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)

21-Aminosteroids (Lazaroids), acting as free radical scavengers and as membrane stabilizers, proved to have beneficial effects in various pathological conditions. In the present study we explored the effectiveness of one of these compounds, U 74389 G, in protecting pigs myocardium against the ischemia-reperfusion damage induced by transient coronary occlusion achieved by clampling the left anterior descending coronary artery. Animals were divided into three groups: control, untreated and treated. Control animals were operated but not subjected to ischemia-reperfusion; the untreated group underwent to ischemia-reperfusion without pharmacological treatment; while the treated group received the aminosteroid (4 mg/kg) before coronary occlusion and at the time of reperfusion. Specimens of myocardial tissue and blood samples were taken for morphological and biochemical studies. In the ischemic-reperfused myocardium of the untreated animals, the dominant morphological features were neutrophil infiltration, intercellular edema and severe swelling of mitochondria. All these alterations, notably neutrophil infiltration, were attenuated by aminosteroid treatment. As for the biochemical findings, the changes in adenine nucleotides and nucleosides levels, thus the reduction of energy charge, were reversed in the treated, but not in the untreated group. Myocardial concentration of malondialdehyde, which was undetectable in the control group, was raised in all the animals after reperfusion, but this effect was significantly less marked with aminosteroid treatment. In addition, the higher myocardial content of ascorbic acid and the reduced serum potential peroxidation exhibited by the treated animals compared with untreated group indicate an enhanced antioxidant protection induced by aminosteroid administration. On the other hand, the serum levels of myoglobin, cardiac troponin I and creatine kinase MB isoenzyme suggest the ability of the aminosteroid to attenuate the modifications of membrane permeability induced by ischemia-reperfusion injury. All these results lead to the conclusion that aminosteroid treatment, at least in the conditions of the present study, is effective in reducing the morphological and biochemical alterations occurring in ischemic-reperfused myocardium.
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PMID:Beneficial effects of the 21-aminosteroid U 74389G on the ischemia-reperfusion damage in pig hearts. 934 76

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

Our objective was to evaluate the safety of coronary anastomosis on the beating heart by measuring the release of cardiac troponin I during minimally invasive coronary artery bypass grafting (MICABG). Cardiac troponin I (cTnI) is a reliable marker of cardiac ischemia during heart operations under cardiopulmonary bypass (CPB). Ten patients (8 males and 2 females, aged 41-63) underwent MICABG with single vessel bypass grafting for left anterior descending coronary artery (LAD) stenosis (n = 7) or occlusion (n = 3). Video-assisted surgery with left anterior minithoracotomy was performed in all patients. Serial venous blood samples were collected for measurement of cTnI before LAD occlusion (T0), during anastomosis (T1) and 10 min (T2), 6 h (T3), 24 h (T4), 48 h (T5), and 72 h (T6) after coronary reperfusion. The assay method used a specific enzyme-linked immunosorbent Stratus autoanalyzer. Control coronary angiography was performed in all patients. There were no operative complications or reoperations for bleeding. The cTnI concentrations were expressed in ng/ml +/- SD. The mean cTnI level was less than 3.05 +/- 0.2 ng/ml (range 0-32.8). Values were T0 = 0, T1 = 0.4 +/- 0.03, T2 = 1.15 +/- 0.2, T3 = 2.16 +/- 0.6, T4 = 1.5 +/- 0.3, T5 = 0.6 +/- 0.02, and T6 = 0.4 +/- 0.01. Angiography showed patent grafts in 9 patients. In one case, early internal thoracic artery (ITA) graft occlusion in a patient with 2 vessel disease was correlated with a higher cTnI concentration (17.8 ng/ml). Percutaneous angioplasty was performed on the right coronary artery, complicated with dissection and cardiac failure. This patient died 3 months after the MICABG despite support from a ventricular assist device. In conclusion, collateral circulation developed in the setting of chronic coronary occlusion may be efficient for myocardial preservation during short periods such as coronary anastomosis. cTnI immunoassay confirmed the safety of coronary anastomosis on the beating heart during minimally invasive coronary operations.
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PMID:Safety of beating heart anastomosis during video-assisted coronary surgery attested by cardiac troponin I. 965 Jun 74

Current markers of myocardial injury lack specificity in patients with end-stage renal disease (ESRD). In particular, a false positive creatine kinase-MB (CKMB) elevation occurs in 5-10% of patients with ESRD. The aim of this study was to ascertain the relationship between CKMB and cardiac troponin I (cTnI), a new, highly sensitive and specific marker for myocardial injury, in the authors' dialysis population and compare their specificities. Blood samples were obtained from 112 dialysis patients (35 in peritoneal dialysis; 77 in hemodialysis). Patients were asymptomatic for cardiac ischemia and skeletal muscle injury. Mean +/- SD CKMB mass was 3.16 +/- 2.26 microg/L (range, 0.34-13.62), and cTnI was 0.025 +/- 0.061 ng/ml (range, 0.001-0.496). CKMB and cTnI levels did not correlate (r2 = 0.002; p = 0.61). CKMB mass concentration was significantly higher in men and in diabetics. No patient had a cTnI level greater than 1.5 microg/L, and eight asymptomatic patients had a CKMB mass greater than 6.7 microg/L. These data suggest a specificity of 100% for cTnI vs 94.6% for CKMB at these cutoff values. It is suggested that cTnI replace CKMB as a marker of myocardial injury in patients with ESRD.
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PMID:Cardiac troponin I in patients receiving renal replacement therapy. 980 66

The main purpose of laboratory tests in patients with acute coronary syndromes is the exclusion of an acute myocardial infarction and the detection of myocardial micronecrosis. Patients with minor myocardial cell damage can best be identified by measurement of cardiac troponin T and possibly also cardiac troponin I levels. Other serum markers of acute ischemia lack specificity and are, therefore, currently of little clinical significance.
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PMID:[Value of laboratory parameters in risk assessment of patients with coronary heart disease and chronic myocardial ischemia]. 982 68

The study was designed to determine the time-course of cardiac troponin I (cTn-I) release in isolated and Langendorff-perfused rat hearts during hypoxia and reoxygenation (H/Reox), and after various durations of total ischemia and subsequent reperfusion (I/R). For this purpose, in H/Reox, cTn-I was measured with the conventional Access immunoassay (ng/ml) and a new immunoassay which operates at pg/ml, and compared with creatine kinase (CK), lactate dehydrogenase (LD) and cardiac troponin T (cTn-T). In I/R, cTn-I was compared with CK and LD. The anti-Tn-I mAbs used in cTn-I assays cross-react with cTn-I of the rat. A clear difference between time-courses and concentration levels of cTn-I in I/R and H/Reox models was found. In I/R, maximum release of cTn-I, CK and LD similarly occurred within minutes following reperfusion; however cTn-I did not return to baseline values. cTn-I levels were not linked to the duration of ischemia. In I/R, we were only able to detect small cTn-I concentrations. In H/Reox experiments, cTn-I, CK and LD increased time-dependently. We found higher cTn-I maximal peak levels detected with the Access immunoassay than with the new assay (median, 0.346 ng/ml per min/g dry wt vs 132 pg/ml per min/g dry wt). cTn-T maximal concentrations were lower than maximal cTn-I levels (median, 0.117 ng/ml per min/g dry wt). Time-courses of cTn-I release were roughly similar with both assays in the H/Reox model (r = 0.90). These data indicate that the cTn-I time-course is related to experimental model (I/R or H/Reox), but also likely depends on the sensitivity of cTn-I assays in such experimental conditions.
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PMID:Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia/reoxygenation and ischemia/reperfusion. 1040 30

To help guide physicians in their evaluation of patients with acute coronary syndromes, we investigated whether elevated cardiac troponin I in patients presenting with unstable angina predicts ischemia on stress testing. Elevated cardiac troponin I in patients who present with chest pain and normal creatine kinase levels is associated with ischemia on stress testing, as well as with future cardiac events.
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PMID:Does elevated cardiac troponin I in patients with unstable angina predict ischemia on stress testing? 1060 19

Rapid, efficient, and accurate evaluation of chest pain patients in the emergency department optimizes patient care from public health, economic, and liability perspectives. To evaluate the performance of an accelerated critical pathway for patients with suspected coronary ischemia that utilizes clinical history, electrocardiographic findings, and triple cardiac marker testing (cardiac troponin I [cTnI], myoglobin, and creatine kinase-MB [CK-MB]), we performed an observational study of a chest pain critical pathway in the setting of a large Emergency Department at the Veterans Affairs Medical Center in 1,285 consecutive patients with signs and symptoms of cardiac ischemia. The accelerated critical pathway for chest pain evaluation was analyzed for: (1) accuracy in triaging of patients within 90 minutes of presentation, (2) sensitivity, specificity, positive predictive value, and negative predictive value of cTnI, myoglobin, and CK-MB in diagnosing acute myocardial infarction (MI) within 90 minutes, and (3) impact on Coronary Care Unit (CCU) admissions. All MIs were diagnosed within 90 minutes of presentation (sensitivity 100%, specificity 94%, positive predictive value 47%, negative predictive value 100%). CCU admissions decreased by 40%. Ninety percent of patients with negative cardiac markers and a negative electrocardiogram at 90 minutes were discharged home with 1 patient returning with an MI (0.2%) within the next 30 days. Thus, a simple, inexpensive, yet aggressive critical pathway that utilizes high-risk features from clinical history, electrocardiographic changes, and rapid point-of-care testing of 3 cardiac markers allows for accurate triaging of chest pain patients within 90 minutes of presenting to the emergency department.
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PMID:Ninety-minute accelerated critical pathway for chest pain evaluation. 1156 82

Calpain is a Ca(2+)-activated neutral protease that supposedly plays a key role in myocardial dysfunction following ischemia/reperfusion, by degrading certain proteins involved in the contraction mechanism. It is possible that overexpression of calpastatin, an endogenous calpain inhibitor, lessens contractile dysfunction in the heart after reperfusion by preventing cardiac troponin I (TnI) degradation. This claim is tested by overexpression of human calpastatin (hCS) in rat hearts ex vivo using an adenovirus vector; the hearts were transplanted heterotopically into the abdomens of recipient rats to allow expression of hCS. On the fourth day after surgery, the hearts were excised and perfused in vitro to study their recovery from 30 min of global ischemia, which was followed by 60 min of reperfusion. The peak recovery of the left ventricular developed pressure (LVDP), and the values of its first derivative (max dP/dt, min dP/dt) in the hCS-overexpressed hearts were 88.9 +/- 4.8%, 90.8 +/- 9.2% and 106.4 +/- 9.8%, respectively; these values were all significantly greater than in the control hearts transfected with LacZ alone (51.4 +/- 6.9%, 52.6 +/- 8.1% and 54.7 +/- 6.6%, P < 0.05). In western blot analysis of ventricular myocardial samples (at 60-min reperfusion) using a monoclonal anti-TnI antibody, two bands corresponding to intact TnI (30 kDa) and TnI fragments (27 kDa) were distinguished. The fraction of 27-kDa TnI (percent of total TnI immunoreactivity) in hCS-overexpressed hearts was significantly less than the controls (5.7 +/- 2.7% vs. 18.1 +/- 3.2%, P < 0.05), implying a protective action of hCS against TnI degradation. These results suggest that adenovirus-mediated overexpression of hCS in the heart could be a novel biological means to minimize myocardial stunning by ischemia/reperfusion.
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PMID:Overexpression of calpastatin by gene transfer prevents troponin I degradation and ameliorates contractile dysfunction in rat hearts subjected to ischemia/reperfusion. 1451 37

Human heart-type fatty acid-binding protein (FABP) has a high potential as an early marker for myocardial infarction (MI) being more specific than myoglobin. FABP is a low molecular mass cytoplasmic protein (15 kDa) that is released early after the onset of ischemia and it may be useful for rapid confirmation or exclusion of acute myocardial infarction (AMI). Immunochemically assayed FABP, cardiac troponin I (cTnI) and enzymatically assayed creatine phosphokinase (CPK) were determined serially in plasma and serum samples from 218 patients presenting with chest pain and suspected MI. In the 94 patients with confirmed MI, FABP rose to a maximum level (577.6 +/- 43.8 microg/L) 3 hours after the onset of symptoms and returned to normal within 30 hours. The FABP level peaked 7-9 hours earlier than CPK (2288 +/- 131 U/L) and cTnI (357.1 +/- 23.9 microg/L). CPK took 50-70 hours to return to normal level and cTnI returned to normal level over 70 hours. The areas under the receiver operating characteristic (ROC) curves for FABP were calculated as 0.871 at admission and 0.995 one hour after admission, whereas for CPK the areas were 0.711 and 0.856 and for cTnI the areas were 0.677 and 0.845, indicating that the FABP test gave a better diagnostic classification at the early stage being reached by cTnI (0.995) only 8 hours after admission. For FABP, both sensitivity and negative predictive value (NPV) increased quickly to 100% for samples monitored just one hour after admission. By using only two samples, one at admission and one 1 hour post admission, sequential FABP monitoring can reliably diagnose AMI patients 1 hour after admission and 100% of non-AMI patients can be excluded with no false negative results. The late markers cTnI and CPK have the similar diagnostic performance only 7 hours later. Thus measurement of FABP in plasma or serum allows the earliest immunochemical confirmation or exclusion of AMI.
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PMID:A superior early myocardial infarction marker. Human heart-type fatty acid-binding protein. 1516 Feb 74


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