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)

Acute ischemic chest pain at rest consistent with unstable angina or non-ST-elevation myocardial infarction is a common problem that may cause death or recurrent myocardial infarction within 30 days unless identified and risk stratified acutely. The latter may be done within 15 minutes by the history, physical exam, and electrocardiogram, and is aided by the measurement of troponin T/I. According to the Agency for Health Care Policy and Research guidelines, low-risk patients can be discharged home and rechecked within 72 hours. Intermediate-risk patients with no ST-segment changes with continuous monitoring and no elevation of troponin should undergo exercise stress testing by electrocardiogram (or nuclear or echocardiographic evaluation if electrocardiogram is non-analyzable). Patients with a negative stress test are low risk (no death or myocardial infarction at 30 days or 6 months) and can be discharged home. Patients with a positive test or who are at high risk according to the Agency for Health Care Policy and Research guidelines should undergo acute invasive testing for possible revascularization. Aspirin and low molecular weight heparin or unfractionated heparin, along with anti-ischemia therapy, is indicated in intermediate- or high-risk patients. The addition of clopidogrel is indicated in these patients, except in those who are potential candidates for coronary artery bypass graft. Platelet glycoprotein IIb/IIIa inhibitors are indicated in high-risk patients likely to undergo percutaneous coronary intervention, should be started early if recurrent ischemia occurs, but are not indicated in lower-risk patients who do not require percutaneous coronary intervention. Intensive secondary prevention should be started before dismissal.
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PMID:Acute coronary syndromes: pathogenesis, acute diagnosis with risk stratification, and treatment. 1553 72

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

S100B is an astrocytic protein assessed in cerebrospinal fluid and serum as a biochemical marker of cerebral injuries. However, increasing evidences suggest the influence of extra cerebral sources on its serum levels. Since it was reported that the injured myocardium expresses S100B, we investigated whether the isolated heart releases this protein. The rat hearts were excised and perfused by the Langendorff technique of isolated heart perfusion. After stabilization, 10 hearts (ischemic group) were submitted to 20 minutes of ischemia and 30 minutes of reperfusion, and 5 hearts (control group) were submitted to 50 minutes of perfusion. The perfusion fluid was collected at pre-ischemia, and 0, 5, 10, 15 and 30 min after ischemia (or equivalent in controls) for S100B and cardiac troponin T (a heart injury marker) assays. In the ischemic group, S100B and troponin T levels increased significantly at time 0 min: S100B values [mug/L, median (IQ25/IQ75)] increased from < or = 0.02 (< or = 0.02/0.03) to 0.38 (0.22/0.84), while troponin T values [mug/L, median (IQ25/IQ75)] increased from 0.31 (0.15/0.45) to 2.84 (2.00/3.63). Our results point to the ischemic heart as an extra cerebral source of S100B.
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PMID:The ischemic rat heart releases S100B. 1592 4

This study shows that relaxin can be effective in the treatment of acute myocardial infarction. In a swine model of heart ischemia-reperfusion currently used to test cardiotropic drugs because of its similarities with human myocardial infarction, human recombinant relaxin (2.5 and 5 microg/kg body weight), given at reperfusion after a 30-min ischemia, markedly reduced the main serum markers of myocardial damage (myoglobin, CK-MB, and troponin T) and the metabolic and histopathologic parameters of myocardial inflammation and cardiomyocyte injury, resulting in overall improvement of ventricular performance (increased cardiac index) compared to the controls. These results provide a background for future clinical trials with human relaxin as adjunctive therapy to catheter-based coronary angioplasty in patients with acute myocardial infarction.
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PMID:Human recombinant relaxin reduces heart injury and improves ventricular performance in a swine model of acute myocardial infarction. 1595 41

The hormone relaxin has been shown to cause coronary vasodilation and to prevent ischemia/reperfusion-induced cardiac injury in rodents. This study provides evidence that relaxin, used as an adjunctive drug to coronary reperfusion, reduces the functional, biochemical, and histopathological signs of myocardial injury in an in vivo swine model of heart ischemia/reperfusion, currently used to test cardiotropic drugs for myocardial infarction. Human recombinant relaxin, given at reperfusion at doses of 1.25, 2.5, and 5 microg/kg b.wt. after a 30-min ischemia, caused a dose-related reduction of key markers of myocardial damage (serum myoglobin, CK-MB, troponin T) and cardiomyocyte apoptosis (caspase 3, TUNEL assay), as well as of cardiomyocyte contractile dysfunction (myofibril hypercontraction). Compared with the controls, relaxin also increased the uptake of the viability tracer 201Thallium and improved ventricular performance (cardiac index). Relaxin likely acts by reducing oxygen free radical-induced myocardial injury (malondialdehyde, tissue calcium overload) and inflammatory leukocyte recruitment (myeloperoxidase). The present findings show that human relaxin, given as a drug to counteract reperfusion-induced cardiac injury, affords a clear-cut protection to the heart of swine with induced myocardial infarction. The findings also provide background to future clinical trials with relaxin as adjunctive therapy to catheter-based coronary angioplasty in patients with acute myocardial infarction.
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PMID:Novel drug development opportunity for relaxin in acute myocardial infarction: evidences from a swine model. 1600 2

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

Calpain-1 is a ubiquitous intracellular Ca2+-activated protease, which has been implicated in the pathogenesis of reversible myocardial depression (i.e. myocardial stunning) that follows ischemia and reperfusion via myofibrillar protein degradation. However, the target proteins of this degradative process in the human myocardium have not yet been identified. In order to compare the levels of Calpain-1 susceptibility within a set of human myofibrillar proteins (titin, alpha-fodrin, desmin, troponin T (cTnT), troponin I (cTnI) and alpha-actinin), crude left ventricular tissue homogenates were incubated for 0.5, 15, 30, 60 or 120 min in the presence of Calpain-1 (1 U or 5 U). Differences in the kinetics and extents of protein degradation were subsequently evaluated by using silver-stained SDS-polyacrylamide gels and Western immunoblot analyses. These assays revealed myofibrillar proteins with high (titin and alpha-fodrin), moderate (desmin and cTnT), or low (cTnI and alpha-actinin) relative Calpain-1 susceptibilities. The level of phosphorylation of cTnI did not explain its relatively low Calpain-1 susceptibility. Moreover, the molecular mass distributions of the truncated alpha-fodrin, desmin and cTnI fragments resulting from Ca2+-dependent autoproteolysis exhibited marked similarities with those of their Calpain-1-clipped products. These in vitro results shed light on a number of structural (titin, alpha-fodrin, desmin and alpha-actinin) and regulatory (cTnT and cTnI) proteins within the contractile apparatus as potential targets of Calpain-1. Their degradation may contribute to the development of postischemic stunning in the human myocardium.
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PMID:Calpain-1-sensitive myofibrillar proteins of the human myocardium. 1618 82

The diagnosis of myocardial damage is preferably based on measurement of the cardiac-specific troponins. However, there is an emerging need for early, specific cardiac markers. One potential candidate is the glycogen phosphorylase BB isoenzyme (GPBB). We investigated the use of a new, commercially available GPBB ELISA assay in 61 patients presenting with an acute coronary syndrome (37 acute myocardial infarction, 24 unstable angina pectoris) in comparison to established cardiac markers such as troponin T, creatine kinase isoenzyme MB (CKMB) mass, and myoglobin. Blood samples were obtained on arrival, as well as 1, 2, 3, 4, 8, 12 and 24 h later. GPBB plasma concentrations were elevated in 90.9% of patients 1 h after onset of chest pain and increased to 100% at 4-5 h. Within the first 6 h, GPBB showed the highest sensitivity (95.5-100%) and high specificity (94-96%) compared to myoglobin (85-95% sensitivity) and CKMB mass (71.4-91.3% sensitivity). As expected, troponin T showed high specificity (100%) and sensitivity >95% later in the time course (>or=3 h). In un-stable angina pectoris patients, a very high rate of elevated GPBB was observed (93.9% at 3 h) compared to myoglobin (66.7%). Cardiac troponin T and CKMB were only elevated in 33.8% and 55.0% of these patients, respectively. In conclusion, GPBB is a promising marker for the early diagnosis of acute coronary syndromes and could probably act as a marker of ischemia. However, further studies on specificity and development of a fast, automated assay are necessary before GPBB can be recommended as a routine diagnostic tool.
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PMID:Glycogen phosphorylase BB in acute coronary syndromes. 1630 72

The present study evaluated whether biomarkers of ischemia, inflammation, myocardial damage, and dysfunction are equally useful in patients who have diabetes mellitus (DM) for prediction of cardiac events in non-ST-elevation acute coronary syndrome (ACS). DM was present in 1,677 of 7,800 patients (21.5%) who had non-ST-elevation ACS and were included in the Fourth Global Utilization of Strategies To Open Occluded Arteries (GUSTO IV) trial. Creatinine, N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), troponin T, C-reactive protein, and interleukin-6 were analyzed in serum samples that were obtained at a median of 9.5 hours from symptom onset. One-year mortality rates were 13.5% among patients who had DM (n = 227) and 6.9% among those who did not (n = 418, p < 0.001). The median level of NT-pro-BNP was 2 times as high in patients who had DM, whereas troponin T levels did not differ by DM status. Mortality increased with ascending quartiles of NT-pro-BNP, with 1-year mortality rates of 3.9% (n = 11) in the bottom quartile and 29% (n = 103) in the top quartile. In multivariable analyses, factors that were predictive of 1-year mortality in patients who did not have DM were also significant for those who did. Presence of ST depression > 0.5 mm had the highest odds ratio of 2.3 (95% confidence interval 1.2 to 4.6). NT-pro-BNP levels > 669 ng/L (odds ratio 2.0, 95% confidence interval 1.1 to 3.6) and interleukin-6 levels > 10 ng/L (odds ratio 1.9, 95% confidence interval 1.2 to 3.0) were significant biomarker predictors. In conclusion, DM confers a high long-term mortality in non-ST-elevation ACS. Despite a larger proportion of ST depression and increased levels of NT-pro-BNP and interleukin-6 at admission, these factors provide independent prognostic information that may improve risk stratification and guidance of treatment.
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PMID:Usefulness of biomarkers for predicting long-term mortality in patients with diabetes mellitus and non-ST-elevation acute coronary syndromes (a GUSTO IV substudy). 1644 56

The European Society of Cardiology and the American College of Cardiology redefined the concept of myocardial infarction in the presence of highly positive markers of myocardial injury associated with at least one of the following: ischemic symptoms; development of pathologic Q waves on the ECG or ECG changes indicative of ischemia (positive or negative deviation of the ST segment), making troponins one of the most important aspects in the evaluation and stratification of patients with chest pain in the emergency room. However, although troponin gives excellent accuracy in the identification of myocardial necrosis, it is known that it can also be elevated in a series of nonatherosclerotic heart diseases. We present the case of a 49-year-old female patient admitted to the Chest Pain Unit with a history of supraventricular tachycardia associated with chest discomfort, nausea and diaphoresis. During risk stratification, the patient presented with a high serum troponin T level (0.143 ng/ml) but with a normal coronary angiography.
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PMID:Elevated troponin levels after prolonged supraventricular tachycardia in patient with normal coronary angiography. 1660 27


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