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)

One of the leading causes of mortality in diabetics is myocardial disease. In the past few years this subject has generated a significant amount of interest with the result that myocardial problems associated with diabetes are far better understood. Though originally thought to occur as a result of atherosclerosis, various studies have shown that heart disease can occur in the absence of atherosclerosis, suggesting a diabetic cardiomyopathy. Using diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Diabetic rat hearts do not respond to conditions of high stress as well as controls. The functional depression is accompanied by altered cardiac enzyme systems. A decrease in myosin ATPase activity which appears to be a result of diabetes-induced hypothyroidism is seen. Also, a depression of sarcoplasmic reticular calcium ATPase, along with a depression of calcium uptake by the SR, is seen in diabetic rat hearts. Na+, K+ ATPase activity has also been shown to be depressed and the depression appears to correlate with depressed atrial contractility. High levels of circulating fats in diabetics may alter the integrity of membranes leading to altered enzyme activities. Insulin treatment has been relatively successful at reversing or preventing myocardial changes in the diabetic rat. Other treatments that have been studied include thyroid hormone treatment, since the depression of myosin ATPase can be corrected by such treatment; and carnitine treatment, as the elevation of long chain acyl carnitines (LCAC) and the resulting depression of calcium uptake in the SR can be so normalized. These treatments have not been successful at normalizing cardiac function. A combination of the two treatments normalized function only partially, suggesting that factors besides myosin ATPase and SR calcium uptake are involved. Other treatments that have been tried include vanadate, methyl palmoxirate, and choline and methionine. Vanadate treatment has proved to be encouraging in that it normalizes both function and hyperglycemia. Methyl palmoxirate, a fatty acid analog, normalized only the elevation of LCAC but did not affect function. Methionine and choline were only partially successful in preventing the functional alterations of diabetic rat hearts. The purpose of the present article is to review our understanding of diabetes-induced myocardial problems and their possible causes. Findings from our laboratory and others are described in which attempts have been made to normalize cardiac function.
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PMID:Diabetes-induced abnormalities in the myocardium. 293 41

Diabetes was introduced in rats by an intravenous injection of streptozotocin (65 mg/kg). Animals were sacrificed 8 weeks later and mitochondria were isolated from the ventricular tissue by differential centrifugation. The state 3 respiration, oxidative phosphorylation rate and Mg2+-dependent ATPase activities were depressed in mitochondria from diabetic hearts. These changes were partially reversible upon 2 weeks of insulin and fully reversible after 4 weeks of insulin therapy. Mitochondrial calcium uptake but not calcium binding, was decreased in diabetes and this change was fully reversible by 2 weeks of insulin administration. The observed alterations in mitochondrial function could not be explained on the basis of any changes in mitochondrial lipid and protein composition or subcellular contamination. These results indicate the presence of a generalized depression in mitochondrial function in chronic diabetes and such a defect is suggested to contribute in the development of cardiomyopathy at late stages of diabetes.
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PMID:Heart mitochondrial function in chronic experimental diabetes in rats. 299 24

A case is presented of a young female with a paraneoplastic subacute cerebellar degeneration, parkinsonian syndrome, autonomic disturbance, profound depression, myopathy and cardiomyopathy. Her paraneoplastic affection preceded the actual detection of carcinoma of the breast by nine months. Block dissection of the carcinoma resulted in alleviation of her muscle weakness and a return of the electrocardiogram to normal.
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PMID:Neurological and cardiac complications of carcinoma of the breast. Case report. 300 85

The UM-X7.1 myopathic and control hamsters at 40, 120 and 280 days of age were employed for the examination of heart sarcolemmal Ca2+-transport activities. Na+-dependent Ca2+ uptake activities were significantly depressed in myopathic animals at 120 and 280 days of age in comparison to the control values. No difference in Na+-induced Ca2+ release activities was found between control and experimental sarcolemmal vesicles. ATP-dependent Ca2+ binding and Ca2+-stimulated, Mg2+ ATPase activities were depressed in the experimental animals at 120 and 280 days of age. Similar alterations in the sarcolemmal Na+-dependent Ca2+ exchange and Ca2+-pump activities were seen upon treating the control hamsters with 40 mg/kg isoproterenol for 24 hr. It is suggested that a depression in the sarcolemmal Ca2+ transport activities may contribute to the development of intracellular Ca2+ overload in the genetically determined cardiomyopathy in hamsters and such a defect may be due to excessive amount circulating catecholamines in these animals.
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PMID:Sarcolemmal Na+-Ca2+ exchange during the development of genetically determined cardiomyopathy. 300 47

A 42-year old man with non-obstructive myocardiopathy complicated by paroxysmal atrial fibrillation treated with amiodarone (200 mg per day) received flecainide in daily doses of 400 mg for undocumented palpitations. Ten syncopes and numerous malaises occurred during the following two months. Electrophysiological testing was performed, showing prolongation of HV to 80 ms and discreet widening of QRS to 100 ms. Programmed atrial stimulation failed to demonstrate a second degree subnodal block and to induce tachycardia. In contrast, ventricular stimulation elicited a critical SH delay (260 ms), always followed by a left delay-type complex preceded by His bundle deflection which suggested reentry within the His-Purkinje system. Three extrasystoles on imposed rhythm started sustained ventricular tachycardia with the same 270 ms cycle morphology and reproducing the symptoms. Each V wave was preceded by an H potential, with HV varying from 100 to 300 ms. Three weeks after flecainide was discontinued, HV was 60 ms, and no ventricular tachycardia could be triggered by programmed stimulation. The patient remained symptom-free throughout the 5-month follow-up. This case illustrates the proarrhythmic effect of the flecainide-amiodarone combination. The mechanism of provoked tachycardia probably involves ventricular reentry through the His bundle branches, induced by a critical depression of conduction below the His bundle.
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PMID:[Bundle branch reentry tachycardia: a possible mechanism of flecainide proarrhythmia effect]. 313 16

Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.
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PMID:Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy. 318 60

Isolated hearts from normal and cardiomyopathic hamsters (160 to 180 days of age) were perfused through the aorta and assessed by echocardiographic and 31P-NMR (nuclear magnetic resonance) techniques. A decreased left ventricular systolic pressure in cardiomyopathic hamsters was associated with diminished cardiac size and left ventricular wall thickness. However, the ratio of inner/outer cross-sectional area and estimated left ventricular volume at any given left ventricular weight was significantly higher, indicating relative left ventricular chamber enlargement in cardiomyopathic hamsters. Left ventricular volumes were increased with an intraventricular balloon. Gradual inflation of the balloon resulted in increments of left ventricular systolic and developed stress that rose to the same values in both groups. At this point, the normalized stress-strain relationship was approximately two times steeper for cardiomyopathic hamsters, while at lower strain values the diastolic stress in cardiomyopathic hamsters was less than in controls, possibly due to cardiac dilatation. Almost the same degree of dilatation was induced in control hearts by the acute addition of 1% alcohol, but it was not followed by increased diastolic stiffness. Examination of hearts by 31P-NMR techniques revealed a decreased phosphocreatine/inorganic phosphate (PCr/Pi) ratio in the cardiomyopathic hamsters that progressed further with balloon inflation and was associated with a relative fall in PCr and adenosine triphosphate (ATP) content. Results suggest increased diastolic stiffness in cardiomyopathic hamsters, which was not seen in acute cardiac depression with alcohol. Diastolic volume overload with increased wall stress is probably the major factor contributing to increased diastolic stiffness early in the cardiomyopathy.
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PMID:Increased left ventricular diastolic stiffness in the early phase of hereditary cardiomyopathy. 341 91

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.
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PMID:[Cardiological findings in acromegaly]. 343 27

45 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 18 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) underwent simultaneous measurements of pulmonary artery pressure and minimal transit times (MTTs) of an intravenously injected bolus of indium-113m-EDTA through the heart at rest and during exercise in supine position. At rest, rate-corrected left and right ventricular MTTs were in the lower normal range, whereas left atrial and, to a lesser degree, right atrial MTTs were abnormally prolonged, indicative of high ventricular ejection fractions and impaired atrial ejection. During exercise, ventricular MTTs rose slightly but remained within the normal range, which corresponds to a slight fall in ventricular ejection fractions. Atrial MTTs exhibited, in contrast, a substantial further prolongation. Together with an abnormal increase in pulmonary artery pressure in the majority of patients, these findings suggest an aggravation of inflow impairment to both ventricles during exercise. There was no quantitative difference between HOCM and HNCM patients suggesting that impaired atrial ejection due to impaired diastolic function is of major pathophysiological importance irrespective of a possible additional role of left ventricular outflow obstruction in HOCM. The influence of surgical therapy (transaortal septal myectomy) was studied in 12 patients with HOCM. A significant increase in left ventricular MTTs to the upper normal range, indicative of a depression of left ventricular ejection fractions to the lower normal range, and a significant shortening of left atrial and pulmonary MTTs were observed, whereas corresponding changes in the right heart were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of therapeutic interventions on minimal cardiac transit times and volume parameters in hypertrophic cardiomyopathy. 343 74

From January 1982 through December 1985, 11 newborn artiodactyls died with clinical and/or pathologic evidence of cardiomyopathy. Clinical signs were inability to rise, depression, failure to nurse, hypothermia, and shivering. Macroscopically, the animals had mild to marked dilatation and thinning of the interventricular septum and left ventricular free wall. Histologic findings included thinning and waviness of myofibers and acute myodegeneration and myocytolysis.
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PMID:Congestive cardiomyopathy in neonatal artiodactyls. 350 27


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