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)

Several studies have shown that depression is an important predictor of morbidity and mortality in patients with ischaemic heart failure. We have investigated whether clinically recognised depression is linked to mortality in patients with non-ischaemic heart failure due to dilated cardiomyopathy (DCM) in the Royal Brompton Hospital (RBH), a tertiary cardiac centre located in London, UK. We retrospectively examined a cohort of 396 consecutive adult patients with DCM who satisfied our inclusion and exclusion criteria identified from an echocardiographic database and the hospital medical records. Mean age was 53+/-15 years. In all, 83 patients (21%) were clinically depressed, the majority of which (60%) were taking antidepressant therapy. After a follow-up period of 48 months, 83 (21%) patients died, 15 (4%) underwent cardiac transplantation and 130 (33%) were readmitted; 29 (35%) of the deaths and 40 (31%) of the readmissions were among clinically depressed patients. After 5 years, clinically depressed patients had significantly higher mortality and readmission rates than non-depressed; 36 vs. 16% (hazards ratio for death, 3.0; 95% CI, 1.4-6.4; P=0.004), and 87 vs. 74% (hazards ratio for readmission, 0.25; 95% CI, 0.07-0.90; P=0.03), respectively. The risk of depression was greatly increased in the presence of other recognised adverse clinical variables at baseline. Depression increases the risk of death and readmission in patients with heart failure secondary to non-ischaemic DCM. The risk associated with depression appears to be greatest among patients with milder disease, those with a shorter duration of symptoms and those demonstrating a lower systolic or diastolic blood pressure, renal impairment, or a restrictive left ventricular physiology on echocardiography. Interventions targeted at reducing depression warrant further study as a possible way to improve quality of life and/or outcome in patients with heart failure.
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PMID:Clinical depression is common and significantly associated with reduced survival in patients with non-ischaemic heart failure. 1279 40

Acquired perforating dermatosis (APD) is characterized by umbilicated 1- to 10-mm-measuring papulonodules with a central adherent oystershell-like keratotic plug, typically on the dorsa of the hands, forearms and over the knees. APD is associated with systemic diseases, especially diabetes mellitus and/or renal failure. Histologically the lesions show transepidermal elimination of altered dermal components into a cup-shaped epidermal depression. We present a 69-year-old man with coexisting APD and Poland syndrome (PS), an association not yet described. PS (OMIM 173800) is a rare congenital anomaly consisting of unilateral partial or total absence of the greater pectoralis muscle and ipsilateral symbrachydactyly. Most cases of PS are sporadic as it was in our case. Our patient had, in addition, an untreated diabetic condition, hyperuricaemia, dilated cardiomyopathy and a very recent pulmonary embolism. He responded to therapy with allopurinol.
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PMID:Acquired perforating dermatosis in a patient with Poland syndrome. 1465 33

ABCA5 is a member of the ABC transporter A subfamily, and a mouse orthologue (mABCA5) in newborn mouse brain and neural cells was identified by reverse transcription-PCR. Full-length cDNA cloning revealed that mABCA5 consists of 1,642 amino acid residues and that its putative structure is that of a full-type ABC transporter having two sets of six transmembrane segments and a nucleotide binding domain. Immunohistochemical studies revealed that mABCA5 is expressed in brain, lung, heart, and thyroid gland. A subcellular localization analysis showed that mABCA5 is a resident of lysosomes and late endosomes. Abca5(-)(/)(-) mice exhibited symptoms similar to those of several lysosomal diseases in heart, although no prominent abnormalities were found in brain or lung. They developed a dilated cardiomyopathy-like heart after reaching adulthood and died due to depression of the cardiovascular system. In addition, Abca5(-)(/)(-) mice also exhibited exophthalmos and collapse of the thyroid gland. Therefore, ABCA5 is a protein related to a lysosomal disease and plays important roles, especially in cardiomyocytes and follicular cells.
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PMID:ABCA5 resides in lysosomes, and ABCA5 knockout mice develop lysosomal disease-like symptoms. 1587 Feb 84

Dilated cardiomyopathy (DCM) is a heart disease characterized by progressive depression of cardiac function and left ventricular dilatation of unknown etiology in the absence of coronary artery disease. Genetic causes and cardiotoxic substances account for about one third of the DCM cases, but the etiology of the remaining 60% to 70% is still unclear. Over the past two decades, evidence has accumulated continuously that functionally active antibodies or autoantibodies targeting cardiac beta(1)-adrenergic receptors (anti-beta(1)-AR antibodies) may play an important role in the initiation and/or clinical course of DCM. Recent experiments in rats indicate that such antibodies can actually cause DCM. This article reviews current knowledge and recent experimental and clinical findings focusing on the role of the beta(1)-adrenergic receptor as a self-antigen in the pathogenesis of DCM.
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PMID:beta(1)-Adrenergic receptor function, autoimmunity, and pathogenesis of dilated cardiomyopathy. 1638 26

Sarcomeric protein abnormalities have been recognized for many years in heart failure due to dilated cardiomyopathy (DCM). In contrast, virtually nothing is known about myofilament abnormalities in heart failure occurring in association with diastolic dysfunction. With the exception of sarcomeric protein mutations that cause DCM, the most important mechanism of myofilament dysfunction in DCM is probably altered post-translational modification, in particular the phosphorylation state of troponins I and T and possibly myosin light chain. Other modifications, including oxidation and glycation, may also play a role. Myosin heavy chain isoform switching occurs in human heart failure, but its functional significance is uncertain. Myofilament abnormalities contribute significantly to myocardial dysfunction in DCM, although their relative importance compared with abnormal calcium handling is debated. One consistent functional abnormality in DCM is increased myofilament calcium sensitivity of tension generation, which contributes to slowed or incomplete relaxation. More recently, decreases in the optimal frequency of myofilament work and power generation have been recognized. These changes may contribute to depression of the force-frequency relation in DCM. Altered mechanoenergetics constitute one of the most important manifestations of myofilament dysfunction in heart failure. DCM and hemodynamic overload are associated with more economical and efficient energy utilization by the contractile machinery, which may be protective of the myocardium. This change is strongly associated with depressed myofibrillar ATPase activity. We speculate that the effectiveness of mechanical therapies such as resynchronization may at least in part be related to improved mechanical function without loss of this mechanoenergetic advantage.
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PMID:Functional consequences of sarcomeric protein abnormalities in failing myocardium. 1641 47

Dilated cardiomyopathy (DCM) is a myocardial disease characterized by progressive depression of myocardial contractile function and ventricular dilatation. Thirty percent of DCM patients belong to the inherited genetic form; the rest may be idiopathic, viral, autoimmune, or immune-mediated associated with a viral infection. Disturbances in humoral and cellular immunity have been described in cases of myocarditis and DCM. A number of autoantibodies against cardiac cell proteins have been identified in DCM. In this study, we have profiled the autoantibody repertoire of plasma from DCM patients against a human protein array consisting of 37,200 redundant, recombinant human proteins and performed qualitative and quantitative validation of these putative autoantigens on protein microarrays to identify novel putative DCM specific autoantigens. In addition to analyzing the whole IgG autoantibody repertoire, we have also analyzed the IgG3 antibody repertoire in the plasma samples to study the characteristics of IgG3 subclass antibodies. By combining screening of a protein expression library with protein microarray technology, we have detected 26 proteins identified by the IgG antibody repertoire and 6 proteins bound by the IgG3 subclass. Several of these autoantibodies found in plasma of DCM patients, such as the autoantibody against the Kv channel-interacting protein, are associated with heart failure.
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PMID:Profiling humoral autoimmune repertoire of dilated cardiomyopathy (DCM) patients and development of a disease-associated protein chip. 1641 13

Unhealthy alcohol use is among the leading causes of morbidity and mortality in the United States. Among military personnel, service members between the ages 18 and 25 had a 27.3% prevalence of heavy drinking in the previous 30 days, compared to 15.3% among civilians in the same age group. In the civilian world, > 100 million patients are treated in U.S. emergency departments (ED) annually; 7.9% of these visits are alcohol related. Alcohol is associated with a broad range of health consequences that may ultimately present in the ED setting: traumatic injuries (e.g., motor vehicle crashes, intentional violence, falls); environmental injuries (e.g., frostbite); cardiovascular problems (e.g., hypertension, dilated cardiomyopathy); gastrointestinal disorders (e.g., hepatitis, pancreatitis, gastrointestinal bleeding); neurological problems (e.g., encephalopathy, alcohol withdrawal, withdrawal seizures), as well as psychological problems (e.g., depression, suicide). Seminal work has been done to create behavioral interventions for at-risk drinkers. These motivational interventions have been found to be successful in encouraging clients to change their risky behaviors. We present such a technique, called the Brief Negotiated Interview as performed in a civilian ED setting, in hopes of adapting it for use in the military context. Military health care providers could easily adapt this technique to help reduce risky levels of alcohol consumption among service members, retirees, or military dependents.
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PMID:Brief interventions to reduce harmful alcohol use among military personnel: lessons learned from the civilian experience. 1680 38

In experimental animals, cardiac work is derived from pressure-volume area and analyzed further using stress-length relations. Lack of methods for determining accurately myocardial mass has until now prevented the use of stress-length relations in patients. We hypothesized, therefore, that not only pressure-volume loops but also stress-length diagrams can be derived from cardiac volume and cardiac mass as assessed by cardiac magnetic resonance imaging (CMR) and invasively measured pressure. Left ventricular (LV) volume and myocardial mass were assessed in seven patients with aortic valve stenosis (AS), eight with dilated cardiomyopathy (DCM), and eight controls using electrocardiogram (ECG)-gated CMR. LV pressure was measured invasively. Pressure-volume curves were calculated based on ECG triggering. Stroke work was assessed as area within the pressure-volume loop. LV wall stress was calculated using a thick-wall sphere model. Similarly, stress-length loops were calculated to quantify stress-length-based work. Taking the LV geometry into account, the normalization with regard to ventricular circumference resulted in "myocardial work." Patients with AS (valve area 0.73+/-0.18 cm(2)) exhibited an increased LV myocardial mass when compared with controls (P<0.05). LV wall stress was increased in DCM but not in AS. Stroke work of AS was unchanged when compared with controls (0.539+/-0.272 vs 0.621+/-0.138 Nm, not significant), whereas DCM exhibited a significant depression (0.367+/-0.157 Nm, P<0.05). Myocardial work was significantly reduced in both AS and DCM when compared with controls (129.8+/-69.6, 200.6+/-80.1, 332.2+/-89.6 Nm/m(2), P<0.05), also after normalization (7.40+/-5.07, 6.27+/-3.20, 14.6+/-4.07 Nm/m(2), P<0.001). It is feasible to obtain LV pressure-volume and stress-length diagrams in patients based on the present novel methodological approach of using CMR and invasive pressure measurement. Myocardial work was reduced in patients with DCM and noteworthy also in AS, while stroke work was reduced in DCM only. Most likely, deterioration of myocardial work is crucial for the prognosis. It is suggested to include these basic physiological procedures in the clinical assessment of the pump function of the heart.
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PMID:A new methodological approach to assess cardiac work by pressure-volume and stress-length relations in patients with aortic valve stenosis and dilated cardiomyopathy. 1772 8

During the past 2 years the number of studies examining psychopathology and quality of life after ICD implantation has increased dramatically. Variables assessed have included recipient age, gender, and social support network. How recipients respond to having the device, particularly after experiencing firing, has been evaluated in light of new depression and anxiety disorder diagnoses as well as premorbid personality structure. Now the picture of what is known is, if anything, cloudier than it was 2 years ago, with little definitive and much contradictory data emerging in most of these categories. It still seems clear that in a significant minority of ICD recipients the device negatively affects quality of life, probably more so if it fires. Education about life with the device before receiving it remains paramount. Reports continue to appear of patients developing new-onset diagnosable anxiety disorders such as panic and posttraumatic stress disorder. Until recently the strongest predictors of induced psychopathology were considered to be the frequency and recency of device firing. It now seems that preimplantation psychologic variables such as degree of optimism or pessimism and an anxious personality style may confer an even greater risk than previously thought. Certainly many variables factor into the induction of psychopathology in these patients. Among these factors are age, gender, and perception of control of shocks, as well as the predictability of shocks and psychologic attributions made by the patient regarding the device. Another source of variability is this population's medical heterogeneity. Some patients receive ICDs after near-death experiences; others get them as anticipatory prophylaxis. Some have longstanding and entrenched heart disease; others were apparently healthy before sudden dangerous arrhythmias. Diagnoses as diverse as myocardial infarction in the context of advanced coronary artery disease and dilated cardiomyopathy after acute viral infection may warrant ICD placement. Moreover the course of cardiac disease after ICD placement may vary from relative stability to continuing disease progression and severe functional compromise. Unless these and other pre- and postimplantation differences are taken into account, it is almost impossible to make meaningful comparisons between studies. Ideally, future research would consist either of large-scale, randomized, prospective studies using validated structured-interview tools to supplement a literature dominated by self-report measures, unstructured assessments, and anecdotal reports, or of smaller studies designed to focus on particular diagnostic subsets. As ICDs become the standard of care for potentially life-threatening arrhythmias, the rate of implantations continues to increase. Because negative emotions have been linked to an increased incidence of arrhythmias, and untreated or unrecognized psychiatric illness can interfere with adaptation to an ICD, assessing and managing both pre-existing and induced psychiatric disorders becomes even more critical. Greater research attention should be paid to determining which patients meet criteria for anxiety disorders before and after implantation and what premorbid traits predispose to postimplantation psychopathology. The authors predict that psychiatrists will be involved increasingly in caring for this population, offering insights into treatment options that increase the likelihood of successful ICD acceptance and decrease the psychosocial costs of these devices.
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PMID:An updated review of implantable cardioverter/defibrillators, induced anxiety, and quality of life. 2110 13

This study was performed to elucidate the relation between in vivo measurements of two-dimensional principal strains and the progression of left ventricle (LV) wall thinning during development of dilated cardiomyopathy in the protein kinase C-epsilon (PKC-epsilon) transgenic (TG) overexpressing mouse heart. Principal two-dimensional strains, E1 and E2, were determined in the LV wall of the anesthetized mouse using cardiac MRI tagging at 14.1 T. PKC-epsilon TG provided a model of pure dilated cardiomyopathy without evidence of hypertrophy (PKC-epsilon TG, n = 6). Ejection fraction, wall thickness, and principal strains were determined at 1-mo intervals in hearts of PKC-epsilon TG vs. age-matched, nontransgenic mice (NTG, n = 5) from age 6 to 13 mo. Through the study, PKC-epsilon TG displayed lower ejection fraction than NTG. At 7 mo, average principal strain E1 in PKC-epsilon TG hearts was lower compared with NTG (PKC-epsilon TG = 0.14 +/- 0.03, NTG = 0.19 +/- 0.03, P < 0.05). The greatest reductions in regional E1 occurred in the lateral segments. The principal strain E2 did not change significantly in either group. At 9 mo, LV wall thinning occurred in PKC-epsilon TG mice (P < 0.01 vs. 8 mo) to 21% below values in NTG (P < 0.001). Average E1 strain diverged between PKC-epsilon TG and NTG hearts by 25-43%. These E1 changes preceded LV wall thinning and predated the eventual transition from a compensated circumstance to the dilated phenotype. The findings indicate a near step function in E1 depression that precedes the onset of LV wall thinning and suggest E1 as a prognostic indicator of dilated cardiomyopathy.
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PMID:Principal strain changes precede ventricular wall thinning during transition to heart failure in a mouse model of dilated cardiomyopathy. 1796 77


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