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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study tested the hypothesis that membrane transport is the major biochemical system of the myocardium altered in furazolidone-induced cardiomyopathy (round heart disease), before the development of myocardial failure, and that metabolic enzymes and contractile proteins are less affected. Compared with controls, maximal percentage depression of activities of myocardium from furazolidone-treated birds were 40 for creatine kinase, 30 for glycolysis, 30 for glycogen, 20 for myofibrils, 20 for Krebs's cycle enzymes, 15 for fatty acid oxidation and 10 for total soluble protein. Sodium and potassium transport, antioxidant system activity, myosin, myosin isoenzyme patterns and amino acid aminotransferases were unaffected. In marked contrast, the calcium-transport ATPase activity of the sarcoplasmic reticulum had undergone a 60 per cent compensatory increase in activity. The pattern of biochemical changes observed is consistent with a role of ischaemia in the pathogenesis of round heart disease and indicates that calcium transport by the sarcoplasmic reticulum is the major biochemical system affected.
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PMID:Myocardial biochemical changes in furazolidone-induced cardiomyopathy of turkeys. 232 37

The discovery of insulin in 1922 aroused immediate clinical interest in its use in heart disease. In severe heart failure, insulin release is suppressed by the combined effect of poor pancreatic perfusion and by increased sympathetic activity. In these circumstances, myocardial metabolism of glucose may break down through the deficiency of insulin. Because of this, glucose, insulin and potassium solution (GIK solution) has been used in cardiopulmonary resuscitation. However, its mechanism is not yet fully known. This study was designed to determine the effect of insulin on cardiac muscle at various temperatures. The mechanical response of papillary muscle isolated from guinea pig ventricle was observed under various thermal conditions (23-37 degrees C). Twitch tension was increased by the administration of 0.2 I.U./ml insulin under each thermal condition. In all circumstances, the increase in contractile force was noted about 2 min after the administration of insulin. The effect of insulin on 20 preparations demonstrated the mean maximum contractile force was 226% ( +/- 34 S.D., n = 5) in 37 degrees C, 194% ( +/- 36 S.D., n = 5) in 30 degrees C, 190% ( +/- 30 S.D., n = 5) in 27 degrees C and 200% ( +/- 36 S.D., n = 5) in in 23 degrees C. The differences between different temperatures was not significant. The effect of insulin during depression Na-K pump by high concentration of ouabain (g-strophanthin, 10(-5) M) was also observed. Insulin (0.2 I.U./ml) was administered when the papillary muscle showed no response to electrical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of isolated guinea pig myocardium to insulin therapy during normothermia and graded hypothermia. 242 78

Of 270 patients successfully resuscitated from out-of-hospital cardiac arrest, 16% had no evidence of coronary heart disease. In these 43 patients, other forms of heart disease were found in 81% (35/43): cardiomyopathy in 18 patients, valvular disease in six, congenital heart disease in two, and primary arrhythmia in nine. Seven patients had evidence of only pulmonary disease and one had pancreatitis as his precipitating event. Nineteen of the 43 patients (44%) had serum potassium less than 3.6 mEq l-1 in the initial blood sample after cardiac arrest. One- and two-year mortalities were 30% and 43%, respectively, for the group, which is similar to one-year (20%) and two-year (35%) mortalities of the 227 resuscitated patients with coronary heart disease. Patients who survive a sudden death experience and who have no evidence of coronary artery disease are a unique but heterogeneous group who usually have identifiable cardiac or pulmonary disease.
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PMID:Clinical characteristics and survival experience of out-of-hospital cardiac arrest victims without coronary heart disease. 245 25

A study was performed to evaluate a user-operated patient-side blood gas and chemistry monitor (GEM-STAT, Mallinckrodt Sensor Systems, Ann Arbor, MI) for the first time in a group of infants and children with congenital heart disease undergoing cardiac surgery. Paired blood samples from 18 patients were analyzed by the test instrument and by standard clinical laboratory instruments. One failure of the test instrument, malfunction of a cartridge, occurred during the evaluation. The integrated and external quality control functions gave readings within the manufacturer's tolerance. The differences between the measurements obtained using the GEM-STAT and the standard laboratory instruments for five of the six variables are summarized as follows (mean +/- SD, units of measure, number of samples): pH (-0.017 +/- 0.02, 132), PaCO2 (-1.90 +/- 3.3 mm Hg, 130), hematocrit (-1.3 +/- 2.3%, 129), potassium (-0.17 +/- 0.20 mmol, 112) and sodium (-2.0 +/- 3.3 mmol, 112). The mean difference in the measurements of PaO2 in the clinically important range defined by the upper quality control limit for oxygen tension of 172 mm Hg for the GEM-STAT is: (-0.20 +/- 7.26 mm Hg, 51). The mean difference between the measurements for PaO2s below the lowest quality control point (60 mm Hg) was (-2.3 +/- 5.5 mm Hg, 30). The values for all variables obtained from the GEM-STAT during the trial period, with the exception of the PaO2 less than 60 mm Hg, showed good correlation with the laboratory over the clinically useful range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of a user-operated patient-side blood gas and chemistry monitor in children undergoing cardiac surgery. 252 Oct 33

Isolated superfused rat atria release [3H]-acetylcholine when depolarized with 57 mM potassium. The depolarization-induced [3H]-acetylcholine overflow was significantly reduced in atria from chronically T. cruzi-infected rats with electrocardiographically characterized cardiopathy. This fact suggests the occurrence of functional alterations of cardiac parasympathetic control in these animals, probably related to cardiac ganglion cell destruction.
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PMID:[3H]-acetylcholine release from rat atria in chronic chagasic cardiopathy. 269 96

The effects of enalapril maleate were studied in a group of 6 patients with arterial hypertension, hypertensive cardiopathy, multiple metabolic disorders and habitual snoring. Earlier treatment with antihypertensive drugs (diuretics, antiadrenergics, calcium antagonists) had been suspended when a marked deterioration was noted in metabolic parameters and plasmatic electrolytes as well as extremely disturbed sleep. The latter is probably attributable to increased respiratory obstruction during the night as a result of the increased hypertonia of the muscles of the upper air ways due to low blood potassium as well as the central and peripheral effects of the antiadrenergic drugs. After the wash-out period there was a marked improvement in laboratory parameters that continued after treatment with enalapril maleate. In particular, apart from a further slight fall in blood cholesterol and uricaemia there was a statistically significant drop in triglyceride levels. The improvement in the laboratory parameters made it possible to reduce the doses of the drugs being taken for the metabolic disorders. A distinct improvement was also noted in the sleep disturbances especially the excessive drowsiness during the day. There was also a statistically significant drop in arterial, systolic, diastolic and mean blood pressure without any significant change in heart beat. The results indicate that enalapril maleate should be the treatment of choice for those patients in whom high blood pressure is accompanied by alterations to the main metabolic parameters and habitual snoring.
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PMID:[Treatment with enalapril maleate in patients with arterial hypertension, pluri-metabolic syndrome and habitual snoring]. 282 86

Glucose-insulin-potassium (GIK) given during myocardial ischemia or anoxemia results in improved myocardial function and augments energy reserves of myocardial glycogen (MG). Because many patients with heart disease also have myocardial hypertrophy, our purpose was to examine whether similar elevations in MG can occur in hypertrophic hearts with GIK administration and to study the effect of hypovolemic shock on those MG levels. Mongrel dogs (n = 5) with myocardial hypertrophy underwent serial myocardial biopsies of the left (LV) and right (RV) ventricles, and blood samples were followed by GIK infusion (14.5 ml/kg/hr) for 2 hr. after which the dogs were subjected to 2 hr of hypovolemic shock (mean arterial pressure = 40 mmHg). It was found that after GIK infusion MG was consistently elevated in both RV (.43 +/- .02 to .60 +/- .04 g%) and LV (.63 +/- .07 to .71 +/- .01 g%) and FFA declined (.20 +/- .05 to .05-.01 mEq/liter). The MG responded to hypovolemia by further significant elevations (RV 1.16 +/- .33; LV .82 +/- .17), as did FFA (.38 +/- .21). These results indicate that hypertrophic hearts can indeed respond to GIK infusion by increasing MG in both the RV and LV, as do normal hearts. These hearts then submitted to hypovolemic shock showed a further elevation of MG. The elevated insulin levels post-GIK resulted in suppression of FFA. Thus GIK administration may have a sparing effect on energy stores of the heart during hypovolemic shock, which could have clinical implications in the treatment of patients with hypertrophic myocardia.
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PMID:Response of hypertrophic heart myocardial glycogen to GIK and hypovolemic shock. 294 28

Inhibition of the angiotensin converting enzyme (ACE) is associated with a decrease in renal vascular resistance, an increase in renal blood flow and a redistribution of intrarenal blood flow toward juxtamedullary nephrons. In general, ACE-inhibition does not affect normal glomerular filtration rate (GFR) but may increase GFR in patients on a low sodium intake prior to treatment. Since the rise in GFR is smaller than the rise in renal blood flow, in most instances a decrease in filtration fraction will result. In contrast to other vasodilator drugs, the decrease in blood pressure induced by ACE-inhibition is not accompanied by sodium retention, but rather by an initial natriuresis. ACE-inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. The initial positive potassium balance after ACE-inhibition may protect patients with heart disease from potentially hazardous arrhythmias. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydrosmotic effect of vasopressin and thus result in a rise in free-water clearance. Finally, based on experimental evidence, long-term treatment with ACE-inhibitors may have a protective effect on renal function by reducing glomerular filtration pressure.
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PMID:[Inhibition of the angiotensin-converting enzyme--effect on kidney function and electrolyte balance]. 306 59

A 72 year old woman was admitted with decompensation of a hypertensive cardiopathy and treated with diuretics. She developed recurrent syncopal torsades de pointes during the 24th hour which were reduced by a bolus intravenous injection of 3 g of magnesium sulphate (Mg SO4). There was a recurrence 30 minutes later which regressed after a second injection of 3 g of Mg SO4. A continuous intravenous infusion of 18 g/day of Mg SO4 prevented further recurrences of the arrhythmia. Biochemical analysis showed intra and extracellular magnesium deficiency at the time of the torsades de pointes but the intracellular potassium was normal. The QT interval was prolonged but this parameter did not change after the bolus of Mg SO4. It returned to normal progressively afterwards. The clinical course was uncomplicated with no recurrences. Metabolic correction was obtained in 3 days. This observation raises the question of the mechanisms relating diuretic therapy, magnesium and torsades de pointes.
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PMID:[Treatment of torsade des pointes by intravenous magnesium]. 309 33

Bidirectional tachycardia is an uncommon arrhythmia that usually occurs in aged persons with severe myocardial disease or digitalis intoxication, and carries a poor prognosis. This is a report of a young woman with familial hypokalemic periodic paralysis, who has a 13-year history of asymptomatic bidirectional tachycardia in the absence of organic heart disease or digitalis intoxication. Association of periodic paralysis and bidirectional tachycardia in this case and four previously reported cases suggests a strong relationship between this arrhythmia and potassium.
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PMID:Long-standing bidirectional tachycardia in a patient with hypokalemic periodic paralysis. 335 12


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