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)

Elevated serum levels of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) are generally present in cases of muscle or heart disease, though there are some exceptions. We treated a 56-year-old man diagnosed as suffering from primary idiopathic hypoparathyroidism (PIHP). The neurologic examination was normal, but serum levels of CPK and LDH, and especially isoenzymes of striated muscle, were elevated. Elevated levels of these enzymes in PIHP are rare. In this case they most probably leaked from muscle into the blood circulation after changes in the muscle cell membrane due to hypocalcemia.
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PMID:[Serum striated muscle enzymes in autoimmune hypoparathyroidism]. 825 99

We report a case of diabetic ketoacidosis (DKA) complicated by acute myocarditis, which was confirmed by cardiac biopsy. A 26-year-old man was hospitalized with severe DKA. On admission, nonspecific ST-T change was noted on the electrocardiogram (ECG). The patient's levels of creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase were slightly elevated, but he did not complain of chest discomfort or symptoms of heart disease. On the first day after admission, ST-T elevation was noted on ECG during treatment of DKA. By cardiac angiography and cardiac biopsy, coronary heart disease was ruled out and postmyocarditic change was histologically confirmed. An episode of upper respiratory viral infection before the onset of acute diabetes suggested that the patient suffered from viral-induced myocarditis and consequent development of IDDM. This possibility was confirmed by the clinical course of ECG change, with elevated CPK and lactate dehydrogenase and a slightly elevated antibody titer for echovirus.
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PMID:A case of myocarditis associated with IDDM. 872 64

The myocardial damage caused by transthoracic direct current countershock was evaluated serologically and histologically. Countershock energy of between 12 and 240 watt-second (ws) discharge was given to rabbits. Total creatine kinase (total CK) and creatine kinase-MB isozyme (CK-MB) activities in plasma were increased after the countershock, with peak values averaging 5690 IU/L (total CK) and 35 IU/L (CK-MB) within 6 h, whereas the CK-MB activity of a rabbit subjected to countershock in the femoral region was within normal range of less than 3 IU/L. Histologically, epicardial alteration was found in electrode-shaped areas which confined to the superficial epicardium in all rabbits. The heart from rabbits that died within a few minutes after countershock showed epicardial alteration in right and left ventricles, and subendocardial alteration with focal hemorrhage was evident in the left ventricle. Subendocardial necrosis and interstitial edema were also revealed in the left ventricle 72 h after countershock. These myocardial damages appeared in the transthoracic pathway between the electrodes. Thus, we conclude that the myocardial damage caused by countershock is distinguishable from heart disease in terms of the characteristic areas and measuring CK levels.
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PMID:A medico-legal approach to the myocardial changes caused by transthoracic direct current countershock. 907 36

ST-segment changes and biochemical signs of myocardial injury, and their relation to sympatho-adrenergic activation and cardiac function, were studied in a case series of 19 alcohol-dependent (DSM-III-R) men undergoing in-hospital treatment for alcohol withdrawal. No patient had any clinically apparent heart disease. Analyses of ST-segment depressions > or = 0.1 mV from 24 h ambulatory electrocardiographic recordings revealed horizontal or downsloping ST-segment depressions in seven of the patients. The serum concentration of creatine kinase (CKMB) the day after admission correlated with the urinary excretion of adrenaline (r = 0.74, P < 0.001) and noradrenaline (r = 0.71, P < 0.001). In the two patients with the highest adrenaline excretion and the highest serum concentrations of CKMB and cardiac troponin T, horizontal ST-segment depressions were detected as well. The left ventricular ejection fraction was > or = 0.65 (range 0.65-0.79) in all of the 17 alcoholic men who were examined by echocardiography. Our study shows that alcohol withdrawal is frequently associated with ST-segment abnormalities in men without impairment of heart function and that sympatho-adrenergic activation during withdrawal seems to influence the release of myocardial enzymes. Alcohol withdrawal should thus be considered a condition in which acute cardiac complications may be expected in susceptible individuals.
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PMID:ST-segment changes and catecholamine-related myocardial enzyme release during alcohol withdrawal. 910 13

The Ontario Laboratory Proficiency Testing Program has regularly monitored the analytical performance of total creatine kinase (CK) (approximately 230 participants) and CK isoenzyme-2 (CK-MB) (approximately 160 participants) throughout the entire province. Consistently, a wide dispersion of results has been observed not only between different analyzer systems but also among identical analyzers. Accordingly, the results of the last three proficiency surveys for these analytes were examined statistically to establish both the extent of these variations and the range of values reported for the male upper reference ranges. The results of many of the analyzer systems were significantly different from each other, as were many of the reference ranges. This unsatisfactory situation may only be remedied by the use of reference materials as shown by others. The consequences of these findings also effect the reliability of epidemiological surveys such as the WHO MONICA Project (Circulation 1994;90:583-612), which monitors deaths due to heart disease and includes cardiac enzyme results in its criteria.
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PMID:Proficiency testing of creatine kinase and creatine kinase-2: the experience of the Ontario Laboratory Proficiency Testing Program. 955 May 69

Acute chest pain patients without ECG-signs of acute myocardial infarction (AMI) on admission need to be earlier and better diagnosed to reduce use of expensive intensive care beds and to treat more patients with acute recirculation therapy. We investigated whether total CK-activity, CK-MB mass, CK-MB2, myoglobin, cardiac troponin I (cTnI) and T (cTnT) measured in venous blood on admission and after 1 and 2 h could be used to identify or exclude acute myocardial damage (AMD) in 22 acute chest pain patients without ECG-signs of AMI admitted to hospital within 6 h after onset of pain. Increases in CK-MB mass, CK-MB2, myoglobin and cTnI identified AMD in three patients classified retrospectively as AMI. Likewise, CK-MB mass, CK-MB2, cTnI and cTnT increased with time in three of seven patients classified as having unstable angina pectoris. CK-MB2 and cTnI increased with time in two patients with tachycardia belonging to the other heart disease group. The remaining seven patients of the non-heart disease group showed no change in any of the cardiac markers. Thus, early serial measurements of selected cardiac markers appear useful in identifying or excluding AMD 3 h after admission in these acute chest pain patients.
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PMID:Serial measurements of cardiac markers to rule in or out acute myocardial damage less than 3 h after admission in acute chest pain patients without ECG-signs of acute myocardial infarction. 974 21

A growing amount of scientific evidence supports the participation of oxygen radicals in heart disease and, consequently, a protective effect of vitamin E (VE), beta-carotene (BC), and other antioxidants. The aim of this study was to correlate plasma VE and BC concentration with the clinical course of the acute myocardial infarction (AMI). We evaluated 120 patients that were admitted at the coronary units within 12 h after the development of AMI symptoms. The AMI was diagnosed by clinical and biochemical criteria and by electrocardiography and echocardiography. Plasma VE and BC concentration was determined by high performance liquid chromatography. The patients were separated according to the plasma concentration of VE (group H, VE > 17.5 microM; group L, VE < 17.5 microM). Clinical history of patients, age, sex, associated cardiovascular risk factors, AMI localization, hemodynamic class, and the treatment received were similar between different groups. The blood levels of creatine phosphokinase (CK) evaluated either 24- or 48-h after admittance, were higher in group L than in group H (24 h: H = 436 +/- 31 U/ml vs. L = 642 +/- 84 U/ml; p < .005; 48 h: H = 242 +/- 21 U/ml; L = 423 +/- 82 U/ml, p < 0.005). The number of deflexions in the electrocardiogram at admittance (ECG-D) was significantly higher in group L than in group H (4.7 +/- 0.3 vs. 3.7 +/- 0.2; p < .005). The number of new Q waves in the ECG of release (ECG-Q) was higher in group L than in group H (2.9 +/- 0.3 vs. 2.2 +/- 0.2; p < .05). The number of segments affected in the echocardiograms (EC-S) was: L = 5.3 +/- 0.6 vs. H = 4.4 +/- 0.2; p = 0.11. No significant differences in CK levels, ECG-D, ECG-Q, and EC-S were observed when the patients were separated according their plasma BC levels. These results indicate that a high concentration of plasma VE, but not BC, was associated with a diminution in the creatine phosphokinase release and with the AMI extension.
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PMID:Tissue damage in acute myocardial infarction: selective protection by vitamin E. 1040 25

Serum cardiac troponin I-values were compared to conventionally obtained diagnosis in 319 consecutive patients suspected of having myocardial infarction, of which 46 patients were given this diagnosis. All patients with troponin I > 20 micrograms/l (n = 40) also had abnormal creatine kinase and abnormal creatine kinase isoenzyme MB activity. All patients with troponin I values in the range 1.0-19.9 micrograms/l (n = 50) had a diagnosis of heart disease (myocardial angina pectoris, myocardial infarction, arrythmia, heart insufficiency). In this patient group, the creatine kinase measurements showed pathological values in only 12 cases. Troponin I seems to be a sensitive indicator of cardiac cell injury, and measurements of troponin I seems to be useful in ruling out cardiac injury.
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PMID:[Measurement of troponin I levels in suspected myocardial infarction]. 1059 46

The concept of antigenic mimicry in autoimmune diseases such as rheumatic fever has been under investigation for decades and the range of cross-reactive tissue antigens for streptococcal-induced antibodies identified in rheumatic heart disease is still expanding. To identify heart tissue-reactive antigens which may be implicated in the secondary immunopathogenesis of rheumatic fever, sera from 56 patients with acute rheumatic heart disease were probed in two-dimensional Western blots for reactivity against heart tissue antigens. After two-dimensional immunoblot analysis, proteins were submitted to N-terminal amino acid sequence analysis. This analysis identified creatine kinase, two mitochondrial proteins and, at a low level, various stress proteins as cross-reactive myocardial antigens. Therefore, in addition to myosin, creatine kinase may represent another major antigen for autoreactive antibodies in rheumatic heart disease. Mitochondrial proteins have been implicated in the pathogenesis of inflammatory heart disease for some years, and in this study we have identified two mitochondrial proteins as relevant antigens in rheumatic heart disease.
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PMID:Autoantibodies in the sera of patients with rheumatic heart disease: characterization of myocardial antigens by two-dimensional immunoblotting and N-terminal sequence analysis. 1093 Nov 41

The diagnosis of myocardial infarction (MI) is established in patients with chest pain and equivocal electrocardiogram changes by demonstrating a rise in blood levels of creatine kinase MB (CK-MB) and/or an increase in cardiac troponin I (cTnI) or cardiac troponin T (cTnT). Previous studies have shown that levels of CK-MB are increased in the left ventricle of individuals with heart disease; however, it has not been established whether there are differences in the ventricular myocardium concentrations of cTnI in diseased compared to healthy hearts. Using a simple extraction technique, concentrations of CK-MB and cTnI were measured in the left ventricle (LV) of six hearts obtained at autopsy from individuals ranging in age from 25 to 79 yr, with and without evidence of cardiac disease. The results show an 86-fold higher concentration of CK-MB and 7.7-fold lower concentration of cTnI in left ventricular myocardium of older men with and without cardiac disease, compared to that of younger men (< age 35 yr) without heart disease. These data suggest that age may need to be considered when setting cutoff limits for these markers for the diagnosis of myocardial infarction.
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PMID:Differences of creatine kinase MB and cardiac troponin I concentrations in normal and diseased human myocardium. 1184 17


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