Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nowadays in many European heart centers the activation of the fibrinolytic system, always occurring during cardiopulmonary bypass, is routinely reduced by high-dose application of the proteinase inhibitor aprotinin (total of > 4 million KIU). In this study parameters of myocardial ischemic injury were investigated with the aim of identifying further benefits of aprotinin, particularly the protection of the myocardium during the ischemic period of aortic crossclamping. Forty patients with coronary artery disease who underwent aorta-coronary bypass grafting were randomly and in a double-blind fashion divided into two groups, one that received high-dose aprotinin therapy and one that received only saline solution. Markers such as troponin T, with high specificity for detection of myocardial ischemia and infarction, and markers with more general specificity such as creatine kinase, its isoenzyme, and lactate dehydrogenase showed significantly increased values after ischemia in both groups. In patients who received high-dose aprotinin therapy 3 days after cardiopulmonary bypass all parameters measured showed significantly lower levels compared with those in the control group. Therefore we can presume that the application of high-dose aprotinin provides myocardial protection from perioperative ischemic injury.
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PMID:Lower cardiac troponin T levels in patients undergoing cardiopulmonary bypass and receiving high-dose aprotinin therapy indicate reduction of perioperative myocardial damage. 753 74

Ischemia is known to produce damage to subcellular organelles, such as nuclei and mitochondria, in myocardial tissue. We tested the hypothesis that during myocardial ischemia various cytoskeletal and contractile proteins also undergo changes. We induced total global ischemia by incubation in buffer of tissue samples from six human left ventricles that were obtained from heart transplant recipients. Samples were removed from the incubation medium at different time intervals and investigated by immunohistochemistry using monoclonal antibodies against myosin, actin, tropomyosin, troponin T, myomesin, desmin, tubulin, and vinculin. The degree of ischemic injury was determined by electron microscopy. Ischemic cardiomyopathic human tissue showed disturbances of the localization pattern of myosin, actin, tropomyosin, and troponin T as early as 10 minutes after the onset of ischemia; this disruption was complete at 20 minutes. Tubulin also started changing at 10 minutes, but complete disruption was only evident after 120 minutes. Desmin and myomesin showed an intermediate response; changes began at 30 to 40 minutes, and disruption was complete at 90 to 120 minutes. Vinculin was most resistant to ischemia. Ultrastructurally, the tissue showed moderate reversible ischemic injury during the entire period of 180 minutes. Measuring the exposure time in seconds allowed quantitation of the intensity of the fluorescence. We reached the following conclusions: (1) Ischemia causes damage to the contractile proteins sooner than to the cytoskeleton and subcellular organelles. (2) Diseased human hearts are extremely susceptible to the effects of ischemia. These findings are important for the situation of induced cardiac arrest in heart operations and for preservation of donor hearts for transplantation.
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PMID:Ischemia induces early changes to cytoskeletal and contractile proteins in diseased human myocardium. 760 73

Cardiac troponin T (TnT) is a new serological marker for use as a diagnostic tool for myocardial damage. A blinded prospective multicentre study representing 298 patients who on admission were suspected of acute myocardial infarction (AMI) to the coronary care units of six Scandinavian hospitals was undertaken to assess the diagnostic performance and prognostic efficacy of a new cardiospecific TnT immunoassay. We used a discriminator value of TnT of 0.20 micrograms/l. One hundred and fifty-five patients (52%) had definite AMI, based on WHO criteria (all had peak S-TnT values > or = 0.20 micrograms/l); 127 patients (43%) had ischaemic heart disease (IHD) without AMI; and 16 patients (5%) had non-IHD (all had peak S-TnT values < 0.20 micrograms/l). The 127 IHD-patients without definite AMI could be subdivided into a group of 44 patients with S-TnT peak values > or = 0.20 micrograms/l, and a group of 83 patients with TnT below this level. A follow-up study was able to define the clinical significance of these findings. The cumulative six months probability of suffering cardiac death or AMI was significantly higher in the subgroup with increased TnT values (14% (6/44)) as compared to the other subgroup (4% (3/83)) (Log-rank test, p = 0.025). The probability of cardiac events was 15% for the patients with definite AMI. We conclude that increased troponin T in serum can detect a subgroup of IHD-patients in whom AMI has been ruled out, but who still have a prognosis as serious as that of patients with definite AMI.
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PMID:[Troponin T in acute myocardial infarction. Diagnosis and prognosis in patients admitted for suspected acute myocardial infarction]. 781 30

Cardiac troponin T (TnT) is a new serological marker for use as a diagnostic tool for myocardial damage. A blinded prospective multicentre study representing 298 patients suspected of having acute myocardial infarction (AMI), and admitted to the coronary care units of six Scandinavian Hospitals was undertaken to assess the diagnostic performance and prognostic efficacy of a new cardiospecific TnT immunoassay. We used a discriminator TnT value of 0.20 microgram l-1. One hundred and fifty five patients (52%) had definite AMI, based on WHO criteria (all had peak S-TnT values of > or = 0.20 micrograms l-1); 127 patients (43%) had ischaemic heart disease (IHD) without AMI; and 16 patients (5%) had non-IHD (all had peak S-TnT values of < 0.20 microgram l-1). The 127 IHD-patients without definite AMI could be subdivided into a group of 44 patients with S-TnT peak values of > or = 0.20 microgram l-1, and a group of 83 patients with TnT below this level. An equal identification of these patients among the centres was seen (mean +/- SD 35 +/- 13%; range 20-55%). A follow-up study was able to define the clinical significance of these findings. The cumulative 6 months probability of suffering cardiac death or AMI was significantly higher in the subgroup with increased TnT values (14% (6/44)) as compared to the other subgroup (4% (3/83)) (Log-rank test, p = 0.025). The probability of cardiac events was 15% for the patients with definite AMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnostic performance and prognostic value of serum troponin T in suspected acute myocardial infarction. 827 56

The time-related frequency of elevated results for the mass concentrations of the MB isoenzyme of creatine kinase and of troponin T were compared with that of creatine kinase and creatine kinase-MB activity in patients with acute myocardial infarction. Patients (322; 175 with and 147 without myocardial infarction) consecutively admitted for evaluation of possible acute myocardial infarction were investigated. Reference limits for troponin T (0.1 microgram/l) and creatine kinase-MB mass concentration (5.0 micrograms/l) were exceeded frequently in patients with unstable angina pectoris (troponin T 43%, creatine kinase-MB mass concentration 24%) in contrast to patients with no acute ischaemic heart disease (both < 5%). Within 4 and between 4-8 hours after onset of chest pain, the frequency of elevated results for creatine kinase-MB mass concentration and troponin T in patients with acute myocardial infarction was considerably higher (20-30%) than for creatine kinase and creatine kinase-MB activity. Creatine kinase-MB mass concentration and troponin T both allowed earlier diagnosis of acute myocardial infarction than creatine kinase and creatine kinase-MB activity, but troponin T was not elevated before the creatine kinase-MB mass concentration.
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PMID:The mass concentrations of serum troponin T and creatine kinase-MB are elevated before creatine kinase and creatine kinase-MB activities in acute myocardial infarction. 830 15

The purpose of this study was to evaluate cardiac troponin T (TnT) in the diagnosis of minor perioperative myocardial tissue damage and small myocardial infarctions during aortocoronary bypass surgery. In 15 patients without enzymatic or electrocardiographic signs of perioperative myocardial ischemia (group 1, uncomplicated bypass surgery), TnT did not exceed 3.55 micrograms/L. In 3 patients with perioperative non-Q-wave infarctions (group 2), TnT was significantly higher than in group 1 patients. In all 3 patients, TnT peak concentrations exceeded 3.5 micrograms/L. Thirteen patients (group 3, borderline cases) showed either signs of perioperative myocardial ischemia by creatine kinase isoenzyme MB (CKMB) activity levels (CKMB > 20 U/L on the first postoperative day, 3 patients) or by electrocardiography (new ST-T segment alterations, 10 patients). TnT concentrations were comparable to group 1 patients and indicated uncomplicated bypass surgery in all 3 patients with solely elevated CKMB activities. On the other hand, TnT concentrations in 3 patients with electrocardiographic signs of perioperative myocardial ischemia were significantly higher than in uncomplicated patients (group 1) with peak values exceeding 3.5 micrograms/L. Thus, TnT indicated perioperative non-Q-wave infarctions not detected by CKMB activity in these 3 patients. These results are in accordance with findings in nonsurgical patients. They suggest a higher sensitivity and specificity of cardiac TnT compared to CKMB activity in the diagnosis of small perioperative myocardial infarctions after bypass surgery.
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PMID:Cardiac troponin T: a new marker of myocardial tissue damage in bypass surgery. 757 27

The new and sensitive serum markers S-troponin T and S-CK MB (mass) can detect minor myocardial damage (MMD) in patients after an episode of acute myocardial ischemia even when accepted criteria for a myocardial infarction are not fulfilled. High-risk MMD patients constitute about one-third of unstable angina pectoris cases. Since 1989 we have compared S-troponin T and S-CK MB (mass concentration) with catalytic S-CK and S-CK MB determinations in several studies comprising more than 600 patients. We conclude that the combination of the two most cardiospecific and sensitive markers, S-troponin T + S-CK MB (mass), is highly informative in studies and evaluations. If only one marker can be routinely used, S-troponin T may replace current tests. Rational utilization of S-troponin T and S-CK MB (mass) requires an adequate number of determinations within the respective diagnostic time windows using a sampling time schedule relating to time of onset pain in each patient. Individual reference values of each marker may easily be obtained by taking baseline samples in a stable phase, e.g. during convalescence. The data are best understood when they are presented as time series in graphic laboratory reports. The relative increases of the myocardial markers are three to five-fold higher when they are plotted relative to the individual baseline value of each patient than when they are plotted against the respective, general discriminator values for infarction.
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PMID:Rational diagnostic strategy in diagnosis of ischemic myocardial injury. S-troponin T and S-CK MB (mass) time series using individual baseline values. 832 51

The diagnostic performance of a new enzyme linked immunosorbent assay for the cardiac structural protein troponin T in the differential diagnosis of ischaemic cardiac damage was assessed. A well documented set of patients admitted to the coronary care unit of a district general hospital were studied. At a cutoff value of 0.2 micrograms/L, troponin T measurements 12-24 h after admission or 12-16 to 24-48 h from onset of chest pain showed an overall efficiency of 97.6% for diagnosis of proven myocardial infarction. Troponin T was not detectable in patients when ischaemic heart disease could be excluded but was present in four patients with angina. Detectable troponin T in these angina patients was associated with subsequent cardiac events.
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PMID:Troponin T for the differential diagnosis of ischaemic myocardial damage. 843 60

A 22-year-old man developed transient unconsciousness during running. He developed fever, nausea, vomiting, diarrhea and general fatigue. Next day, he was admitted to National Hospital Nayoro because of high serum CK level of 13,610U/l. Biochemical analyses revealed elevated serum myoglobin, increased CK-MM isozyme, aldolase and lactate dehydrogenase, increased serum osmolality, increased uric acid, and decreased serum potassium levels. Therefore, he was diagnosed as having rhabdomyolysis. In addition, serum CK-MB isozyme, cardiac myosin light chain I and troponin T were increased, suggesting the damage of cardiac muscle. Electrocardiogram showed elevated ST segment and inverted T on V2-4, which were not observed previously. He had no preceding infectious disease, drug ingestion or an underlying metabolic disorder. The rhabdomyolysis may be precipitated by the superimposition of dehydration and loss of potassium due to diarrhea and vomiting. The myocardial injury, probably produced by transient myocardial ischemia, should be paid attention in case of rhabdomyolysis.
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PMID:[A case of rhabdomyolysis complicated with myocardial injury]. 856 47

The functional significance of the developmental transition from slow skeletal troponin I (ssTnI) to cardiac TnI (cTnI) isoform expression in cardiac myocytes remains unclear. We show here the effects of adenovirus-mediated ssTnI gene transfer on myofilament structure and function in adult cardiac myocytes in primary culture. Gene transfer resulted in the rapid, uniform, and nearly complete replacement of endogenous cTnI with the ssTnI isoform with no detected changes in sarcomeric ultrastructure, or in the isoforms and stoichiometry of other myofilament proteins compared with control myocytes over 7 days in primary culture. In functional studies on permeabilized single cardiac myocytes, the threshold for Ca2+-activated contraction was significantly lowered in adult cardiac myocytes expressing ssTnI relative to control values. The tension-Ca2+ relationship was unchanged from controls in primary cultures of cardiac myocytes treated with adenovirus containing the adult cardiac troponin T (TnT) or cTnI cDNAs. These results indicate that changes in Ca2+ activation of tension in ssTnI-expressing cardiac myocytes were isoform-specific, and not due to nonspecific functional changes resulting from overexpression of a myofilament protein. Further, Ca2+-activated tension development was enhanced in cardiac myocytes expressing ssTnI compared with control values under conditions mimicking the acidosis found during myocardial ischemia. These results show that ssTnI enhances contractile sensitivity to Ca2+ activation under physiological and acidic pH conditions in adult rat cardiac myocytes, and demonstrate the utility of adenovirus vectors for rapid and efficient genetic modification of the cardiac myofilament for structure/function studies in cardiac myocytes.
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PMID:Slow skeletal troponin I gene transfer, expression, and myofilament incorporation enhances adult cardiac myocyte contractile function. 914 57


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