Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.1 (ACS)
 78,556 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was undertaken to evaluate a Card Test called "Spectral Diagnostics Inc Cardiac STATus CK-MB/Myoglobin" (Toronto, Canada), which is distributed by Dade International Inc, Miami, FL, for the simultaneous qualitative determination of CK-MB and myoglobin levels in human serum. The Card Test is advertised by the manufacturer as an aid in diagnosing acute myocardial infarction (AMI) in the emergency department (ED). Fifty-eight consecutive serum samples were obtained from 25 patients being evaluated for AMI in an ED. Qualitative CK-MB and myoglobin results from the Card Test were compared with quantitative CK-MB and myoglobin results using the ACS-180 instrument (Ciba Corning Diagnostics, Medfield, MA) and Stratus IIntellect T (Dade International Inc, Miami, FL), respectively. Qualitative results from the STATus CK-MB/Myoglobin Card Test were similar, diagnostically, to quantified results using these automated instruments.
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PMID:Evaluation of the cardiac STATus CK-MB/myoglobin card test to diagnose acute myocardial infarctions in the ED. 914 93

Acute coronary syndrome encompasses the entities acute MI, unstable AP and sudden cardiac death. The syndrome of unstable AP covers a very heterogenous group of patients. Recent pathological post-mortem investigations have revealed, that unstable AP leading to MI or sudden cardiac death is frequently preceded by microinfarctions. Despite the fact that thrombus formation is recognized as the major cause, the role of coronary artery spasm seems also important. Therefore, the pathological hallmark of ACS is at present thought to be caused by an active coronary plaque (the culprit lesion), which is often the site of intermittent occlusion and of thrombus formation, with or without vasospasm. The release of myocardial cell constituents in connection with these microinfarctions is to be expected. In order to detect these, diagnostic tools sensitive to myocardial injury and specific for myocardial tissue must be employed. According to WHO the criteria for the diagnosis of acute MI are based on clinical history, electrocardiographic changes, and enzymes in serum. Although these criteria are quite adequate in most cases, they are not present or easily discernible in all acute MI patients. The clinical symptoms are and will remain insensitive and nonspecific indicators of acute MI. Electrocardiographic alterations are carefully described, but sometimes less applicable due to non-interpretable ECG's. During the last decades, activity measurements of cardiac enzymes, and especially the isoenzymes of CK and LD, have become the final arbiters by which myocardial damage is diagnosed or excluded. However, they are not fully cardiospecific and have a low sensitivity to detect MMI, retaining a high specificity. Improved immunoassays have therefore been developed measuring the mass concentration of CK-MB instead of its catalytic activity, as well as immunoassays measuring structural proteins of the heart i.e., TnT, a tropomyosin-binding protein of the troponin regulatory complex located on the thin filament of the contractile apparatus of the myocyte; and MLC, a component of the thick filament of the contractile apparatus of the myocyte. We, and others, have shown that minor ischaemic myocardial injury can be detected by CK-MB mass immunoassays in around one-fourth to one-third of patients with unstable AP or in whom an acute MI has been ruled out. However, the prognostic significance of this identification has not been investigated. A priori, it is known that 5-20% of patients with unstable AP have a poor prognosis, with progression to acute MI or cardiac death within the first year. Additional, non-Q wave MI may also be considered a relatively unstable condition associated with a lower initial mortality but a higher risk of later MI/cardiac death. It is of further importance, that although the incidence of unrecognized MI is less than that of clinically apparent MI, the long-term prognosis for unrecognized MI appears to be similar to, and as serious as, that following detected MI. Therefore, in order to follow-up this subgroup identification based on CK-MB mass levels, we subsequently carried out a prognostic study. It demonstrated a significantly increased risk of cardiac events (i.e., non-fatal acute MI, cardiac death) in patients with significant fluctuations of CK-MB mass in serum. A similar observation has been supported by others using the rate of change in serial samples of CK-MB mass. Further, we demonstrated a good correlation between elevated CK-MB mass levels and a poor prognosis, when using a fixed discrimination limit. However, an increasing number of CK-MB mass immunoassays have been developed, and a standardization of CK-MB mass is urgently needed, as at present each laboratory determines its own reference levels and discriminatory values leading to the risk of diagnostic confusion. (ABSTRACT TRUNCATED)
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PMID:Creatine kinase isoenzyme MB mass, cardiac troponin T, and myosin light chain isotype 1 as serological markers of myocardial injury and their prognostic importance in acute coronary syndrome. 950 65

It has been shown that the 2-h Stratus II delta creatine kinase-MB (CK-MB) is more sensitive and is equally specific compared to a 2-h Stratus II CK-MB and to a 2-h Stratus II delta cardiac troponin-I (DeltacTnI) for identification of acute myocardial infarction and adverse outcome (AO). Because the newest generation of Stratus (Stratus CS) cTnI assay has an analytical sensitivity of 0.03 ng/mL, compared to 0.35 ng/mL for the first generation assay, we undertook a small pilot study of 120 chest pain patients to compare sensitivities and specificities for 30-day AO of the Stratus CS DeltacTnI immunoassay to the DeltaCK-MB and DeltacTnI, as measured by the Abbott Axsym immunoassay, and to the DeltaCK-MB, as measured by the Stratus CS. A Stratus CS DeltacTnI > or = +0.02 ng/mL in 2 h was more sensitive (61.9%) than an Axsym DeltaCK-MB > or = +1.3 ng/mL (38.1%; p = 0.03), a Stratus CS DeltaCK-MB > or = +0.4 ng/mL (38.1%; p = 0.03), and an Axsym DeltacTnI > or = +0.3 ng/mL (33.3%; p = 0.03) for 30-day AO. There were no differences in specificities. Our data support enhanced identification of ACS with a second generation cTnI assay. Pending larger studies, patients with a rise in DeltacTnI of > or = +0.02 ng/mL in 2 h, as measured by the Stratus CS immunoassay, should receive consideration for aggressive anti-ischemic therapy and further diagnostic testing prior to making an exclusionary diagnosis of non-ischemic chest pain.
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PMID:Improved identification of acute coronary syndromes with second generation cardiac troponin I assay: utility of 2-hour delta cTnI > or = +0.02 ng/mL. 1185 18

CVD are on the first place among death causes in the world. The half of all death at middle age persons is CVD causality, the most often because of ischaemic heart diseases, and there are a few clinic forms: acute coronary syndrome, stabile pectoral angina, variant pectoral angina, syndrome x, and silent myocardial ischemia. Toward definition ACS include clinical manifestation causality of myocardial ischemia due of atherosclerotic plague rupture. ACS include: non-stable pectoral angina non-Q infarction, Q myocardial infarction and sudden cardiac death. Consequence of plague rupture is occlusive thrombus which produces typical ST elevation on ECG after that appearance Q-in ECG with blood markers elevation (Troponin I, T, CK and CK-MB). There are sometimes non-typical ST elevation on ECG with blood markers elevation and chest pain. On that way becomes non-Q infarction. Smaller thrombus make non stable pectoral angina and appearance of ST depression on ECG without blood markers elevation. Sometimes sudden cardiac death is the first sign of coronary disease in the diagnostic management coronary disease due of: clinical symptom of chest pain, ECG (with or without ST elevation) and appearance appsence biochemical blood markers (at myocardial necrosis troponins are present in blood during 14 days, CK-MB is present 3 days). Sometimes echocardiography examination is helpful in estimate of regional kinetic disorders. European society of cardiologists made guidelines for management od ACS without ST elevation and guidelines management of acute myocardial infarction with ST elevation.
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PMID:[New approach in the diagnosis of acute coronary syndrome]. 1520 7

This paper provides a comprehensive up-to-date review of the medical and invasive management of patients with non- ST-segment elevation acute coronary syndromes (NSTE-ACS). The authors have summarized findings from key clinical trials published recent years that contribute to clinicians' understanding of how best to optimize therapy. The goals for the management of NSTE-ACS are rapid and accurate risk stratification, appropriate and institution-specific triage to interventional versus medical strategies and optimal pharmacologic therapy--all of which provide for a smooth and seamless transition of care between the emergency department and the cardiology service. High-risk features or absolute treatment trigger criteria that support more aggressive medical therapy (i.e., addition of small-molecule GP IIb/IIIa inhibitor to a core regimen of aspirin, enoxaparin, and in most cases, clopidogrel) and/or that would direct clinicians toward percutaneous, mechanical/interventional strategies as the preferred modality include, but are not limited to, the presence of one or more of the following: (1) elevated cardiac markers (troponin and/or CK-MB); (2) elevated levels of inflammatory markers (particularly CRP > 3 microg/dl); (3) age > 65 years; (4) presence of ST-T wave changes; (5) TIMI Risk Score greater than or equal to 4; (6) diabetes; and/or (7) clinical instability in the setting of suspected NSTE-ACS. Specific clinical, ECG and/or biochemical trigger points modulate the aggressiveness of both the medical therapy and the propensity to perform early angiography with or without subsequent revascularization in patients with NSTE-ACS. Although additional refinements and changes in ACS management are still to come, evidence-based strategies suggest that prompt mechanical revascularization is associated with the best possible clinical outcomes, particularly for patients with high-risk features and in whom benefits of adjunctive, pharmacoinvasive antithrombotic therapies can be consolidated. Patient transfer for cardiac catheterization/percutaneous coronary intervention (PCI) is strongly recommended in patients who manifest high-risk features and/or aggressive treatment trigger criteria, so that this high-risk subgroup may receive definitive, interventional and/or cardiology-directed specialty care at appropriate sites of care. When available, interventional management is preferred in these patients. The importance of safe and effective anticoagulation in the spectrum of management strategies has been confirmed, and the evidence in support of enoxaparin and other antithrombotic agents has been reviewed. Dosing recommendations for enoxaparin use in the setting of PCI have been issued by the CATH Panel and have been summarized in this consensus report. Similar recommendations have been presented for the use of oral antiplatelet agents and GP IIb/IIIa antagonists. The addition of statins, ACE-inhibitors and beta-blockers is also stressed as part of a comprehensive secondary cardioprotective strategy for patients with coronary heart disease.
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PMID:Strategies for optimizing outcomes in the NSTE-ACS patient The CATH (cardiac catheterization and antithrombotic therapy in the hospital) Clinical Consensus Panel Report. 1719 14

The field of diagnostic cardiac biomarkers has grown exponentially since the development of an assay for aspartate transaminase activity to diagnose myocardial infarction in 1954. The clinician now has a vast array of clinical tools, which include biomarkers of inflammation, ischaemia and necrosis as well as sensitive imaging technology and coronary anatomy intervention at their disposal when evaluating acute coronary syndromes. Previously the World Health Organisation (1979) defined a myocardial infarction (MI) in the presence of two of the following triad: History of chest pain, electrocardiographic (ECG) changes and a rise in cardiac enzymes to twice the upper limit of normal. At this time, creatine kinase and its MB isoenzyme were the preferred biochemical markers. The clinical requirements of early diagnosis, risk stratification and effective treatment have stimulated the development of numerous new and cardiac specific biomarkers (e.g. cardiac troponins). Cardiac troponins are now integral to the diagnosis of MI and have led to the reclassification of MI into either ST elevated MI (STEMI) or non-ST elevated MI (NSTEMI). Subsequent to the release of each new cardiac specific assay there typically follows an array of studies supporting or refuting its efficacy. Many cardiac biomarkers originally proposed with high sensitivity and specificity for ACS are now of questionable clinical value or require the addition of significant caveats once they have been fully evaluated. Indeed, acute exercise often stimulates perturbations in cardiac biomarkers; such as elevations in creatine kinase, cardiac troponins or reductions in Ischemia Modified Albumin (IMA). Such an influence of exercise upon commercially available cardiac biomarkers may hamper or distort the viability of such assays in the clinical arena. The purpose of this review is to examine the influence of exercise upon a number of established and novel cardiac biomarkers, including markers of necrosis, inflammation, cardiac function and ischemia. We will also address the clinical relevance of such exercise-induced perturbations.
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PMID:The influence of exercise upon cardiac biomarkers: a practical guide for clinicians and scientists. 1758 54

This paper provides a comprehensive up-to-date review of the medical and invasive management of patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS), and ST-elevation myocardial infarction (STEMI), as supported by recent updates to the ACC/AHA Guidelines. The authors have summarized findings from key clinical trials published in recent years that contribute to clinician's understanding of how best to optimize therapy. The goals for the management of NSTE-ACS and STEMI are rapid and accurate risk stratification, appropriate and institution-specific triage to interventional versus medical strategies and optimal pharmacologic therapy - all of which provide for a smooth and seamless transition of care between the emergency department and the cardiology service. High-risk features or absolute treatment trigger criteria that support more aggressive medical therapy (i.e., addition of a small molecule gylcoprotein [GP] IIb/IIIa inhibitor to a core regimen of aspirin, enoxaparin or other anticoagulants, and in most cases, clopidogrel) and/or that would direct clinicians toward percutaneous interventional strategies as the preferred modality include, but are not limited to the presence of one or more of the following: 1) elevatedcardiac markers (troponin and/or CK-MB); 2) age older than 65 years; 3) presence of ST-T-wave changes; 4) TIMI Risk Score >/= 5; 5) clinical instability in the setting of suspected NSTE-ACS. Although additional refinements and changes in ACS management are still to come, evidence-based strategies suggest that prompt mechanical revascularization is associated with the best possible clinical outcomes, particularly for patients with high-risk features and in whom benefits of adjunctive, pharmacoinvasive antithrombotic therapies can be consolidated. Transfer for cardiac catheterization/percutaneous coronary intervention (PCI) is strongly recommended in patients who manifest high-risk features and/or aggressive treatment trigger criteria, so that this high-risk subgroup may receive definitive, interventional and/or cardiology-directed specialty care at appropriate sites of care. When available, interventional management is preferred in these patients. The importance of safe and effective anticoagulation in the spectrum of management strategies has been confirmed, and the evidence in support of enoxaparin and other antithrombotic agents has been reviewed. Dosing recommendations for enoxaparin use in the setting of PCI have been issued by the CATH Panel and have been summarized in this consensus report. Similar recommendations have been presented for the use of oral antiplatelet agents and GP IIb/IIIa antagonists. The addition of statins, angiotensin-converting enzyme (ACE) inhibitors and beta-blockers is also stressed as part of a comprehensive secondary cardioprotective strategy for patients with coronary heart disease.
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PMID:Pharmacoinvasive management of acute coronary syndrome: incorporating the 2007 ACC/AHA guidelines: the CATH (cardiac catheterization and antithrombotic therapy in the hospital) Clinical Consensus Panel Report--III. 1818 May 24

The purpose of this study was to compare cardiac markers in the pericardial fluid and serum in order to evaluate preoperative myocardial injury. Thirty patients were divided into three groups. The first group (AVR; n=10) received an aortic valve replacement. The second group (SA; n=10) included patients with stable angina who underwent elective coronary artery bypass grafting (CABG). The third group (ACS; n=10) included patients with acute coronary syndrome who underwent urgent CABG. Pericardial fluid and venous samples were taken after opening the pericardium and 24 h postoperatively. Serum and pericardial concentration of troponin I (cTnI), creatine kinase (CK), its MB isoenzyme (CK-MB) and myoglobin were determined. Preoperative pericardial cTnI was significantly (P<0.01) higher than in serum in all groups. Preoperative pericardial CK, CK-MB and myoglobin were significantly (P<0.01) lower than in serum in groups AVR and SA. Preoperative pericardial and serum cTnI were significantly higher in the ACS than in AVR and SA groups (P<0.01). Postoperative pericardial concentration of all markers was significantly higher (P<0.01) than in serum in all groups. We conclude that preoperative pericardial accumulation of cTnI may reflect subclinical injury which may not be demonstrated by the usual laboratory tests.
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PMID:Biochemical markers of myocardial injury in the pericardial fluid of patients undergoing heart surgery. 1825 49

This study investigated D-dimer levels in 241 patients admitted to the emergency department with sudden-onset chest pain. The patient group included those diagnosed with acute coronary syndrome (ACS; i.e., unstable angina pectoris [USAP], non-ST elevated myocardial infarction [NSTEMI], ST-elevated myocardial infarction [STEMI]); the control group included those diagnosed with non-cardiac chest pain. Mean serum levels of D-dimer, creatine kinase-MB (CK-MB) and troponin I (TPI) were compared between the groups. Levels of D-dimer, CK-MB and TPI in the patient group were significantly higher than in the control group. There were also significantly higher D-dimer, CK-MB and TPI levels in the STEMI and NSTEMI patient subgroups compared with the control group. Only the D-dimer level was significantly higher in the USAP subgroup versus the control group. The sensitivity and specificity of D-dimer for ACS were 83.7% and 95.4%, respectively, suggesting that evaluating D-dimer levels might be useful in the emergency room for diagnosing ACS and predicting mortality in patients presenting with acute chest pain.
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PMID:The role of serum D-dimer level in the diagnosis of patients admitted to the emergency department complaining of chest pain. 2130 92

Pitavastatin is the newest member of the HMG-CoA reductase inhibitor family and is approved as adjunctive therapy to diet to reduce elevated levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (Apo) B, and triglycerides and to increase levels of high-density lipoprotein (HDL) cholesterol in adult patients with primary hyperlipidemia or mixed dyslipidemia. Pitavastatin undergoes minimal metabolism by cytochrome P450 (CYP) enzymes and, therefore, has a low propensity for drug-drug interactions with drugs metabolized by CYP enzymes or the CYP3A4 substrate grapefruit juice. In clinical trials, pitavastatin potently and consistently reduced serum levels of total, LDL, and non-HDL cholesterol, and triglycerides in patients with primary hypercholesterolemia where diet and other non-pharmacological measures were inadequate. Mean reductions from baseline in serum total and LDL cholesterol and triglyceride levels were 21-32%, 30-45%, and 10-30%, respectively. Moreover, a consistent trend towards increased HDL cholesterol levels of 3-10% was seen. Long-term extension studies show that the beneficial effects of pitavastatin are maintained for up to 2 years. Pitavastatin produces reductions from baseline in serum total and LDL cholesterol levels to a similar extent to those seen with the potent agent atorvastatin and to a greater extent than those seen with simvastatin or pravastatin. In the majority of other studies comparing pitavastatin and atorvastatin, no significant differences in the favorable effects on lipid parameters were seen, although pitavastatin was consistently associated with trends towards increased HDL cholesterol levels. Pitavastatin also produces beneficial effects on lipids in patients with type 2 diabetes mellitus and metabolic syndrome without deleterious effects on markers of glucose metabolism, such as fasting blood glucose levels or proportion of glycosylated hemoglobin. Pitavastatin appears to exert a number of beneficial effects on patients at risk of cardiovascular events independent of lipid lowering. In the JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) study, pitavastatin was non-inferior to atorvastatin at reducing plaque volume in patients with ACS undergoing percutaneous coronary intervention. Further beneficial effects, including favorable effects on the size and composition of atherosclerotic plaques, improvements in cardiovascular function, and improvements in markers of inflammation, oxidative stress, and renal function, have been demonstrated in a number of small studies. Pitavastatin is generally well tolerated in hyperlipidemic patients with or without type 2 diabetes, with the most common treatment-related adverse events being musculoskeletal or gastrointestinal in nature. Increases in plasma creatine kinase levels were seen in <5% of pitavastatin recipients and the incidence of myopathy or rhabdomyolysis was extremely low. In summary, pitavastatin, the latest addition to the statin family, produces potent and consistent beneficial effects on lipids, is well tolerated, and has a favorable pharmacokinetic profile. The combination of a potent decrease in total and LDL cholesterol levels and increase in HDL cholesterol levels suggest that pitavastatin may produce substantial cardiovascular protection.
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PMID:Are all statins the same? Focus on the efficacy and tolerability of pitavastatin. 2144 76


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