|Year : 2018 | Volume
| Issue : 1 | Page : 42-51
Heart-type fatty-acid-binding protein is a prognostic biomarker for sepsis outcome and sepsis-related left-ventricular dysfunction: a comparison with troponin I
Mohamed Abul Wafa, Hossam M Sherif, Ayman Gaber, Wael Sami
Critical Care Medicine Department, Faculty of Medicine, Cairo University, Cairo, Egypt
|Date of Web Publication||24-Jan-2018|
Hossam M Sherif
Critical Care Center, Cairo University Hospitals, El Manial, Cairo, 11562
Source of Support: None, Conflict of Interest: None
Background Using heart-type fatty-acid-binding protein (H-FABP) in critically ill patients provides a superior results than the conventional cardiac biomarkers.
Objective The aim of the study was to estimate the prognostic significance of H-FABP in patients with septic shock and the prevalence of sepsis-related myocardial dysfunction in comparison to troponin I.
Patients and methods Fifty ICU patients with sepsis were enrolled in this study. All patients were evaluated using Acute Physiology and Chronic Health Evaluation II score on admission and every 24 h during ICU stay. Serum levels of both H-FABP and troponin I were investigated during the first 24 h after admission. Using modified Simpson’s method, echocardiographic left-ventricular end-diastolic volume (LVEDV), left-ventricular end-systolic volume (LVESV), and left-ventricular ejection fraction (LV%EF) were calculated on admission and after 24 h.
Results The patients were divided into two groups: group 1, which included 12 patients (mean age: 50.2±21 years) suffering from sepsis; and group 2, which included 38 patients (mean age: 58.4±19.2 years) with septic shock. Compared with group 1, H-FABP of group 2 showed significant higher values (76.3 vs. 33.3% of patients, P<0.05). In both groups, compared with patients with negative H-FABP, patients with positive H-FABP showed significantly increased values (66 vs. 34%, P<0.05). The positive H-FABP patients showed significantly increased left ventricular volumes (LVEDV=105 vs. 77 ml, P<0.05; and LVESV=49 vs. 33 ml, P<0.05). The mortality rate was significantly higher in group 2 compared with group 1 (78.9 vs. 41.7%, P<0.05). H-FABP was a better prognostic marker than troponin I; it showed an increased prevalence of mortality (88 vs. 35%, P<0.001) with good correlation (r=0.54, P<0.05).
Conclusion In septic shock, H-FABP can be used as a prognostic marker for mortality rathar than troponin I. The positive H-FABP patients showed a significant relation with sepsis-related left-ventricular systolic myocardial dysfunction.
Keywords: heart-type fatty-acid-binding protein, left-ventricular dysfunction, multiorgan dysfunction syndrome, sepsis, troponin I
|How to cite this article:|
Abul Wafa M, Sherif HM, Gaber A, Sami W. Heart-type fatty-acid-binding protein is a prognostic biomarker for sepsis outcome and sepsis-related left-ventricular dysfunction: a comparison with troponin I. Res Opin Anesth Intensive Care 2018;5:42-51
|How to cite this URL:|
Abul Wafa M, Sherif HM, Gaber A, Sami W. Heart-type fatty-acid-binding protein is a prognostic biomarker for sepsis outcome and sepsis-related left-ventricular dysfunction: a comparison with troponin I. Res Opin Anesth Intensive Care [serial online] 2018 [cited 2019 Mar 18];5:42-51. Available from: http://www.roaic.eg.net/text.asp?2018/5/1/42/223838
| Introduction|| |
In sepsis, up to 50% of patients may suffer from cardiac dysfunction that contributes to an elevated mortality rate compared with those without cardiovascular impairment . In this regard, some cardiac biomarkers such as cardiac troponins (troponin I), MB-isoenzyme of creatine kinase, and B-type natriuretic peptides are commonly used in the ICU .
However, interpretation of these biomarkers may be confounded by a lot of factors including severity of the disease, multiorgan dysfucntion, and altered synthesis/clearance . Therefore, it is still necessary to find additional novel biomarkers for clinical use ,.
Heart-type fatty-acid-binding protein (H-FABP), an emerging cardiac biomarker, is a small cytosolic protein abundant in cardiomyocyte that binds to and has a role in uptake and transport of long-chain fatty acids. It is rapidly released from cardiomyocytes into the circulation shortly after the onset of cell damage .
H-FABP has been reported to be a promising biomarker of myocardial damage and clinical outcome in acute coronary syndrome , and useful in the prediction of cardiac dysfunction and adverse outcomes in congestive heart failure, pulmonary embolism, and cardiac surgery with cardiopulmonary bypass .
In contrast, serum troponin I, which is a well-known biomarker of myocardial injury, was found to be increased in patients with sepsis ,. Several theories explained why troponin I is elevated in septic patients including stress-mediated myocarditis and microthrombosis ,. However, due to lack of specificity, its use is limited in the diagnosis of sepsis-related myocardial dysfunction .
H-FABP offers better sensitivity than troponin I in detecting ongoing myocardial damage in congestive heart failure  and has better discriminatory ability for pulmonary embolism-related complications than troponin I and N-terminal-pro-B-type natriuretic peptide . The superiority of H-FABP over classic biomarkers may result from its faster increase and more rapid clearance that make it more sensitive in detection of cardiac dysfunction . The low molecular weight and relative tissue specificity of H-FABP may also contribute to the advantage in reflecting minor myocardial damages during sepsis .
Few studies ,,,, however, have investigated the utility of H-FABP in critically ill patients with sepsis or septic shock; whether H-FABP offers similar or even superior power to the conventional cardiac biomarkers in critically ill septic patients is to be further elucidated.
Our aim in this study was to find the prognostic value of H-FABP for the adverse outcomes and mortality in septic patients (sepsis or septic shock) without prior cardiovascular impairment in comparison to the routinely used cardiac biomarker troponin I.
| Patients and methods|| |
This prospective cohort study included 50 patients admitted from March 2013 until March 2014 to the Critical Care Department, Cairo University Hospitals. This investigation was approved by the Ethical Committee Review Board of the Faculty of Medicine, Cairo University. Consents were acquired from each patient before the enrollment in the study.
According to the hemodynamic instability, all patients were classified according to the degree of their sepsis into :
- Group 1: sepsis.
- Group 2: septic shock.
Criteria for sepsis and septic shock had followed the modification of the third International Consensus Definitions for Sepsis and Septic Shock (Sepsis 3) .
The variables used for patients’ stratification were as follows :
- Fever (>38.3°C).
- Hypothermia (core temperature<36°C).
- Tachycardia (>100 beats/min).
- Tachypnea (>20 breaths/min).
- Altered mental status.
- Significant edema all over the body or positive fluid balance (>20 ml/kg/24 h).
- Hyperglycemia (plasma glucose>140 mg/dl) without a history of diabetes mellitus.
- Leukocytosis [white blood cell (WBC) count>12 000/µl] or leukopenia (WBC count<4000/µl) or normal WBC count with more than 10% immature cells.
- Plasma C-reactive protein (CRP) more than 2 SD above the normal value and the serum concentration of CRP less than 10 mg/l in 99% of normal samples .
- Arterial hypotension: systolic blood pressure less than 90 mmHg, mean arterial blood pressure less than 70 mmHg, or systolic blood pressure decrease more than 40 mmHg.
Organ dysfunction variables
- Arterial hypoxemia (PaO2/FiO2<300).
- Acute oliguria (urine output<0.5 ml/kg/h for at least 2 h despite adequate fluid resuscitation).
- Serum creatinine increase more than 0.5 mg/dl.
- Coagulation abnormalities (international normalized ratio>1.5 or activated partial thromboplastin time>60 s).
- Ileus (absence of bowel sounds).
- Thrombocytopenia (platelet count<100 000/µl).
- Hyperbilirubinemia (plasma total bilirubin>4 mg/dl).
Tissue perfusion variables
- Decreased capillary refill or mottling.
- Increase serum lactate level less than 2 mmol/l.
- History of heart, hepatic, or renal diseases.
- Evidence of acute myocardial ischemia.
- Evidence of acute pulmonary embolism.
During the first 24 h, all patients were subjected to the following:
- Full history and clinical examination.
- Laboratory blood tests:
- Complete blood counts on admission.
- Liver function tests to detect the presence of liver dysfunction including aspartate transaminase, alanine aminotransferase, and serum albumin.
- Kidney function tests: blood urea and serum creatinine.
- Coagulation profile.
- Arterial blood gasses.
- 12-Lead ECG and plain chest radiograph.
- Acute Physiology and Chronic Health Evaluation II (APACHE II) score : calculated using 12 routine physiological measurements.
- Serum level of H-FABP:
- H-FABP was measured using a colloidal gold rapid test strip of human H-FABP at room temperature. The result was shown as the appearance of one or two red bands in the test-card window after 15 min. Two red bands at the test and control zones were considered as a positive result and one band at the control zone was considered as a negative result. No band would develop at both zones if the trial were invalid ([Figure 1]). The test strip was then placed into the Quick-Sens Omega 100 analyzer (8sens Biognostic GmbH, Berlin, Germany) and the level of H-FABP could be read on the screen. The test was considered positive when H-FABP concentration was more than 10 ng/ml. The sensitivity of this technique was 95.3% and the specificity was 96.2% .
|Figure 1 Heart-type fatty acid binding protein test strip. The purple control line (C-line) indicates that the test works properly. The test should be repeated if the control line does not appear and if the test line (T-line) appears without C-line.|
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- All the procedures were performed by laboratory technicians who were blinded to our clinical data.
- Serum level of troponin I:
- The laboratory test was carried out as a quantitative determination of the serum troponin I using an assay protocol and carried out on an acssess analyzer ; all reagents and samples were at room temperature (18–26°C) before its use in the assay. Positioning was marked for blank/standard/sample/control on the protocol sheet. Troponin I values 0.02 ng/ml or less were considered as normal.
- Each patient was examined in the left lateral decubitus position following the American Society of Echocardiography recommendations. Images were aquired from each part of the examination sequence together with lead-II of ECG and were stored on a videotape for subsequent analysis .
We utilized a Philips/ATL HDI 5000 color-Doppler echocardiography machine with a 3.5 MHz transducer, available in the Critical Care Center, Cairo University Hospitals, to record two-dimensional-echocardiography (2DE) and M-mode in the classic three views: long, short parasternal, and apical.
Evaluation of left ventricular systolic function
- The standard views of the 2DE were used in each patient:
- Parasternal long axis view.
- Parasternal short axis view at different levels [great vessels, left ventricule (LV) at mitral valve leaflets and papillary muscles].
- Apical views: four-chamber, five-chamber, and two-chamber views.
- The biplane Simpson’s method :
- Estimation of LV volumes and left ventricular ejection fraction (LV%EF) were carried out using manual tracing of sequential short-axis views of LV from the apex to the mitral annulus. Following selection of LV long-axis view, end-diastolic (the first frame before closure of the mitral valve) and then end-systolic (the first frame before the opening of the mitral valve) datasets were selected. This resulted in the generation of equidistant cross-sections of LV. The computer displayed similar short-axis view in a static display for manual endocardial tracing. When manual tracing of the short-axis was completed, the system calculated the volume of 3-mm thick slice by summing up the voxels included in the traced area. Slice by slice, the system summed corresponding subvolumes and finally calculated left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV). The system then calculated the values of LV%EF.
- Two-dimensional study parameters included:
- Assessment of LV contractility.
- Assessment of LV regional function.
- Under the guidance of 2DE, using parasternal views, the M-mode cursor was positioned at the level of the mitral valve leaflets tips to measure the followings:
- The left-ventricular end-systolic dimension (LVESd) and left-ventricular end-diastolic dimension (LVEDd) (normal: ≤5.6 cm) were measured at the end of T-wave and R-wave of the ECG, respectively.
- The LV fractional shortening percentage was calculated as: [(LVEDd−LVESd)/LVEDd]×100 (normal: 25–45%).
- The LV%EF (systolic dysfunction was defined as LV%EF below 55%).
- Posterior wall thickness diameter.
- Interventricular septal thickness diameter.
- The right ventricular end-diastolic diameter.
- Aortic root.
- Left atrium.
- Septal flattening and notch.
Numerical variables were described as mean±SD. Categorical variables were described as percentages. Comparisons were carried out using Student’s t-test for numerical variables and χ2-test for categorical variables. Correlations were plotted, and r values were calculated using Spearma’s correlation. Paired t-test was used to compare baseline and follow-up measurements. We used analysis of variance test for analyzing the differences among multiple groups’ means. Kaplan–Meier curves were plotted to assess mortality between sepsis and septic shock groups and between positive and negative H-FABP states. P value was considered significant if 0.05 or less. Statistics were calculated using SPSS 12.0 (SPSS Inc., Chicago, Illinois, USA) software.
| Results|| |
A total of 50 patients (52% male) were enrolled in this study. The patients were divided into two groups ([Table 1]).
In our study, three patients had no organ dysfunction, 19 had single-organ dysfunction, and 28 patients had multiorgan dysfunction; acute kidney injury was encountered in 76% patients, altered neurological manifestations in 56%, hepatic dysfunction in 30%, and respiratory failure in 2%.
Compared with group 1, patients in group 2 had a statistically significantly higher prevalence of multiorgan dysfunction syndrome (MODS) with more number of affected organs (1.8±0.8 organs for group 2 vs. 1.1±0.5 organs for group 1, P<0.001).
In all patients, the positive values of H-FABP and troponin I showed a statistically significantly higher percentage (66 and 22%, respectively) ([Figure 2]).
|Figure 2 Cardiac biomarkers in all patients. H-FABP, heart-type fatty acid binding protein.|
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Compared with group 1, patients in group 2 showed statistically significantly more positive H-FABP values [29/38 (76%) patients in group 2 vs. 4/12 (33%) patients in group 1, P<0.05]. However, with troponin I the data were comparable between both groups; 10 (26%) patients in group 2 and one (8%) patient in group 1 showed increased troponin I values.
Only 33% of positive H-FABP patients had positive troponin I, whereas in all negative H-FABP patients, the troponin I was negative (r=0.38, P=NS).
Need for mechanical ventilation or vasopressors
Eighty-six percent of all patients needed vasopressors (VPs) and 80% needed mechanical ventilation (MV) ([Table 2]).
Need for mechanical ventilation
Patients who needed MV showed statistically significantly higher prevalence for positive H-FABP than patients with positive troponin I values (77.5 vs. 27.5% for positive troponin I) ([Table 3]).
Need for MV showed a good correlation with positive H-FABP (r=0.49, P<0.001), but poor correlation with positive troponin I values (r=0.27, P=NS).
Need for vasopressors
Patients who needed VP showed statistically significantly higher prevalence for positive H-FABP than patients with positive troponin I values (72.1 vs. 23.3% for positive troponin I) ([Table 4]).
Need for VP showed a good correlation with positive H-FABP (r=0.32, P<0.05), but no correlation could be detected with positive troponin I values.
Acute Physiology and Chronic Health Evaluation II score
The mean value of APACHE II score in all patients was 28.14±11.1. Compared with the values in group 1, patients in group 2 showed statistically significantly lower values (16.2±7.1 vs. 31.9±9.3, P<0.001).
Compared with patients with both negative H-FABP and negative troponin I values, patients with positive H-FABP or positive troponin I values showed significantly higher APACHI II score reflecting the severity of the clinical illness ([Table 5]).
Prevalence of multiorgan dysfunction syndrome
Patients with positive H-FABP showed a higher prevalence of MODS, but the data were comparable with troponin I ([Figure 3]).
|Figure 3 Cardiac biomarkers and prevalence of multiorgan dysfunction syndrome (MODS) in all patients. H-FABP, heart-type fatty acid binding protein.|
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Echocardiographic examination of all patients showed good LV%EF (54.5±12%), LVEDV (95.4±43.9 ml), and LVESV (43.9±25.3 ml).
Compared with group 1, patients in group 2 showed statistically significantly higher LVEDV. In contrast, LVESV and LV%EF were comparable in both groups ([Table 6]).
Our data showed that more the number of organ dysfunction, higher the values of LV systolic and diastolic volumes, but the data were statistically comparable ([Figure 4]).
|Figure 4 The organ dysfunction and left ventricular (LV) volumes. LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; MODS, multiorgan dysfunction syndrome.|
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Compared with patients with negative H-FABP, patients with positive H-FABP showed statistically significant increased LV volumes, but the data were comparable for LV%EF 24 h after admission. In contrast, the echocardiography data of both groups were comparable with troponin I ([Table 7]).
The mortality rate
In our study, the mortality rate was 70% for all patients. Compared with group 1, the death rate showed statistically higher prevalence in group 2 (85 vs. 33.3%, P<0.05). In group 2, the length of ICU stay was statistically significantly less (6.3±1.1 days) compared with group 1 (16.2±5.5 days) (P<0.05) ([Figure 5]).
Besides a good correlation between positive H-HABP and mortality rate (r=0.54, P<0.05), compared with patients with positive H-FABP, the death rate showed statistically significantly higher prevalence than patients with negative H-FABP (88 vs. 35%, P<0.05) ([Table 8] and [Figure 6]). In contrast, compared with patients with positive troponin I values, the mortality rate was comparable with patients with negative troponin I values ([Table 8]).
|Table 8 Mortality rate in both heart-type fatty acid binding protein groups|
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|Figure 6 Kaplan–Meier curve for survival duration in positive and negative heart-type fatty acid binding protein (H-FABP) patients.|
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Multivariate regression analysis showed that the number of organ dysfunction with positive H-FABP raised the odds of mortality. Each increase in organ dysfunction increased the odds of mortality by 6.1 times (P<0.05). The total organ dysfunction with positive H-FABP increased the odds of mortality by 7.5 times (P<0.05).
| Discussion|| |
Sepsis syndrome is a common problem in ICU worldwide and is associated with significantly higher morbidity and mortality rates . Septic shock refers to a state of unexplained acute circulatory dysfucntion and is considered as a multifactorial condition including causal microorganism, patient predisposition, comorbidity, and response to therapy ,,,. For better follow-up of sepsis-induced cardiac dysfucntion different cardiac biomarkers such as MB-isoenzyme of creatine kinase, B-type natriuretic peptides, and troponins are now regularly used in ICU ,,.
In our study, we investigated prognostic value of H-FABP in the prediction of adverse outcomes in septic patients without prior cardiovascular impairment in comparison to a known cardiac biomarker, troponin I, and the usefulness of H-FABP as an independent risk factor predictor for mortality in such patients.
Despite its superiority over the classic biomarkers, few studies have investigated H-FABP in sepsis and septic shock with sepsis-induced LV dysfunction, which was a major limitation for our discussion, but this great subject still in need for further elucidation.
Analysis of our results showed that 66% of all patients had elevated H-FABP values, whereas only 22% of our patients had elevated troponin I values. H-FABP was positive in most of the patients in group 2 compared with group 1 (76 vs. 33%, P<0.05). However, only 26% of group 2 patients had positive troponin I values with an insignificant difference. In agreement with our results, Zhang et al. , who studied 93 patients, and Jo et al. , who studied 99 patients with septic shock, stated that H-FABP was positive in 64 and 34% of the patients, respectively. In addition, in a prospective cohort study conducted by Wang et al. , who evaluated 44 patients with septic shock 24-h post-ICU admission, showed that troponin T in patients with or without LV dysfunction showed comparable results.
In our study, 33% of positive H-FABP patients had positive troponin I values, whereas in all negative H-FABP patients the troponin I was negative (r=0.38, P=NS). However, in study by Zhang et al. , patients with H-FABP positive had significantly higher troponin I level than negative H-FABP patients (1.5±0.1 vs. 0.8±0.1 ng/ml, P≤0.001). But, and in agreement with our study, they found that the prevalence of positive H-FABP in septic shock was higher than the prevalence of positive troponin I.
Our study showed that both positive H-FABP and positive troponin I patients showed significantly high clinical severity score (APACHE II: 32.3±8.7 and 36.2±7.2, respectively). Our data showed a clear agreement with both Zhang et al.  (APACHE II: 19.8±2.9 in H-FABP positive patients) and Jo et al.  (APACHE II: 25.7±8.3 in H-FABP positive patients). The worse APACHE II score in our study can be explained by the fact that 70% of our patients were diagnosed as a septic shock, whereas most of the patients in Zhang et al.’s  study were diagnosed as sepsis. Moreover, the need for VPs in our study reached 86%, whereas it was only 58% in Zhang et al.’s  study and 78% in Jo et al.’s  study. Another point that was in agreement with our data was that of Jo et al. , who showed that both APACHE II score and H-FABP positivity were independent prognostic factors in patients with septic shock; the higher the severity scores, the higher the mortality rates were.
In our study, positive H-FABP patients showed significantly higher prevalence of MODS (1.8±0.8 vs. 1.2±0.7 organs, P<0.05), but the data were comparable with troponin I (1.6±0.9 vs. 1.6±0.8 organs, P=NS). This was in agreement with both Zhang et al.  and Jo et al. . They found that H-FABP positivity was significantly higher in patients with MODS. In contrast, John et al.  showed that troponin I-positive patients had more possibility of MODS, but in this study the troponin I level was measured on the third day of ICU admission.
Our data showed good LV systolic function in all patients 24 h post-ICU admission, but data analysis of both groups showed that patients of group 2 had statistically significantly higher LVEDV values than group 1 (69.8±24.8 vs. 103.4±45.7 ml, P<0.05), but LVESV and LV%EF were comparable in both groups. Compared with patients with negative H-FABP, patients with positive H-FABP showed statistically significantly increased LV volumes (LVEDV: 105.1±48.6 vs. 76.5±24.3 ml, P<0.05; and LVESV: 49.3±28.8 vs. 33.2±10.8 ml, P<0.05), but the data were comparable for LV%EF. In contrast, the echocardiography data showed comparable results with troponin I. Our results also showed that the more the number of organ dysfunction, the higher the values of LV volumes, but the data were statistically insignificant.
Zhang et al.  demonstrated that in septic shock patients H-FABP was a superior cardiac biomarker in diagnosing sepsis-related myocardial disease. They found that H-FABP-positive patients were more likely to have cardiac dysfunction (84.5 vs. 31.4%, P<0.001) and compared with patients with H-FABP negative, patient with positive H-FABP showed significantly lower LV%EF (50±6 vs. 65±9%, P<0.001). Also, H-FABP level was negatively correlated to LV%EF (r=−0.56, P<0.001). Important to mention here is that they used the term sepsis-related myocardial disease for patients with LV%EF less than 45%.
However, in our study, patients with positive H-FABP had significantly higher LV volumes. This can be explained by the results of Vieillard-Baron , who stated that normal pericardium in septic-shock patients restrains acute LV dilatation with normal LV%EF. This proposal would explain the disagreement between our study and Zhang et al.’s  study. Moreover, in agreement with our study, Favory and Neviere  showed that most of LV contractility indexes are affected by peripheral vasodilatation and changes in loading conditions observed in septic shock. Also, catecholamine stress seen in sepsis stimulates the myocardium and may, therefore, mask the myocardial depression .
In our study, the total mortality rate was 70%, but because of less disease severity, it was only 26.8% in Zhang et al.’s  study and 38.3% in Jo et al.’s  study.
Our findings suggested that H-FABP can be used as a useful prognostic biomarker in sepsis patients; our patients with positive H-FABP showed significantly higher prevalence of mortality (88 vs. 35%, P<0.001), but the data were comparable with troponin I-positive patients (82 vs. 67%, P=NS). The multivariate regression analysis showed that in positive H-FABP, the odds of mortality increased 7.5 times (P<0.05). Cox’s regression analysis showed that H-FABP had a significant impact on survival duration (P<0.001), whereas troponin I did not have.
In agreement with our study, Zhang et al.  and Jo et al.  found that H-FABP is an independent factor for determining mortality at 28 days of ICU stay and more accurate than troponin I. Positive H-FABP was associated with increased risk for death during the 28-day follow-up period ,. In disagreement to our stuy, a large randomized study including 598 patients conducted by John et al.  found that troponin I is a good prognosticator of mortality in septic shock patient, but in their study troponin I was evaluated after 72 h of the onset of the organ failure .
| Limitations|| |
Besides the limited number of patients, in this study we measured H-FABP of our patient only at the time of enrollment, but it actually can be used a strength factor. In this study, we have shown the impact of using this biomarker as an independent outcome predictor in sepsis and sepsis–LV dysfunction patients, but further investigation would be of an added value to elucidate the emerge of this biomarker.
| Conclusion|| |
H-FABP is a good independent prognostic biomarker and a risk factor predictor for mortality in sepsis patients including prediction of MODS, more than troponin I. During the first 24 h post-ICU admission, the positive H-FABP could predict the significantly increased LV volumes in sepsis-related LV systolic myocardial dysfunction.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Bentzer P, Russell JA, Walley KR. Advances in sepsis research. Clin Chest Med 2015; 36:521–530.
Peng D, Liu X. Research advances in biomarker for sepsis. In: Fu X, Liu L, editors. Advanced trauma and surgery. Springer nature Singapore Pte Ltd.; 2017. 235–251.
Valle HA, Riesgo LG-C, Bel MS, Gonzalo FE, Sanchez MS, Oliva LI. Clinical assessment of heart-type fatty acid binding protein in early diagnosis of acute coronary syndrome. Eur J Emerg Med 2008; 15:140–144.
Muehlschlegel JD, Perry TE, Liu K-Y, Fox AA, Collard CD, Shernan SK et al.
Heart-type fatty acid binding protein is an independent predictor of death and ventricular dysfunction after coronary artery bypass graft surgery. Anesth Analg 2010; 111:1101–1109.
Ivády B, Béres BJ, Szabó D. Recent advances in sepsis research: novel biomarkers and therapeutic targets. Curr Med Chem 2011; 18:3211–3225.
Niizeki T, Takeishi Y, Takabatake N, Shibata Y, Konta T, Kato T et al.
Circulating levels of heart-type fatty acid-binding protein in a general Japanese population: effects of age, gender, and physiologic characteristics. Circ J 2007; 71:1452–1457.
Puls M, Dellas C, Lankeit M, Olschewski M, Binder L, Geibel A et al.
Heart-type fatty acid-binding protein permits early risk stratification of pulmonary embolism. Eur Heart J 2007; 28:224–229.
O’Donoghue M, de Lemos JA, Morrow DA, Murphy SA, Buros JL, Cannon CP et al.
Prognostic utility of heart-type fatty acid binding protein in patients with acute coronary syndromes. Circulation 2006; 114:550–557.
Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M et al.
The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315:801.
Devran Ö, Karakurt Z, Adıgüzel N, Güngör G, Moçin Ö, Balcı M et al.
C-reactive protein as a predictor of mortality in patients affected with severe sepsis in intensive care unit. Multidiscip Respir Med 2012; 7:47.
Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med 1985; 13:818–829.
Hasegawa T, Yoshimura N, Oka S, Ootaki Y, Toyoda Y, Yamaguchi M. Evaluation of heart fatty acid-binding protein as a rapid indicator for assessment of myocardial damage in pediatric cardiac surgery. J Thorac Cardiovasc Surg 2004; 127:1697–1702.
Gottdiener JS, Bednarz J, Devereux R, Gardin J, Klein A, Manning WJ et al.
American Society of Echocardiography recommendations for use of echocardiography in clinical trials. J Am Soc Echocardiogr 2004; 17:1086–1119.
Otterstad JE, Froeland G, St John Sutton M, Holme I. Accuracy and reproducibility of biplane two-dimensional echocardiographic measurements of left ventricular dimensions and function. Eur Heart J 1997; 18:507–513.
Potz BA, Sellke FW, Abid MR. Endothelial ROS and impaired myocardial oxygen consumption in sepsis-induced cardiac dysfunction. J Intensive Crit Care 2016; 2:pii:20.
Wang Z, Li H, Yao G, Zhu X. Impacts of sepsis-induced myocardial dysfunction on hemodynamics, organ function and prognosis in patients with septic shock. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2015; 27:180–184.
Lv X, Wang H. Pathophysiology of sepsis-induced myocardial dysfunction. Mil Med Res 2016; 3:30.
Landesberg G, Jaffe AS, Gilon D, Levin PD, Goodman S, Abu-Baih A et al.
Troponin elevation in severe sepsis and septic shock. Crit Care Med 2014; 42:790–800.
Zhang Z, Dai H, Yu Y, Yang J, Hu C. Usefulness of heart-type fatty acid-binding protein in patients with severe sepsis. J Crit Care 2012; 27:415.e13–415.e18.
Jo YH, Kim K, Lee JH, Rhee JE, Lee JH, Kang KW et al.
Heart-type fatty acid-binding protein as a prognostic factor in patients with severe sepsis and septic shock. Am J Emerg Med 2012; 30:1749–1755.
John J, Woodward DB, Wang Y, Yan SB, Fisher D, Kinasewitz GT et al.
Troponin-I as a prognosticator of mortality in severe sepsis patients. J Crit Care 2010; 25:270–275.
Vieillard-Baron A. Septic cardiomyopathy. Ann Intensive Care 2011; 1:6.
Favory R, Neviere R. Significance and interpretation of elevated troponin in septic patients. Crit Care 2006; 10:224.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]