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)

Myocardial blood flow was estimated using the technique of selective xenon-133 solution injection into the coronary artery, in 20 patients with mitral stenosis, 8 patients with mitral insufficiency, 8 patients with primary cardiomyopathy, and in 7 healthy subjects. The mean value of myocardial blood flow in mitral stenosis (60.9 +/- 10.5 ml/min/100 g) and in mitral insufficiency (58.5 +/- 7.7) did not differ from the mean value obtained in the control group (66.0 +/- 9.1). On the other hand, myocardial blood flow in primary congestive cardiomyopathy was significantly diminished (54.1 +/- 8.6). Myocardial blood flow was also lowered in patients with class IV of heart failure (48.3 +/- 7.6), as compared to healthy subjects. A positive correlation was found between myocardial blood flow and the left ventricular work index (r = 0.48, p less than 0.05), as well as between myocardial blood flow and the right ventricular work index (r = 0.47, p less than 0.05). A weak correlation was noticed between myocardial blood flow and left ventricular end-diastolic pressure (r = 0.38, p less than 0.05), as well as between myocardial blood flow and right ventricular end-diastolic pressure (r = 0.34, p less than 0.05).
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PMID:Myocardial blood flow in mitral valve disease and in primary congestive cardiomyopathy, and its relation to some haemodynamic indices. 126 Dec 75

The present study investigated the effects of celiprolol a novel beta 1-antagonist with partial beta 2-agonist activity on the human failing heart. Experiments were performed on isolated electrically driven atrial and ventricular cardiac preparations and in membrane preparations from the left ventricles of nine patients (four with dilated cardiomyopathy; five with ischemic cardiomyopathy) undergoing cardiac transplantation for terminal heart failure. Celiprolol produced a negative inotropic effect in atrial and ventricular heart muscle. However, in the presence of forskolin--which activates the catalyst of the adenylate cyclase-or the cAMP phosphodiesterase inhibitor milrinone, celiprolol produced concentration-dependent positive inotropic effects and positive lusitropic effects. Experiments with the beta 1-and beta 2-selective antagonists CGP 207.12A and ICI 118.551, respectively, suggest that the positive inotropic response is mediated by beta 2-adrenoceptors. In radioligand binding experiments, a selectivity of 15.7 [-Gpp(NH)p] or 23.9 [+Gpp(NH)p] as judged from the Ki values--of binding to beta 2-adrenoceptors was measured in the failing human ventricular myocardium. Competition curves with celiprolol alone and in the presence of the guanine nucleotide Gpp(NH)p revealed no evidence for agonist activity at beta 1- or beta 2-adrenoceptors. It is concluded that amplification of the cAMP response is able to unmask partial agonist activity of celiprolol in the failing human heart at beta 2-adrenoceptors. The inotropic measurements are a more sensitive approach than radioligand binding studies. Whether the pharmacological profile of celiprolol will be useful in conditions like heart failure is questionable with respect to the potential downregulation of beta 2-adrenoceptors by its partial agonist activity.
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PMID:Positive inotropic effects due to partial agonistic activity of the beta-adrenoceptor antagonist celiprolol following amplification of cAMP formation in failing human myocardium. 127 96

The purpose of the study was to evaluate the effect of enalapril on the frequency of ventricular premature beats in patients with congestive heart failure. The study group consisted of 30 patients with a mean age of 47 +/- 0.6 years with chronic congestive heart failure (NYHA classes III and IV) due to primary dilated cardiomyopathy and cardiomyopathy in the course of ischaemic heart disease. Initial therapy with digitalis and diuretics was supplemented with enalapril at a dose of 5-20 mg daily. Initially and at three months after enalapril, the following parameters were evaluated: NYHA functional class, the presence of premature ventricular beats in 24-hour ECG recording and left ventricular function by echocardiography. The scheduled therapy was completed by 23 patients; in 5 patients, the intake was discontinued because of hypotension, one patient died after 14 days due to worsening heart failure, and one patient was submitted for pacemaker implantation. Clinical improvement manifesting itself by a shift to lower NYHA classes was found in 20 patients. A reduced number of premature ventricular beats was observed in 52% of the patients. Termination of cardiac arrhythmias, especially of complex beats, was parallel to the circulatory improvement.
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PMID:The effect of enalapril on cardiac arrhythmias in patients with congestive heart failure. 128 55

The cardiomyoplasty is a new surgical procedure that uses a skeletal muscle electrostimulated in order to reinforce or even substitute partially the cardiac muscle. We present the electrophysiology aspects in a patient with dilated cardiomyopathy that underwent cardiomyoplasty. First the latissimus dorsi muscle was prepared with a neurostimulant ITREL II. During the surgical procedure a dual-chamber pacemaker mode DDD brand CPI was placed. After three months, ablation radiofrequency of the AV node was performed in order to control the atrial fibrillation that caused heart failure. By means of the AV block we obtained synchrony between the ventricular stimulation and the latissimus dorsi muscle, and by this the patient improved. Using the modern pacemakers and radiofrequency we can control the bradyarrhythmias as well as the tachyarrhythmias frequent in patients with dilated cardiomyopathy, increasing the success rate of cardiomyoplasty.
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PMID:[The usefulness of electrophysiology in a patient undergoing cardiomyoplasty]. 128 59

End-stage human heart failure is the common final manifestation of a group of heterogeneous diseases, and it is usually accompanied by myocardial hypertrophy. Studies on animal models have shown that myocardial hypertrophy is an adaptational process accompanied by characteristic changes in the expression of cardiac genes: reinduction of fetal isoforms of the myofilaments actin and myosin, downregulation of SR Ca(2+)-ATPase and phospholamban, downregulation of beta-adrenoceptors and increased expression of inhibitory G proteins (Gi). These alterations lead to reduced shortening velocity, slowed relaxation, and to desensitization of adenylyl cyclase, thereby probably increasing myocardial economy and lowering energy demand. Gene expression in human end-stage heart failure due to dilated cardiomyopathy exhibits some clear differences, but also significant parallels to gene expression in experimental hypertrophy: there is no isoform shift because fetal isoforms of the myofilaments are already predominant in the adult ventricle. However, like in animal models expression of SR Ca(2+)-ATPase and phospholamban is decreased, correlating with slowed relaxation of the diseased myocardium, beta-adrenoceptors are downregulated, and the expression of Gi is increased, leading to desensitization of the adenylyl cyclase pathway. These results suggest that alterations of gene expression in human end-stage myocardial failure, known so far, are secondary to chronic overload and are not a primary cause in the pathogenetic process. They are probably initially favorable adaptive processes to chronic overload, but finally cause a further deterioration of contractile performance of the myocardium.
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PMID:[Changes in gene expression in terminal myocardial failure]. 129 Mar 4

To assess the prognostic role of echocardiographic indexes and their relation to clinical conditions, 225 patients with dilated cardiomyopathy were studied prospectively. All cases had a normal coronary angiogram and non specific endomyocardial biopsy findings. 163 men (72.4%) and 62 women (27.6%), mean age 41.5 +/- 12.3 (range 8-61), were studied. Clinical, electrocardiographic and echocardiographic parameters, normalized for body surface area, were tested according to NYHA class and presence of segmental or diffuse wall motion abnormalities. One hundred-four patients were in NYHA class I-IIa, 94 were in class IIb-III and 27 were in class IV. Left ventricular end systolic diameter index, right ventricular end diastolic diameter index, left atrial diameter index, left ventricular fractional shortening and ejection fraction, and radius to wall thickness ratio were significantly more impaired in patients with more severe symptoms. Twenty-eight patients (13%) showed segmental wall motion abnormalities and had smaller left ventricular end systolic and left atrial diameter index and higher left ventricular fractional shortening and ejection fraction. During a mean follow up of 23 +/- 15 months (range 1-67 months), 25 patients (11.1%) died from cardiac causes and 16 (7.1%) underwent heart transplant because of refractory heart failure. Prognostic evaluation was performed separately for cardiovascular mortality alone and for cardiac events (cardiovascular mortality and heart transplantation). At Cox multivariate analysis only right ventricular end diastolic diameter index (p < 0.005) predicted cardiovascular mortality, while left atrial diameter index (p < 0.001), right ventricular end diastolic diameter index (p < 0.01) and left ventricular ejection fraction (p < 0.05) were significant independent predictors of cardiac events.
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PMID:[Clinical and prognostic significance of echocardiographic parameters in dilated cardiomyopathy: a prospective study on 225 patients. The Italian Multicenter Study of Cardiomyopathies Group]. 129 25

Region-specific characteristics of hypertrophic cardiomyopathy (HC) and dilated cardiomyopathy (DC) were compared for 108 relevant patients living in Dubai (United Arab Emirates) and Moscow (Russia). Out of 49 citizens of Dubai 17 had HC, 32 DC, and 59 Moscow patients had HC in 23, DC in 36 cases. It was found that HC in Dubai tends to run a silent latent course, involving mainly basal septum and right ventricle. Apical lesions were more typical for Moscow citizens who also display more severe myocardial impairment. DC in Dubai produces weaker cardiac insufficiency and arrhythmia. Incidence of idiopathic and periportal DC proved higher in Dubai, while alcohol and virus infection underlie DC more frequently in Moscow.
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PMID:[The characteristics of cardiomyopathy in different geographical regions]. 129 16

24 d of rapid ventricular pacing induced dilated cardiomyopathy with both systolic and diastolic dysfunction in conscious, chronically instrumented dogs. We studied mechanical properties and intracellular calcium (Ca2+i) transients of trabeculae carneae isolated from 15 control dogs (n = 32) and 11 dogs with pacing-induced cardiac failure (n = 26). Muscles were stretched to maximum length at 30 degrees C and stimulated at 0.33 Hz; a subset (n = 17 control, n = 17 myopathic) was loaded with the [Ca2+]i indicator aequorin. Peak tension was depressed in the myopathic muscles, even in the presence of maximally effective (i.e., 16 mM) [Ca2+] in the perfusate. However, peak [Ca2+]i was similar (0.80 +/- 0.13 vs. 0.71 +/- 0.05 microM; [Ca2+]o = 2.5 mM), suggesting that a decrease in Cai2+ availability was not responsible for the decreased contractility. The time for decline from the peak of the Cai2+ transient was prolonged in the myopathic group, which correlated with prolongation of isometric contraction and relaxation. However, similar end-diastolic [Ca2+]i was achieved in both groups (0.29 +/- 0.05 vs. 0.31 +/- 0.02 microM), indicating that Cai2+ homeostasis can be maintained in myopathic hearts. The inotropic response of the myopathic muscles to milrinone was depressed compared with the controls. However, when cAMP production was stimulated by pretreatment with forskolin, the response of the myopathic muscles to milrinone was improved. Our findings provide direct evidence that abnormal [Ca2+]i handling is an important cause of contractile dysfunction in dogs with pacing-induced heart failure and suggest that deficient production of cAMP may be an important cause of these changes in excitation-contraction coupling.
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PMID:Abnormalities in intracellular calcium regulation and contractile function in myocardium from dogs with pacing-induced heart failure. 131 23

An eight-month-old was admitted for acute congestive heart failure with fever. The respective parts played by hypocalcemia (due to vitamin-D deficiency rickets) and acute Epstein-Barr virus infection are discussed. Hypocalcemia was sufficiently marked to induce heart failure per se but replenishment of calcium stores was followed by only partial improvement in cardiac manifestations. Initial management was difficult because of the risks associated with concomitant administration of calcium and digitalis. After eighteen months during which the patient's status remained stable, evaluation showed that clinical features were consistent with sequelae of acute viral myocarditis. The possibility of primary hypokinetic dilated cardiomyopathy was then considered. Esterified carnitine levels were found to be increased leading to further investigations which outruled mitochondrial cytopathy.
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PMID:[Acute heart insufficiency in an 8-month-old infant presenting with hypocalcemia and Epstein-Barr virus infection: acute myocarditis? Or primary hypokinetic dilated cardiomyopathy?]. 131 31

Single cardiac myocytes were isolated from the ventricles of failing and non-failing human hearts. The contraction amplitude, time-to-peak shortening and time to 50% and 90% relaxation were measured in cells stimulated at 0.2 Hz at 32 degrees C. The effects of increasing extracellular calcium and isoproterenol were investigated using cumulative concentration/response curves. Maximum contraction amplitude in high calcium or velocities of contraction or relaxation were not impaired in cells from failing hearts. Beta-adrenoceptor function in a single cell was assessed by the maximum contraction amplitude in the presence of isoproterenol relative to that with high calcium in the same cell (isoproterenol/calcium ratio). A decrease in the isoproterenol/calcium ratio correlated positively with an increase in the isoproterenol EC50 (concentration for half-maximal effect) for a cell (P less than 0.02, n = 39). The isoproterenol/calcium ratio in left ventricular myocytes decreased with increasing severity of disease, correlating with failure as defined by New York Heart Association class (P less than 0.001, n = 26 patients), left ventricular ejection fraction (P less than 0.001, n = 24), left ventricular end diastolic pressure (P less than 0.05, n = 21) and amount of diuretics prescribed (P less than 0.001, n = 26). In right ventricular myocytes, only increasing NYHA class correlated with decreasing isoproterenol/calcium ratios. There was a correlation of the isoproterenol/calcium ratio between right and left ventricular cells from patients with ischemic heart disease (P less than 0.05), n = 11). Beta-adrenoceptor subsensitivity occurred in mitral valve disease, ischemic heart disease, congenital abnormalities and congestive cardiomyopathy, but not in the right ventricle of patients with myocarditis. The isoproterenol/calcium ratio correlated negatively with the age of the patient (P less than 0.001, n = 26, left ventricle). Multiple regression indicated that the maximum contraction amplitudes in either high isoproterenol or high calcium declined significantly with age only, but that both age and severity of disease contributed to the decrease in isoproterenol/calcium ratio. Time-to-peak tension in isoproterenol, as well as relaxation times in high calcium also decreased with the age of the patient. Analysis of variance showed that between-patient variation was significantly greater than between-cell for most of the parameters measured. Beta-adrenoceptor desensitisation may be detected in individual myocytes from failing hearts, and this relates more to the severity of disease and the age of the patient rather than the etiology of heart failure. A decline in absolute contractility of muscle cells with age was detected.
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PMID:Isolated ventricular myocytes from failing and non-failing human heart; the relation of age and clinical status of patients to isoproterenol response. 132 14


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