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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause. We tested the hypothesis that IDCM was associated with a myocardial metabolic defect by determining a comprehensive biochemical profile of metabolite concentrations and enzyme activities for the major metabolic pathways of the myocardium. We used the Doberman pinscher breed as a naturally occurring canine model of IDCM and compared its myocardial profile with that of healthy adult mongrels. Compared with controls, myocardium in IDCM had markedly reduced mitochondrial electron transport activity and myoglobin concentration, in association with acidosis and energy depletion following anoxic challenge: 60% decreased NADH dehydrogenase and 50% decreased ATP synthetase activities; 90% decreased myoglobin concentration; and 30% reduced ATP and 50% increased lactate and proton concentrations. Sarcoplasmic reticulum Ca(2+)-transport ATPase was decreased by 42%. There was a 15% compensatory increase in fatty acid oxidation and Krebs cycle activity. Other biochemical changes were mild by comparison with the mitochondrial defects. We conclude that IDCM is associated with a marked impairment of mitochondrial production of ATP, arising from decreased activity of the mitochondrial electron transport system, including myoglobin. These changes may be secondary to an underlying genetic defect or may indicate a deficiency of the mitochondrial respiratory chain that predisposes this breed to heart failure.
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PMID:Respiratory chain defect of myocardial mitochondria in idiopathic dilated cardiomyopathy of Doberman pinscher dogs. 133 76

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

Postoperative changes in serum myoglobin levels have been studied in 47 patients undergoing open heart surgery. The patients were retrospectively divided into two groups according to the time to peak myoglobin level during reperfusion. In 38 patients, myoglobin levels increased rapidly to a peak within 3 hours after reperfusion, after which it was cleared from the blood (group 1). Contrarily, a rise in myoglobin levels was persistent for 24 hours and its time to peak was greater than 3 hours after reperfusion in nine patients (group 2). There were no differences in preoperative and early reperfusion (within 1 hour of reperfusion) values of myoglobin between the two groups. At 3, 6, and 12 hours of reperfusion, myoglobin levels were significantly greater in group 2: 448 +/- 196 vs 1,149 +/- 900 ng/ml, 359 +/- 172 vs 2,653 +/- 3,179 ng/ml, 184 +/- 95 vs 1,896 +/- 1,387 ng/ml, respectively, p less than 0.0001 in each. The maximum activities of both myoglobin and CK-MB were significantly higher in group 2 (myoglobin-max: 771 +/- 257 vs 3,221 +/- 3,024 ng/ml, p less than 0.0001; CK-MBmax: 107 +/- 60 vs 227 +/- 219 IU/L, p less than 0.005). Five of nine patients in group 2 required post-operative assistance with intra-aortic balloon pumping (p less than 0.0005 compared with one of 38 in group 1) and perioperative myocardial infarction developed in three patients (33.3 percent) in this group (p less than 0.005 compared with 0 percent in group 1). Thus, patients with a delayed peak of serum myoglobin level exhibited detrimental cardiac failure postoperatively. These findings suggest that myocardial injury accelerated by reperfusion following ischemia might progress in these patients.
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PMID:Delayed time to peak serum myoglobin level as an indicator of cardiac dysfunction following open heart surgery. 203 22

In 1984-88 the authors examined in 813 subjects with the chest pain syndrome of varying aetiology (acute myocardial infarction, myocarditis, pericarditis, vertebrogenic algic syndrome, embolism of the pulmonary artery, patients lacking detectable organic causes of pain) the trend of myoglobin serum levels. They found significantly elevated values only in patients with myocardial infarction and myocarditis whereby the two diseases differ in particular as regards the shape of the curve of myoglobin values. In chest pain with another aetiology the myoglobin levels rose only rarely or not at all. From the differential diagnostic aspect it is particularly valuable that myoglobin was not elevated in any patient with embolism of the pulmonary artery and only very rarely in angina pectoris. Where in exceptional instances the myoglobin levels were elevated in patients with other investigated causes of chest pain, this increase was always due to another basic disease (right-sided cardiac failure, renal insufficiency, neuromuscular disease), whereby for these conditions prolonged persistence of the elevated serum myoglobin values was typical and the levels were never above 8 nmol/l.
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PMID:[The significance of myoglobin determination in the differential diagnosis of chest pain syndrome]. 205 2

The primary cause of death following i.v. injection of the basic phospholipase A2 (PLA2) from Naja nigricollis venom has been attributed to its direct cardiotoxicity. In view of our recent findings that cardiac failure caused by the basic PLA2 from Naja m. mossambica is primarily due to hyperkalemia resulting from cellular damage and possibly also from hemolysis, the cause of death due to the basic PLA2 from Naja nigricollis was re-investigated. In the anesthetized mice and rats, the PLA2 (0.3 micrograms/g, i.v.) produced a transient hypotension followed by recovery and subsequently by cardiac failure with ECG changes suggestive of hyperkalemia, such as P-R prolongation, tall T-wave, biphasic QRS-T complex, low voltage of QRS, A-V block, etc. Analysis of blood chemistry revealed marked increases in the plasma levels of K+, CPK, LDH, GOT, GPT, inorganic phosphate and hemoglobin (probably a mixture of hemoglobin and myoglobin). In the atrial preparation, however, no marked cardiotoxicity was observed except for a slight negative inotropic effect at 30 micrograms/ml. When 200 micrograms of the enzyme was injected into the coronary circulation in the Langendorff preparation, also no marked cardiotoxic effect was observed except for a decrease (about 40%) of coronary flow. From these results, it is concluded that the primary cause of death following i.v. injection of the basic PLA2 from Naja nigricollis is apparently cardiac failure due to hyperkalemia, resulting from cellular damage and possibly also from hemolysis, rather than direct cardiotoxicity.
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PMID:Is direct cardiotoxicity the primary cause of death following i.v. injection of the basic phospholipase A2 from Naja nigricollis venom? 252 Mar 58

In patients with Duchenne muscular dystrophy (DMD), heart failure appears in later stage of the disease due to myocardial degeneration and respiratory insufficiency, and sometimes causes death. However, there have been no adequate parameters which can be used easily to evaluate the grade of heart failure in DMD, except cardiac enlargement and pulmonary congestion observed by chest X-ray picture. Thus, we measured the plasma concentrations of atrial natriuretic peptide (ANP) in the patients with muscular dystrophy of various types, and studied a relationship between plasma ANP concentration and heart failure, expecting that it could be an index of heart failure in DMD patients. The plasma ANP concentrations in patients with DMD were 35.5 +/- 3.3pg/ml (mean +/- SE) and higher than in normal subjects (19.3 +/- 1.0pg/ml). In the patients with limb-girdle muscular dystrophy, facioscapulohumeral muscular dystrophy and neurogenic muscular atrophy, the plasma ANP concentration showed a tendency to elevate. However, no elevation of plasma ANP levels was observed in the patients with other types of muscular dystrophy. In DMD, number of the patients having a high plasma ANP concentration was increased with progress of disability grade, and decrease in serum creatine kinase activity and serum myoglobin concentration. There was a significant correlation (p less than 0.01) between plasma ANP concentration and cardiothoracic ratio or PEP/LVET, but no correlation between the concentration and respiratory failure. Immunohistochemistry of the atrial cardiac muscle of an autopsied DMD case revealed many ANP-positive atrial muscle cells, indicating the preservation of ANP-secreting function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Secretion and clinical significance of atrial natriuretic peptide in patients with muscular dystrophy]. 252 1

The present study was undertaken to determine whether near-infrared spectroscopy can be used to noninvasively assess skeletal muscle oxygenation in patients with heart failure. The difference between light absorption at 760 and 800 nm was used to assess hemoglobin-myoglobin oxygenation. Initial studies conducted in isolated canine gracilis muscle demonstrated that 760-800-nm absorption correlated closely (r = -0.97 +/- 0.01) with venous hemoglobin O2 saturation when the muscle was stimulated to contract at 0.25-5.0 Hz. In normal subjects (n = 6) and patients with heart failure (n = 8), 760-800-nm absorption changes from the vastus lateralis muscle were monitored at rest, during progressive maximal bicycle exercise, and during thigh cuff inflation to suprasystolic pressure, an intervention designed to assess minimal hemoglobin-myoglobin oxygenation. Absorption changes were expressed relative to the full physiologic range noted from rest to thigh cuff inflation. During exercise, normal subjects exhibited an initial increase in hemoglobin-myoglobin oxygenation followed by a progressive decrease in oxygenation to 27 +/- 13% of the physiologic range at the peak exercise workload of 140 +/- 9 W. In contrast, patients exhibited an initial decrease in hemoglobin-myoglobin oxygenation with the first workload, followed by a progressive further decrease to 26 +/- 13% of the physiologic range at a peak exercise workload of 60 +/- 8 W, less than half the peak workload noted in the normal subjects. At all exercise loads, hemoglobin-myoglobin oxygenation was significantly less in the patients than in the normal subjects. These data suggest that near-infrared spectroscopy can detect impaired skeletal muscle O2 delivery in patients with heart failure. This technique could provide a valuable method of assessing muscle O2 delivery in patients, particularly before and after therapeutic interventions.
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PMID:Noninvasive detection of skeletal muscle underperfusion with near-infrared spectroscopy in patients with heart failure. 259 29

The aim of the present study is to evaluate the real need and the sensitivity of serum myoglobin levels as an early index for the diagnosis of acute myocardial infarction. A total of 62 patients (38 suffering from acute myocardial infarction, 16 from "angina pectoris", 8 from heart failure) and 20 healthy volunteers were included in the study. The patients with acute myocardial infarction were divided in 3 subgroups according to the time passed between the beginning of the pain and their admittance to our Department (Coronary Care Unit), that was, less than 6 hours, between 6 and 12 hours, between 12 and 24 hours. Among the patients with "angina", 8 presented spontaneous crisis whereas 4 had crisis only during treadmill test. 8 of the healthy volunteers received intramuscular injections of physiological solution every 12 hours during the 3 days preceding the study. In all subjects serum myoglobin level were measured by radioimmunoassay; in patients with acute myocardial infarction serum CK and MBCK levels with enzymatic method were measured too. No variation of plasma myoglobin levels was seen in patients with angina, neither in healthy volunteers had they received or not intramuscular injections. The low increase in plasma myoglobin levels observed in patients with heart failure might be due to a deficit of renal function. Serum myoglobin levels were significantly elevated in all the patients with acute myocardial infarction, whereas plasma CK and MBCK levels were significantly high only 6 hours after the necrosis. In myocardial infarction the levels of myoglobin rise during the first hours, peak at 10 hours and return to normal in 20 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in plasma myoglobin levels in ischemic heart disease]. 261 6

The informative value of various functional and laboratory diagnostic methods was reviewed in 150 patients with unstable angina (UA). High informativeness (92%) and sensitivity (83%) of isometric hand grip under computerized electrocardiographic monitoring was demonstrated for the diagnosis and control of treatment in these patients. Isometric loading brought out a dramatically reduced coronary reserve, latent heart failure and electrical instability of the myocardium. The cold test with a small area of skin exposure is of low diagnostic value in UA cases and cannot be recommended for clinical use. Serial myoglobin assays add to the accuracy of diagnosis and have high predictive value.
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PMID:[Methods of diagnosing unstable stenocardia and monitoring its treatment]. 286 42

Chronic cardiac insufficiency can be produced by a variety of causes which may be partly determined by means of macroscopic, histological and electron microscopic investigations. By using quantitative histochemical methods, changes of substances in the myocardium can be observed indicating myocardial insufficiency and giving an explanation of its cause. Hypertrophied hearts without insufficiency show cardiac muscle fibres having increased in width, volume and dry weight up to a maximum value which will not be exceeded even in further progressing cardiac hypertrophy. The biochemically determined amount of collagen increases significantly with the growing weight of the myocardium. Both the myocardial amount of DNA and the amount of myoglobin, correlated with the width of the fibres, have also increased. The heart muscle nuclei showed a polyploidization which is also correlated with the weight of the myocardium. In insufficient hearts suffering from myocardial hypertrophy, the increase of the total DNA content is significantly decreased as compared to non-insufficient hearts. The mean ploidy level is increased in case of lower weights of the myocardium and decreased in higher weights in comparison to non-insufficient hearts of the same weight. In insufficient hearts a more significantly increased amount of the connective tissue cells is observed than in the case of cardiac hypertrophy alone. In contrast to this, the increase of the heart muscle cells is significantly reduced. A lack of contractile proteins, decreased DNA synthesis, increased fibrozation and, in particular, the reduced number of cardiac muscle cells must be considered as essential factors for cardiac insufficiency.
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PMID:Histochemically determinable changes in cardiac insufficiency and their functional significance. 294 64


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