Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stress-echocardiography represents a new non-invasive, alternative approach in the assessment of patients with coronary artery disease. By means of dynamic or pharmacological stress or by atrial pacing regional wall motion abnormalities can be induced, which can be identified by 2D-echocardiography. Beyond the indirect detection of ischemia this approach allows a better quantification of the amount of ischemia and of global LV function, which is advantageous compared to stress ECG recording or myocardial scintigraphy. Disadvantageous is however, the subjective reading of the echo itself. In experienced hands stress-echocardiography has proven to be as sensitive and specific as myocardial scintigraphy. Recently, in addition the diagnostic potential of myocardial cell injury has been improved by the detection of specific antibodies versus Troponin T. In comparison with conventional biochemical markers of myocardial cell necrosis Troponin T analysis has been proven to be superior in postoperative or traumatic cardiac damage or in the setting of acute myocardial infarction. In this situation the time window is improved by an earlier rise compared to CK and a longer detection rate compared to lactate dehydrogenase.
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PMID:[New diagnostic methods--ultrasound and clinico-chemical procedures in diagnosis of ischemia]. 815 50

Human heart fatty acid-binding protein (HH-FABP), which is a low molecular weight protein and abundant in the cytoplasm of myocardial cells, is reported to be released into the circulation shortly after the onset of acute myocardial damage. However, the changes in serum HH-FABP levels in open heart surgery have not been elucidated. To determine whether HH-FABP enables the earlier detection of myocardial damage caused by ischemia-reperfusion in open heart surgery, we measured the serial levels of serum HH-FABP, CK-MB and Troponin T (TnT) at every 15 min for 48 hours after reperfusion in 10 adult patients with coronary artery bypass graft. The serum HH-FABP levels reached the peak within 60 min after reperfusion (mean +/- SD; 49 +/- 7 min), and this was significantly (p < 0.001) earlier than CK-MB (212 +/- 108 min) and TnT (244 +/- 150 min). The peak value of serum HH-FABP had a significant correlation to the peak value of serum CK-MB or TnT (r = 0.815, p = 0.02; r = 0.925, p = 0.0001, respectively). These results indicate that serum HH-FABP enables the earlier detection of myocardial damage than the other markers in the patients with open heart surgery.
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PMID:[The earlier detection of myocardial damage in open heart surgery using serum human heart fatty acid-binding protein]. 875 83

It is still uncertain to what extent PTCA contributes to a rise of the myocardial ischemic marker troponin T. The purpose of this study was to determine the release of troponin T in patients with unstable and stable angina pectoris pre- and post-PTCA. Serial troponin T measurements were performed in 66 patients with unstable angina (group A) and 55 patients with stable angina pectoris (group B) pre-PTCA and 4, 8 and 24 hours post-PTCA. In group A, 39 (59%) patients with unstable angina pectoris showed pathologic troponin T concentrations (troponin T > or = 0.1 ng/ml); in 27 (41%) patients already pre-PTCA the troponin T was elevated beyond the normal values. Medians of troponin T rose from initially 0.045 ng/ml pre-PTCA to a maximum of 0.21 ng/ml 8 hours post PTCA. In group B medians of troponin T were at all times within normal limits; there was no rise in the observation interval. Using the Chi-square test there were statistically significant differences between group A and B regarding the troponin T values pre- and post-PTCA. In group A medians of total creatine kinase ranging between 24 U/L and 30 U/L were to all times within normal limits. Also in group B medians of total creatine kinase were always within normal limits. Statistically significant differences between the two groups could not be shown. Our study could show a difference in the periinterventional course of the ischemic marker troponin T in patients with unstable and stable angina pectoris. The data indicate a PTCA induced reversible ischemia of the cardiac muscle cell with additional release of the cytoplasmatic bound part of troponin T in patients with unstable angina pectoris. Troponin T also appears to be a more sensitive marker of very short myocardial ischemia than creatine kinase.
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PMID:[Release of troponin T following PTCA in patients with unstable and stable angina pectoris]. 1064 59

In this study we addressed the question of whether the measurement of cardiac Troponin T (cTnT) and cardiac Troponin I (cTnI) is able to detect myocardial cell damage in an ischemia-reperfusion model in pigs. To answer the question 3 pigs were anaesthesized and a cardiac arrest was induced by electric fibrillation. After 5 minutes of global ischemia the cardiac arrest was reversed by electric defibrillation until normal perfusion was restored. We could clearly demonstrate an increase of cTnT and cTnI 30 minutes after reperfusion indicating myocardial injury during ischemia and subsequent reperfusion. The cTnT as well as the cTnI serum levels increased till 180 minutes after reperfusion. This ischemia-reperfusion injury is likely induced by oxygen radicals generated during hypoxia and subsequent reperfusion We conclude from our first results that troponin measurements with commercial available test kits may also reflect myocardial cell damage in pigs as it was recently demonstrated in rats. Further studies are needed for correlation of troponin serum levels and histopathological damage in this model especially if it is used to test beneficial or toxicological effects of radical neutralizing drugs.
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PMID:Cardiac troponin I and cardiac troponin T increases in pigs during ischemia-reperfusion damage. 1096 91

Introduction and objectives. Troponin T (TnT) is a very specific marker of myocardial damage. Our objective was to describe TnT behavior after dobutamine stress echocardiography (EDOB) and evaluate its usefulness for improving the diagnostic power of EDOB.Methods. Blood levels of TnT were measured at baseline and 3, 6, 12, and 24 h after EDOB in 63 patients (mean age: 69 9; 38 males). Coronary angiography was performed on 36 patients.Results. EDOB was positive in 29 patients and there was an increase over baseline values in 15 of them (51%); EDOB was negative in 34 patients and there was only a rise in TnT in 7 (20%; p < 0.01). The TnT increment was higher in patients with a positive response to EDOB (0.033 0.02 vs. 0.026 0.01; p < 0.01). The ischemia score index was higher in patients in which a significant increase in TnT values was later detected (0.41 0.31 vs. 0.38 0.20; p < 0.01). Coronariography was performed in 36 patients. EDOB was positive in 22 of the 29 patients with coronary artery disease (76%) and TnT was raised in 14 of them (48%; p < 0.05).Conclusion. The rise in TnT levels during EDOB suggests that this test may produce myocardial damage associated with the appearance of contractility disorders during dobutamine infusion.
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PMID:[Dobutamine stress echocardiography and troponin T as a marker of myocardial injury]. 1201 25

Patients with renal insufficiency can have elevations of serum troponin without suspected clinical coronary ischemia. Although cardiovascular disease is the main cause of death in patients with renal failure, the process of elevation of serum troponin is not well known. Troponin T is more frequently elevated than troponin I in these patients which leads to uncertainty in the clinical interpretation of results. There are studies suggesting that troponin elevations are associated with a higher risk and increased mortality. To explain the process leading to troponin increases in this kind of pathology and to confirm its usefulness in the diagnosis, evolution and prognosis it would be necessary to carry out more clinical studies monitoring troponin and studying the stratification of risk.
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PMID:[Value of troponins in acute coronary syndrome in patients with renal failure]. 1553 31

Troponin T levels have been monitored in baboons (n = 8) undergoing pig heterotopic heart transplantation, and correlated with a decrease in graft contractions and graft survival. Pig heart graft survival was from 12 to 139 days (mean 45, median 33), and graft failure was associated with predominant thrombotic microangiopathy and ischemia, with focal hemorrhage, and edema. An increase in troponin T levels 5 to 6 days before graft failure correlated closely with diminished graft contractions. An increase in troponin T was a reliable indicator that graft dysfunction was occurring.
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PMID:Troponin T levels in baboons with pig heterotopic heart transplants. 1565 86

Considerable effort by clinicians and scientists focuses on the utility of biomarkers to prevent, diagnose and manage adverse cardiac events as well as provide information on a specific patient's underlying pathology. Although troponins I and T (TnI and TnT) are cardiac specific markers that yield diagnostic and prognostic value in patients with myocardial injury, troponins cannot be utilized in all clinical settings. Troponins have limited utility for the diagnosis of early ischemia and preoperative myocardial infarction. Troponin T also lacks specificity in patients with renal failure. New markers, such as ischemia modified albumin (IMA) and CD40 ligand, and new technologies, such as proteomics, are under investigation to advance our knowledge of heart disease.
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PMID:Laboratory diagnosis of acute myocardial injury. 1591 1

The term "acute coronary syndrome" encompasses a range of thrombotic coronary artery diseases, including unstable angina and both ST-segment elevation and non-ST-segment elevation myocardial infarction. Diagnosis requires an electrocardiogram and a careful review for signs and symptoms of cardiac ischemia. In acute coronary syndrome, common electrocardiographic abnormalities include T-wave tenting or inversion, ST-segment elevation or depression (including J-point elevation in multiple leads), and pathologic Q waves. Risk stratification allows appropriate referral of patients to a chest pain center or emergency department, where cardiac enzyme levels can be assessed. Most high-risk patients should be hospitalized. Intermediate-risk patients should undergo a structured evaluation, often in a chest pain unit. Many low-risk patients can be discharged with appropriate follow-up. Troponin T or I generally is the most sensitive determinant of acute coronary syndrome, although the MB isoenzyme of creatine kinase also is used. Early markers of acute ischemia include myoglobin and creatine kinase-MB subforms (or isoforms), when available. In the future, advanced diagnostic modalities, such as myocardial perfusion imaging, may have a role in reducing unnecessary hospitalizations.
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PMID:Diagnosis of acute coronary syndrome. 1704 41

We have previously found that uridine 5'-triphosphate (UTP) significantly reduced cardiomyocyte death induced by hypoxia via activating P2Y(2) receptors. To explore the effect of UTP following myocardial infarction (MI) in vivo we studied four groups: sham with or without LAD ligation, injected with UTP (0.44microg/kg i.v.) 30min before MI, and UTP injection (4.4microg/kg i.v.) 24h prior to MI. Left ventricular end diastolic area (LVEDA), end systolic area (LVESA) fractional shortening (FS), and changes in posterior wall (PW) thickness were performed by echocardiography before and 24h after MI. In addition, we measured different biochemical markers of damage and infarct size using Evans blue and TTC staining. The increase in LVEDA and LVESA of the treated animals was significantly smaller when compared to the MI rats (p<0.01). Concomitantly, FS was higher in groups pretreated with UTP 30min or 24h (56+/-14.3 and 36.7+/-8.2%, p<0.01, respectively). Ratio of infarct size to area at risk was smaller in the UTP pretreated hearts than MI rats (22.9+/-6.6, 23.1+/-9.1%, versus 45.4+/-7.6%, respectively, p<0.001). Troponin T and ATP measurements, demonstrated reduced myocardial damage. Using Rhod-2-AM loaded cardiomyocytes, we found that UTP reduced mitochondrial calcium levels following hypoxia. In conclusion, early or late UTP preconditioning is effective, demonstrating reduced infarct size and superior myocardial function. The resulting cardioprotection following UTP treatment post ischemia demonstrates a reduction in mitochondrial calcium overload, which can explain the beneficial effect of UTP.
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PMID:Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct. 1693 82


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