[N-terminal pro-brain natriuretic peptide (NT-proBNP) and ischemia modified albumin (IMA) in exercise induced ischemia in patients with stable coronary artery disease].
Ključne riječi
Sažetak
BACKGROUND
Preliminary data indicate that B type natriuretic peptides' levels may rise in exercise induced myocardial ischemia in patients with stable coronary artery disease. Such findings hint at a potential broader application of these markers reaching beyond its present use in chronic heart failure and acute coronary syndromes. Ischemia modified albumin (IMA) is a novel diagnostic marker in acute coronary syndromes as its value increases in states of myocardial ischemia and necrosis. The role of this marker in the assessment of exercise induced myocardial ischemia in stable coronary artery disease has not been extensively investigated and remains unknown.
OBJECTIVE
To examine changes in N-terminal pro-brain natriuretic peptide (NT-proBNP) and ischemia modified albumin (IMA) during an ECG stress test in patients with stable coronary artery disease and to assess the potential of these markers to detect exercise induced myocardial ischemia.
METHODS
Patients with angiographically confirmed coronary atherosclerosis were included into the study. In all of them prognostic ECG stress test according to Bruce protocol was performed. The test was considered true positive (ischemia present) in case of significant ST-segment depression in the presence of significant coronary stenosis. The test was considered true negative (ischemia absent) when no significant ST depression was noted in the absence of significant coronary stenosis. In all patients echocardiography was performed and blood was drawn for NT-proBNP, IMA, serum albumin and creatinine before and within the first five minutes after exercise.
RESULTS
41 patients with unequivocal stress test result corresponding to coronary angiogram were included in the final analysis (out of 51 examined patients). 21 patients demonstrated ischemia during exercise, 20 did not. NT-proBNP concentration was significantly higher after the stress test than before in the whole group: 127.9 (10.7-994.2) pg/ml and 110 (10.5-990.2) pg/ml respectively; p < 0.0001. NT-proBNP increase was higher in the ischemic than in the non-ischemic group; however, the difference was not statistically significant: deltaNT-proBNP 12.3 (1.0-172.3) pg/ml and 4.2 (1.0-77.1) pg/ml respectively; p = 0.09. This manifested itself in poor sensitivity and specificity of NT-proBNP in detecting exercise induced myocardial ischemia: 62 and 55% respectively (AUC 0.589). In the whole group the increase of NT-proBNP depended on baseline NT-proBNP concentration (r = 0.54; p = 0.0003), the magnitude of ST-segment depression (r = 0.38; p = 0.01), creatinine concentration (r = 0.34; p= 0.03) and history of myocardial infarcion: log deltaNT-proBNP in post-MI patients and in patients without prior MI 1.19 ( +/- 0.54) i 0.61 ( +/- 0.57) respectively; p = 0.004. In multiple regression analysis the only factor independently determining NT-proBNP increase during exercise was the history of myocardial infarction (beta = 0.342; p = 0.01) but not left ventricle ejection fraction. IMA decreased during exercise in all patients significantly--the mean value before and after exercise was 88.20 (7.72) and 78.05 (8.33) U/ml respectively; p = 0.0001. Decrease in IMA correlated only with increase in albumin concentration measured before and after exercise (r = -0.6; p < 0.0001).
CONCLUSIONS
Exercise induced myocardial ischemia has little influence on NT-proBNP increase. The test measuring it has therefore insufficient ability to detect exercise induced ischemia in stable coronary artery disease. In patients with stable coronary artery disease without severe impairment of left ventricular function the history of myocardial infarction is the main factor determining NT-proBNP increase during exercise. Changes in serum albumin concentration during exercise seem to exclude the use of IMA in the assessment of exercise induced myocardial ischemia.
