In spite of early contemporary reperfusion therapy by primary percutaneous intervention (PPCI), ST – elevation myocardial infarction (STEMI) can lead to systolic and/or diastolic dysfunction with decreased cardiac output, leading to acute heart failure, acute kidney injury, suden cardiac death and increased mortality. Neutrophil gelatinase – associated lipocalin (NGAL) is a novel early marker of acute kidney injury for which has been shown that it can also be released from the injured myocardium.
Our aim was to correlate urine NGAL with markers of in-hospital heart failure (NT-proBNP ≥ 400 pmol/l, Kilip class ≥ II, ejection fraction of left ventricle < 50 %) in patients with acute STEMI after PPCI.
We performed an observational prospective monocentric study with patients addmitted with acute STEMI to the Department of Medical Intensive Care (ICU) University Medical Centre Maribor. We prospectively included 61 consecutive STEMI patients after PPCI between April 2010 and July 2011 and estimated admission and in-hospital urine NGAL, serum creatinine, troponin I, leucocytes, CRP, NT-proBNP and ejection fraction by echocardiography. Urine NGAL levels were measured on admission and after 12 h. We compared urine NGAL levels between patients with and without heart failure defined as serum NT-proBNP ≥ 400 pmol/l. Urine NGAL levels on admission and after 12 h were correlated to markers of heart failure (NT-proBNP, EF), inflammation (CRP), kidney function (creatinine) and markers of ishemic necrosis (troponin I).
Urine NGAL levels were within normal levels (137 ng/ml) in most of our patients. Average urine NGAL levels on admission were 24.5 ± 42.1 ng/ml and after 12 h 27.7 ± 42.7 ng/ml. When comparing participants with heart failure (NT-proBNP ≥ 400 pmol/l) to those with NT-proBNP below 400 pmol/l, the urine NGAL levels on admission (45.0 ± 65.2 ng/ml, vs. 14.8 ± 19.2 ng/ml; p < 0.01) and after 12 h (53.8 ± 63.6 ng/ml, vs. 15.5 ± 18.3 ng/ml, p < 0.01) as well as CRP levels (59.5 ± 74.9 mg/l, vs. 21.3 ± 23.3 mg/, p < 0.01) were all significantly higher among those with heart failure. The two groups did not differ in creatinine levels on admission (117.3 ± 60.7 μmol/l, vs. 96.4 ± 34.4 μmol/l, p > 0.05), leucocyte count on admission (12.6 ± 5.1 x 1012/l, vs. 10.5 ± 3.7 x 1012/l, p > 0.05), troponin I levels after 12 h (65.3 ± 37.7 μg/l, vs. 50.8 ± 36.5 μg/l, p > 0.05), peak troponin I levels (75.6 ± 44.6 μg/l, vs. 58.8 ± 36.2 μg/l, p > 0.05) and amount of contrast material used (160.3 ± 69.6, vs. 142.0 ± 67.3 ml, p > 0.05). Urine NGAL level of 50 ng/ml had 90% specifity for heart failure, its sensitivity was low at 25%. Comparison of participants with NGAL levels < 50 ng/ml and ≥ 50 ng/ml at admission and after 12 h revealed a significant difference in NT-proBNP levels, left ventricle ejection fraction, markers of inflammation and of kidney function. Urine NGAL level was independently associated with NT-proBNP level.
The level of urine NGAL early after myocardial infarction is correlated with NT-proBNP concentration. Even NGAL levels below 137 ng/ml, the usually reported normal cut-off value, had high specificity for heart faiure in our sample.|