Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ATP-ase activity of myosin; the level of SH-groups and the concentration of myosin were studied in various clinical groups of patients with mitral, mitral-aortic and mitral-aortic-tricuspid valve defects. Proceeding from the duration of the history of the disease, the mitral cases were grouped in the following way: Group 1 -- heart disease of under 10-years duration; Group 2 -- under 20 years; Group 3 -- over 20 years; Group 4 -- three patients with combined heart diseases; Group 5 -- four lethal cases due to postoperative cardiovascular failure. The papillary muscle was taken for biochemical tests in all surgical procedures for mitral valve replacement. The conducted investigations demonstrated that the ATP-ase activity of myosin was the lowest in those dying after surgery of cardiovascular failure. The earliest sign of the deteriorating structure of the contractile proteins in lasting mitral heart disease is the growing content of thiol compounds of myosin.
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PMID:[Contractile myocardial proteins in patients with acquired heart defects]. 12 76

Oxygen tension in the blood and tissues, lipid peroxidation (LP) intensity (content of malonic blood dialdehyde and activity of superoxide dismutase in erythrocytes), spectrum of fatty acids and phospholipid composition of erythrocytic membranes, their passive K(+) permeability, total ATP content in erythrocytes, some other metabolic indices were investigated in 24 patients with blue type congenital heart disease. It was shown that these patients showed a reduced oxygen tension in the blood and tissues, LP intensification, changes of the lipid phase of erythrocytic membranes, disorders of their permeability, decrease of intraerythrocytic ATP reserves. Beta-adrenoblocking agents (obsidan, anaprilin were used in 10 patients. Reported are clinico-metabolic findings indicating a favourable effects of these drugs on LP processes, lipid spectrum of erythrocytic membranes, their permeability and bioenergy reactions.
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PMID:[Lipid peroxidation and erythrocyte membrane function in congenital heart defects in relation to the use of beta-adrenoblockers]. 136 25

Our purpose in this article is to examine the hypothesis that both myocardial disease and ischemia can alter the electrophysiologic function of the ion channels responsible for the cellular electrical activity of the heart. Changes in the intracellular and extracellular milieus occur during ischemia and can alter the electrophysiology of several species of ionic channels and the cellular electrophysiologic activity of cardiac myocytes. Included are 1) changes in extracellular [K+] and pH and in intracellular [Na+], [Ca2+], and pH; 2) accumulation of noxious metabolic products such as lysophosphatidylcholine; and 3) depletion of intracellular ATP. Finally, ischemia or disease (e.g., hypertrophy) can alter the electrophysiology of at least two types of K+ channels, the A-like channels underlying the transient outward current and the inward rectifier, by mechanisms that apparently do not involve alteration of either the intra- or extracellular milieus. Findings suggest that the expression of cardiac A-like channel function can be altered by hypertrophy and that at least one intrinsic conductance property of the inward rectifier can be altered by ischemia. We speculate that the control of expression, function, and regulation of cardiac ion channels can be affected at the molecular level by heart disease and myocardial ischemia.
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PMID:Connections: heart disease, cellular electrophysiology, and ion channels. 137 69

Tissue oxygen tension, peroxidation of lipids (malonic dialdehyde levels, superoxide dismutase activity), fatty acid, spectrum and phospholipid composition in the red blood cells, Na+, K(+)-ATPase were studied in 11 healthy children and 21 with cyanotic heart disease. The beta-adrenoblocker obsidan was used in the multimodality treatment of 10 patients. Unlike healthy children, the patients had decreased tissue oxygen tension, intensified lipid peroxidation, an altered lipid profile in the red blood cell membranes, their abnormal permeability, diminished intracellular ATP depot. The conventional tools of intensive care (oxygenation, cardiotropic drugs, goal-oriented fluid therapy) are low beneficial. There is evidence for the supplementation of obsidan, a beta-adrenoblocker, to a therapeutical complex for this group of patients. Clinical and metabolic evidence for the positive action of the drug on lipid peroxidation, lipid spectrum in the red blood cell membranes, their permeability and biological energy reactions.
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PMID:[Erythrocyte membranes in patients with congenital cyanotic heart disease before and after obsidan therapy]. 166 48

A comprehensive intraoperative examination of myocardial contractility and energy function in patients with acquired heart disease with predominant stenosis has enabled the significant correlations to be established between the complex of the functional indices of right ventricular myocardial and the levels of energy substrates in the myocardium of the left atrial auricular and coronary arteriovenous ATP difference. The magnitudes of changes were found in the functional parameters, which indicated myocardial energy deficiency.
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PMID:[Relation between the energetic and contractile functions of the myocardium]. 204 53

There are obviously several causes of myocardial dysfunction but energy deficiency of the myocytes may play a significant role and probably is a common mechanism during the progression of myocardial failure. Theoretically, a poor utilization efficiency of oxygen may be due to exhaustion of the myocardial stores of bioenergetics. In this report the authors review their biochemical results from measurements of coenzyme Q10 (CoQ10) levels in blood and human endomyocardial biopsies using an HPLC method from patients with suspected myocardial disease (n = 45). The levels of CoQ10, which has a key role in the respiratory chain and the synthesis of ATP, was found to be significantly decreased in various groups of patients with myocardial failure (dilated and restrictive cardiomyopathy and alcoholic heart disease) as compared to "normal" myocardium (0.42 +/- 0.04 micrograms/mg dry weight). The deficiency of CoQ10 was more pronounced with increasing symptoms; e.g. patients with dilated cardiomyopathy in NYHA Classes III and IV had lower tissue CoQ10 content than those of Classes I and II (0.28 +/- 0.04 vs. 0.37 +/- 0.06 micrograms/mg, p less than 0.001). Nearly two thirds of a series of 40 patients in severe heart failure (Classes III and IV) treated with CoQ10, 100 mg daily, in an open, controlled design showed subjective and objective improvement. Clinical responders were 69% and 43% of patients with cardiomyopathy and ischaemic heart disease, respectively. The results suggest that CoQ10 is a novel and effective breakthrough in heart-failure therapy and it appears safe, as no adverse reactions were registered. The through in heart-failure therapy and it appears safe, as no adverse reactions were registered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. 227 93

Extract of Tan-Shen (Salvia miltiorrhiza, Labiatae), a Chinese traditional crude drug, was reported to show beneficial activity for heart disease. Chemical examination on the extract was performed on the basis of screening for protective action on the ischemic myocardium. Isolated hearts were subjected to hypoxic perfusion for 20 min, followed by 45 min reoxygenation, and the recovery of cardiac contractile force and changes in UV absorbance of the perfusate were examined. Among the components isolated, tanshinone I, cryptotanshinone, and tanshinone VI elicited a significant enhanced recovery of the contractile force upon reoxygenation. This was associated with a decrease in the increase in UV absorbance of the perfusate, suggesting the preservation of ATP metabolites in the myocardium. This, in turn, may enhance the restoration of ATP upon oxygen-replenishment. The results suggest that tanshinone I, cryptotanshinone, and tanshinone VI can protect the myocardium against ischemia-induced derangements.
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PMID:Possible active components of tan-shen (Salvia miltiorrhiza) for protection of the myocardium against ischemia-induced derangements. 271 90

This study investigates the influence of inadequate oxygen supply on CK and CK-MB release rate in congenital cyanotic heart disease in fourteen patients. Eleven patients had Tetralogy of Fallot and 3 Transposition of great vessels. Their age ranged between 10 days and 10 years (mean 50.48 +/- 31.82 months). The corrective repair was carried out under CPB with systemic hypothermia (20 degrees-25 degrees C) and intermittent St. Thomas Cardioplegia perfusion in the aortic root until the septal temperature was below 16 degrees C. Three blood samples were taken before, during and 10 minutes after CPB to quantitate the CK and CK-MB. In 6 cases of Fallot, two simultaneous biopsies, one from the right and another from the left ventricular walls were taken at the end of the 10 first minutes of reperfusion to evaluate the ATP, CP and glycogen contents. CK and CK-MB levels showed an increasing evolution; the CK-MB per cent increased sharply after aortic clamp release and then fell abruptly to low values at the 10th minute after CPB arrest. Comparative evaluation between the 3 values for C K showed significant differences (P less than 0.001) in all, except when the first values were compared to the second (P greater than 0.05) and for CK-MB an overall significant differences were found at P less than 0.025 and P less than 0.001. On the other hand, quantification of ATP, CP and glycogen contents from simultaneous biopsies from the left and the right ventricular walls did not demonstrate significant differences between the two ventricles after the ischemic period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Profile of creatine phosphokinase (CK) and its isoenzyme MB (CK-MB) during corrective procedures of congenital cyanotic heart disease. 274 16

We have previously identified the adenine nucleotide translocator (ANT), an intrinsic protein of the inner mitochondrial membrane, as an auto-antigen in dilated cardiomyopathy (DCM). Further immunochemical characterization by crossed immunoelectrophoresis, indirect solid phase radioimmunoassay and immunoadsorption studies on the isolated translocator protein and mitochondria from heart, kidney and liver showed the existence of organ-specific antigenic determinants although partial crossreactivity between the three proteins was observed. Sera from 18 patients with histologically proven dilated cardiomyopathy were studied for their capacity to bind to the translocator protein. Seventeen of 18 patients showed significant binding, while in the sera of patients with coronary heart disease, suspected alcoholic heart disease or healthy blood donors, no anti-ANT antibodies were observed. Further studies showed organ-specific and functionally active autoantibodies, which decreased the ADP/ATP exchange rate from heart mitochondria. A close correlation was found between the antibody-titer and the hemodynamic function. These results give new evidence for autoimmunological events in dilated cardiomyopathy.
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PMID:Immunological analysis of auto-antibodies against the adenine nucleotide translocator in dilated cardiomyopathy. 299 41

Supraventricular tachycardia is one of the most frequent arrhythmias in childhood. It may accompany congenital heart disease. W.P. W. syndrome, or a normal state of health. A re-entry circuit is the most commonly observed electrophysiological mechanism. Persistence is followed by decompensation. Drug management is based on digitalis, ATP, amiodarone, and verapamil. Atrial and ventricular pacing and surgery are alternatives when other means fail. Persistent tachycardia (i.e. its presence over long periods) is much less frequent that the paroxysmal form, and its aetiology is generally unknown. Even here, the clinical picture is substantially related to decompensation. Digitalis + amiodarone is the best treatment, though the arrhythmia may resolve spontaneously.
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PMID:[Supraventricular tachycardia in children]. 665 30


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