Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with end-stage liver disease usually show a hyperdynamic circulatory state. It has previously been reported that patients who develop myocardial depression in the early post-liver transplantation period are more prone to organ failure and death. We reviewed the records of 754 adult patients undergoing liver transplantation at our institution and identified 7 patients who initially showed hyperdynamic circulation, but then developed reversible dilated cardiomyopathy in the early posttransplantation period. All identifiable causes of cardiac dysfunction, such as myocardial ischemia, thyroid dysfunction, and electrolyte imbalances, were excluded. Left ventricular ejection fraction decreased from a preoperative median baseline of 60% to 20% (P = .02), with four-chamber dilatation on echocardiogram. All these patients required supportive care, including mechanical ventilation, afterload reduction, inotropic support, and monitoring in the intensive care unit. Cardiac function subsequently improved in all patients, with ejection fraction increasing to a median of 50%. All patients were discharged from the hospital. At a median follow-up of 15 months, there was no recurrence of heart failure. The increased peripheral resistance seen after successful liver transplantation may be an important causative factor.
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PMID:Post-liver transplantation myocardial dysfunction. 972 77

A novel dilated cardiomyopathy (DCM) in 12 related Portuguese Water Dogs was identified by retrospective analysis of postmortem and biopsy case records. Male and female puppies born to clinically healthy parents typically died at 13 (+/- 7.3) weeks of age (range, 2-32 weeks) because of congestive heart failure. Puppies died suddenly without previous signs or with mild depression followed by clinical signs of congestive heart failure 1-5 days before death. There was no sex predilection. The hearts were enlarged and rounded, with marked left ventricular and atrial dilation. No other significant structural cardiac defects were noted. The histologic changes in the myocardium were diffuse and characterized by myofibers of irregular sizes separated by an edematous interstitium. The myofibers had multifocal swollen, cleared segments often involving perinuclear areas that contained granular, phosphotungstic-acid-hematoxylin-positive material consistent with mitochondria. There was loss of the cross-striation pattern, and intercalated discs were difficult to identify. There was no evidence of concurrent myocardial fibrosis; rare chronic inflammatory infiltrates were noted in one dog. Noncardiac skeletal muscles were not affected. The underlying cause is unknown. From the pedigree analysis, an autosomal recessive pattern of inheritance is suspected. Based on the histologic findings, this DCM is most likely due to an underlying molecular (biochemical or structural) defect. The early onset and rapid progression of the disease makes this a clinically distinctive form of canine DCM.
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PMID:Familial dilated cardiomyopathy of young Portuguese water dogs. 1005 66

Alcoholism is a very important cause of congestive cardiomyopathy in man. The aim of this study was to examine a short-term effect of ethanol in rat cardiac muscle, using histologic, morphometric and biochemical methods. Experiments were carried out in Wistar male albino rats, divided into two groups: the control group consisting of eight animals receiving tap water, and the experimental group comprising eight animals received ethyl alcohol for ten days, in a single daily dose of 3 g ethanol/kg body weight, per os, using esophageal intubation. The mean volume weighted nuclear volume of cardiac myocytes was estimated by point sampled intercept method, by objective x 100. The mean cubed nuclear intercept length was multiplied by pi and divided by 3. For biochemical analysis, a 10% water tissue homogenate from the left ventricle was made. In the experimental group, the mean volume-weighted nuclear volume (15.08 +/- 5.20 microm3) was significantly lower than in the control group (51.32 +/- 7.83 microm3) (p < 0.001). The treatment of experimental animals with ethanol caused significant increase of aldolase (p < 0.0001) and aspartate transaminase (p < 0.05) activity in the rat cardiac tissue; at the same time, the enzyme activity of creatine phosphokinase, alanine transaminase and alkaline phosphatase were not changed in the experimental group compared to the control values. The amount of the glucose in the cardiac muscle was greater in the experimental group compared to the control animals. Our results suggest that there is depression of cardiomyocyte nuclei in experimental animals treated with ethanol. Alcohol intake results in the loss of Krebs cycle enzymes and as a consequence there is greater utilization of fatty acids for energy production.
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PMID:Morphometric and biochemical characteristics of short-term effects of ethanol on rat cardiac muscle. 1066 13

This study investigated beat-to-beat QT variability in patients with panic disorder and depression, and normal control subjects using an automated algorithm to compute QT intervals. An increase in QT variability appears to be associated with symptomatic patients with dilated cardiomyopathy and also with an increased risk for sudden death. QT(vm) (QT variability normalized for mean QT interval) and QT(vi) (a log ratio of QT variance normalized for mean QT over heart rate variability normalized for mean heart rate) were significantly higher in patients with panic disorder and depression in supine as well as standing postures (P=0.002 and 0.0001 for QT(vm) and QT(vi), respectively). In another analysis, QT(vi) was significantly higher in patients with panic disorder compared to control subjects in supine as well as standing postures during spontaneous breathing as well as 12, 15 and 20 per minute breathing (P=0.005). These findings are important especially in view of the recent reports of increased risk for cardiovascular mortality and sudden death in patients with anxiety and depression and the utility of QT(vi) as a noninvasive measure of temporal repolarization lability.
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PMID:Increased QT variability in patients with panic disorder and depression. 1076 Mar 81

This study investigated beat-to-beat QT variability in patients with panic disorder before and after treatment with nortriptyline (n = 13) and paroxetine (n = 16), using an automated algorithm to compute QT intervals. An increase in QT variability appears to be associated with symptomatic patients with dilated cardiomyopathy and also with an increased risk for sudden cardiac death. QTvi (QT variability index: a log ratio of QT variance normalized for mean QT over heart rate variability normalized for mean heart rate) was significantly higher in supine posture in patients with panic disorder treated with nortriptyline (P = 0.006) but not paroxetine. Thus paroxetine may be a better drug of choice especially in patients with coexisting cardiac disease. These findings are important especially in view of the recent reports of increased risk for cardiovascular mortality and sudden death in patients with anxiety and depression. QTvi can be a valuable noninvasive measure of temporal repolarization lability, especially to study the side effects of medications which affect cardiac autonomic function.
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PMID:Effects of nortriptyline and paroxetine on QT variability in patients with panic disorder. 1087 54

Ca(2+) sensitizers may be advantageous for treatment in human heart failure by increasing cardiac force without increasing the Ca(2+) transient or energy consumption. To study the mode of action of the Ca(2+) sensitizers EMD 57033 (EMD) and CGP 48506 (CGP), their influence on butanedione monoxime (BDM)-mediated depression of cross-bridge cycling was analyzed in human myocardium (explanted hearts, dilated cardiomyopathy, n = 19). In Triton X (1%)-skinned fiber preparations of left ventricular myocardium from patients suffering from dilated cardiomyopathy, troponin I was extracted by vanadate (10 mM) treatment, resulting in a Ca(2+)-independent contraction. In troponin I-depleted fibers BDM (5-50 mM) was applied in the absence and presence of EMD (10 microM) or CGP (10 microM). To analyze the influence on cross-bridge kinetics, tension cost (ratio of ATPase activity and tension development) was studied. BDM exerted a dose-dependent force inhibition in troponin I-depleted fibers (IC(50) = 7.22 mM), which was antagonized by EMD (IC(50) of BDM + EMD = 19.97 mM) and CGP (IC(50) of BDM + CGP = 15.30 mM). EMD increased Ca(2+) sensitivity of force and maximal force in Triton X-skinned fibers. The Ca(2+)-sensitizing effect of CGP was accompanied by an increased Ca(2+) sensitivity of myosin-ATPase activity, an increased slope of the Ca(2+) force and Ca(2+) ATPase curve, as well as a reduced maximal myosin ATPase activity. CGP and EMD reduced tension cost. In conclusion, EMD and CGP antagonize the BDM-mediated relaxation in troponin I-depleted cardiac muscle fibers. The Ca(2+)-sensitizing effect of CGP seems to be dependent on an improvement of the myofilament cooperativity, whereas EMD seems to operate by increasing the force per cross-bridge.
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PMID:Different effect of the Ca(2+) sensitizers EMD 57033 and CGP 48506 on cross-bridge cycling in human myocardium. 1108 66

To determine whether selective impairment of cardiac sarcoplasmic reticulum (SR) Ca(2+) transport may drive the progressive functional deterioration leading to heart failure, transgenic mice, overexpressing a phospholamban Val(49) --> Gly mutant (2-fold), which is a superinhibitor of SR Ca(2+)-ATPase affinity for Ca(2+), were generated, and their cardiac phenotype was examined longitudinally. At 3 months of age, the increased EC(50) level of SR Ca(2+) uptake for Ca(2+) (0.67 +/- 0.09 microm) resulted in significantly higher depression of cardiomyocyte rates of shortening (57%), relengthening (31%), and prolongation of the Ca(2+) signal decay time (165%) than overexpression (2-fold) of wild type phospholamban (68%, 64%, and 125%, respectively), compared with controls (100%). Echocardiography also revealed significantly depressed function and impaired beta-adrenergic responses in mutant hearts. The depressed contractile parameters were associated with left ventricular remodeling, recapitulation of fetal gene expression, and hypertrophy, which progressed to dilated cardiomyopathy with interstitial tissue fibrosis and death by 6 months in males. Females also had ventricular hypertrophy at 3 months but exhibited normal systolic function up to 12 months of age. These results suggest a causal relationship between defective SR Ca(2+) cycling and cardiac remodeling leading to heart failure, with a gender-dependent influence on the time course of these alterations.
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PMID:Superinhibition of sarcoplasmic reticulum function by phospholamban induces cardiac contractile failure. 1132 20

Heart failure is characterized by the inability of the myocardium to shorten sufficiently or to eject an adequate stroke volume to maintain normal perfusion of both the cardiac and the extracardiac organs. Irrespective of etiologic reasons, the depression of myocardial contractility represents one of the major mechanisms that contributes to low output in heart failure. Despite their intrinsic negative inotropic effects, beta-receptor-blocking agents have been used in numerous studies for treating the failing heart, especially in dilated cardiomyopathy and ischemic heart disease. In this regard, specific therapeutic aims of the use of beta-receptor-blocking agents in chronic heart failure have been described. e.g., reduction of an increased heart rate in tachycardia, blood pressure reduction in hypertensive heart failure, improvement of supraventricular and ventricular arrhythmias, depression of an increased sympathetic tone (e.g., in hyperthyrioidism, pheochromocytoma), increase in the amount of downregulated beta-receptors, and anti-ischemic effects in coronary artery disease. For chronic heart failure, therefore, some special indications may be established and may be individually used; for acute heart failure, only very rare indications are present (e.g., hypertensive crisis, life-threatening cardiac arrhythmias). The actual rationale for the use of beta-receptor blocking agents in heart failure is therefore analyzed with regard to pathophysiology, clinical effects, and clinical outcome of treated patients.
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PMID:Beta-blocking agents in heart failure: modern concepts and overview. 1152 16

The Ras-like Rab GTPases regulate vesicle transport in endocytosis and exocytosis. We found that cardiac Rabs1, 4, and 6 are upregulated in a dilated cardiomyopathy model overexpressing beta(2)-adrenergic receptors. To determine if increased Rab GTPase expression can contribute to cardiomyopathy, we transgenically overexpressed in mouse hearts prototypical Rab1a, the small G protein that regulates vesicle transport from endoplasmic reticulum to and through Golgi. In multiple independent mouse lines, Rab1a overexpression caused cardiac hypertrophy that progressed in a time- and transgene dose-dependent manner to heart failure. Isolated cardiac myocytes were hypertrophied and exhibited contractile depression with impaired calcium reuptake. Ultrastructural analysis revealed enlarged Golgi stacks and increased transitional vesicles in ventricular myocytes, with increased secretory atrial natriuretic peptide granules and degenerative myelin figures in atrial myocytes; immunogold studies localized Rab1a to these abnormal vesicular structures. A survey of hypertrophy signaling molecules revealed increased protein kinase C (PKC) alpha and delta, and confocal microscopy showed abnormal subcellular distribution of PKCalpha in Rab1a transgenics. These results indicate that increased expression of Rab1 GTPase in myocardium distorts subcellular localization of proteins and is sufficient to cause cardiac hypertrophy and failure.
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PMID:Increased myocardial Rab GTPase expression: a consequence and cause of cardiomyopathy. 1173 71

Dilated cardiomyopathy (DCM) is a myocardial disease characterized by progressive depression of myocardial contractile function and by ventricular dilatation. Abnormalities of the cellular and humoral immune system are present in patients with myocarditis and DCM. Various circulating cardiac autoantibodies have been detected among patients suffering from DCM. The relative contribution of cardiac antibodies to cardiac malfunction in DCM remains to be elucidated. Extraction of antibodies by immunoadsorption has been successfully used for treatment of various autoimmune diseases. In this review we report recent studies, which indicate that immunoadsorption improves cardiac function of patients with DCM. The data from these studies indicate that activation of the humoral immune system, with production of cardiac autoantibodies, may play a functional role in cardiac malfunction of patients with DCM.
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PMID:Improvement of cardiac function after immunoadsorption in patients with dilated cardiomyopathy. 1190 80


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