UMLS:C0018801 - FACTA Search

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

Alcohol decreases myocardial contractility through direct, toxic effect. Ingestion of more than 150 g per day for more than 10 years carries a high risk of developing alcoholic cardiomyopathy. The discontinuance of alcohol intake--if put into effect early in the natural history of patients with alcoholic cardiomyopathy--commonly but not invariably results in remission of heart failure. In order to evaluate the left ventricular (LV) function and to find out a possible correlation between the degree of cardiac dysfunction and the severity of the morpho-functional aspects of alcoholic liver disease, 20 chronic alcoholic patients without clinical evidence of heart disease were examined. Echocardiography, systolic time intervals, mechanical polygraphic recordings and liver biopsy were obtained. According to the morphological alterations showed by the needle biopsy of the liver, we separated 12 patients with liver steatosis (Group I) from 8 subjects with alcoholic hepatitis and fibrosis. In Group I LVET, ICT, PEP/LVET indices and LV fractional shortening (delta %) were not statistically different from control subjects. Patients of Group II showed marked impairment of myocardial function, as revealed by significant ICT, PEP, PEP/LVET prolongation and by an equally significant reduction of fractional shortening of the LV. The noninvasive method has proved to be quite useful in detecting early LV dysfunction in asymptomatic chronic alcoholics and has revealed a correlation between the severity of the morphological involvement of the liver and the impairment of cardiac performance.
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PMID:[Non-invasive evaluation of left ventricular function in chronic alcoholics. Histo-morphological and echo-polygraphic correlations]. 718 10

The hemodynamic effect of 2-[(2-methoxy-4-methylsulfinyl)phenyl]- 1H-imidazo[4,5-b]pyridine (AR-L 115 BS), a new positive-inotropic substance, was studied in 10 Patients with chronic congestive heart failure after i.v. infusion of increasing does of 1.8 mg/min, 2.7 mg/min and 3.6 mg/min over a period of 40 min each. Prior to each infusion an i.v. bolus of 16 mg was given. The hemodynamic changes were measured by means of a Swan Ganz balloon tipped catheter and by echocardiography. The heart rate remained unchanged whereas systolic, diastolic and mean arterial pressures fell slightly by about 5%. The mean and diastolic pulmonary pressures decreased by 30% with a concomitant increase in cardiac output of 15%. The total peripheral and pulmonary resistance was reduced by 20% and 40%, respectively. The echocardiographically measured fraction of systolic fiber shortening of the left ventricle was increased by 15%. In parallel the ratio of PEP/LVET decreased by 10%. While the increase of the infusion dose from 1.8 mg/min to 2.7 mg/min was followed by an increase in the hemodynamic changes, no further alterations were observed after the dose was increased from 2.7 mg/min to 3.6 mg/min despite a marked increase in the blood level of AR-L 115 BS. The effect was still present 75 min after the infusion had been stopped. The blood level at that time had returned to the level achieved with the dose of 2.7 mg/min. The results are consistent with findings in animals which have shown that AR-L 115 BS exerts not only a positive-inotropic action on the heart, but also exhibits a vasodilating effect, predominantly in the capacitance vessels. As the substance can also be administered orally it could prove to be a useful agent in the management of severe cases of heart failure.
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PMID:The acute effect of a new positive inotropic agent (AR-L 115 BS) on cardiac hemodynamics and contractility in patients with severe chronic congestive heart failure. 719 35

Serial electrocardiograms, phonocardiograms and echocardiograms were recorded in a prospective study of 45 closely-followed patients receiving chemotherapy with Adriamycin (doxorubicin hydrochloride, Adria Labs.). QRS voltage, systolic time intervals (STI), echocardiographic ejection fraction (EF) and rate of ventricular circumferential fiber shortening (Vcf) were compared as indicators of Adriamycin cardiotoxicity. Seven patients (16%) developed a decline in left ventricular function. Four of these seven patients (57%) developed symptoms and signs of congestive heart failure (CHF). The pre-ejection period/left ventricular ejection time (PEP/LVET) was earliest to change and was the least specific of the noninvasive parameters. The ejection fraction was the most specific parameter in predicting clinical cardiotoxicity. In every case of congestive heart failure, significant changes in ejection fraction, Vcf and PEP/LVET preceded the onset of symptoms, suggesting that measurement of the ejection fraction and systolic time intervals will allow early prediction and avoidance of heart failure. A fall in the ejection fraction of greater than or equal to 10% may represent sufficient grounds for discontinuing Adriamycin.
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PMID:Comparative analysis of noninvasive cardiac parameters in the detection and evaluation of adriamycin cardiotoxicity. 725 65

Systolic time intervals were measured from simultaneous high speed recordings of the electrocardiogram, phonocardiogram, and carotid artery pulse in 15 men with chronic severe anaemia not in heart failure and with a normal heart size, and in 15 normal men. Heart rates, electromechanical systole (QS2), pre-ejection period index (PEPI), left ventricular ejection time index (LVETI), and the ratio of pre-ejection period to left ventricular ejection time (PEP/LVET) did not differ significantly in the two groups. After the intravenous administration of frusemide in 10 of the anaemic patients, the pre-ejection period index was prolonged, the PEP/LVET ratio increased, heart rate increased, and the left ventricular ejection time index shortened. Intravenous digoxin did not alter the QS2 interval and heart rate significantly in the anaemic subjects. Left ventricular function in chronic severe anaemia as measured by systolic time intervals does not differ from that of normal controls. The effect of frusemide on the systolic time intervals is explained as an effect of the fall in preload, bringing cardiac function further down on the ascending limb of the Frank-Starling curve. Other related studies are discussed.
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PMID:Systolic time intervals in chronic severe anaemia and effect of diuretic and digitalis. 727 17

The cardiac function in Hegglin syndrome (HS; prolonged QT interval and shortened QS2) remains unclear. In order to estimate cardiac function of HS, left ventricular echocardiographic parameters and systolic time intervals (STI) were analyzed, and compared with those of normal subjects (N) (n = 20). Forty-six patients (pts) of HS are constituted of 23 pts with chronic renal failure, 7 with cardiomyopathy, 5 with ischemic heart disease, 5 with essential hypertension, 4 with acquired valvular disease, 1 with effusive pericarditis and 1 with Romano-Ward syndrome. Corrected preejection period (PEPc) and PEP/ET were significantly larger (0.15 +/- 0.02 vs 0.13 +/- 0.01, p less than 0.001; 0.48 +/- 0.13 vs 0.35 +/- 0.04, p less than 0.001, respectively) in HS. Corrected ejection time (ETc) was significantly smaller (0.37 +/- 0.02 vs 0.41 +/- 0.01, p less than 0.001) in HS. Mitral EF slope (DDR), ejection fraction (EF), and mean ventricular circumferential fiber shortening (mVCF) were significantly decreased (58 +/- 29 vs 92 +/- 25, p less than 0.001; 0.52 +/- 0.15 vs 0.62 +/- 0.07; p less than 0.005; 0.98 +/- 0.33 vs 1.18 +/- 0.20; p less than 0.05, respectively) in HS, but cardiac index (C.I.) did not differ. Thus, patients with Hegglin syndrome showed heart failure pattern in STI and hypodynamic cardiac function in echocardiographic parameters, and our data suggest that hypodynamic cardiac function of HS is caused by both lowered pump function and decreased myocardial contractility.
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PMID:[Systolic time intervals and echocardiographic parameters in Hegglin syndrome (author's transl)]. 732 May 60

The effects of intravenous disopyramide phosphate on myocardial function were evaluated by non-invasive indices of cardiac performance (systolic time intervals, STI) in 15 patients with atherosclerotic heart disease and different degrees of cardiac failure. Disopyramide (1.5 mg/Kg) was given intravenously over a period of 5 min. This drug induced in patients in I-II classes of NYHA a significant decrease of LVETc, while PEP, ICT, and PEP/LVET ratio rose significantly. STI were affected much more markedly in patients in III-IV classes of NYHA. Particularly affected were contractility indices (PEP, ICT, PEP/LVET), which were reduced significantly more in patients in III-IV classes as compares to patient in I-II classes. In contrast, LVETc, which correlates to stroke volume and cardiac output, was similarly worsened by the drug in the 2 groups of patients. Therefore, this study shows that disopyramide has relevant depressant effects on myocardial performance, simultaneously reducing stroke volume and contractility, and that the effect on contractility is more marked in patients with severe left ventricular impairment.
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PMID:Effects of intravenous disopyramide on myocardial function in patients with different degrees of cardiac failure. 737 60

Patients with Becker muscular dystrophy (BMD) have milder muscular impairment and better prognosis than patients with Duchenne muscular dystrophy (DMD). Another difference is that while cardiac failure due to myocardial involvement is a frequent cause of death in BMD, respiratory failure is the most common cause of death in DMD. We examined cardiac function and the mechanism of cardiac failure in 21 BMD patients aged 3 to 63 years (mean, 40.4) by electrocardiography, mechanocardiography, echocardiography, and post-mortem examination. Diagnosis of BMD was made by characteristic symptoms, dystrophic change in muscle histology, and the followings: 1) a deletion in the dystrophin gene, 2) "patchy" staining of dystrophin on immunocytochemical analysis, 3) abnormal dystrophin size on Western blotting, and 4) presence of a definite carrier in the family. To be diagnosed as BMD, patients exhibited one or more of 1)-3). Patients who were diagnosed only by 4) had a relative who had been diagnosed as BMD by one of 1)-3). The control group included 43 DMD patients (age 4-26 years, mean 16.2) and 20 healthy males (age 15-60 years, mean 33.3). Electrocardiogram showed prominent Q waves in leads II, III, aVF and V6, and tall R in V1, suggesting myocardial injury in the posteroinferior and lateral walls. The ratio of ejection time to pre-ejection period (ET/PEP) decreased to 2.0-3.3 in BMD, and was significantly lower than that in DMD patients with comparable muscle weakness. Left ventricular dilatation became more prominent with age, and end-diastolic left ventricular dimension (EDLVD) averaged 52.3 mm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical feature and mechanism of cardiac failure in patients with Becker muscular dystrophy]. 819 65

We investigated the usefulness of the plasma concentration of brain natriuretic peptide (BNP) for evaluating cardiac function in patients with Duchenne muscular dystrophy (DMD). The plasma BNP concentration was measured by immunoradiometric assay in 55 patients with DMD and in 34 healthy subjects. Cardiac function was evaluated by the cardiothoracic ratio (CTR) on chest roentgenogram, left ventricular end-diastolic dimension (LVDd) and fractional shortening (FS) on echocardiogram, and the ratio of ejection time to pre-ejection period (ET/PEP) on mechanocardiogram. The function of skeletal muscle was evaluated in terms of the disability of lower limb function, serum creatine kinase (CK) activity and % vital capacity (% VC). The plasma concentration of BNP was increased in patients with DMD (32.7 +/- 14.8 pg/ml, mean +/- SEM) compared with that in normal subjects (4.3 +/- 0.5 pg/ml). Two of the DMD patients had symptoms of heart failure, with markedly increased plasma BNP concentrations. The other DMD patients with increased plasma BNP concentrations showed abnormal cardiac function but no symptoms of heart failure. In addition, in patients with DMD, the plasma BNP concentration showed significant positive correlations with CTR and LVDd (p < 0.01), and negative correlations with ET/PEP and FS (p < 0.01). In severe DMD patients who had advanced disability and decreased CK activity, the plasma BNP concentration tended to be elevated. There was no significant correlation between the plasma BNP concentration and % VC. These findings suggest that the plasma BNP concentration is useful for evaluating cardiac dysfunction, whether manifest or latent, in patients with DMD, in whom accurate evaluation of cardiac function by conventional methods is difficult due to severe muscle atrophy and deformity of the thorax.
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PMID:[Estimation of cardiac function by plasma concentration of brain natriuretic peptide in patients with Duchenne muscular dystrophy]. 868 97

To determine the effect of left ventricular and endocrine functions on linear growth in children with rheumatic heart disease (RHD) we studied 100 children and adolescents with RHD over a period of 1 year. The mean +/- SD for age of onset and duration of RHD were 7.3 +/- 3.8 years and 4.4 +/- 2.8, respectively. The cardiac lesions were mitral incompetence (n = 31), combined mitral and aortic incompetence (n = 64), and mitral stenosis (n = 5). Growth was assessed by determining both height standard deviation scores (HtSDS) and growth velocity standard deviation score (GVSDS) every 4 months, and sexual maturity was assessed according to Tanner's criteria. Two-hundred age-matched normal children served as controls for the growth data. Endocrine evaluation was performed in the 30 children with RHD who had age above 14 years (mean age 15.4 +/- 1.5 years), 20 age- and sex-matched normal children, and 20 age-matched children with constitutional delay of growth (normal variant short stature) (NVSS). Circulating concentrations of estradiol (E2) in girls, testosterone (T) in boys, and free T4 (FT4) were measured. Growth hormone (GH) response to clonidine provocation, LH and FSH response to LHRH stimulation, and in boys testosterone (T) response to HCG were evaluated. Echocardiographic evaluation of the left ventricular parameters was performed using a colour-coded echodoppler. The HtSDS and GVSDS of children with RHD were significantly lower than those for the normal control group. Delayed onset of puberty was evident in 16/30 of the children with RHD, and 6/ 30 more had sexual maturity score below 10th percentile for age and gender. In comparison with the age-matched normal group, those with RHD had significantly lower sexual maturity score (1.8 +/- 0.4 v. 3.25 +/- 0.8). All the children had normal GH response to clonidine provocation and normal FT4 concentrations. Basal and HCG stimulated T concentrations were significantly low in adolescents with RHD and E2 levels were non-significantly lower in girls with RHD compared to normal controls. LH response to LHRH was significantly decreased in RHD patients v. controls denoting delayed maturation of the hypothalamic-pituitary gonadal axis. HtSDS and GVSDS were correlated significantly with the left ventricular echocardiographic parameters, including left ventricular end diastolic diameter (LVEDD) (r = 0.57, and 0.617, respectively; P < 0.01), left ventricular end systolic diameter (LVESD) (r = 0.49, and 0.546, respectively; P < 0.01), left ventricular end diastolic volume (LVEDV) (r = 0.33 and 0.31, respectively; P < 0.05), left ventricular end systolic volume (LVESV) (r = 0.325 and 0.33, respectively; P < 0.05), peak velocity of circumferential fibres (Vcf) (r = 0.25 and 0.38, respectively; P < 0.05), and with pre-ejection period/ejection time (PEP/ET) (r = 0.14 and 0.47, respectively; P < 0.05). It appears that linear growth of children with RHD, without heart failure, depends on the left ventricular function. In addition, they have high incidence of delayed sexual development secondary to delayed maturation of their hypothalamic-pituitary gonadal axis.
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PMID:Growth parameters and endocrine function in relation to echocardiographic parameters in children and adolescents with compensated rheumatic heart disease. 907 21

Diastolic heart failure (DHF) is characterized by the clinical presentation of heart failure in the setting of preserved left ventricular systolic function and evidence of diastolic dysfunction. It is estimated to be present in at least one-third of patients, who represent the signs and symptoms of heart failure, and is especially prevalent among the elderly population. Despite an increasing understanding of the pathophysiology of this disease and the improvement of diagnostic and prognostic assessment, the management of DHF remains to be established. Medical therapy consists of the cautious use of diuretics, and some studies suggested the beneficial role of beta-blockers and calcium antagonists. The rationale of current therapy is largely dependent on understanding the pathophysiology of DHF and observations from clinical trials that included relatively small numbers of patients. Large, multicenter, randomized, controlled studies are needed to define the role of various therapeutic agents in DHF, and whether the prognosis of the disease will be altered. The SWEDIC trial observed that carvedilol treatment in patients with DHF was associated with an improvement in diastolic indices measured by Doppler echocardiography. The CHARM-Preserved trial reported a non-significant reduction of cardiovascular death or admission for heart failure. Other studies which are underway include PEP-CHF and the Hong Kong Diastolic Heart Failure study. They will play a pivotal role in ascertaining the therapeutic efficacy of various agents and will help experts to set up treatment guidelines for this common condition.
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PMID:Update in the management of diastolic heart failure. 1532 Aug 27

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