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)

Renal dysfunction is an important predictor of mortality in patients with acute coronary syndrome. Until recently, the Cockcroft-Gault (C-G) equation has been most commonly used to estimate renal function, although the Modification of Diet in Renal Disease (MDRD) equation is now recommended. Which equation better predicts mortality is unclear. Consecutive patients without ST elevation on the initial electrocardiogram admitted for exclusion of myocardial ischemia were included. Admission creatinine was used to estimate renal function, and 30-day and 1-year mortality were compared after classifying patients as having no (estimated glomerular filtration rate [eGFR] > or =60 ml/min/m(2)), moderate (eGFR 30 to 59 ml/min/ m(2)), or severe (eGFR <30 ml/min/m(2)) renal dysfunction using the 2 equations. Of the 4,343 patients (49% women, 64% African-American) included, 16% had troponin I elevations consistent with myocardial infarction, and 1-year mortality was 10%. Agreement between the 2 equations was high (r = 0.87 p <0.001, concordance 86%). Mortality was similar in the 2 renal function classifications, with no significant differences based on race or troponin I status at 30 days or 1 year. However, the area of the receiver operator characteristic curve was significantly larger for predicting 1-year mortality with the C-G equation (0.75 [0.72 to 0.77] vs 0.71 [0.68 to 0.73]; p <0.01); both were superior to creatinine alone (0.68 [0.66 to 0.71]; p <0.01 for both C-G and MDRD). Results for 30-day mortality were similar. In conclusion, the C-G equation appears to be superior to the MDRD equation for predicting short- and long-term mortality in patients admitted for exclusion of ischemia, although differences are minor.
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PMID:Comparison of the modification of diet in renal disease and the Cockcroft-Gault equations for predicting mortality in patients admitted for exclusion of myocardial ischemia. 1860 10

The diagnosis of a postoperative myocardial infarction (PMI) is important in the orthopedic population because these events can be associated with significant cardiac morbidity. Plasma troponin I (cTnI) analysis has markedly increased our ability to detect myocardial damage. Using cTnI analysis for evidence of a PMI, we prospectively assessed all of our patients for (1) the 1-year incidence of PMI, (2) the clinical consequences of a PMI in relation to the level of the cTnI release, and (3) 6-month follow-up for cardiac complications. During a 12-month period, patients at risk for perioperative myocardial ischemia were assessed for a PMI by serum cTnI levels and daily serial ECGs. Patients with cTnI levels above the reference level (> or = 0.4 ng/ml) were also assessed for new cardiac regional wall motion abnormalities with an echocardiogram and 6-month postdischarge adverse cardiac events. Of the 758 patients who were assessed for a PMI, 49 patients had detectable cTnI levels (> or = 0.4 ng/ml); the incidence of a PMI was 0.6% of all surgical cases and 6.5% of those patients were at risk for a cardiac event. A PMI was more common after hip arthroplasty than other orthopedic procedures. Twenty-three patients had a cTnI level >3.0 ng/ml, and 74% these patients (17/23) had anginal symptoms and/or ischemic ECG changes. Nine of these patients (9/23) had new postoperative echocardiographic changes, five (5/23) required emergency transfer to a cardiac care unit, and 10 (10/23) had postoperative cardiac complications. In contrast, 15 patients with levels of cTnI <3.0 ng/ml and without ischemic ECG changes and/or anginal symptoms had no postoperative cardiac complications. Fourteen patients (14/47) had cardiac complications 6 months after discharge, including four cardiac deaths, one fatal stroke, and four patients with unstable anginal episodes that required a change in medical management, and six patients required coronary revascularization. Orthopedic surgical patients with cTnI level <3 ng/ml and without symptoms or ECG changes suggestive of myocardial ischemia (15/49) may have different risks than those with higher-level cTn1.
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PMID:The one year incidence of postoperative myocardial infarction in an orthopedic population. 1875 68

Matrix metalloproteinase-2 (MMP-2) has emerged as a key protease in various pathologies associated with oxidative stress, including myocardial ischemia-reperfusion, heart failure or inflammation. Peroxynitrite (ONOO(-)), an important effector of oxidative stress, was reported to activate some full length MMP zymogens, particularly in the presence of glutathione (GSH), but whether this occurs for MMP-2 is unknown. Treating MMP-2 zymogen with ONOO(-) resulted in a concentration-dependent regulation of MMP-2, with 0.3-1 microM ONOO(-) increasing and 30-100 microM ONOO(-) attenuating enzyme activity. The enzyme's V(max) was also significantly increased by 1 microM ONOO(-). Comparable responses to ONOO(-) treatment were observed using the intracellular target of MMP-2, troponin I (TnI). GSH at 100 microM attenuated the effects of ONOO(-) on MMP-2. Mass spectrometry revealed that ONOO(-) can oxidize and, in the presence of GSH, S-glutathiolate the MMP-2 zymogen or a synthetic peptide containing the cysteine-switch motif in the enzyme's autoinhibitory domain. These results suggest that ONOO(-) and GSH can modulate the activity of 72 kDa MMP-2 by modifying the cysteine residue in the autoinhibitory domain of the zymogen, a process that may be relevant to pathophysiological conditions associated with increased oxidative stress.
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PMID:Activation and modulation of 72kDa matrix metalloproteinase-2 by peroxynitrite and glutathione. 1904 43

The effects of mexicor (ethylmethylhydroxypyridine succinate) at doses of 50 and 100 mg/kg on myocardial infarct size, serum levels of myocardial markers, and severity of ischemia- and reperfusion-induced arrhythmias were studied in the rat model of myocardial ischemia-reperfusion injury. It was shown that pre-ischemic intravenous infusion of mexicor at a dose of 50 mg/kg resulted in significant reduction of myocardial infarct size and troponin I level. When the dose of mexicor was increased up to 100 mg/kg the infarct-limiting effect was reversed. Both doses of mexicor tested in this study failed to protect the heart from ischemic tachyarrhythmias but decreased the occurrence of persistent reperfusion-induced ventricular fibrillation.
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PMID:[The effects of modulation of cardiac metabolism and antioxidant state on myocardial ischemia-reperfusion injury]. 1906 30

Complement activation has been shown to play an important role in the inflammation and tissue injury following myocardial ischemia and reperfusion (MI/R). Several recent studies from our laboratory demonstrated the importance of mannose-binding lectin (MBL) as the initiation pathway for complement activation and the resulting pathological effects following MI/R. However, other studies from the past suggest an important role of the classical pathway and perhaps natural antibodies. In the present study, we used newly generated genetically modified mice that lack secreted IgM (sIgM), MBL-A, and MBL-C (sIgM/MBL null) in a plasma reconstitution mouse model of MI/R. Following 30 min of ischemia and 4 h of reperfusion, left ventricular ejection fractions were significantly higher in sIgM/MBL null mice reconstituted with MBL null or sIgM/MBL null plasma compared with reconstitution with wild-type (WT) plasma or WT mice reconstituted with WT plasma following MI/R. Serum troponin I concentration, myocardial polymorphonuclear leukocyte infiltration, and C3 deposition were dependent on the combined presence of sIgM and MBL. These results demonstrate that MI/R-induced complement activation, inflammation, and subsequent tissue injury require both IgM and MBL. Thus MBL-dependent activation of the lectin pathway may not be completely antibody independent in I/R models.
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PMID:Myocardial ischemia and reperfusion injury is dependent on both IgM and mannose-binding lectin. 1974 70

The specific persistent sodium current blocker F 15845 was tested in two myocardial ischemia-reperfusion models in the pig in order to evaluate its cardioprotective effects. In the first protocol, the left circumflex coronary artery was ligated for 60-min and then reperfused for 48-h. F 15845 (2.5+2.5 and 5+5mg/kg) was administered by i.v. infusion, starting before ischemia to the beginning of reperfusion. The second protocol attempted to evaluate F 15845 (5+5mg/kg) response in a more pathological state of the heart. To this end, a non necrotic ligation of the left circumflex coronary artery was applied for 15 min one week before the actual 60 min occlusion. For both protocols, infarct size was determined at the end of the reperfusion period and was assessed by histochemistry (tetrazolium staining). Plasma levels of biochemical markers (myoglobin and troponin I) were also evaluated. In protocol 1, F 15845 significantly reduced the infarct size by 27+/-3 and 43+/-5% at 2.5+2.5 and 5+5mg/kg, respectively. At 5+5mg/kg, F 15845 decreased plasma levels of myoglobin and cardiac troponin I. In protocol 2, F 15845 (5+5mg/kg) significantly reduced myocardial infarct size by 54+/-15% and lowered the plasma myoglobin and troponin I levels relative to vehicle-treated animals. In conclusion, the highly effective persistent sodium current blocker F 15845 exerts remarkable cardioprotective activities. It reduces both myocardial infarct size and the release of biochemical markers in healthy pigs as well in pigs previously exposed to an ischemic episode.
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PMID:Myocardial protection by F 15845, a persistent sodium current blocker, in an ischemia-reperfusion model in the pig. 1977 35

Chronic obstructive pulmonary disease patients are at increased risk for mortality, particularly from cardiovascular conditions. Acute exacerbation increases heart burden and may lead to release of troponin I. This study investigates the long-term prognostic value of elevated troponin I detected during acute exacerbation of chronic obstructive pulmonary disease. The records of 182 patients with acute exacerbation in whom troponin I levels were sampled during their hospitalization were reviewed retrospectively. Receiver operator curve was used to determine the cut-off level for troponin I that discriminated survivors and non-survivors, and predictors for all-cause mortality were tested in a multivariate analysis. The results showed that, during a mean observation time of 50.1 +/- 45.6 months, 66 (36.3%) patients died, providing 1, and 3-year survival rates of 84%, and 54%, respectively. Troponin I levels were significantly higher in non-survivors compared with survivors, mean troponin I +/- SD in microg x L(-1): 1.35 +/- 3.17 vs. 0.53 +/- 2.08, respectively, p = 0.0033. ROC curve analysis identified troponin I > 0.03 microg x L(-1) as the optimal cut-off level for prediction of mortality. Kaplan-Meier survival analysis revealed that the probability of survival was significantly lower in patients with troponin I > 0.03 microg x L(-1) (log-rank test p = 0.0058). On multivariate analysis, only ischemic heart disease (HR = 2.335, p = 0.0017) and troponin I level (HR = 1.31541, p = 0.2513) were independent predictors of mortality. In conclusion, it was found that a mildly elevated troponin I level measured in patients with chronic obstructive pulmonary disease during acute exacerbation is a strong independent predictor of mortality following discharge.
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PMID:Cardiac troponin-I predicts long-term mortality in chronic obstructive pulmonary disease. 1981 68

A 58 year old male patient was hospitalized numerous times due to an elevated troponin I level in spite of the absence of specific chest pain and ischemic changes on ECG. The patient had undergone two coronary angiography procedures and numerous cardiac studies without evidence of ischemic heart disease. The elevated troponin level remained unchanged in between hospitalizations while the patient was asymptomatic. Further workup revealed that the troponin I level was normal when tested with an alternative laboratory kit. The troponin T level was also normal. This case report underscores the problematic nature of relying on an elevated troponin level as the sole component in the diagnosis of coronary disease.
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PMID:[Recurrent hospitalizations due to false positive troponin in a patient presenting with chest pain]. 1990 97

A 70-year-old woman with a history of undifferentiated connective tissue disease was admitted for work-up of shortness of breath and progressive weakness over the course of 1 year. She had been treated with hydroxychloroquine (HCQ) for last 5 years. Her evaluation revealed diffuse muscle weakness and hyperpigmentation of the skin consistent with HCQ deposition, although this did not entirely explain the patient's dyspnea. The patient underwent cardiac evaluation because of occasional substernal chest pain and persistent elevation in serum troponin I, but her ECG and adenosine thallium study did not show any signs of ischemic heart disease. The diagnosis of HCQ-induced myopathy was made with electromyography and muscle biopsy. HCQ was discontinued, with improvement of the patient's signs and symptoms over the course of the next 18 months.We propose that this patient was experiencing myocardial toxicity as a consequence of HCQ deposition disease with her clinical picture of skeletal muscle myopathy and HCQ deposition in the skin. A Medline search yielded several case reports as well as a case series of patients with antimalarial-induced myopathy. HCQ-induced myopathy may be less recognized because of its presentation with signs, symptoms, and laboratory results which suggest other critical diseases. Moreover, this medication is often prescribed to treat illnesses whose clinical manifestations may include myopathy.
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PMID:Hydroxychloroquine-induced myopathy. 2005 53

Small elevations in serum creatinine may reflect significant kidney damage and be associated with poor patient outcomes, thus rendering creatinine to be a late marker of acute kidney injury (AKI). AKI researchers refer to the AKI biomarker quest as the "search for the renal troponin I," implying that such putative earlier AKI biomarker use could allow for earlier intervention. We consider the analogy to troponin I and its acceptance to prompt evaluation and therapeutic intervention to treat myocardial ischemia and prevent myocardial infarction an informative and potentially applicable model to the AKI field. Because AKI does not hurt, there is no validated equivalent of chest pain or anginal equivalent to increase suspicion for AKI presence on the part of the clinician. So, although biomarkers may ultimately be validated to detect AKI early, unless nephrologists and intensivists can define "renal angina" to initiate "renal troponin I" assessments, AKI biomarkers may never realize their full potential to improve patient care and outcomes. The purpose of this article is to review both adult and pediatric AKI literature to devise a definition for a renal anginal syndrome equivalent.
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PMID:Renal angina. 2037 43


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