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

To assess forearm exercise capacity and exercise energy metabolism in relationship to forearm muscle mass and blood flow in patients with chronic heart disease, 22 patients (NYHA class I (C1) 8, class II(C2) 10, class III (C3) 4) and 10 normal subjects were studied using Phosphorus-31 magnetic resonance spectroscopy (31P-MRS). First, the maximal cross sectional area (MCA) of the forearm flexor muscles was estimated in each individual using magnetic resonance imaging. Then, during multistage forearm flexor exercise, 31P-MRS was performed to estimate phosphocreatine (PCr), inorganic P (Pi), and intracellular pH. Forearm blood flow was measured by plethysmography. An initial work load of forearm exercise was decided by MCA as 1 J/cm2, and multistage exercise was done with an increment of 1 J/min/cm2 to the point of maximal muscle exhaustion. The maximal load (J/min) was decreased in cardiac groups as NYHA class advanced. However, the difference among all groups except group C3 was not significant when the max load was adjusted for muscle MCA. As the work load was increased during forearm exercise, PCr and intracellular pH decreased, and Pi increased in every group. Standardized PCr [PCr/(PCr + Pi)] was lower in group C2 and C3 than in group N at each work load. At high work loads, intracellular pH tended to be lower in group C2 and C3 than in group N and C1. Forearm blood flow during forearm exercise was not different among the four groups. In the maximal exercise test using upright ergometer, peak oxygen uptake and anaerobic threshold were lower in group C1, C2 and C3 than in group N.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study of forearm muscle metabolism in patients with chronic heart disease]. 188 57

In valve replacement operations on 78 patients with acquired heart disease, the efficiency of phosphocreatine in intraoperative protection of ischemic myocardium was evaluated by clinical, morphologic, and biochemical methods. Phosphocreatine (8 to 10 mmol/L) in a blood cardioplegic solution was used in operations on 41 patients; in the control group (37 patients) standard blood cardioplegia was used. In the group with phosphocreatine treatment we observed more rapid recovery of hemodynamics after release of the aortic cross-clamp, a decreased frequency of fibrillation, and more frequent restoration of sinus rhythm even if there were sinus rhythm disturbances before aortic cross-clamping. Analysis of the biopsy samples taken from the right ventricle showed protection of the sarcolemma against ischemic damage afforded by phosphocreatine and complete preservation of high-energy phosphates. The results obtained confirm the conclusion made by Robinson, Braimbridge, and Hearse (J Thorac Cardiovasc Surg 1984; 87:190-200) that phosphocreatine is an effective additional cardioprotective agent when used in cardioplegic solutions.
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PMID:Protection of ischemic myocardium by exogenous phosphocreatine. II. Clinical, ultrastructural, and biochemical evaluations. 331 24

1. Exercise tolerance is impaired in congenital heart disease. To examine the possible contribution of abnormalities in skeletal muscle bioenergetics, we used 31P nuclear magnetic resonance spectroscopy to investigate muscle metabolism in 10 subjects with congenital heart disease with cyanosis (median age 17.3 years) and in eight healthy age-matched control subjects. Spectra were collected from the gastrocnemius muscle at rest and during exercise and recovery. 2. In resting muscle there were significant elevations in cytosolic pH and in the cytosolic concentration of inorganic phosphate in the patients, and a strong positive correlation between cytosolic pH and blood haemoglobin concentration in all subjects. 3. During plantar flexion exercise the patients showed increased phosphocreatine depletion and cytosolic acidification over a shorter duration of exercise. The rise in calculated cytosolic ADP concentration was similar in both groups. 4. After cessation of exercise, the recovery half-times of phosphocreatine, ADP and phosphate were two to three times longer in the patients, and the initial rate of phosphocreatine resynthesis (a measure of the rate of mitochondrial ATP synthesis) was half the control value, consistent with a reduction in the effective maximum rate of oxidative ATP synthesis (expressed per volume of muscle). Also, recovery was faster in the young control subjects than in our earlier studies of older healthy control subjects. 5. The high phosphate concentration in resting muscle and the abnormalities found in exercise and recovery are consistent with a decrease in oxidative ATP synthesis due to reduced oxygen delivery by the blood in chronic hypoxaemia. The correlation between cytosolic pH and haemoglobin concentration remains to be explained.
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PMID:Abnormalities in skeletal muscle metabolism in cyanotic patients with congenital heart disease: a 31P nuclear magnetic resonance spectroscopy study. 814 86

We use the hyperbolic relationship between cytosolic [ADP] and the rate of phosphocreatine (PCr) resynthesis after exercise to estimate the apparent maximum rate of oxidative ATP synthesis (QMAX). We examine data from some human diseases in which mitochondrial oxidation may be impaired (due to reduced mitochondrial numbers, intrinsic mitochondrial defect or impaired vascular supply). Muscle responds to impaired oxidation by stimulating anaerobic ATP synthesis and/or by increasing [ADP], the stimulus to the mitochondrion. However, these responses interact: [ADP] depends on pH and [PCr], and lactic acid production tends to lower [ADP] (by lowering pH), while proton efflux has the opposite effect. We identify four patterns of results: (A) in mitochondrial myopathy, apparent QMAX is reduced and [ADP] is appropriately increased, because increased proton efflux reduces the pH change in exercise despite increased lactic acid production; (B) in some conditions (e.g., cyanotic congenital heart disease) apparent QMAX is reduced but there is no compensatory rise in [ADP], probably because anaerobic ATP synthesis during exercise is increased without increase in proton efflux; (C) in other conditions (e.g., myotonic dystrophy) [ADP] is increased during exercise but apparent QMAX is normal, suggesting either an increase in proton efflux and/or decrease in anaerobic ATP synthesis during exercise; (D) there are also conditions (e.g., respiratory failure) where, despite impaired oxygen supply, both apparent QMAX and end-exercise [ADP] are normal. We also discuss the metabolic conditions under which end-exercise [ADP] is increased by a mitochondrial defect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative analysis by 31P magnetic resonance spectroscopy of abnormal mitochondrial oxidation in skeletal muscle during recovery from exercise. 826 62

The reproducibility of the phosphocreatine to adenosine triphosphate ratio (PCr/ATP) was assessed from cardiac phosphorus-31 (31P) NMR spectra of the human left ventricle acquired with three different localization techniques. Cardiac 31P-NMR spectra (n = 68) were obtained at rest from 16 healthy subjects with three-dimensional (3D) image selected in vivo spectroscopy (ISIS), 1D spectroscopic imaging (SI), or with a combination of 2D ISIS and the 1D SI technique (ISIS + SI). The average PCr/ATP ratios were 1.41 +/- 0.20 for ISIS + SI and 1.31 +/- 0.19 for ISIS and were in the lower range of values obtained in previous studies, mainly because of a lower saturation correction factor for the cardiac PCr/ATP ratio. The SI experiment yielded an average PCr/ATP value of 0.98 +/- 0.20, significantly lower as compared to the correct values obtained with ISIS + SI and ISIS (p < 0.001), underscoring the need for 3D localization to avoid contamination of the NMR signal by liver tissue. Intersubject standard deviations of the PCr/ATP ratio were comparable to values reported previously. For all three localization techniques the absolute intra-examination differences in PCr/ATP (0.06 for ISIS to 0.15 for ISIS + SI) were significantly smaller (p approximately 0.03) than inter-examination differences (0.24 for ISIS to 0.29 for ISIS + SI). Therefore, consecutive acquisition of cardiac 31P-NMR spectra from the same patient during a single examination, e.g. under various cardiac loading conditions, appears to be a reliable approach for metabolic evaluation of heart disease.
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PMID:Reproducibility of human cardiac 31P-NMR spectroscopy. 906 3

Localized (1)H-MR spectroscopy is sensitive to motion and has mostly been applied to the brain. For the human heart, cardiac and respiratory motion lead to displacements on the order of the localized voxel and lead to substantial variations of voxel content, lineshape, water suppression, and signal phase and amplitude. Combined respiratory and cardiac double triggering can avoid these complications to a large extent. Three methods of double triggering are evaluated, with reproducibility established in nine subjects for a method based on respiratory modulation of the ECG amplitude and a visual feedback mechanism. Quantitated with respect to water, within-subject reproducibilities for this setup were 9% for trimethylammonium compounds, 10% for creatine/phosphocreatine, and 13% for lipids. ANOVA showed significant differences between subjects which may relate to natural variability between subjects or exact location within the heart. Unresolved issues for this technique are its susceptibility to precise placement of ECG electrodes and the reasons for failure in 20% of examination. With this technique it is possible to investigate open questions in cardiac pathophysiology, such as the creatine content in chronic heart disease. Variants of this triggering method may also improve cardiovascular MRI methods relying on data acquired in several heartbeats. Magn Reson Med 42:903-910, 1999.
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PMID:Methods and reproducibility of cardiac/respiratory double-triggered (1)H-MR spectroscopy of the human heart. 1054 49

Magnetic resonance spectroscopy (MRS) can noninvasively provide a window into the metabolic status of the heart. This technique has shown abnormalities in the phosphocreatine-to-adenosine triphosphate ratio in patients with severe cardiomyopathies, either dilated or hypertrophic. Data indicate that abnormal metabolic parameters can risk stratify patients with dilated cardiomyopathy and provide independent prognostic information. Finally, the use of MRS in patients after cardiac transplantation is being explored. The information from cardiac MRS will likely provide the investigator and clinician with unique data and assist in the diagnosis and management of patients with various forms of heart disease.
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PMID:Magnetic resonance spectroscopy in human cardiomyopathies. 1154 32

Hemochromatosis is a hereditary iron overload syndrome characterized by increased iron storage, followed by liver cirrhosis and is often associated with restrictive cardiomyopathy. The purpose of this study was to detect alterations of cardiac high-energy phosphate metabolism in patients with hereditary hemochromatosis (HHC) prior to the development of structural heart diseases. Therefore cardiac phosphorus-31 two-dimensional chemical shift imaging ((31)P 2D CSI) was employed. Twenty-four male patients (mean age 47.2 +/- 12 years) homozygous for the C282Y mutation in the hemochromatosis associated HFE gene and twenty-four male healthy volunteers (mean age 47 +/- 11 years) as age-matched controls were included in this study. Using a 1.5-Tesla whole-body magnetic resonance scanner, electrocardiograph-triggered transversal 31P 2D CSI was performed. Left ventricle mean phosphocreatine (PCr) to beta-adenosine triphosphate (beta-ATP) ratios of patients with HHC (1.60 +/- 0.41) were significantly decreased in comparison to healthy volunteers (1.93 +/- 0.36; p = 0.004). Furthermore, we detected moderate, negative correlations between left ventricular PCr to beta-ATP ratios and transferrin saturation, cholesterol, low-density lipoprotein as well as triglyceride. This study shows that 31P 2D CSI permits the detection of alterations of cardiac high-energy phosphate metabolism in patients with HHC, but without any evidence for heart disease. The decreased PCr to beta-ATP ratios in HHC might be caused by mitochondrial impairment due to cardiac iron overload.
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PMID:Cardiac phosphorus-31 two-dimensional chemical shift imaging in patients with hereditary hemochromatosis. 1512 Jan 71

In myotonic dystrophy type 2 (DM2/PROMM), cardiac muscle involvement is usually more benign than in DM1, but clinically severe cardiomyopathy has been reported in some patients. Using a novel method of magnetic resonance spectroscopy (MRS), we examined the left ventricular myocardium and the left gastrocnemius muscle in 11 unselected DM2/PROMM patients without overt cardiac disease. Data on cardiac morphology and function were obtained by gradient echo two-dimensional cine magnetic resonance imaging (MRI); no significant differences were found between DM2 patients and healthy controls, but using a median split approach older patients showed mildly increased left ventricular (LV) volumes, i.e., 59% increase of end-systolic volume index (ESVI) and 35% increase of end-diastolic volume index (EDVI), and an increase of LV mass (26%). On cardiac MRS, DM2/PROMM patients showed a reduction of phosphocreatine (PCr) and adenosine triphosphate (ATP) by 25 and 20% compared to matched healthy controls. No significant differences were found between younger and older patients. In skeletal muscle of the DM2 patients, no significant decrease of PCr and ATP concentrations was found. However, in older patients, who commonly show overt hip flexor muscle weakness, we observed reduced values for PCr and ATP. Our MRS and MRI findings reveal evidence for subclinical cardiomyopathy in DM2/PROMM patients without overt heart disease. Future prospective studies are needed to clarify the risk of developing overt cardiac disease in DM2 and to define prognostic factors.
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PMID:Cardiac and skeletal muscle involvement in myotonic dystrophy type 2 (DM2): a quantitative 31P-MRS and MRI study. 1545 41

The cognitive deficits observed in children with cyanotic congenital heart disease suggest involvement of the developing hippocampus. Chronic postnatal hypoxia present during infancy in these children may play a role in these impairments. To understand the biochemical mechanisms of hippocampal injury in chronic hypoxia, a neurochemical profile consisting of 15 metabolite concentrations and 2 metabolite ratios in the hippocampus was evaluated in a rat model of chronic postnatal hypoxia using in vivo 1H NMR spectroscopy at 9.4 T. Chronic hypoxia was induced by continuously exposing rats (n = 23) to 10% O2 from postnatal day (P) 3 to P28. Fifteen metabolites were quantified from a volume of 9-11 microl centered on the left hippocampus on P14, P21, and P28 and were compared with normoxic controls (n = 14). The developmental trajectory of neurochemicals in chronic hypoxia was similar to that seen in normoxia. However, chronic hypoxia had an effect on the concentrations of the following neurochemicals: aspartate, creatine, phosphocreatine, GABA, glutamate, glutamine, glutathione, myoinositol, N-acetylaspartate (NAA), phosphorylethanolamine, and phosphocreatine/creatine (PCr/Cr) and glutamate/glutamine (Glu/Gln) ratios (P < 0.001 each, except glutamate, P = 0.04). The increased PCr/Cr ratio is consistent with decreased brain energy consumption. Given the well-established link between excitatory neurotransmission and brain energy metabolism, we postulate that elevated glutamate, Glu/Gln ratio, and GABA indicate suppressed excitatory neurotransmission in an energy-limited environment. Decreased NAA and phosphorylethanolamine suggest reduced neuronal integrity and phospholipid metabolism. The altered hippocampal neurochemistry during its development may underlie some of the cognitive deficits present in human infants at risk of chronic hypoxia.
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PMID:In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus. 1609 7


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