Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

During the past 2 decades, randomized trials have proved the efficacy of several treatments for non-ST-elevation acute coronary syndromes (NSTE-ACSs), including aspirin, beta blockers, and coronary revascularization. However, the cumulative effectiveness of these evolving therapies in actual clinical practice remains unknown. The Atherosclerosis Risk In Communities (ARIC) surveillance study uses rigorous prospective community surveillance to monitor the epidemiology of coronary heart disease among subjects who are 35 to 74 years of age and reside in 4 United States communities, with a population totaling 370,000 subjects. We identified 6,379 ARIC surveillance patients who were hospitalized with NSTE-ACS (defined as cardiac chest pain and ST depression or T-wave inversion on the presenting electrocardiogram) between 1987 and 2000 and then analyzed 30-day and 1-year mortalities by calendar year of admission. Using logistic regression, 30-day mortality was modeled first using predictor variables of the calendar year, ARIC community, and indicators of severity and co-morbidity and then by adding variables for treatment with aspirin, beta blockers, and coronary revascularization to this model. Crude 30-day mortality decreased from 8.6% in 1988 to 3.6% in 2000 (p for trend <0.001), a trend that remained significant (p = 0.006) after adjustment for case severity and co-morbidity. The trend became nonsignificant after adjustment for treatment variables, suggesting that newer treatments may explain the improved survival. In conclusion, 30-day mortality from NSTE-ACS has decreased as treatment has improved.
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PMID:Fourteen-year (1987 to 2000) trends in the attack rates of, therapy for, and mortality from non-ST-elevation acute coronary syndromes in four United States communities. 1627 76

Myotrophin is a 12 kDa protein initially isolated from hypertrophied hearts of spontaneously hypertensive rats and acts by modulating NF-kappaB (nuclear factor kappaB) activity. We have reported previously the presence of myotrophin in patients with human systolic heart failure; however, its role as a predictor of MACE (major adverse cardiac events) in patients with ACS (acute coronary syndrome) is unclear. In the present study, we sought to investigate this and compared myotrophin with NTproBNP (N-terminal pro-B-type natriuretic peptide), a marker of MACE. We studied 356 patients with ACS {276 men; mean age, 63.0+/-12.8 years; 80.6% STEMI [ST segment elevation MI (myocardial infarction)]; and 19.4% NSTEMI (non-STEMI)}. Blood measurement was made at 25-48 h after the onset of chest pain. The plasma concentration of myotrophin and NTproBNP was determined using in-house non-competitive immunoassays. Patients were followed-up for the combined end point of death, MI or need for urgent revascularization. Over the median follow-up period of 355 (range 0-645) days, there were 28 deaths, 27 non-fatal MIs and 73 patients required urgent revascularization. Myotrophin was raised in patients with MACE compared with survivors [510.7 (116.0-7445.6) fmol/ml compared with 371.5 (51.8-6990.4) fmol/ml respectively; P=0.001; values are medians (range)]. Using a Cox proportional hazards model, myotrophin {HR (hazard ratio), 1.64 [95% CI (confidence interval), 0.97-2.76]; P=0.05} and Killip class above 1 [HR, 1.52 (95% CI, 0.93-2.42); P=0.10] were the only independent predictors of MACE. A Kaplan-Meier survival curve revealed a significantly better clinical outcome in patients with myotrophin below the median compared with those with myotrophin above the median (log rank, 7.63; P=0.006). In conclusion, after an ACS, levels of myotrophin are more informative at predicting MACE than NTproBNP and may be useful to risk stratify patients.
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PMID:Myotrophin is a more powerful predictor of major adverse cardiac events following acute coronary syndrome than N-terminal pro-B-type natriuretic peptide. 1701 19

The majority of patients presenting to a primary care physician with acute chest pain will have non-life-threatening etiologies. Nevertheless, catastrophic cause of chest pain such as ACS, AD, PE, esophageal perforation, and pericarditis must be considered in the differential diagnosis. Often, these deadly conditions have atypical clinical presentations that must be recognized. Furthermore, the physical examination can be deceptively benign in patients harboring a catastrophic etiology of chest pain. By identifying these atypical presentations, recognizing the utility of the physical examination, and understanding of the limitations of traditional diagnostic imaging, primary care physicians can effectively diagnose patients who have life-threatening cause of acute chest pain.
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PMID:Identifying chest pain emergencies in the primary care setting. 1708 52

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

The GRACE (Global Registry of Acute Coronary Events) risk score has been shown to offer predictive power with regard to death and AMI (acute myocardial infarction) in patients with ACS (acute coronary syndromes). NT-proBNP (N-terminal pro-B-type natriuretic peptide) has also been found to be useful in predicting mortality following ACS. In the present study, we sought to investigate the use of the GRACE score and NT-proBNP levels at predicting risk of early and late deaths following ACS. We studied 1033 patients (740 men, mean age 66.5+/-12.7 years) with AMI. Blood was drawn once within 24 h following the onset of chest pain. The plasma concentration of NT-proBNP was determined using an in-house non-competitive immunoassay. Patients were GRACE risk scored. The 30-day mortality was 3.7% and the 6-month mortality was 7.8%, and all were related to higher GRACE risk scores (P=0.001 for trend). Higher NT-proBNP levels were also related to increased mortality (P<0.0001). In a Cox proportional hazards model, independent predictors of 30-day and 6-month mortality included NT-proBNP levels and the GRACE risk score. The receiver-operating curve for the GRACE risk score was complemented by NT-proBNP levels for prediction of 30-day mortality [AUC (area under the curve), 0.85] and 6-month mortality (AUC, 0.81). NT-proBNP gives complementary information to the GRACE risk score for predicting early and late mortality. The inclusion of the NT-proBNP blood test is useful in risk-stratifying patients after ACS.
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PMID:N-terminal pro-B-type natriuretic peptide complements the GRACE risk score in predicting early and late mortality following acute coronary syndrome. 1917 Jun 58

In the United States alone, nearly 6 million patients present annually to emergency departments with complaints of chest pain suggestive of acute coronary ischemia. Most of these patients have a non-negligible risk for acute coronary syndrome(s) (ACS) and undergo extended observation and workup for an ischemic cause. Of those admitted for extended observation, less than 30% of patients have true ACS. In patients with a low to intermediate probability, cardiac CT performs well in ruling out coronary artery disease, and American College of Cardiology and American Heart Association guidelines deem this application to be "appropriate." This article reviews the application of CT for the evaluation of acute chest pain the emergency department.
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PMID:Cardiac CT in the emergency department. 1976 15

Anginal chest pain is one of the most common complaints in the outpatient setting. While much of the focus has been on identifying obstructive atherosclerotic coronary artery disease (CAD) as the cause of anginal chest pain, it is clear that microvascular coronary dysfunction (MCD) can also cause anginal chest pain as a manifestation of ischemic heart disease, and carries an increased cardiovascular risk. Epicardial coronary vasospasm, aortic stenosis, left ventricular hypertrophy, congenital coronary anomalies, mitral valve prolapse, and abnormal cardiac nociception can also present as angina of cardiac origin. For nonacute coronary syndrome (ACS) stable chest pain, exercise treadmill testing (ETT) remains the primary tool for diagnosis of ischemia and cardiac risk stratification; however, in certain subsets of patients, such as women, ETT has a lower sensitivity and specificity for identifying obstructive CAD. When combined with an imaging modality, such as nuclear perfusion or echocardiography testing, the sensitivity and specificity of stress testing for detection of obstructive CAD improves significantly. Advancements in stress cardiac magnetic resonance imaging enables detection of perfusion abnormalities in a specific coronary artery territory, as well as subendocardial ischemia associated with MCD. Coronary computed tomography angiography enables visual assessment of obstructive CAD, albeit with a higher radiation dose. Invasive coronary angiography remains the gold standard for diagnosis and treatment of obstructive lesions that cause medically refractory stable angina. Furthermore, in patients with normal coronary angiograms, the addition of coronary reactivity testing can help diagnose endothelial-dependent and -independent microvascular dysfunction. Lifestyle modification and pharmacologic intervention remains the cornerstone of therapy to reduce morbidity and mortality in patients with stable angina. This review focuses on the pathophysiology, diagnosis, and treatment of stable, non-ACS anginal chest pain.
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PMID:Nonacute coronary syndrome anginal chest pain. 2038 Sep 51

Acute chest pain is a common symptom but triage decisions in these patients remain a challenge. Patient's history, cardiac enzyme levels, or electrocardiograms often are unspecific. Nowadays, multidetector-row computed tomography (CT) currently represents the imaging modality of choice for diagnosing or excluding pulmonary embolism (PE) or acute aortic syndrome (AAS). Furthermore, recent studies have demonstrated advantages for non-invasive imaging of the coronary arteries by CT. The so called triple rule-out CT allows the depiction of the pulmonary arteries, the thoracic aorta, and the coronary arteries within a single examination with a simultaneous attenuation of these three vessel territories. This enables the detection of life-threatening such as PE, AAS and ACS, as well as of non-life-threatening diseases causing acute chest pain.
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PMID:[Use of multislice CT in the evaluation of patients with acute chest pain]. 2044 22

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

1. Patients presenting with ACS are at high risk of subsequent events and if ischaemic sounding chest pain is associated with either a raised troponin, dynamic ECG changes or other high risk features, inpatient coronary angiography should be arranged within 72 hours. 2. Patients with either ongoing chest pain and ECG changes despite medical treatment, ventricular arrythmias, or cardiogenic shock / haemodynamic compromise require emergency coronary angiography. 3. For patients with suspected ACS but no high risk features (Table 4) a non invasive test for myocardial ischaemia prior to discharge is recommended 4. In patients with renal impairment (creatinine .220) and chronically elevated troponin in whom an acute coronary syndrome is suspected additional cardiac markers such as CK or CK-MB as well as consecutive troponin measurements on admission and 12 hours are helpful to identify whether the patient sustained acute cardiac damage.
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PMID:Management of Non-STEMI and suspected Acute Coronary Syndrome. 2160 2


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