Discrimination Between Myocardial and Skeletal Muscle Injury by Assessment of the Plasma Ratio of Myoglobin Over Fatty Acid–Binding Protein

Nieuwenhoven, Frans A. van; Kleine, Appie H.; Wodzig, K.W.H.; Hermens, Wim Th.; Kragten, Hans; Punt, C. D.; Dieijen, Marja P. Van; Vusse, Ger J.; Glatz, Jan F. C.

doi:10.1161/01.cir.92.10.2848

Cited by 193 publications

(116 citation statements)

References 23 publications

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“…Moreover, in patients with acute myocardial infarction, it has been observed that the H type of FABP released from damaged or ischemic cardiac muscle appears in blood at the acute phase. 14 Recently, in comparison with the creatinine kinase MB-isoform or troponin-T, the blood concentration of H-type FABP was most sharply increased in patients visiting emergency departments for chest pain. Sandwich ELISA was found to be particularly useful for discovery of acute coronary syndrome within 6 h after its onset.…”

Section: Discussionmentioning

confidence: 99%

Renal L-Type Fatty Acid–Binding Protein in Acute Ischemic Injury

Yamamoto

Noiri

Ono

et al. 2007

Journal of the American Society of Nephrology

325

291

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Fatty acid-binding proteins (FABPs) bind unsaturated fatty acids and lipid peroxidation products during tissue injury from hypoxia. We evaluated the potential role of L-type FABP (L-FABP) as a biomarker of renal ischemia in both human kidney transplant patients and animal models. Urinary L-FABP levels were measured in the first urine produced from 12 living-related kidney transplant patients immediately after reperfusion of their transplanted organs, and intravital video analysis of peritubular capillary blood flow was performed simultaneously. A significant direct correlation was found between urinary L-FABP level and both peritubular capillary blood flow and the ischemic time of the transplanted kidney (both P Ͻ 0.0001), as well as hospital stay (P Ͻ 0.05). In human-L-FABP transgenic mice subjected to ischemiareperfusion injury, immunohistological analyses demonstrated the transition of L-FABP from the cytoplasm of proximal tubular cells to the tubular lumen. In addition, after injury, these transgenic mice demonstrated lower blood urea nitrogen levels and less histological injury than injured wild-type mice, likely due to a reduction of tissue hypoxia. In vitro experiments using a stable cell line of mouse proximal tubule cells transfected with h-L-FABP cDNA showed reduction of oxidative stress during hypoxia compared to untransfected cells. Taken together, these data show that increased urinary L-FABP after ischemic-reperfusion injury may find future use as a biomarker of acute ischemic injury.

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Section: Discussionmentioning

confidence: 99%

Renal L-Type Fatty Acid–Binding Protein in Acute Ischemic Injury

Yamamoto

Noiri

Ono

et al. 2007

Journal of the American Society of Nephrology

325

291

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“…Serum DNase I activity was significantly elevated within 3 hours of the onset of acute chest pain in the patients with AMI, whereas the serum levels of CK-MB and troponin T were slightly elevated and exceeded the cutoff levels in approximately 45% of those patients; we were thus able to detect the elevation of the serum DNase I activity earlier than that of CK-MB and troponin T. As an early marker for myocardial necrosis, the serum myoglobin level is a sensitive test but lacks cardiac specificity, because there may be an elevation in the serum levels of myoglobin secondary to musculoskeletal injury. 13 However, the serum DNase I activity level does not rise after trauma, and surgical trauma has been reported to induce no elevation of the activity, 14 suggesting that DNase I may be a more specific marker for AMI than myoglobin. Furthermore, there is a slight overlap between the levels of activity in patients with AMI and patients with OD (Figure, C).…”

Section: Discussionmentioning

confidence: 99%

Diagnostic Use of Serum Deoxyribonuclease I Activity as a Novel Early-Phase Marker in Acute Myocardial Infarction

et al. 2004

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Background-The delayed release of serum cardiac markers such as creatine kinase isoenzyme MB and equivocal early electrocardiographic changes have hampered a diagnosis of acute myocardial infarction (AMI) in the early phase after its onset. Therefore, a reliable serum biochemical marker for the diagnosis of AMI in the very early phase is desirable. Methods and Results-Serum samples were collected from the patients with AMI, unstable angina pectoris, stable angina pectoris, and other diseases. Levels of serum deoxyribonuclease I (DNase I) activity in the patients were determined. An abrupt elevation of serum DNase I activity was observed within approximately 3 hours of the onset of symptoms in patients with AMI, with significantly higher activity levels (21.7Ϯ5.10 U/L) in this group compared with the other groups with unstable angina pectoris (10.4Ϯ4.41 U/L), angina pectoris (10.8Ϯ3.70 U/L), and other diseases (9.22Ϯ4.16 U/L). Levels of the DNase I activity in serum then exhibited a marked time-dependent decline within 12 hours and had returned to basal levels within 24 hours. Conclusions-We suggest that serum DNase I activity could be used as a new diagnostic marker for the early detection of AMI. Key Words: myocardial infarction Ⅲ enzymes Ⅲ diagnosis I n patients with acute myocardial infarction (AMI), the infarct size is an important determinant of both mortality and morbidity. 1 When revascularization and thrombolytic therapies are initiated rapidly, there is a greater potential for reduction in the infarct size. The release of cardiac proteins from injured cardiac tissue into plasma has been used as a diagnostic marker for the exclusion or confirmation of AMI. 2 However, it is often difficult to make a diagnosis of AMI in the very early phase, ie, within 3 hours of onset. This is partly due to a delay in the appearance in the serum of the biochemical markers specific for myocardial damage. 2,3 Deoxyribonuclease I (DNase I, EC 3.1.21.1), one of the well-known enzymes, was the first enzyme to be recognized as specific for DNA. 4 One of its proposed roles is DNA breakdown during apoptosis. 5 DNase I has been detected in human myocardium, and it has been reported that the activity level increases in heart failure due to idiopathic dilated cardiomyopathy. 6 However, the association between serum DNase I activity level and coronary heart disease (CHD) has not yet been clarified. In the present study, we assessed the serum DNase I activity in patients with AMI and related CHD and found that there is a specific elevation of serum DNase I activity in the very early stages of AMI. Methods Patients and Sample CollectionWe assessed 53 consecutive Japanese patients with AMI admitted to our hospitals between September 2002 and May 2003. The clinical diagnosis of AMI and unstable angina pectoris (UAP) was made according to the European Society of Cardiology/American College of Cardiology Committee criteria. 7 The mean lapse time between the onset of symptoms and hospital admission was 10.7Ϯ13.8 hours. Emergent coronary ang...

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“…H-FABP is produced mainly in the heart, but to a lesser extent, it is also produced in skeletal muscle (58 ). When patients suffered skeletal muscle injury as a result of cardioversion, multiorgan failure, postoperative states, or vigorous exercise such as running (59 ) or rowing (60 ), H-FABP was released into the blood.…”

Section: Clinical Interpretation Of Plasma H-fabp Concentrationsmentioning

confidence: 99%