Ischemia-modified albumin (IMA) has been proposed as a biological marker of myocardial ischemia (1, 2 ). Exposure to ischemic myocardium modifies circulating albumin at its NH 2 terminus by different mechanisms, and this modification is the basis of IMA measurement by the albumin cobalt binding (ACB) test (3 ). The tissue-specific nature of the mechanism by which ischemia modifies albumin remains undetermined. Together with a nondiagnostic electrocardiogram and negative troponin values, IMA concentrations within the reference interval have high negative predictive value of myocardial ischemia in patients with suspected acute coronary syndromes (1, 2 ). However, IMA cardiospecificity has not been validated and needs an evidence base before routine clinical use. A recent report showed significant IMA increases 24 -48 h after a marathon race, with exercise-promoted gastrointestinal and/or delayed skeletal muscle ischemia being evoked as possible causes of such increases (4 ). However, because IMA has shown rapid kinetics of increase (in minutes) and return to baseline no longer than 12 h after angioplastic procedures (5 ), long-duration skeletal muscle ischemia (i.e., occurring during marathons) does not appear to be the most appropriate model to investigate the effect of such ischemia on IMA values or the kinetics of IMA occurring during acute coronary syndromes. The aim of this work was to analyze the possible contribution of skeletal muscle ischemia to IMA by investigating its short-term kinetics in an isolated skeletal-muscle ischemia model. Because lactate and ammonia concentrations increase sharply after a forearm ischemia test, their possible influence in the ACB assay was studied.Ten healthy volunteers (4 men and 6 women) from our laboratory staff (age range, 48 -61 years; median, 53 years) with no personal or family history of cardiovascular disease and no known cardiovascular risk factors after a medical examination underwent a forearm ischemia test (6 ). Briefly, after an overnight fast (10 -12 h) and 30 min of previous rest, a preexercise (0 min) blood sample was drawn, and blood systolic pressure was recorded twice within a 5-min interval. Thereafter, forearm ischemia was produced by inflating the blood pressure cuff up to 20 -30 mmHg higher than the maximum systolic pressure registered. Under these ischemic conditions, a hand-grip exercise at maximum possible strength was performed for 1 min. Thereafter, the cuff was removed, and serial blood samples were drawn at 1, 3, 5, 10, 15, and 30 min. Serum for IMA, creatine kinase, and potassium; EDTA plasma for ammonia; and fluoride plasma for lactate and glucose were collected at each time point into Vacutainer ® Tubes (Becton Dickinson). To establish reference values, IMA was tested in a group of 86 fasting (10 -12 h), ambulatory (median age, 57 years; 38 women) sedentary individuals who underwent blood sampling after health examinations or before minor surgical procedures. Individuals with cardiovascular risk factors or past or present signs or symptoms o...

No abstract

No abstract

Serum creatine kinase isoenzyme 2 concentrations (CK 2 mass) were measured in marathon runners during training and 1 and 2 days after a race and compared with values from 36 acute myocardial infarction (AMI) patients whose total CK and (or) CK 2 activities were similar to those of runners in the basal state. During training, runners had CK and CK 2 activities 53% and 43% above reference values, respectively, and 36% had CK 2 activity > 5% of total CK. Nine runners (26%) showed CK 2 mass values > 6 micrograms/L but < or = 10 micrograms/L; 35 of the AMI subjects, despite having CK activities similar to those of runners, had values > 10 micrograms/L. The ratio of CK 2 mass to total CK activity was significantly (P < 0.0002) different between sexes for runners. At 1 and 2 days after racing, 100% of CK and CK 2 activities and 71% and 57% of the percentages of CK 2 activity, respectively, were abnormally high; 57% and 43% of CK 2 mass values were > 10 micrograms/L, being comparable with those observed for the AMI group. Basal CK 2 mass values of the runners appeared only slightly higher than that for sedentary subjects, but after exercise half the subjects presented increased values similar to those observed for AMI subjects. The ratio of CK 2 mass to total CK activity appeared unaltered by exercise in all but one of the samples assayed, indicating its utility in evaluating CK 2 mass increases originating in skeletal muscle.

Acutely dyspneic patients are challenging, because their symptoms can be due to cardiac, pulmonary or other diseases. B-type natriuretic peptide testing offers higher diagnostic accuracy (85%-90%) than clinical assessments for identifying heart failure as the cause of dyspnea. On the other hand, the high clinical sensitivity and negative predictive value of natriuretic peptides permit to rule out heart failure with an accuracy > 90%. Natriuretic peptides are the most powerful, single prognostic markers of complications associated with acute dyspnea and permit the early recognition of high-risk patients. It has been shown that systematic natriuretic peptide testing reduces the economic expenses associated with clinical management of acutely dyspneic patients. Finally, whether these biomarkers could be used to guide heart failure therapy in the acute setting remains to be elucidated.