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)

Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.
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PMID:Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I. 801 1

Recent reports have demonstrated the presence of two isoforms of troponin I in the human fetal heart, namely, cardiac troponin I and slow skeletal muscle troponin I. Structural and physiological considerations indicate that these isoforms would confer differing contractile properties on the myocardium, particularly on the phosphorylation-mediated regulation of contractility by adrenergic agonists. We have investigated the developmental expression of these isoforms in the human heart from 9 weeks of gestation to 9 months of postnatal life, using Western blots revealed with troponin I antibodies to detect troponin protein isoforms and Northern blots to detect the corresponding mRNAs. The results show the following: 1) Slow skeletal muscle troponin I is the predominant isoform throughout fetal life. 2) After birth, the slow skeletal isoform is lost, with cardiac troponin I being the only isoform detectable by 9 months of postnatal development. 3) The protein isoforms and their corresponding mRNAs follow the same pattern of accumulation, suggesting that the transition in troponin expression is regulated at the level of gene transcription. The developmental transition in troponin I isoform content has implications for contractility of the fetal and postnatal myocardium. We further analyzed right and left ventricular muscle samples from 17 hearts in end-stage heart failure resulting from pulmonary hypertension, ischemic heart disease, or dilated cardiomyopathy. Cardiac troponin I mRNA remained abundant in each case, and slow skeletal muscle troponin I mRNA was not detectable in any of sample. We conclude that alterations in troponin I isoform content do not therefore contribute to the altered contractile characteristics of the adult failing ventricle.
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PMID:Troponin I gene expression during human cardiac development and in end-stage heart failure. 847 26

Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.
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PMID:Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle. 1070 39

We evaluated whether recent cocaine use alters the specificity of CK-MB, myoglobin, and cardiac troponin I for acute myocardial infarction (AMI) in patients who are seen in the emergency department for chest pain. Patients <60 years old with potential myocardial ischemia underwent a standardized history and physical examination and routine CK-MB assays every 8 to 12 hours and had study serum obtained at presentation for CK-MB, myoglobin, and cardiac troponin I immunoassays, as well as benzoylecgonine, cocaine's main metabolite. We enrolled 97 patients, 19 (20%) of whom had recent used cocaine. Patients with and without cocaine use were similar with regards to sex, race, renal and muscular disease, diabetes, family history, and hypertension and rate of AMI (12% vs 11%, p = 1.0). In patients without MI, the mean myoglobin level was higher in cocaine users than noncocaine users (179 vs 74 ng/ml; Mann-Whitney p = 0.003), but the mean values were similar for CK-MB (2.2 vs 2.1 ng/ml; Mann-Whitney p = 0.58) and for cardiac troponin-I (0.02 vs 0.02 ng/ml; Mann-Whitney p = 0.87). The specificities of the markers in patients with and without cocaine use were as follows: cardiac troponin I, 94% vs 94%, (p = 1.0); CK-MB, 75% vs 88% (p = 0.24); and myoglobin, 50% vs 82%, (p = 0.02), respectively. Our data demonstrate that the specificity of myoglobin was altered by recent cocaine use. The specificity of CK-MB was affected less and the specificity of cardiac troponin I was not affected by recent cocaine use.
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PMID:Effect of recent cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. 948 72

A prospective single center study was performed to determine the minimal preoperative incidence of unrecognized cardiac injury in patients suffering aneurysmal and presumed aneurysmal subarachnoid hemorrhage (SAH). When caring for such patients in the pre- and post operative period clinicians must be aware of the possibility of cardiac injury even when a history of previous cardiac symptomatology is not present. Forty-seven consecutive patients suffering from SAH over a five-month period underwent serum measurements of the cardiac muscle marker troponin I (cTnI) immediately upon admission. Repeat studies, if possible, were done 24 hours later. EKG was performed in all patients and was available for review in 44 of the 47 cases. Echocardiography was performed in four of eight patients with elevated cTnI levels. Signs and symptoms relating to cardiac ischemia were recorded by the patients' physicians and nurses. Eight individuals (17%) had elevations in cardiac troponin I levels. Because surgical treatment is generally carried out as soon as possible following the hemorrhage, many patients with normal troponin I levels within twenty-four hours of their hemorrhage were operated upon before a repeat enzyme could be obtained or possibly before elevations could be recorded. In addition, a number of patients were referred to our center several days post-hemorrhage at a time when marker levels may have normalized. Therefore, the 17% incidence of elevated cTnI may be an underestimate. Only two of the eight patients had clinical abnormalities in cardiac function. Four patients with elevated levels had echocardiograms, three of which were abnormal. One additional patient died of a myocardial infarction before an echocardiogram could be obtained. EKG was abnormal in six of the seven patients with elevated troponin who had tracings available for review. Recordings consistent with recent myocardial ischemia were present in four of these. Of the 39 patients with negative troponin I levels, 37 had EKG available for review. None had recordings clearly consistent with recent myocardial ischemia although 13 were suggestive of ischemic changes. None of these 39 patients had pre- or post-operative clinical changes in cardiac function. Elevations in troponin I appeared to be unrelated to the patient's Hunt and Hess grade or Fisher score although our numbers were too small to draw any meaningful conclusions.
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PMID:The use of cardiac troponin-I (cTnI) to determine the incidence of myocardial ischemia and injury in patients with aneurysmal and presumed aneurysmal subarachnoid hemorrhage. 952 14

To study the comparative value of the levels of cardiac troponin I (cTnI), creatine kinase-MB isoenzyme (CK-MB), and myoglobin in the detection of acute ischemic myocardial injury, we serially measured plasma concentrations of these cardiac proteins in 12 pigs with myocardial ischemia subtending severe coronary artery stenoses and in 5 pigs with a sham operation performed, but without coronary artery stenosis. In the stenosis group, flow in the left anterior descending (LAD) artery was reduced by 36% and maintained for 24 hours (n = 3), 7 days (n = 6), or 4 weeks (n = 3). Flow in the coronary artery was measured by a flowmeter, and regional left ventricular dysfunction was monitored by echocardiography. Myocardial infarction was identified with triphenyltetrazolium chloride staining. All pigs with stenosis of the LAD had significant ultrastructural abnormalities consisting of loss of myofibrils and an increase in mitochondria and glycogen deposition. Cardiac proteins were released in all pigs with stenosis of the LAD artery during the development of myocardial ischemia; the levels of cTnI, CK-MB, and myoglobin increased significantly relative to the baseline. The sensitivity and specificity for cTnI were higher than for CK-MB or myoglobin. Results of this study show that cTnI is the better marker for the detection of acute ischemic myocardial injury. Increased levels of cTnI can be found in reversible and irreversible myocardial ischemic injury in this model.
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PMID:Comparison of cardiac troponin I, creatine kinase-MB, and myoglobin for detection of acute ischemic myocardial injury in a swine model. 966 24

Sudden cardiac death due to lethal arrhythmia may be the initial presenting symptom of ischemic heart disease. In many cases, in the absence of trauma, a majority of these deaths will be visually inspected by a medical examiner and released with death being ascribed to atherosclerotic cardiovascular disease, coronary artery disease, arrhythmia, myocardial infarction, or a similar diagnosis. When an autopsy is performed, there may be significant cardiovascular disease but no gross or histologic evidence of an acute myocardial infarct unless the patient survived for several hours following the event. Biochemical assays of creatine kinase MB fraction (CKMB) performed on serum have been used to document myocardial injury in the absence of morphologic changes. Newly developed assays for cardiac troponin I (cTnI) may detect myocardial injury with a greater sensitivity than CKMB. A prospective study was performed on 28 autopsied patients at the Office of the Chief Medical Examiner of the state of Maryland. Subclavian blood was sampled for subsequent analysis of serum CKMB and cTnI. In 3 cases of cardiac-related death, there was insufficient plasma for analysis of both CKMB and cTnI, and only CKMB was quantitated. In 12 cases, hemolysis rendered interpretation questionable. Of the remaining 16 cases, the mean serum CKMB level was 857.9 ng/ml (n = 7) and the cTnI level was 93.4 ng/ml (n = 4) for cardiac-related deaths, compared with mean CKMB levels of 116.4 ng/ml (n = 9) and mean cTnI levels of 16.6 ng/ml (n = 9) for non-cardiac-related deaths. The differences in serum elevation of both CKMB and cTnI noted between the cardiac- and non-cardiac-related deaths were statistically significant. Serum cTnI concentrations >40 ng/ml were only noted in cardiac-related deaths. These data suggest that an elevated postmortem serum concentration of cTnI reflects ischemic heart disease and supports its use in determining cause of death. Quantitation of this analyte may prove useful when death may be due to an arrhythmia following a morphologically undetectable microinfarct.
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PMID:Serum concentrations of cardiac troponin I in sudden death: a pilot study. 988 25

Despite advances in diagnosis and management, ischemic heart disease remains the leading cause of death in the USA. Serum cardiac enzymes, one of the three fundamental criteria for establishing the diagnosis of myocardial infarction, are not specific for cardiac muscle and have a narrow time-window. The recent development of monoclonal antibodies to cardiac troponin I and troponin T has resulted in cardiac-specific assays. Several published studies have documented the utility of troponin proteins in the evaluation of myocardial necrosis. A brief overview of the characteristics and clinical utility of troponin T and I is presented here.
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PMID:Acute coronary ischemia: troponin I and T. 1061 30

Cardiomyopathy is a multifactorial disease, and the dystrophin-glycoprotein complex has been implicated in the pathogenesis of both hereditary and acquired forms of the disease. Using mouse models of cardiomyopathy made by ablating genes for components of the sarcoglycan complex, we show that long-term treatment with verapamil, a calcium channel blocker with vasodilator properties, can alleviate the severe cardiomyopathic phenotype, restoring normal serum levels for cardiac troponin I and normal cardiac muscle morphology. Interruption of verapamil treatment leads again to vascular dysfunction and acute myocardial necrosis, indicating that predilection for cardiomyopathy is a continuing process. In contrast, verapamil did not prevent cardiac muscle pathology in dystrophin-deficient mdx mice, which neither show a disruption of the sarcoglycan complex in vascular smooth muscle nor vascular dysfunction. Hence, our data strongly suggest that pharmacological intervention with verapamil merits investigation as a potential therapeutic option not only for patients with sarcoglycan mutations, but also for patients with idiopathic cardiomyopathy associated with myocardial ischemia not related to atherosclerotic coronary artery disease.
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PMID:Prevention of cardiomyopathy in mouse models lacking the smooth muscle sarcoglycan-sarcospan complex. 1116 Jan 28

An analytical and clinical evaluation of cardiac troponin I (cTnI) on the IMMULITE system is presented. The assay results were compared with those of the Stratus II and the Dimension RxL-HM. A between-run imprecision CV < 20% was found at a cTnI concentration of 0.23 microg/L (functional limit of detection). On the basis of a reference study including 215 patients without ischemic heart disease (97.5th percentile: 0.294 microg/L) and 36 patients clinically classified as having stable angina pectoris (<0.22 microg/L) a preliminary cutoff level of 0.3 microg/L was defined. Assay linearity, sample stability, influence of sample material and method comparison studies were performed. In patients with Duchenne's disease, chronic hemodialysis treatment, pulmonary embolism, coronary artery bypass surgery and minimally cardiac surgery the cTnI results of the IMMULITE agreed better with the Dimension RxL-HM than with the Stratus II data. Of 142 samples from patients with unstable angina 67 samples were classified as cTnI positive with the IMMULITE, 76 with the Dimension RxL-HM, and 62 with the Stratus II. In conclusion, the new assay is sensitive for the determination of cTnI and easy to perform within 45 min.
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PMID:Comparison of diagnostic performance of cardiac troponin I on the IMMULITE system with other automated troponin I assays in minor myocardial damage. 1138 9


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