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)

Three patients presented with severe congestive cardiomyopathy of unknown cause. All three had a profound depression of serum phosphorus levels resulting from the chronic ingestion of large quantities of a phosphorus-binding antacid. Results of physical examination and echocardiograms were consistent with cardiomegaly and severe myocardial dysfunction, and chest films showed enlargement of the cardiac silhouette with interstitial pulmonary edema. Serum phosphorus was restored to normal levels, and within 2 to 5 weeks the results of physical examination and echocardiogram of each patient returned to normal. We conclude that these patients had reversible hypophosphatemic cardiomyopathy and show the importance of inorganic phosphorus in myocardial metabolism and function. Serum phosphorus measurements should be a part of the routine evaluation of patients with congestive cardiomyopathy because, at least in some patients, hypophosphatemia appears to be a reversible cause of this disorder.
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PMID:Reversible severe congestive cardiomyopathy in three cases of hypophosphatemia. 634 61

Myoglobin is known to protect the mechanical function of the heart from hypoxia by acting as a sarcoplasmic oxygen reservoir and shuttle. We postulated a role for myoglobin in the pathogenesis of congestive heart failure. Several models of congestive heart failure were employed to test the hypothesis, including spontaneous inherited dilated cardiomyopathy in Doberman Pinschers, and heart failure produced by rapid ventricular pacing in dogs, volume overload in chickens and furazolidone toxicity in turkeys. Myocardial myoglobin was decreased by approximately 50% for all models (P less than 0.05). In Doberman Pinschers dogs which are predisposed to the development of dilated cardiomyopathy and have mild subclinical depression of cardiac performance, myocardial myoglobin (1.05 +/- 0.22 mg/g) is approximately 50% decreased compared to healthy mongrel dogs (2.15 +/- 0.52 mg/g), approximately twice as much as dobermans with heart failure (0.47 +/- 0.25 mg/g) but similar to the concentration found in dogs paced to heart failure (1.09 +/- 0.34 mg/g). Myocardium from poultry had remarkably decreased myoglobin compared to mammals (34 +/- 4 micrograms/g) with heart failure produced either by furazolidone or salt toxicity causing a further 50% reduction. In the canine models of heart failure, myocardial myoglobin concentration was demonstrated to be correlated with biochemical and physiological indicators of myocardial performance, namely, mitochondrial and sarcoplasmic reticular ATPase activities, and cardiac output, systemic vascular resistance, pulmonary capillary wedge pressure and mean arterial pressure, respectively. Our data implicates a role for myoglobin deficiency in the pathogenesis of congestive heart failure and in the predisposition of doberman pinschers to dilated cardiomyopathy.
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PMID:Myocardial myoglobin deficiency in various animal models of congestive heart failure. 140 11

Doxorubicin (Adriamycin, ADR) is an effective antineoplastic agent with a major side effect of dilated cardiomyopathy. Previously we showed ADR selectively decreased alpha cardiac (alpha c) actin mRNA in the rat heart when compared to other mRNAs examined in heart and skeletal muscle. The present study determined if this effect was selective for mRNAs within the thin filament, related to inhibitory effects on mitochondrial transcription, and modified by pretreatment with the cardioprotective chelating agent ICRF-187. Adult Sprague-Dawley rats received ADR at 8 mg/kg intraperitoneally (ip) with or without pretreatment with ICRF-187 given at 80 mg/kg ip. After 3 days, rats were killed and myocardial RNA was extracted, electrophoresed, transferred to nitrocellulose, and hybridized with the [32]cDNA probes alpha c actin, troponin C (TnC), BamHI fragment of mouse mitochondria (MM), and glyceraldehyde-3-phosphate dehydrogenase (G3PD). Results showed a major depressive effect of ADR on rat myocardial alpha c actin mRNA. No depression of the other mRNAs examined (TnC, MM, or G3PD) was seen. ICRF-187 did not modify the effect. We conclude that the ADR-induced decrease in alpha c actin mRNA was: (1) selective within the thin filament; (2) not related to inhibitory effects on mitochondrial transcription; and (3) not related to free radical formation. Possible subcellular mechanisms are discussed.
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PMID:Selective alterations in rat cardiac mRNA induced by doxorubicin: possible subcellular mechanisms. 170 8

The evolution of several mechanical parameters of left ventricular function was studied in 32 control subjects, 171 chronic chagasic and 60 primary dilated cardiomyopathy patients, which were submitted to an extensive invasive and non-invasive protocol. Preload and afterload (end-diastolic and end-systolic stress), contractile status (ejection fraction), the magnitude (mass/index) and adequacy of hypertrophy (mass/volume ratio) and afterload (systolic stress/volume ratio) were derived from the invasive explorations. There was an increased afterload in 25% of chronic chagasic patients without other evidence of early myocardial damage, which was accompanied by signs of inadequate hypertrophy. Both findings increased further with the progression of the disease. Systolic performance was initially preserved, but showed a progressive depression paralleling the clinical evolution. Patients with dilated cardiomyopathy showed a mechanical profile similar to chagasic patients with advanced degree of myocardial damage. The hemodynamic determination of mass index, mass/volume ratio, end-systolic and end-diastolic stress seem to be the best parameters for detection of early abnormalities in loading conditions of the heart in chronic Chagas, disease, and for indication and evaluation of the results of vasodilator therapy in both groups of patients.
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PMID:[Left ventricular mechanics in Chagas' disease and primary dilated myocardiopathies. A hemodynamic study]. 177 15

A novel, simple, rapid and reproducible microassay is used for kinetic analysis of Ca-sequestration by homogenates of myocardium of turkeys with furazolidone-induced congestive cardiomyopathy. The assay monitors Ca in real-time using dual-emission ratiometric spectrofluorometry and the Ca-indicator dye indo-1. Using this assay and isolated SR studies we make several novel findings regarding the mechanism of SR failure in furazolidone cardiomyopathy. Qualitative differences in Ca-sequestration were not detected between groups. However, compared to controls the furazolidone treatment resulted in: 1) 50% depression in maximal activities (1.54 +/- 0.36 vs 0.73 +/- 0.12 microM/sec); 2) 2-fold increases in post-sequestration concentrations of ionized Ca (79 +/- 23 vs 141 +/- 13 nmol Ca/L homogenate); 3) 2-fold increases in Ca half-life (415 vs 790 msec); and 4) 25% increased passive Ca-binding capacity of homogenates. The Ca-ATPase specific activity of isolated sarcoplasmic reticulum was 60% increased in congestive cardiomyopathy (543 +/- 140 vs 873 +/- 108 nmol ATP hydrolyzed/min/mg membrane protein) although membrane yield was 20% decreased (0.79 +/- 0.09 vs 0.63 +/- 0.03 mg/g heart). The increased ATPase and decreased Ca-uptake activities in combination with the occurrence of 36% cardiac hypertrophy and 19% decreased body weights resulted in estimates of the relative energy cost to the animal for myocardial Ca transport being 5.5-fold increased with cardiomyopathy (20.5 vs 111 nmol ATP hydrolyzed per microM decrease of sarcoplasmic free Ca/kg body weight). These data indicate that congestive cardiomyopathy is associated with markedly increased permeability of sarcoplasmic reticulum to Ca and compensatorily increased Ca-ATPase activity. Accelerated energy consumption due to the increased energy cost of Ca transport and increased time of myocyte activation are predicted to predispose the myocardium to fatigue and irreversible failure.
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PMID:Myocardial Ca-sequestration failure and compensatory increase in Ca-ATPase with congestive cardiomyopathy: kinetic characterization by a homogenate microassay using real-time ratiometric indo-1 spectrofluorometry. 182 61

Isovolumic left ventricular (LV) preparations were used to assess myocardial failure associated with dietary taurine deficiency in cats. Adult female cats (n = 12) were fed a purified diet devoid of taurine for 6-8 mo. Six of the cats received 1,000 mg of crystalline taurine orally once daily. The remaining six cats were not provided taurine replacement. Compared with control preparations, hearts isolated from taurine-deficient cats generated significantly lower values for developed LV systolic pressure (107 +/- 6 vs. 66 +/- 15 mmHg; P less than 0.05), maximal rate of LV pressure rise (+dP/dtmax; 1,103 +/- 38 vs. 718 +/- 172 mmHg/s; P less than 0.05), and fall (-dP/dtmax; 930 +/- 46 vs. 587 +/- 129 mmHg/s; P less than 0.05). LV function curves generated by hearts from taurine-deficient cats were shifted downward and to the right of control curves, demonstrating inotropic depression. In addition, end-diastolic pressure-volume (compliance) relationships in hearts from taurine-deficient cats were shifted downward and to the right of controls in the direction of increased chamber compliance or distensibility. Ten millimolar taurine significantly improved inotropic indexes only in hearts from taurine-deficient cats but failed to affect diastolic compliance. Myocardial contractile dysfunction and LV chamber dilatation in hearts from taurine-deficient cats verify a causal association between dietary deficiency of this amino acid and dilated cardiomyopathy in this species.
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PMID:Systolic and diastolic dysfunction of the left ventricle induced by dietary taurine deficiency in cats. 185 11

A stained-glass artisan with depression and a retired junkyard worker with congestive cardiomyopathy had increased mobilizable body burdens of lead by calcium ethylenediaminetetaacetic acid testing. Although both patients improved with several months of intramuscular chelation therapy, the efficacy of such therapy in chronic lead poisoning is controversial. Recognition of unusual manifestations of chronic lead poisoning may at least interrupt further exposure, even if specific therapy is not undertaken.
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PMID:Adult chronic lead intoxication. A clinical review. 188 36

To determine whether the development of cardiomyopathies is associated with alterations in creatine kinase function, the functional properties of cardiac contractile apparatus and mitochondria were studied in two different models of cardiomyopathies, the Syrian hamster (hereditary dilated cardiomyopathy, strain UM-X7.1, 200 days old) and the diabetic rat (4-6 weeks after injection of streptozotocin) using ventricular skinned fibers. After Triton X-100 treatment, the hereditary cardiomyopathic fibers demonstrated decreased maximal calcium-activated tension and unchanged calcium sensitivity, whereas fibers from diabetic hearts exhibited unchanged maximal tension and increased calcium sensitivity, when compared with their respective controls. In both cases myofibrillar creatine kinase appeared unchanged. The functional properties of total tissue mitochondria were evaluated using saponin-skinned fibers. Coupling between oxidation and phosphorylation was not altered in cardiomyopathies. Respiration rate (per unit of tissue dry weight) was normal in hereditary cardiomyopathy but was considerably lower in diabetic fibers compared with control fibers. In both models of cardiomyopathies, creatine-stimulated respiration was significantly lower than in controls, thus indicating the depression of functional activity of mitochondrial creatine kinase.
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PMID:Creatine kinase and mechanical and mitochondrial functions in hereditary and diabetic cardiomyopathies. 191 31

We performed an ultrastructural, morphometric comparison of mitochondria and myofibrils of cardiomyocytes using endomyocardial biopsy specimens in hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Biopsies came from the right ventricular side of the interventricular septum in nine patients with HCM, nine with DCM, and nine controls with arrhythmia and/or ST depression. Morphometric analysis was carried out using electron microscopic photographs and an image analyser. Mitochondria were significantly greater in number and smaller in size in HCM than in the control group. In DCM, the size of mitochondria was also significantly smaller than in the control group, although their number was similar to that of the control group. No statistically significant difference was found regarding the size of mitochondria between HCM and DCM. The percentages of both mitochondrial and myofibrillar areas in cytoplasm were smaller in the DCM than the HCM and control groups, though no difference was seen between the latter two. The ratio of mitochondrial area to myofibrillar area was almost the same in each group. These results suggest increased mitochondrial function to match hypertrophic cardiomyocytes in HCM, and decreased mitochondrial function and cardiomyocytic contractility in DCM.
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PMID:Morphometric comparison of mitochondria and myofibrils of cardiomyocytes between hypertrophic and dilated cardiomyopathies. 211 Jun 95

These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia. Simple ventricular arrhythmias occur among athletes with the same frequency as in the general population, but they usually disappear with exercise. The occurrence of complex ventricular forms of arrhythmia should always prompt cardiologic examination in search of underlying cardiac disease, particularly hypertrophic or dilated cardiomyopathy. The presence of ventricular arrhythmias without evidence of underlying heart disease does not indicate a special or increased risk of sudden cardiac death. A higher incidence of right and/or left ventricular hypertrophy, exercise-reversible ST elevation, and exercise-reversible changes in T waves (T negativity, sharp and/or excessive T waves) can be considered physiologic changes in the ECGs of athletes. These changes correlate closely with the type of sports activity and degree of training and are reversible when the activity is stopped. Horizontal ST segment depression are by contrast very rare in athletes and should always be clarified by cardiologic examination. Exercise-induced sudden cardiac death in athletes is unusual without preexisting heart disease. The cause of sudden cardiac death among athletes less than 40 years of age can be predominantely ascribed to congenital heart diseases (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes more than 40 years of age and with increasing age, coronary heart disease is the most frequent autopsy finding. A corresponding risk stratification should take these partial dangers into account.
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PMID:ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. 219 78


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