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)

In end-stage heart failure, cardiac beta-adrenoceptors are decreased and cardiac Gi protein is increased. We assessed beta-adrenoceptors, G proteins, and effects of several beta-adrenoceptor agonists, histamine, and 5-HT on adenylyl cyclase activity in right and left atria and left ventricles and on left ventricular contractility in six potential heart transplant donors (nonfailing hearts; NFHs) and in nine patients with end-stage dilated cardiomyopathy (DCM) and 11 patients with end-stage ischemic cardiomyopathy (ICM) to establish whether the functional responsiveness of all cardiac Gs-coupled receptors is reduced. Beta-adrenoceptors were reduced in all three tissues; in DCM, beta1-adrenoceptors were more markedly downregulated; in ICM, both beta1- and beta2-adrenoceptors were diminished. In all three tissues, isoprenaline-, terbutaline-, histamine- and 5-HT-induced adenylyl cyclase activation was reduced similarly in DCM and ICM. Moreover, in DCM and ICM, guanosine triphosphate (GTP)- (involving Gs and Gi) activated adenylyl cyclase was significantly diminished, whereas NaF-activated (involving only Gs) and Mn2+-activated (acting at the catalytic unit of the enzyme) adenylyl cyclase was unaltered. Left ventricular positive inotropic responses to beta1- (noradrenaline, dopamine, and dobutamine), beta2- (terbutaline), and beta1- and beta2-adrenoceptors (isoprenaline, adrenaline, and epinine), as well as H2-receptor (histamine) stimulation were significantly reduced. The extent of reduction was not different for each agonist in ICM and DCM. We conclude that in DCM and ICM, functional responsiveness of all cardiac Gs-coupled receptors is similarly reduced.
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PMID:Diminished responsiveness of Gs-coupled receptors in severely failing human hearts: no difference in dilated versus ischemic cardiomyopathy. 955 9

Endoventricular circular patch plasty (Dor operation) was used to treat end-stage dilated ischemic cardiomyopathy in 13 patients from January to December, 1997. There were 10 men and three women aged from 57 to 78 years (mean 63 years). Single, double, triple and left main trunk coronary disease was present in one, two, eight and two patients, respectively. Mean ejection fraction was 22% (6-30%) and signs of congestive heart failure were clear in all patients [New York Heart Association (NYHA) class III in eight patients and class IV in five patients]. Angina pectoris was present in five patients. Six patients had associated significant mitral regurgitation. Coronary artery bypass grafting (mean 3.2 grafts) was used in 11 patients and mitral valve reconstruction was performed in 6 patients (4: replacement and 2: repair) combined with akinetic area exclusion by the Dor technique. All patients were successfully weaned from cardiopulmonary bypass without mechanical support and no perioperative death occurred. Three patients died in hospital at 1-2 postoperative months due to pneumonia, stroke and heart failure, respectively. Two patients died during the late period due to stroke and sudden death. Among the eight survivors, six patients were in NYHA class I-II and two patients in class III. Ejection fraction increased from 22% to 36%, end-diastolic and systolic volume indices decreased from 168 +/- 58 to 123 +/- 39 ml/m2 and from 131 +/- 60 to 81 +/- 33 ml/m2, respectively. Pulmonary capillary wedge pressure decreased from 19 +/- 10 to 14 +/- 5 mmHg. The Dor procedure is an effective surgical alternative for patients with end-stage ischemic cardiomyopathy who are considered to be candidates for cardiac transplantation.
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PMID:[Dor operation for end-stage ischemic cardiomyopathy]. 955 80

Accumulating evidence suggests that endogenous endothelin-1 (ET-1) may contribute to the development of heart failure. In this study we determined sites of ET-1 synthesis and production in the failing human myocardium by immunohistochemistry and in situ hybridization for ET-1 and endothelin-converting enzyme-1 (ECE-1). Myocardial tissues were obtained from 19 patients with heart failure and from four noncardiac patients as controls. In both failing and nonfailing hearts, apparent immunoreactivity for ET-1 and ECE-1 was consistently seen in cardiac myocytes. Endothelial cells of intramyocardial coronary arteries and veins had only weak or focal ET-1 and apparent ECE-1 immunoreactivities. On the other hand, in situ hybridization showed strong signals for ET-1 and ECE-1 mRNAs in vascular endothelial cells but a lesser intensity of signals in cardiac myocytes. Apparent immunoreactivity and strong hybridization signals for both ET-1 and ECE-1 were seen in macrophages, which were abundant in infarcted regions of ischemic cardiomyopathy and in myocardium of septic patients but were rare in healthy hearts. These results suggest that, in failing human heart, vascular endothelial cells and macrophages rather than cardiac myocytes appear to be the principal ET-1 synthetic sites, although ET-1 peptides are abundantly present in cardiac myocytes of both failing and nonfailing hearts. Endogenous ET-1 may play a pathophysiologic role in human heart failure.
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PMID:Expression of endothelin-1 and endothelin-converting enzyme-1 mRNAs and proteins in failing human hearts. 959 1

Heart failure continues to plague a large population worldwide, and its incidence is increasing annually as a result of an aging population. It is associated with lengthy hospital stays, multiple hospital readmissions, and decreased quality of life because of its clinical manifestations. Although cardiac transplantation has become the therapy of choice for patients with heart failure, scarcity of donor hearts and age limitations prohibit its widespread use. Despite major advances in medical management, researchers continue to explore alternative surgical therapies to help augment cardiac function. This article explores surgical interventions in the management of heart failure, many of which are still experimental or in clinical trials. Coronary artery bypass surgery, dynamic cardiomyoplasty, and partial left ventriculectomy for the management of heart failure are discussed in detail. Descriptions of each surgical procedure, special care needs, and clinical outcomes are presented. However, because readers are familiar with the coronary artery bypass procedure and postoperative patient care, the discussion will focus on issues related to coronary artery bypass grafting in the presence of ischemic cardiomyopathy.
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PMID:Surgical alternatives in the treatment of heart failure. 963 72

The aim of the present study was to determine the kinetics of recovery of muscle oxygenation (MO) from comparable levels of exercise in chronic heart failure (CHF) patients and normal subjects and to relate MO kinetics to the level of exercise intolerance. The rationale is based on the observation that the O2 debt is increased in patients with heart failure and repayment of the debt is relatively slow. Ten patients with stable CHF (mean age 47 +/- 10 years) and nine healthy control subjects (47 +/- 6 years) were studied. All patients had ischemic cardiomyopathy (ejection fraction 33 +/- 7%). On different days, all subjects performed an upright incremental cycle ergometer exercise test with gas-exchange analysis to determine peak VO2, and a 6-minute constant work-rate (CWR) protocol at 60% of peak VO2. Oxygenation of the vastus lateralis muscle was continuously monitored during exercise and recovery using near-infrared spectroscopy (NIRS). Both MO and VO2 responses to recovery were described by a monoexponential model with a time delay. The time constant and time delay were combined to calculate a mean response time (MRT). Recovery VO2 and MO MRTs for the incremental and constant work rate exercise test were longer in CHF patients than in control subjects (p < 0.05). Both VO2 and MO MRTs were inversely related to peak VO2 (r = -0.73 and -0.52, respectively; p < 0.05 for both). However, both kinetics were not significantly different within each group between the two exercise intensities. In conclusion, the greater the cardiac dysfunction, as assessed by peak VO2, the more the recovery of muscle and total body oxygenation from both maximal and submaximal exercise is delayed.
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PMID:Muscle oxygenation kinetics measured by near-infrared spectroscopy during recovery from exercise in chronic heart failure. 977 11

During end-stage heart failure, plasma levels of interleukin-6 (IL6) are elevated. This cytokine exerts a negative inotropic influence on the myocardium. The production site of IL6 is unclear. We examined the hypothesis that IL6 in end-stage heart-failure patients is produced in the myocardium itself and is differentially regulated according to etiology. Cardiac tissue was obtained from 27 patients (idiopathic dilated cardiomyopathy, (DCM) 9/6 m/f, age 46 +/- 14 y; ischemic cardiomyopathy (ICM), 11/1 m/f, age 55 +/- 8 y) at the time of transplantation. The tissue was subjected to IL6 Northern-blot analysis. Signals were quantified by densitometric scanning after normalization to G3 PDH mRNA. Data were compared by Mann-Whitney test between DCM and ICM patients, divided by chamber origin. IL6 transcripts were found in all patients. In DCM, left-ventricular IL6 mRNA expression was higher than in ICM (p = 0.006). Median right-ventricular as well as left- and right-atrial IL6 mRNA expression was not significantly different in both groups. In summary, in end-stage heart failure, IL6 mRNA is consistently expressed in the myocardium. Left-ventricular expression is higher in DCM than in ICM. These data support the concept of a potentially reversible inflammatory component in the etiology of DCM which is more pronounced than in patients with ICM of comparable clinical severity.
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PMID:Left-ventricular expression of interleukin-6 messenger-RNA higher in idiopathic dilated than in ischemic cardiomyopathy. 977 95

Investigations of calcium antagonists in patients with advanced heart failure have raised concern over an increased risk of worsening heart failure and heart failure deaths. We assessed the effect of amlodipine on cause-specific mortality in such patients enrolled in a randomized, double-blind, placebo-controlled trial. In total, 1,153 patients in New York Heart Association class IIIb or IV heart failure were randomized to receive amlodipine or placebo, along with angiotensin-converting enzyme inhibitors, diuretics, and digitalis. Over a median 14.5 months of follow-up, 413 patients died. Cardiovascular deaths accounted for 89% of fatalities, 50% of which were sudden deaths and 45% of which were due to pump failure, with fewer attributed to myocardial infarction (3.3%) or other cardiovascular causes (1.6%). Amlodipine treatment resulted in a greater relative reduction in sudden deaths (21%) than in pump failure deaths (6.6%) overall. When patients were classified by etiology of heart failure (ischemic or nonischemic), cause-specific mortality did not differ significantly between treatment groups in the ischemic stratum. In the nonischemic stratum, however, sudden deaths and pump failure deaths were reduced by 38% and 45%, respectively, with amlodipine. Thus, when added to digitalis, diuretics, and angiotensin-converting enzyme inhibitors in patients with advanced heart failure, amlodipine appears to have no effect on cause-specific mortality in ischemic cardiomyopathy, but both pump failure and sudden deaths appear to be decreased in nonischemic heart failure patients treated with amlodipine.
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PMID:Effect of amlodipine on mode of death among patients with advanced heart failure in the PRAISE trial. Prospective Randomized Amlodipine Survival Evaluation. 978 71

We report a 51-year-old man with severe ischemic cardiomyopathy and heart failure in whom incessant bigeminal ventricular ectopy failed to generate a detectable arterial pressure. This created a mechanical bradycardia despite an adequate electrical heart rate. Dual chamber pacing increased the effective heart rate and allowed discontinuation of an intraaortic balloon pump from which the patient could not otherwise be weaned.
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PMID:Concealed mechanical bradycardia: an indication for permanent pacemaker implantation. 979 2

In patients with an elevated left ventricular filling pressure, the mitral A wave is diminished while the pulmonary venous A wave is augmented because of decreased left ventricular compliance. We examined whether an increase in the ratio of pulmonary venous to mitral A velocity might be a marker for an elevated mean pulmonary capillary wedge pressure. Forty-one patients who had left ventricular systolic dysfunction underwent transthoracic Doppler echocardiography simultaneously or within 24 hours of right heart catheterization. There were 29 men and 12 women 61 +/- 12 (mean +/- SD) years of age. Underlying heart disease was ischemic cardiomyopathy in 27 and nonischemic cardiomyopathy in 14 patients. The same Doppler-hemodynamic study was performed on 8 patients after optimal management of heart failure. The ratio of pulmonary venous to mitral A velocity correlated strongly with mean pulmonary wedge pressure (r = 0.72, P < .0001). When the cutoff value of the ratio was set at 0.5 or higher, the sensitivity for predicting a pulmonary capillary wedge pressure of 15 mm Hg or more was 88%, and the specificity was 80%. The serial Doppler-hemodynamic study showed that the ratio decreased markedly after treatment of heart failure. The value was 0.84 +/- 0.29 before treatment and 0.36 +/- 0.17 after treatment (P = .001). An increased ratio of pulmonary venous to mitral A velocity is a useful marker for elevated pulmonary capillary wedge pressure among patients with left ventricular systolic dysfunction.
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PMID:Ratio of pulmonary venous to mitral A velocity is a useful marker for predicting mean pulmonary capillary wedge pressure in patients with left ventricular systolic dysfunction. 980 1

The distinction of left ventricular (LV) dysfunction caused by fibrosis from that arising from viable (hibernating and/or stunned) myocardium has important implications for the management of patients with ischemic cardiomyopathy. In many of these patients, LV function can improve significantly after revascularization. Using positron emission tomography (PET), increased glucose uptake in dysfunctional segments with reduced blood flow at rest (PET mismatch) indicates presence of viable myocardium, whereas a concordant reduction in blood flow and glucose uptake (PET match) reflects myocardial scar. The average positive and negative predictive accuracies of PET for predicting improved function after revascularization are 76% and 82%, respectively. The greater the number of viable myocardial segments, the greater is the probability that revascularization will improve global LV function and, consequently, improve heart failure symptoms and survival. Early revascularization affords a more complete recovery of LV function. In patients with PET mismatch, early referral to revascularization improves long-term survival over medical therapy, regardless of symptoms. In patients without PET mismatch, long-term survival is similar with medical therapy or revascularization especially if minimal or no anginal symptoms are present. Noninvasive evaluation of myocardial viability should be an important component of the diagnostic evaluation of patients with heart failure due to coronary artery disease. This approach will likely enhance the selection of patients with poor cardiac function in whom revascularization will likely improve both the quality and quantity of life.
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PMID:Predicting improved function after myocardial revascularization. 982 74


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