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 frequency, clinical characteristics, and outcome of patients admitted with heart failure to a district general hospital in North-West London serving a population of approximately 155,000 was assessed over a six-month period. The number of patients with heart failure was determined by both a prospective ward survey and a retrospective study of all patient records with diagnostic codes for heart failure or pulmonary oedema. During those six months, 2,877 patients were admitted to the medical and geriatric services of whom 140 (4.9%) had heart failure. Only 29 patients in heart failure were under the age of 65 years. In 86 patients the mode of presentation was acute pulmonary oedema. Fifty-two (37%) patients had an arrhythmia at the time of admission of whom 48 had atrial fibrillation. An electrocardiogram, a chest X-ray, and an echocardiogram were performed in 137, 136, and 81 patients respectively. The aetiology of heart failure was considered to be coronary artery disease (41%), valve disease (9%), hypertension (6%), cor pulmonale (4%), a dilated cardiomyopathy (1%), congenital heart disease (1%), thyrotoxicosis (1%), and unknown (36%). During the period of hospital stay 42 patients (30%) died; a further 20 patients (14%) died in a one-year follow-up. In a district general hospital heart failure is a common reason for admission and patients remain in hospital for a considerable time. Arrhythmias are commonly associated with heart failure. The prognosis is poor and the hospital mortality high. The management of heart failure is an important consideration in allocating hospital resources in a district general hospital.
 ...
PMID:Heart failure in a district general hospital. 842 54

Twenty-seven patients with peripartum cardiac failure were seen at the Royal Victoria Hospital, Banjul over a 2-year period while one further patient presented 6 months after delivery with a cerebral embolus secondary to a dilated cardiomyopathy. Five (18%, P less than 0.001) patients had twin pregnancies. Seventeen (63%) patients attended for follow-up, of whom eight had evidence of continuing cardiac dysfunction and required treatment with diuretics; two patients were known to have died. In five asymptomatic patients the electrocardiogram had reverted to normal and three patients had further pregnancies without relapse. The bipolar distribution of onset of symptoms in relation to pregnancy was suggestive of two different pathological processes. There was no evidence that cultural habits played any significant part in the aetiology of peripartum cardiac failure in The Gambia.
 ...
PMID:Peripartum cardiac failure in The Gambia. 159 75

It has been suggested that chronically reduced myocardial adenosine triphosphate (ATP) content causes contractile dysfunction in dilated cardiomyopathy. Because total adenine nucleotides (ATP, adenosine diphosphate and monophosphate) may reflect chronic changes in energy metabolism better than may ATP alone, myocardial ATP, and adenosine diphosphate and monophosphate were determined in endomyocardial biopsy specimens from 19 patients with dilated cardiomyopathy, and decreased left (30 +/- 2%) and right (34 +/- 3%) ventricular ejection fractions, and from 11 patients with ischemic cardiomyopathy (left ventricular ejection fraction 38 +/- 3%), and compared with those from 28 normal control subjects (ejection fraction greater than 55%) to assess myocardial energy metabolism in heart failure. Myocardial norepinephrine was measured simultaneously in the same biopsy specimens to assess if the myocardium studied for adenine nucleotide content was metabolically altered. Myocardial total adenine nucleotides as well as ATP levels in 19 patients with dilated cardiomyopathy (39 +/- 3 and 23 +/- 3 nmol/mg of noncollagen protein, respectively) were unchanged in comparison with those of control subjects (37 +/- 4 and 23 +/- 3, respectively); patients with ischemic cardiomyopathy were not significantly different (30 +/- 3 and 19 +/- 3, respectively). Myocardial norepinephrine in the same biopsy specimens from patients with dilated (5.8 +/- 1.1 pg/micrograms of noncollagen protein) or ischemic (5.7 +/- 1.3) cardiomyopathy was significantly decreased compared with that of normal control subjects (12 +/- 1.1).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Myocardial adenine nucleotide concentrations and myocardial norepinephrine content in patients with heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. 159 72

In isolated papillary muscle strips from nonfailing donor hearts (NF) and from the hearts of patients with dilated cardiomyopathy with severe heart failure (NYHA IV), the force-frequency relationship was studied. Experiments were performed under basal conditions and in the presence of 0.01 microM or 0.1 microM isoprenaline and 0.02 microM ouabain. In NF, there was a positive inotropic effect following an increase of the stimulating frequency, whereas in NYHA IV, the force gradually declined under these conditions. Low concentrations (0.01 microM) of isoprenaline prevented the negative inotropic effect in NYHA IV, whereas at 0.1 microM the mechanical function deteriorated in NF and NYHA IV. Ouabain had no effect on the force-frequency relationship compared to basal conditions. It is concluded that a reduction of high frequencies does improve the contractility in the failing myocardium. It is not unreasonable to speculate that this mechanism might be involved in the beneficial effects of drugs which reduce the heart rate, such as beta-adrenoceptor antagonists and cardiac glycosides, in the condition of congestive heart failure in which the sympathetic tone is high.
 ...
PMID:Force-frequency relationship and inotropic stimulation in the nonfailing and failing human myocardium: implications for the medical treatment of heart failure. 160 Mar 53

Compensation for heart failure can be influenced by cardiac loads due to organ failure. This investigation studied the effect of secondary organ failure on the hemodynamics of acute heart failure. Of 106 patients with acute heart failure due to myocardial infarction or dilated cardiomyopathy, 49 (46%) patients had secondary organ failure, either kidney, liver, brain or blood. Their acute heart failure was sustained for significantly longer than that of 57 patients without organ failure. A transient but severe decompensation induced secondary organ failure, although the left ventricular ejection fraction was not different from that of the control without heart failure. Hypervolemia in cases of renal failure, bradycardia in loss of consciousness, hyperdynamic state in anemia and low blood pressure in liver dysfunction caused the sustained acute heart failure. These results suggested that secondary organ failure might occur in 46% of patients with acute heart failure, and might disrupt compensation by different kinds of hemodynamic loads in low cardiac function.
 ...
PMID:Effects of secondary organ failure on compensation of acute heart failure in patients with myocardial infarct and dilated cardiomyopathy. 160 1

Heart transplantation is currently the most effective therapy for patients with severe heart failure due to dilated cardiomyopathy, although long-term survival without transplantation has been described in a few patients. We have identified five patients with severe heart failure who experienced a significant clinical and hemodynamic improvement while they were waiting for heart transplantation. At initial assessment, all five patients were symptom-class 4; left ventricular end-diastolic pressure was 33 +/- 4 mm Hg, left ventricular ejection fraction was 0.20 +/- 0.01, left ventricular end-systolic volume was 130 +/- 3 ml/min/m2, and cardiac index was 2.1 +/- 0.1 L/min/m2. These patients showed a marked improvement at two to ten months after initial assessment, while they were waiting for a donor heart. After a follow-up of 10 to 31 months (mean follow-up, 20 months), the five patients were still alive and their clinical and hemodynamic condition remained stable. On the contrary, survival was less than 15 percent at six months for the remaining patients with indications for heart transplantation but in whom transplant could not be performed because of the existence of contraindications or lack of donors; all these patients were dead at 18 months after initial assessment. The five patients who developed spontaneous favorable outcome showed a trend to have higher serum sodium values, shorter symptomatic history, lesser need for intravenous inotropic support, and better response to medical therapy than the other patients. Our findings suggest that some patients with transplants could have experienced a sustained and spontaneous clinical and hemodynamic recovery with medical therapy alone, although it seems currently difficult to identify patients with this favorable outcome.
 ...
PMID:Spontaneous clinical and hemodynamic improvement in patients on waiting list for heart transplantation. 162 3

A patient with mitochondrial encephalomyopathy who died from progressive intractable cardiac failure at the age of 18 is reported. At the age of 4, he presented with short stature, but multiorgan disorders including deafness, focal glomerulosclerosis, epilepsy and dilated cardiomyopathy appeared later in his clinical course. Laboratory tests showed hyperlactatemia and hyperpyruvatemia. Histopathological findings demonstrated mitochondrial myopathy with ragged red fibers and focal cytochrome C oxidase-deficient fibers in skeletal and cardiac muscles. The activity of cytochrome C oxidase was 30% less than the control level in skeletal muscle. Sequencing of the entire mitochondrial tRNA genome revealed a novel point mutation in the tRNA(Ile) region (nt 4269). This A-to-G substitution was found in none of the 30 controls by screening using mispairing PCR and Ssp I digestion methods, suggesting that this new mutation was pathogenic in our case.
 ...
PMID:Mitochondrial tRNA(Ile) mutation in fatal cardiomyopathy. 163 86

In patients with congestive heart failure, down-regulation of beta-adrenoceptors is present, probably as a result of sympathetic overstimulation. In end-stage dilated cardiomyopathy, beta 1-adrenoceptor density is markedly reduced, while beta 2-adrenoceptor density is normal. This latter finding does not necessarily imply normal sensitivity to beta 2-stimulation, due to possible alterations in the beta-adrenoceptor/adenylate cyclase complex beyond the receptor. In some disease states, such as ischemic cardiomyopathy and mitral valve disease, there seems to be a concomitant reduction of the beta 1- and beta 2-adrenoceptor density. The finding of beta-adrenoceptor down-regulation has stimulated the search for novel therapeutic approaches in heart failure patients. Beta-agonists could even further down-regulate beta receptors, and this perhaps explains why they seem not to be useful in long-term use. Agents that directly stimulate adenylate cyclase activity, such as forskolin, or that increase cyclic adenosine monophosphate degradation, such as the phosphodiesterase inhibitors, are being tested. Beta-adrenoceptor blocking agents were used in treatment of heart failure before beta-adrenoceptor down-regulation was recognized in these patients. It is tempting to speculate that the beneficial clinical and hemodynamic effects seen in these patients treated with metoprolol is indeed due to an antagonism of the beta-adrenoceptor down-regulation. Studies testing whether beta-adrenoceptor blocking agents can improve survival in congestive heart failure patients are on-going.
 ...
PMID:Receptor function in heart failure. 164 66

To examine whether the downregulation of beta-adrenoceptors is accompanied by reduced beta-adrenoceptor-mediated effects in atrial as well as in ventricular myocardium, we investigated the beta-adrenoceptor-effector coupling in atrial and papillary muscle strips from patients with terminal heart failure (heart transplantation because of dilated cardiomyopathy; New York Heart Association Class IV, NYHA IV) and moderate heart failure (mitral valve replacement, NYHA II-III) and in tissue from non-failing hearts. The isometric force of contraction induced by isoprenaline (0.001-1 mumoll-1) or Ca2+ (1.8-15 mmoll-1) in atrial muscle strips and papillary muscle strips has been measured. We also examined the number of beta-adrenoceptors in both tissues by radioligand binding. The degree of heart failure affected neither the potency (EC50: control: 0.01 (0.001-0.082) mumoll-1; NYHA II-III: 0.01 (0.001-0.125) mumoll-1; NYHA IV: 0.01 (0.001-0.160) mumoll-1) nor the efficacy (NYHA IV: 7.8 +/- 1.0 mN; NYHA II-III: 6.1 +/- 0.7 mN; control: 7.7 +/- 0.9 mN) of the isoprenaline-mediated increase in force of contraction in atrial muscle strips. This is in spite of a reduced number of beta-adrenoceptors in moderately (NYHA II-III) and terminally (NYHA IV) failing atrial myocardium compared to non-failing atrial myocardium (P less than 0.05). In contrast, in papillary muscle strips increasing degrees of heart failure were accompanied by a progressive reduction of the isoprenaline-mediated increase in force of contraction (P less than 0.05) as well as by a progressive decrease of beta-adrenoceptors (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Different beta-adrenoceptor-effector coupling in human ventricular and atrial myocardium. 165 13

Circulating plasma concentrations of norepinephrine, renin, angiotensin and vasopressin are increased in congestive heart failure. By increasing ventricular afterload, heart failure is further worsened, which in turn--in a vicious cycle--stimulates neurohumoral vasoconstrictor mechanisms. Furthermore, because of the compensatory but excessive stimulation of the sympathomimetic system, a down-regulation and desensitization particularly of the myocardial beta 1 receptors and depletion of myocardial catecholamine occurs in chronic heart failure. These defects may be restored toward normal by interventions that attenuate the activity of the sympathetic nervous system. A direct approach to modify the excessive vasoconstriction is to administer systemic vasodilator drugs, but despite favorable short-term effects, tolerance developed to most of these drugs during long-term treatment. One reason for the loss of effectiveness is the reflex activation of the sympathetic system, which increases vasoconstrictor hormone concentrations. Activation of the renin-angiotensin system can be modified effectively by angiotensin-converting enzyme inhibitors that have shown favorable responses in patients with chronic heart failure. Beta-blocking agents interfere with endogenous sympathetic activation and have produced beneficial effects in patients with congestive cardiomyopathy. Long-term treatment is associated with up-regulation of the number of beta receptors and an improved responsiveness to catecholamines. Owing to the negative inotropic effects of beta-blocking agents, some of the patients with severe heart failure deteriorated hemodynamically and clinically. Theoretically, it should be advantageous to have a substance that combines protection against excessive beta stimulation with a mild inotropic support to prevent cardiac decompensation. This may be achieved by a selective beta 1-partial agonist like xamoterol.
 ...
PMID:Interrupting the adaptive changes in congestive heart failure. 167 86


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