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

The prognosis is poor for patients with left ventricular enlargement associated with large infarcts. We studied 78 patients using gated single-photon emission computed tomography (SPECT, to assess left ventricular volumes), right heart catheterization (to measure pulmonary wedge pressure and cardiac output), and conventional planar radionuclide ventriculography (to estimate ejection fraction), 2-6 days, 3-5 weeks, and 5-8 months after their first myocardial infarction. Patients were assigned to a large or small infarct-size group based on creatine kinase analysis. In 37 patients with large infarcts, left ventricular volume increased and was greater than 27% after 5-8 months than after 2-6 days (p less than 0.05). Although ejection fraction remained significantly depressed, stroke volume, which initially declined, was restored as a result of dilation and thus returned to normal by 3-5 weeks, indicating that enlargement of the left ventricle compensated for the loss of contractile myocardium and depression of global ejection fraction. The progressive nature of left ventricular dilation suggested that this process is of major pathophysiologic importance and that it plays an etiologic role in the genesis of heart failure and perhaps of sudden death following myocardial infarction. Dilation preceded hemodynamic deterioration, which became evident on exercise after 5-8 months in patients with large infarcts.
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PMID:Serial changes in left ventricular size after acute myocardial infarction. 183 92

On the basis of a case history, the clinical and paraclinical manifestations of hypothyroidism are reviewed. Exertion dyspnoea without signs of cardiac insufficiency occurs frequently. The minute and stroke volume and heart rate are reduced. The blood pressure may rise (reversible) and hypertension may occur. The function of the left ventricle is reversibly reduced. A tendency to formation of exudates has been observed. X-ray of the thorax may revial massive relatively asymptomatic pleural exudates and cardiomegaly. Pericardial exudate occurs frequently and is demonstrated best by echocardiography. Inter- and intracellular deposits, infiltrations and fibroses have been demonstrated in the myocardium and these probably contribute to some of the non-specific, reversible ECG changes (low voltage, flattening/inversion of T waves, sinus bradycardia). The plasma concentrations of several different enzymes (including creatine kinase (CK), CK-MB and LDH) may be raised in myxoedema. The reason for this is perhaps compromized membrane function in the skeletal muscle cells. The diagnosis of myocardial infarction in myoedema requires that CK-MB constitutes at least 6% of the total CK and that the increase is transient. In patients with coronary sclerosis, substitution treatment should be initiated carefully because the risk of ischaemic symptoms is otherwise considerably increased. It is not elucidated whether the hypothyroidism per se can increase atheroma formation.
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PMID:[Cardiovascular manifestations of hypothyroidism]. 186 65

The increase of serum ASTm activity might reflect the severity of damage at the subcellular level of the myocardium. 50 patients with acute myocardial infarction (AMI) were observed. The mean peak ASTm activity was 34.34 +/- 34.60 IU/L and 48 patients (96%) greater than or equal to 9 IU/L (two times median value of normal subject). The peak time (36 h) came later and the duration (120 h) was longer than that of CK-MB. ASTm/ASTt ratio in groups of AMI, non-AMI heart failure and acute ictero-hepatitis was 0.25 +/- 0.10, 0.02 +/- 0.05 and 0.05 +/- 0.02 respectively. The former was significantly greater than other two groups (P less than 0.01). The activity of ASTm in AMI cases with heart function at I, II and III + IV (Killip classification) was 21.8, 40.2 and 76.2 IU/L respectively (F = 8.407 P less than 0.01) and it was 84.9 and 24.7 IU/L in the death and surviving groups (P less than 0.01). The result showed that the estimation of serum ASTm level was helpful to the establishment of diagnosis in the patients with AMI who were sent delayed to the hospital. It held special significance in evaluating the severity of myocardial damage, heart function and in predicting the prognosis of AMI.
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PMID:[Serum mitochondrial aspartate aminotransferase (ASTm) in acute myocardial infarction]. 191 59

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

The enzymatic activity of creatine kinase-MB isoenzyme (CK-MB), a sensitive and specific marker of myocardial damage, was measured in 32 children following scorpion envenomation. CK-MB activity, total creatine phosphokinase (CPK) and serum glutamine oxalacetic transaminase (SGOT) levels were examined for relationship with electrocardiographic (ECG) results and the clinical state of the children. Twenty-seven out of the 32 children had signs of systemic intoxication ("symptomatic" cases), while the other five children had only local signs ("asymptomatic" cases). Thirteen out of the 27 symptomatic children had enzymatic myocardial involvement characterized by high total CPK level, elevated CK-MB level and a CK-MB/CK ratio exceeding 6%. Six of these 13 children had ECG changes consistent with myocardial damage, and only one child had clinical signs of myocardial injury. None of the asymptomatic children, nor five healthy control children, had any evidence of myocardial damage as judged by CK-MB levels, clinical signs and ECG. Our study suggests that CK-MB activity is specific and highly sensitive in detecting myocardial damage in children following scorpion envenomation, and appears superior to ECG and clinical parameters. We speculate that the myocardial lesions are too small to cause heart failure in most cases, but they may account for the cardiovascular changes frequently seen in scorpion envenomation.
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PMID:Myocardial injury without heart failure following envenomation by the scorpion Leiurus quinquestriatus in children. 204 53

A prospective study in 76 newborn with perinatal asphyxia searching for myocardial ischemia was carried out. The disease was found in 51% of the patients. With electrocardiogram, myocardial enzymes, X ray and clinical manifestations the diagnosis was elaborated. No difference in the sex was present, the mean of gestational age was 35 weeks, and with mean birth weight 2,216 g, respiratory distress was present in all the people; only 20.5% developed heart failure and two had heart murmurs; 61.5% showed cardiomegaly. The creatine kinase MB isoenzyme at twelve hours after birth was raised in most of the patients. Respiratory distress syndrome was the principal diagnosis in 38%; hypoxic ischemic encephalopathy and peri-intraventricular hemorrhage was present in 50 and 33% of the patients, respectively. Mortality rate was 33%. Also a comparative study in the infants with and without myocardial ischemia was carried out appearing significative difference in: 1. Cardiomegaly, 2. Hypoxic-ischemic encephalopathy and 3. Creatine kinase MB isoenzyme.
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PMID:[Transient myocardial ischemia in newborn babies with perinatal asphyxia (hypoxic cardiomyopathy)]. 209 33

To address the hypothesis that impaired ATP synthesis rates caused by changes in the creatine kinase system is an important mechanism underlying cardiac failure, we measured total creatine kinase activity, isoenzyme composition and creatine content in two animal models of hypertrophy with cardiac dysfunction, the spontaneously hypertensive rat in the transition to failure and the creatine-depleted hyperthyroid rat heart challenged by hypoxia. During the transition from stable compensated hypertrophy to failure characterized by decreased functional capacity, we found that total creatine kinase activity and particularly mitochondrial creatine kinase activity decreased. The decrease in functional capacity, the further increase in heart size and the derangements in the creatine kinase system did not occur if these animals were treated for 6 months with the antihypertensive agents, guanethidine or hydralazine. These results suggest that changes in the creatine kinase system occur coordinately with the transition to failure. To assess whether the changes in the creatine system may be causally linked to decreased functional capacity, we used 31P NMR spectroscopy of isolated perfused hearts to define the high energy phosphate content and cardiac performance of creatine-depleted (approximately 50%) hypertrophied hearts challenged by hypoxia. These hearts displayed greater susceptibility to hypoxic injury with regard to both systolic and diastolic function during and following hypoxia. We also measured total creatine kinase activity in right ventricular biopsy specimens from patients with various forms of cardiomyopathy and low ejection fractions, and found a positive correlation between total creatine kinase activity and ejection fraction. Taken together, these results support the hypothesis that decreasing the energy reserve for ATP synthesis renders the heart more susceptible to systolic and diastolic failure.
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PMID:Energetic correlates of cardiac failure: changes in the creatine kinase system in the failing myocardium. 214 77

Transgenic mice expressing atrial natriuretic factor-SV40 T-antigen fusion genes (ANF-TAG) developed cardiac tumors asymmetrically in the right atrium. Features associated with cardiac failure, including increased plasma creatine kinase activity (MM and MB) and ventricular dysrhythmias, also were associated with atrial tumor growth. These atrial tumors were able to grow at histocompatible sites (subcutaneously in syngeneic animals) for protracted periods of time yielding a series of transplantable atrial tumor lineages. The transplantable tumors displayed several cardiac-specific characteristics, such as endogenous electrical activity and expression of cardiac-specific proteins. These transplantable atrial tumors constitute a novel experimental resource for developing cell lines which display an adult cardiac phenotype.
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PMID:Cardiac tumors and dysrhythmias in transgenic mice. 215 Oct 59

A case of 25-year-old woman with glycogen storage myopathy is reported here. She was hospitalized for acute heart failure after alcohol drinking. The electrocardiogram on admission showed marked ST elevation. Laboratory data showed elevated levels of serum myogenic enzymes but no rise in cardiomyogenic enzyme: CK 3862 IU/l CK-MB 35 IU/l, LDH 427 IU/l, GOT 203 IU/l. After several days, she recovered from acute heart failure and could walk without supporting. ST elevation in ECG and elevated myogenic enzymes were also normalized. The occurrence of acute myocardial infarction was ruled out because a coronary angiogram and 99 Tcm scintigram were normal. Physical examination revealed proximal muscular weakness and mental retardation (WAIS, total 72). Venous lactate response was normal after semi-ischemic forearm exercise. PAS staining of muscle specimen showed an excess deposit of glycogen. Ragged-red fibers were not seen on Gomori-trichrome stain. By electron microscopy, a large amount of glycogen particles were demonstrated in the subsarcolemma, but there were no abnormal mitochondrial changes. Biochemical analysis showed accumulation of glycogen in muscles: 28.7 mg/g muscle (normal 11.4 +/- 4.2 mg/g muscle). The activities of enzyme in the pathway of glycogen and glycogenosis (alpha-glucosidase, amylo-1,6-glucosidase, phosphorylase a, phosphorylase kinase, phosphofructokinase, etc.) were within normal limits. The spectrum of glycogen iodine complex was normal. Our case was different from any type of muscle glycogen storage disease previously reported. The etiology of an excess of glycogen deposit in muscles is unknown.
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PMID:[A case of glycogen storage myopathy with acute heart failure]. 220 34

The numerous metabolic abnormalities encountered in chronic purgative abusers were investigated and the new concept of autonomous pseudo-Bartter's syndrome documented. Detailed metabolic screening tests were performed in 9 women aged 17-54 years. Two patients underwent further studies, including serum renin and aldosterone, blood volume, total body potassium, urinary chloride and prostaglandin determinations, and each underwent renal biopsy on admission and after 1 year free from laxative abuse. Clinical complications included confusion, convulsions, coma, skeletal muscle weakness with or without paralysis or rhabdomyolysis, cardiac failure, urinary tract infections and bone disease (osteomalacia, secondary hyperparathyroidism and osteoporosis). Hypokalaemia, hypomagnesaemia, hypocalcaemia and hypophosphataemia were frequent findings. Serum creatine kinase correlated inversely with the product of the potassium and serum phosphate (r = -0.86; P less than 0.03), suggesting that hypokalaemia and hypophosphataemia act synergistically to produce muscle damage. After laxative withdrawal, oedema and weight gain, followed by diuresis, ensued in 7 patients. In the other 2, ongoing chloruresis, kaliuresis, hyper-reninaemia and raised urinary prostaglandin secretion persisted. Renal biopsies in these 2 patients showed the features of juxtaglomerular apparatus hyperplasia as well as medullary interstitial cell hyperplasia. In conclusion, pseudo-Bartter's syndrome was documented in 9 chronic laxative abusers. Because patients often indulged in more than one aberrant habit, e.g. laxative and/or diuretic abuse or bulimia, the clinical syndrome produced a myriad of confounding metabolic derangements, which we termed 'metabolic madness'. Laxative withdrawal was complicated by temporary pseudo-idiopathic oedema, which persisted in 2 patients. Further studies in these 2 women strongly supported the concept of 'autonomous pseudo-Bartter's syndrome'.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic laxative abusers with pseudo-idiopathic oedema and autonomous pseudo-Bartter's syndrome. A spectrum of metabolic madness, or new lights on an old disease? 225 4


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