in 48 h. The estimated value of renal clearance was 0.314 +/- 0.129 ml/min/kg. When compared to control cardiac patients, the data showed that the apparent volume of distribution for dihydroquinidine is smaller in patients with congestive heart failure and as a result of this diminished volume, the clearance rate of dihydroquinidine was slower. The net effect of these differences was the production of higher plasma concentrations of dihydroquinidine in the heart failure group.
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PMID:Pharmacokinetics of dihydroquinidine in congestive heart failure patients after intravenous quinidine administration. 49 5

Forty-one infants and children with the combination of patent ductus arteriosus (PDA) and ventricular septal defect (VSD) were encountered over 20 years. Twenty-four presented in infancy with congestive cardiac failure. Pulmonary hypertension was present in 32, the cause in 19 being increased pulmonary blood flow. Increased pulmonary vascular resistance (PVR) was detected in 13 (indicated by a pulmonary to systemic resistance ratio (Rp : RS) greater than 0.24:1 and PVR greater than 4 units). Thus 22% had a pulmonary artery systolic pressure less than 30 mmHg and 68% had a pulmonary vascular resistance below four units, indicating an unusually mild form of the combined condition in these patients. Surgical management is discussed, and in particular the question of simultaneous closure of the defects during infancy. Cardiac failure, resistant to drug treatment, and increased PVR are indications of operation. The PDA should be closed and only if there is no substantial fall in pulmonary artery pressure is the VSD repaired.
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PMID:Pulmonary hypertension accompanying ventricular septal defect and patent ductus arteriosus. Management in infancy and early childhood. 50 40

In a study of 31 cases and a review of the literature, Staphylococcus aureus endocarditis was distinguished from that due to other organisms by the absence of prior valvular disease, by the presence of debilitating illness or acute onset, and by a toxic fulminant course. Availability of semi-synthetic penicillins decreased mortality from 90% to about 50%, with death due to heart failure rather than sepsis. Valvular replacement may improve survival if employed at the first signs of cardiac decompensation, rather than after medical therapy has failed to stabilize a downhill course.
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PMID:S aureus endocarditis: a review and plea for early surgery. 50 30

Tienilic acid (TA) is a common new diuretic agent with a potent uricosuric action. In a double-blind cross-over study its antihypertensive effect was compared to that of hydrochlorothiazide (HCT). 20 patients with essential hypertension were studied: after I weeks of placebo wash-out 10 patients received TA (dose range 250-750 mg/die) and 10 HCT (dose range 50-150 mg/die), for 5 weeks. Systolic and diastolic blood pressures were significantly and equally reduced (p < 0.001) after the first week of treatment in both groups. While serum uric acid concentration increased after HCT, it was significantly reduced (p < 0.001) after TA treatment. Serum potassium was slightly reduced with both treatments. Serum tryglicerides, unchanged after HCT, showed a slight tendency to reduction on TA treatment. Ten patients with congestive heart failure, on full digitalis treatment, were given TA (dose range 250-1000 mg/die): in each patient a prompt diuretic effect was observed, associated to a significant reduction of body weight and to a marked improvement of the clinical signs of heart failure. Therefore, TA is an effective diuretic agent which may be conveniently used in the treatment of arterial hypertension and congestive heart failure, as it induces a diuretic effect comparable to that obtained with HCT, reducing at the same time, serum uric acid levels.
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PMID:[Tienilic acid in the treatment of arterial hypertension and congestive cardiac insufficiency]. 54 82

Since April 1974 until January 1978 permanent pacemakers were implanted in 21 children. The patient age at the time of operation averaged 4.5 years; the youngest patient was 3 months old. Indications for pacemaker implantation were: congenital total a-v block (TAVB) (n = 4), sick syndrom (S-S-S) (n = 4), postoperative TAVB (n = 13). Cardiac failure was present in all patients despite optimal medical treatment. Pacemakers were implanted under general anesthesia and intubation. The stimulation electrodes were positioned by the transvenous route in 16 subjects and by direct fixation upon the ventricle and the atrium in 5 patients. 5 children obtained an atrial triggered, 14 patients R-inhibited demand pacemaker and 2 subjects an asynchronous pacemaker. After a mean observation time of 16.4 months mean pacemaker function is normal in 14 patients. 6 children died 1 to 33 months after implantation despite functioning pacemakers because of congestive heart failure. Pacemaker malfunction was observed in 4 patients. The type of malfunction induced: failure of the impulse generator (n = 2), dislodgement of the electrode (n = 2), threshold increase (n = 1). In 5 children generators were changed 9 to 36 months (m = 23 plus or minus 10) after implantation because of battery depletion. The use of the pacemakers in small children is connected with several specific problems: 1. Application of large generators is hazardous because of impending perforation and secondary infection. 2. Until now miniaturization of pacemakers decreases function time and therefore implies frequent surgical intervention. 3. Stretching and dislodgement of transvenous electrodes may occur due to growth of the child. 4. Threshold increase may limit the life-span of myocardial electrodes. 5. Physiological changes in natural frequency requires changes in stimulation rate. 6. To guarantee normal physical activity demand related adaptation of heart rate is necessary. Because of these reasons a pacemaker system for children should have the following criteria: low weight, small wolume, high energy capacity, atrial or programmable stimulation, a thin elastic perhaps coiled electrode.
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PMID:[Pacemaker therapy in infants (author's transl)]. 55 59

Congestive heart failure with dilated left ventricle developed in two patients with symptomatic hypertrophic obstructive cardiomyopathy. Both patients previously underwent cardiac surgery for relief of their outflow obstruction. Alterations in structure and function of the left ventricle during their episode of cardiac failure and thereafter were documented by echocardiography. The findings suggest that progression to left ventricular dilatation is a potential complication in patients with hypertrophic obstructive cardiomyopathy.
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PMID:Progression to left ventricular dilatation in patients with hypertrophic obstructive cardiomyopathy. 57 Dec

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
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PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

Congestive heart failure in neonatal thyrotoxicosis is attributed to sympathetic overstimulation of the myocardium with resulting high-output cardiac failure. An additional case of neonatal thyrotoxicosis with congestive heart failure is discussed; three possible causes (thyrotoxicosis, maternal propranolol therapy, and ventricular septal defect) were present. Along with the usual procedures, the echocardiogram is of value in separating these factors. In addition, we discuss the potential dangers to the newborn of a mother receiving long-term propranolol hydrochloride therapy during pregnancy.
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PMID:Neonatal hyperthyroidism and heart failure. A differential approach. 57 68

d-3-Acetoxy-cis-2,3-dihydro-5-]2-(dimethylamino)ethyl]-2-(p-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one hydrochloride (diltiazem HCl) was orally administered to 9 patients with chronic congestive heart failure (Class IIb to III, NYHA) to examine whether the drug induces sodium retention and aggravates congestive heart failure. Renal hemodynamics and urinary electrolytes excretion were measured for 3 h after the medication in 6 out of 9 patients. Four of the rest of patients had received chronic administration of the drug for about 2 weeks. There was a significant increase in urinary sodium excretion without noticeable change in renal hemodynamics after diltiazem administration, demonstrating the presence of its direct inhibitory action on renal tubules. The increase in urinary sodium excretion was more marked in patients with heart failure than in those without. This difference in the response to diltiazem may be due to the functional constriction of renal cortical vessels in heart failure. This constriction may be related to renin-angiotensin system which diltiazem was reported to antagonize. The chronic administration of the drug did not induce sodium retention and edema. There was no deterioration of symptoms due to congestive heart failure such as dyspnea and body weight increase. It may be concluded that diltiazem does not aggravate congestive heart failure through its diuretic action and probably its systemic vasodilating action.
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PMID:The effect of diltiazem hydrochloride upon sodium diuresis and renal function in chronic congestive heart failure. 58 67

A case of the carpal tunnel syndrome is described which occurred simultaneously with congestive cardiac failure. As the cardiac failure responded to treatment the carpal tunnel syndrome improved dramatically.
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PMID:The carpal tunnel syndrome in congestive cardiac failure. 59 82


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