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)

Risk stratification of patients with acute coronary syndromes (ACS) is pivotal for correct allocation of health resources and for maximizing the benefit of available treatment modalities. However, clinical and electrocardiographic indicators of high risk lack sufficient sensitivity for the detection of major cardiac events. The complementary information provided by the measurement of different biomarkers is believed to be very useful. Specifically, elevations of cardiac troponin I (cTnI) and T (cTnT) are strongly associated with a high-risk profile both at short- and long-term. This has been definitely demonstrated in many studies as well as in cumulative meta-analysis. The role of different biomarkers, such as those reflecting activation of hemostasis and the presence of inflammation, is however less defined. At the moment, no study has prospectively evaluated these biomarkers in the whole spectrum of unselected patients with ACS. It is also unclear whether these biomarkers add independent prognostic value to the clinical and electrocardiographic indicators of adverse outcome and whether they offer additional information when compared to each other. The Early Prognostic Value of Biochemical Markers of Myocardial Damage, Activation of Hemostatic Mechanism and Inflammation in Acute Ischemic Syndromes (EMAI) study has been prospectively designed to solve these issues. In this study, we have evaluated the prognostic value of cTnI and cTnT, D-dimer, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT) and C-reactive protein (CRP) in patients with ACS at the time of admission. We have enrolled in 31 Italian Coronary Care Units 1971 patients with rest anginal pain within 12 h from admission and electrocardiographic evidence of myocardial ischemia. Of these, 730 patients resulted to have ST-segment elevation myocardial infarction eligible for a reperfusion strategy and 1241, an acute coronary syndrome without persisting ST-segment elevation. Primary outcome measure of the study is the composite of death and non-fatal MI within 30 days from admission, which has occurred in 8.9% of the study population.
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PMID:Cardiac markers and risk stratification: an integrated approach. 1155 47

Cardiac disease is the major cause of death in patients with end-stage renal disease (ESRD), accounting for about 45% of all deaths. In dialysis patients about 20% of cardiac deaths are attributed to acute myocardial infarction (AMI). The survival of dialysis patients after AMI is poor, with nearly three-quarters of patients dead at 2 years after AMI. The definition of AMI is based on symptoms, electrocardiography, and cardiac biomarkers. In the non-ESRD population, it has been recognized that sensitive markers of myocardial injury (cardiac troponin I and troponin T) define a group of patients who are increased risk for adverse cardiac outcomes and who are more likely to benefit from treatment. Elevated cardiac troponin levels in nonhospitalized ESRD patients without other evidence of ongoing myocardial ischemia may also prospectively identify a subgroup of ESRD patients at increased risk for death. This editorial is an overview of cardiac biomarkers (specifically troponin I and troponin T) in the management of acute coronary syndromes in ESRD patients. A potential role of cardiac troponin testing for risk stratification in the outpatient dialysis unit is also presented.
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PMID:Cardiac biomarkers in the new millennium. 1167 96

An elevated cardiac troponin I (cTnI) and a positive dobutamine echocardiography are powerful predictors for future cardiac events in patients with coronary artery disease. Investigating their correlation also should be helpful in understanding their clinical usefulness in evaluating patients with acute coronary syndromes (ACS). Dobutamine echocardiography and a blood sampling for cTnI were performed on 117 patients with ACS 70 +/- 2 hours after arriving at the hospital. CTnI was considered elevated when its value was greater than 2.0 ng/ml. Dobutamine echocardiography was positive in 86 (73.5%) patients, and cTnI was elevated in 37 (31.6%). The occurrence of positive dobutamine echocardiography in patients with elevated cTnI was significantly higher than in those with normal cTnI (86.5% vs. 67.5%, P = 0.042). More patients in the elevated cTnI group developed myocardial ischemia before or at the stage of dobutamine 20 microg/kg/min (43.2% vs. 15%, P = 0.002). When compared with patients with normal cTnI, patients with elevated cTnI had a lower ischemic threshold during dobutamine echocardiography, and more frequently had baseline echocardiographic wall-motion abnormalities, a history of myocardial infarction, and a positive dobutamine echocardiography. Using multivariate analysis, we found that only a lower dobutamine echocardiography ischemic threshold (P = 0.0008) and baseline wall-motion abnormalities (P = 0.0004) were associated independently with the elevation of cTnI. Our results suggest that in patients with ACS, dobutamine echocardiography can offer information regarding wall-motion abnormalities and ischemic threshold, which are suggested to have a clinical value similar to elevated cTnI.
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PMID:Relationship between dobutamine echocardiography and the elevation of cardiac troponin I in patients with acute coronary syndromes. 1173 66

To evaluate the sensitivity of the serum cardiac troponin I level in detecting stress test-induced myocardial ischemia, the authors conducted a prospective study including patients admitted for chest pain to the telemetry floor of Our Lady of Mercy Medical Center at Bronx, NY. Consecutive 134 telemetry patients that agreed to participate in this study were included. All of these patients had a nuclear stress test and were divided into various groups based on the prestress test probability of having coronary artery disease. To assess serum cardiac troponin I levels, blood samples were drawn before and after stress testing and compared with the stress test results. Overall, 30 patients (22%) had reversible perfusion defects on stress images, and none (0%) had increased serum cardiac troponin I levels. One patient of 18 patients (6%) in group C with negative stress test results had an elevated serum cardiac troponin I level after the stress test, but none of group A or group B patients had elevated troponin I levels. These data show that serum cardiac troponin I levels do not increase with stress test-induced myocardial ischemia.
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PMID:Does the serum cardiac troponin I level increase with stress test-induced myocardial ischemia? 1214 81

Human albumin has the ability to bind cobalt at the N-terminus. The exposure of circulating albumin to ischemic tissue alters the ability of albumin to bind cobalt, probably through a mechanism involving free-radical production. The Albumin Cobalt Binding (ACB) test measures the alteration in albumin metal binding, and elevation of the ACB test is thought to be an early indicator of myocardial ischemia. In a previous multicenter study of chest pain patients presenting to the emergency department (ED), this test demonstrated high negative predictive value and sensitivity in the sample collected at presentation for predicting cardiac troponin I (cTnI)-negative or cTnI-positive results 6-24 h later. Since the completion of that report, the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) have redefined the criteria for the diagnosis of acute myocardial infarction (AMI). The data from the multicenter ACB study were re-examined using the new diagnostic criteria for AMI to determine if combining the ACB test with troponin improved the sensitivity of either assay used alone for early diagnosis of AMI. Assay values were compared to either the final discharge diagnosis made at each site or to a diagnosis of AMI using the strict application of the ESC/ACC guidelines. Using the criterion of physician's discharge diagnosis and using blood collected at ED presentation, the cTnI test alone had a sensitivity of 23.9%, and the ACB test alone had a sensitivity of 39.1%, but the sensitivity significantly increased to 55.9% (p < 0.001 over cTnI alone) when both tests were used in combination. The sensitivity of the combination of ACB and cTnI tests at the 1- to 6-h time-point was 86.7% and at the >6- to 12-h time-point was 93.5%, but they were not significantly improved over the cTnI test alone. In conclusion, using the new ESC/ACC criteria, the combination also resulted in a statistically significant higher diagnostic sensitivity on blood collected at presentation. These data indicate a possible role of the ACB test in the early triage of patients with chest pain.
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PMID:Analysis of the Albumin Cobalt Binding (ACB) test as an adjunct to cardiac troponin I for the early detection of acute myocardial infarction. 1221 87

The pericardial fluid was examined in 26 patients without morphological signs of severe damage to cardiac histiocytes, who died unexpectedly from ischemic heart disease (IHD)--main group. The control group comprised 26 persons, who died from other (not heart diseases-asphyxia, acute blood loss, crania-cerebral trauma). The mean age of the died was 57.4 +/- 1.5 years in the main group and 51.8 +/- 2.7 years in the control group. Cardiac markers were examined in the pericardial fluid of the died in both groups, i.e. the activity of aspartate aminotransferase (AsAT), of creatine kinase (CK), of isoenzyme KK-MB, of lactate dehydrogenase (LDG), and its isoenzyme spectrum, and, finally, the content of the cardiac troponin I (cTnI). The statistically reliable differences were found between the two groups according to the activity of AsAT, LDG, its isoenzyme spectrum and the cTnI content. Isoenzymes LDG1 and LDG2 constituted up to 60% of the LDG activity in the pericardial fluid of those who unexpectedly died from IHD. As for the control group, the LDG activity was virtually evenly distributed between all isoenzymes. No differences were found in the activity of CK and isoenzyme KK-MB between the main and control groups. Thus, the obtained data are indicative of the "cardiac" origin of enzymes in the pericardial fluid. Finally, a number of assumptions were put forward on mechanisms of hyper-fermentation in the ischemic damage of the cardiac muscle.
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PMID:[Cardiac markers in the pericardial fluid in sudden coronary death]. 1282 98

Troponins are highly sensitive and specific biochemical markers of myocardial injury that are released into the circulation during myocardial ischemia. We describe changes in cardiac troponin I (cTnI) prior to and following clinical evidence of severe myocardial dysfunction in a child with hemolytic uremic syndrome (HUS). A previously healthy, 22-month-old girl presented with typical HUS and stool cultures positive for Escherichia coli O157:H7. She required dialysis, blood and platelet transfusions, and insulin for HUS-related diabetes mellitus. On the 6th hospital day she had sudden circulatory collapse with a blood pressure of 70/40 mmHg and an oxygen saturation of 88%. She responded rapidly to emergency resuscitation but had diminished left ventricular function (ejection fraction 18%). Four days after the acute event an echocardiogram showed normal ventricular size and contractility. She underwent hemodialysis for 22 days, and renal function was normal after 33 days. cTnI levels were measured with a microparticle enzyme immunoassay. cTnI was normal (>0.4 microg/l) 32 h prior to cardiac collapse, mildly increased (2.1 microg/l) 8 h before the cardiac collapse, severely elevated shortly after the cardiac event (43.1 microg/l), and peaked (140.6 microg/l) at 24 h. It then fell gradually and was normal at discharge. These results suggest that measurement of cTnI may be a useful predictor of cardiac involvement in severely affected children with HUS.
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PMID:Troponin I levels in a hemolytic uremic syndrome patient with severe cardiac failure. 1468 41

Pericardial fluid reflect the composition of cardiac interstitium in myocardial ischemia. This study investigated the value of the pericardial and serum myoglobin (MG) measurements for the diagnosis of perioperative myocardial infarction (MI) after coronary artery bypass grafting (CABG). Postoperative arterial and pericardial blood samples were taken in 64 subjects undergoing elective CABG allocated to two groups according to the 12-lead electrocardiogram (ECG) abnormalities observed during the first postoperative 24h. Group 1=normal and nonspecific ECG abnormalities, and Group 2=perioperative Q-wave MI. The occurrence of perioperative MI was associated with a dramatic increase in both serum and pericardial cardiac troponin I (CTnI) and MG concentrations. Pericardial concentrations were higher than serum concentrations during the first postoperative 24h in all subject. However, pericardial/serum CTnI ratio in subjects in Group 2 was not statistically different from Group 1 at the time of admission to the intensive care unit (ICU) and did not significantly change at time intervals. On the other hand, more than two-fold increase in the pericardial/serum MG ratio was determined for all patients who experienced perioperative Q-wave MI with the lowest value as 2.75, whereas only 1 of 59 patients in group 1 had the ratio higher than 2 with the highest value as 2.15 at the time of admission to the ICU. In conclusion, determination of pericardial/serum MG ratio may be a useful tool for the early diagnosis of the perioperative MI after CABG.
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PMID:Determination of the pericardial to serum myoglobin ratio for the early diagnosis of perioperative myocardial infarction after coronary artery bypass grafting. 1522 66

A 74-year-old man was admitted for chest infection with acute exacerbation of chronic obstructive pulmonary disease. He was incidentally found to have an increased serum level of cardiac troponin I, despite the absence of symptoms and electrocardiographic evidence of ischaemic heart disease. Troponin I became undetectable after the serum was treated with polyethylene glycol, which removed any interfering antibodies. Serum cardiac troponin T was also undetectable after this treatment. Interference of the cardiac troponin I assay by heterophilic antibodies was thus confirmed. Because of the possibility of false-positive results due to immunoassay interference, clinicians should be alerted whenever laboratory findings are incompatible with the clinical picture, and should be ready to perform additional laboratory tests.
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PMID:A patient with an increased troponin level without evidence of ischaemic cardiac injury. 1529 74

All novel markers of myocardial ischemia (ischemia-modified albumin, choline, unbound free fatty acids) lack cardiac specificity. Therefore, for the specific detection of myocardial ischemia selective blood sampling from an inserted coronary sinus catheter is needed, which limits the applicability of these markers in most clinical routine settings. In addition, the superiority of these novel markers over the calculation of myocardial lactate production, the current criterion standard for the laboratory diagnosis of myocardial ischemia, has not been demonstrated so far, and even comparative data is frequently lacking. Further the superiority of these new candidate markers over lactate determination for the diagnosis of myocardial ischemia in peripherally drawn blood samples has not been demonstrated either, and these novel parameters appear not to be a breakthrough for laboratory diagnosis of myocardial ischemia during or after percutaneous coronary interventions or coronary artery bypass grafting. The determination of cardiac troponin I or troponin T is the current criterion standard for the laboratory diagnosis of myocardial damage due to their higher sensitivities and specificities compared to creatine kinase isoenzyme MB. According to current knowledge, troponin increases in peripherally drawn blood samples must be regarded as an indicator of myocardial necrosis which, however, may be limited, only detectable by troponin and may be missed by creatine kinase isoenzyme MB determination. After on-pump coronary artery bypass grafting the generally applied troponin discriminator limits are not valid as there is limited, inevitable cardiac tissue damage occurring during the surgical procedure. Therefore, troponins are significantly increased after reperfusion of the arrested heart over values seen before bypass and also in patients without complications. Perioperative myocardial infarctions can be reliably identified by their characteristic troponin time courses, and both peak concentrations and time of peak values are diagnostic criteria. Troponin release is lower in off-pump compared to on-pump bypass surgery. Despite the controversy over the significance of troponin elevations after clinically uncomplicated and successful procedures, it is tempting to postulate that less myocardial damage as detected by troponin release is beneficial for the patient. After elective percutaneous coronary interventions, only troponin increases >8-fold the upper reference limit were associated with increased mortality in long-term follow-up.
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PMID:Markers for perioperative myocardial ischemia: what both interventional cardiologists and cardiac surgeons need to know. 1609 33


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