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)

Incidence and significance of pericardial effusion in patients with acute myocardial infarction (AMI) have not been established. To evaluate these issues, we studied prospectively 138 consecutive patients with AMI. An echocardiogram was obtained in each 1, 3, and 10 days and 3 and 6 months after admission. Fifty four patients with unstable angina and 57 without heart disease were studied as controls. Echocardiographic diagnostic criteria of pericardial effusion were established from 33 additional patients undergoing surgery. Pericardial effusion was found in 28% of patients with AMI. Twenty-five percent of patients with AMI had pericardial effusion on the third day, vs 8% of patients with unstable angina (p less than .02) and 5% of patients without heart disease (p less than .01). At 1, 3, and 10 days and 3 and 6 months prevalence of pericardial effusion was 17%, 25%, 21%, 11%, and 8%, respectively. There was no case of tamponade. Pericardial effusion was more common in anterior AMI (p less than .02) and in patients with heart failure (p less than .05) but it was not significantly associated with early pericarditis, peak creatine kinase-MB, the level of anticoagulation, or mortality. Thus, pericardial effusion is a common event in patients with AMI (incidence of 28%), but does not result in specific complications. The reabsorption rate of pericardial effusion is slow and, in our experience, mild or moderate pericardial effusion does not preclude heparin therapy.
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PMID:Pericardial effusion in the course of myocardial infarction: incidence, natural history, and clinical relevance. 394 64

A nonionic contrast medium (iohexol) was evaluated for safety and efficacy in pediatric angiocardiography in this study of 15 patients, age 6 to 82 months. Patients carried a preliminary diagnosis of congenital heart disease. Subjects were injected with iohexol, 350 mg iodine/ml of solution with an average volume of 2.46 ml/kg of body weight at a rate of 9 to 14.5 ml/sec. The parameters evaluated included vital signs, intravascular BP, ECG changes, discomfort, and adverse reactions. No adverse reactions were noted in 14 of 15 patients. No significant changes in axillary temperature of ECG were observed. Intravascular blood pressure showed only moderate changes. After 24 hours, creatine phosphokinase (CPK) plasma concentrations increased significantly. Serum electrolytes remained unchanged. Image quality was deemed excellent considering variations in injection site and flow condition of the heart. Iohexol caused remarkably little discomfort and no adverse effects.
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PMID:Pediatric angiocardiography with iohexol. 397 30

Human myocardial tissue obtained at autopsy from ten patients was examined for content of the MB isoenzyme of creatine kinase (CK-MB). We wished to determine whether this isoenzyme is distributed homogeneously throughout the heart. In eight cases, there was no history or pathological evidence of heart disease. Two had a history of previous myocardial infarction; in these, tissue was obtained from sites distant from the scar. Difference was found between the CK-MB content of the right atrium and the left atrium, and between the right ventricle and left ventricle. In all cases, the CK-MB content of the right side of the heart significantly exceeded that of the left side of the heart. Statistically significant differences were also found between the CK-MB content of the anterior interventricular septum and that of the posterior septum. These topographical variations in CK-MB content may be related to differences in the density of contractile elements in various parts of the heart and, moreover, are not taken into account in the enzymatic estimation of infarct size.
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PMID:Regional distribution of the MB isoenzyme of creatine kinase in the human heart. 689 37

Serum creatine kinase (EC 2.1.3.2) isoenzyme MM was resolved by isoelectric focusing into a five-band pattern, a pattern that gradually changed after the onset of myocardial infarction. Similar changes were also demonstrated in patients undergoing coronary-bypass surgery. The evolution of two CK-MB sub-bands was studied in both cases. We found that three electrophoretic bands (CK-MM, pI 7.10; MM1, pI 6.88; MB1, pI 5.61) were predominant in patterns for sera collected during the early phase of myocardial infarction, but rapidly disappeared during the following hours, whereas bands of increased electrophoretic mobility (MM2, pI 6.70; MM3, pI 6.45; MM4, pI 6.25; MB2, pI 5.34) gradually increased. MM3 was always the major band at the end of the observation period in acute myocardial infarction (mean, 61.4% of total creatine kinase activity 36 h after the peak value for total creatine kinase in serum). The CK-MM bands were also present in the serum of patients without heart disease. Changes in the electrophoretic pattern were induced by a thermolabile factor in normal human serum, which transformed the muscular or myocardial MM and MM1 bands after their release into the blood stream.
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PMID:Further heterogeneity demonstrated for serum creatine kinase isoenzyme MM. 696 2

Abnormal creatine kinase (CK) isoenzyme patterns were observed in the serum of a 64-year-old woman with severe heart disease. Agarose electrophoresis revealed the presence of all the usual CK isoenzymes (MM, MB, and BB) plus an extra band between MM and MB. Total serum CK activity was within the normal range. Within 2 h after the patient suffered cardiorespiratory arrest, a fifth CK isoenzyme appeared, cathodal to MM. After cardiac valve replacement, the patient's serum showed a high activity of CK, but the isoenzyme pattern showed only MM and, transiently, an MB band. With return of the serum CK activity to normal, the CK isoenzymes pattern also became normal, virtually ruling out genetic variant(s). The abnormal CK isoenzyme patterns might have been the consequence of severe hypoxemia in the patient, thus such patients may represent an ominous prognostic sign. The association of the abnormal pattern upon admission with rapid deterioration of the condition of the patient suggests prompt attention for the prevention of complications.
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PMID:Five creatine kinase isoenzymes in serum of a patient with severe heart disease. 712 50

In adults, plasma elevations of creatine kinase isoenzymes are highly specific for myocardial necrosis, however, the diagnostic sensitivity and specificity of MB CK in children have not been determined. Accordingly, we analyzed the CK isoenzyme activity in serial plasma samples from 147 patients, aged 2 days to 18 months. Forty-two patients underwent routine checkups and served as controls. Fifty-seven patients underwent cardiac catheterization for congenital heart disease, an additional 16 underwent non-cardiac surgery, and 32 cardiac surgery. Blood samples were obtained prior to surgery and catheterization and q6H x 3 thereafter. Total plasma CK and MB CK in normals averaged 62 +/- 22 (SD) and 1.7 +/- 0.8 IU/L respectively. Despite a fivefold increase in total plasma CK after catheterization and surgery, MB CK remained normal. After cardiac surgery, total CK increased from 68 +/- 18 to 905 +/- 231 IU/L, and MB CK increased from 1.7 +/- 0.6 to 13 +/- 7 IU/L. Thus, MB CK is specific for cardiac injury and would be a valuable adjunct in the diagnosis of myocarditis or in assessing interventions to minimize cardiac injury during surgery.
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PMID:Plasma creatine kinase isoenzyme determinations in infants and children. Characterization in normal patients and after cardiac catheterization and surgery. 739 87

Many infants who require cardiac surgery have cyanotic heart disease. We assessed the relative tolerances to ischemia of hearts from immature normoxemic rabbits versus hearts from immature rabbits subjected to hypoxemia since birth. Normoxemic animals were raised from birth in an environment where the inspired fractional concentration of oxygen (FIO2) was 0.21; for the hypoxemic studies FIO2 was reduced to 0.09. Hearts (n = 6/group) from normoxemic and chronically hypoxemic rabbits at 7-12, 21-28, 35-44, and 51-56 days of age underwent aerobic "working" perfusion with Krebs bicarbonate buffer, and cardiac function was measured. Hearts were then arrested by a 3-min infusion with either cold (14 degrees C) Krebs buffer (hypothermia alone group) or St. Thomas' Hospital II solution (hypothermia plus cardioplegia group) before 6 h of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic creatine kinase leakage and recovery of function were measured. For hearts protected with hypothermia alone, recovery of aortic flow was better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (78 +/- 7 vs. 60 +/- 6%, P < 0.05) and 21-28 days old (81 +/- 12 vs. 26 +/- 28%, P < 0.05). Protection with hypothermia plus cardioplegia was also better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (74 +/- 8 vs. 63 +/- 10%, P < 0.05) and 21-28 days old (84 +/- 3 vs. 71 +/- 5%, P < 0.05). Protection with hypothermia alone and hypothermia plus cardioplegia was no different within chronically hypoxemic age groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance of the developing heart to ischemia: impact of hypoxemia from birth. 790 Aug 70

Because many infants who require cardiac operation have cyanotic heart disease, we determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is optimal to protect the immature rabbit heart hypoxemic from birth during subsequent ischemia. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting chronically hypoxemic (PaO2 = 34 +/- 11 mmHg, SaO2 = 63% +/- 3%) versus normoxemic (PaO2 = 76 +/- 11 mmHg, SaO2 = 92% +/- 3%) immature hearts (7 to 12 days old) during ischemia. Hearts (n = 6 per group) underwent aerobic 'working' perfusion with Krebs bicarbonate buffer and cardiac function was measured. The hearts were then arrested with a 3 minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or modified St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile was observed for recovery of postischemic aortic flow but not for postischemic creatine kinase leakage, with improved protection occurring at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.4 mmol/L, which was significantly better than with hypothermia alone or standard St. Thomas' II solution. We conclude that the existing calcium concentration of St. Thomas' II solution is responsible, in part, for its inadequate protection of immature myocardium hypoxemic from birth during ischemia.
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PMID:Calcium and cardioplegic protection of the ischemic immature heart: impact of hypoxemia from birth. 794 63

Myocardial involvement is frequently present in Xp21-linked muscular dystrophy, due to a lack of dystrophin in cardiac fibres. We describe a 41-yr-old man affected by dilated cardiomyopathy with sporadic episodes of myoglobinuria induced by effort and increased levels of serum creatine kinase. Very mild signs of skeletal myopathy were clinically evident. His mother was affected by an indefinite cardiopathy and suddenly died when she was 36 yr old. Muscle biopsy of the patient showed a dystrophic process. Dystrophin analysis together with a genetic DMD locus study led us to diagnose Becker type muscular dystrophy, with truncated dystrophin and a gene deletion extending from exon 45 to 48. Prevalent cardiac involvement in a Becker type mutation of the dystrophin gene further confirms clinical variability of dystrophinopathies.
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PMID:Prevalent cardiac involvement in dystrophin Becker type mutation. 798 95

A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLC1) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial blood-samples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC1 assay was compared with total creatine kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD1), troponin T (TnT) and mitochondrial-aspartate aminotransferase (m-ASAT). The detection limit of HVMLC1 was 0.4 microgram/l (linear range 0-20 micrograms/l). Sera from 190 reference persons did not contain detectable levels of HVMLC1 (< 0.4 microgram/l; 99% percentile). The coefficients of variation were 13% (1.0 microgram/l) and 3.1% (17.7 micrograms/l). Cross-reactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 +/- 2.0, LD1 43.4 +/- 3.2, HVMLC1 72.9 +/- 7.0, and m-ASAT 67.3 +/- 5.6 h. Time-curves of HVMLC1 and m-ASAT were similar, whereas time-curves for HVMLC1 and TnT were quite different in most cases. Peak value of HVMLC1 was five times higher than CK peak value and eight times that of LD1. HVMLC1 appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLC1 in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLC1 assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLC1 and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
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PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43


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