Diagnostic value of heart fatty-acid binding protein in early hospitalized patients with non ST elevation acute coronary syndrome

BACKGROUND: Heart fatty-acid-binding protein (FABP) is supposed to be the most sensitive biomarker of myocardial necrosis in patients with Q-wave myocardial infarction (MI) and non-diagnostic ECG during first hours after onset of symptoms. However, diagnostic value of FABP in patients with non-ST elevation acute coronary syndrome (NSTEACS) is not well established. AIM: To elucidate diagnostic value of FABP in patients with NSTEACS hospitalized within time interval considered to be too early for a majority of biochemical tests. MATERIAL AND METHODS: FABP levels were measured by immunofluorometry (HyTest, Finland) in 44 patients (26 men, mean age 69+/-8.9 years) at admission within 6 hours (median - 2 h) from onset of index attack of angina and in 6, 12, 24 hours after onset of pain. Cut off FABP level was 12 ng/ml. Serum cardiac troponin I was measured for diagnosis of MI on admission and twice during first 24 hours of hospital stay. Cut off TnI level was 0.4 ng/ml. RESULTS: Acute MI was diagnosed by TnI above cut off in 31 patients (70.5%). There were no new-Q-wave MIs. Average ratio of observed serum FABP level to diagnostic cut off value on admission and in 6, 12, 24 hours after onset of pain was higher in patients with MI than in patients with unstable angina (1.01, 1.53, 0.81, 0.66 and 0.78, 0.51, 0.65, 0.56, respectively). The difference was maximally significant in 6 hours after onset of pain (p=0.018). Among patients with MI admission FABP compared with admission TnI more frequently exceeded diagnostic level (in 18 vs 9 patients, respectively, p=0.009). Sensitivity and specificity of admission levels of FABP and TnI for diagnosis of MI were 58 and 85%, 29% and 100%, respectively. CONCLUSION: In patients with NSTEACS during first 6 hours after pain onset FABP compared with TnI has greater sensitivity for detection of MI and sufficient specificity. FABP can be used as additional diagnostic tool for MI detection in early admitted patients with NSTEACS.     

Prognostic value of serial determination of CPK in acute myocardial infarction (author's transl)]

Serial determinations of CPK enzyme were performed every 4 hours during a 72 hour period in 40 patients with acute myocardial infarction (AMI) admitted to the Coronary Care Unit in the first 6 hours (average 2.6) from the appearance of symptoms. The peak ratio of activity of CPK was 708 mU/ml +/- 48 E.S. as medium value in the whole group was reached in a medium period of 21,1 +/- 0,74 E.S. hours from the attack. Half value of the peak ratio activity was reached after a medium time of 19,1 +/- 1,0 E.S. hours. A significant statistical correlation between the CPK peak ratio and the prognostic index of Selvini et al. was found. The peak ratio resulted in 571 +/- 41 E.S. in patients with uncomplicated AMI, whereas in those with complications such as arrhythmias and heart failure the average value was 901 +/- 136 E.S. No significant correlation between CPK values and ST wave evolution of the ECG peak ratio of 1638 mU/ml was found; however, one patient who died of cardiac rupture showed a low level of 395 mU/ml. The diagnostic and prognostic value of the serial determination of CPK during the first 48 hours of a coronary attack is emphasized.     

Tumor necrosis factor alpha in patients with acute myocardial infarction

Acute myocardial infarction (AMI) is a myocardial necrosis occurring due to persistent coronary ischemia, in which inflammation plays an important role and heart failure is a common complication. The present work was undertaken to clarify the role of Tumor Necrosis Factor Alpha (TNF-alpha) in acute myocardial infarction (AMI). The study was conducted on 20 newly diagnosed AMI patients and 10 healthy age and sex matched controls. Sequential estimation of plasma TNF alpha level was carried out at admission, 24 and 48 hours post admission using ELISA. AMI patients showed a significant increase of plasma TNF-alpha level on admission, and 24 hours post admission but not after 48 hours. However, a significant increase was still seen at 48 hours post admission in patients with signs of heart failure but not in those without signs of heart failure. A significant positive correlation was found between plasma TNF-alpha level and CPK level at admission. On the other hand a significant negative correlation was found between these 2 parameters at 24 and 48 hours post admission. It is concluded that TNF-alpha may be an early marker of myocardial damage because of the early increase of its level after ischemic injury instead of being late consequence of extensive tissue necrosis. TNF-alpha level may be an important indicator of the severity of AMI and the occurrence of heart failure.     

Prognostic significance of heart fatty acid binding protein in patients with non-ST elevation acute coronary syndrome: results of follow-up for twelve months

Value of heart fatty acid binding protein (FABP) for medium term prognosis in patients with non-ST elevation acute coronary syndrome (NSTEACS) is not well established. AIM: To compare prognostic value of FABP levels with those of troponin I (TnI) and creatine kinase MB (CK MB) activity in patients with NSTEACS. METHODS: Serum FABP and TnI levels (HyTest), CK MB activity (Biocon) were measured in 203 patients with NSTEACS (mean age 63.9+/-11.5 years, 52.2% male). Blood was sampled at admission within 12 (median 3.83) hours and in 6 and 12 hours after onset of pain. Upper limits of normal range (ULN) for TnI and CK MB were 0.4 ng/ml and 25 U/l, respectively. Serum FABP was measured in 53 healthy volunteers (mean age 44.3+/-13.3) and 95th percentile was used as ULN (4.67 ng/ml). Deaths and nonfatal MIs (events) were registered during one year follow-up. RESULTS: There were 47 events (23%, 23 deaths and 24 nonfatal MIs). Patients with events compared with those without events had significantly higher TnI and CK MB 12 hours after onset of pain and significantly higher FABP at all time points of blood sampling. Multivariate (step-up) analysis selected the following independent predictors of events: elevated FABP 6 hours after pain onset (OR 2.45, 95% CI 1.14-5.24; p=0.021), T-wave inversion on admission ECG, age >65 and regular use of nitrates before hospitalization. Sensitivity of elevated FABP 6 hours after pain onset was 78.4%, specificity -- 45.1%. After exclusion from analysis of all or just admission and 6 hours FABP data elevated TnI 12 hours after onset of pain became an independent predictor of events. CONCLUSION: In this group of patients with NSTEACS among markers of myocardial necrosis (FABP, TnI, MB CK) obtained serially during first 12 hours after pain onset elevated FABP was the best predictor of events during 1 year follow up for subjects in whom blood sample could be done 6 hours after pain onset.     

Biochemical markers of ischaemia for the early identification of acute myocardial infarction without St segment elevation

Blood was collected on admission and after 1-2 h in 130 consecutive patients admitted with typical chest pain in order to assess the capacity of myoglobin, fatty-acid-binding protein (FABP), CK-MB mass, and troponin I (TnI) in the early identification of acute myocardial infarction (AMI) without ST elevation. Using the maximum value within 6 h of onset of symptoms, AMI was detected with a 90-95% sensitivity and a 81-94% specificity by FABP at a cut-off level 8-12 midrog/l, or 81-86% and 89-93%, respectively, by myoglobin at a cut-off level 70-90 microg/l. CK-MB mass and TnI had low sensitivity, albeit very high specificity. As almost all AMI patients were identified within 6 h, serial measurements of FABP or myoglobin ruled out AMI with a very high degree of certainty. Due to the low prevalence of AMI (16%), the positive predictive values were modest (47-73%), yet increasing the probability of AMI by a factor 3-4. Myoglobin and FABP are very useful markers in the early triage of chest pain patients.     

Heart fatty acid binding protein in patients hospitalized because of worsening heart failure. Relation to prognosis of death

PURPOSE: We tested the hypothesis that serum heart fatty-acid binding protein (FABP), an early marker of myocardial necrosis, is related to prognosis of patients hospitalized because of worsening heart failure (HF). METHODS: Sixty nine patients (64% men, age 66.6 +/- 11.0 years) with NYHA class II, III, IV HF (1, 18, and 50 patients, respectively) at hospital admission were followed for 6-12 (mean 11.6 +/- 1.3) months. Forty seven patients (68.1%) had history of myocardial infarction (MI), 56 (81.2%) - hypertension, 15 (21.7%) -- diabetes, and 17 (24.6%) had echocardiographical signs of aortic stenosis. Median left ventricular ejection fraction was 28%. Serum FABP, cardiac troponin I (Tn I) and N-aminoterminal pro brain natriuretic peptide (NT proBNP) were measured within 3 days after admission ( " admission " levels) and 2 weeks later (minimal hospital stay). Manufacturer recommended upper limits of norm (ULN) were 4.0 ng/ml for FABP, 0.35 ng/ml for Tn I, 0.1 ng/ml for NT proBNP. RESULTS: Median admission FABP was insignificantly higher than level measured 2 weeks later (4.17 vs 4.03 ng/ml, p=0.069). FABP exceeded ULN in 38 (55.1%) patients and in 35 (50.7%) patients at admission and in 2 weeks, respectively (p=0.65). Median admission NT proBNP was significantly higher than 2 weeks level (13.23 vs 6.02 ng/ml, p < 0.0001). Median admission and 2-weeks levels of Tn I were similar and greatly lower than ULN. There were 27 all cause deaths (39.1%) during follow up. Median admission levels of TnI, FABP and NT proBNP were similar in patients who died and survived. Two weeks NT proBNP was significantly higher in patients who died (8.65 vs 3.62 ng/ml, p=0.012). ROC curve derived cut-off levels of FABP and NT proBNP (3.31 ng/ml and 3.5 ng/ml, respectively) were used in univaritate regression analysis. According to this analysis FABP >or= 3.31 ng/ml was related to occurrence of death (OR 3.54; 95% CI 1.03-12.17, p=0.044). FABP and variables with p > 0.1 (age, history of MI and diabetes, regular treatment with nitrates, signs of aortic stenosis, pulmonary rales at admission, and 2 weeks level of NT proBNP >or = cut-off) were included into multivariate logistic regression model. Independent predictors of death were aortic stenosis (OR 31.67; 95% CI 6.11-164.00) and NT proBNP >or= 3.5 ng/ml (OR 5.75; 95%CI 1.69- 19.52). CONCLUSION: In this group of patients hospitalized due to worsening of HF admission values of neither FABP nor other biomarkers studied were predictors of death during about 1 year of follow up. FABP level after 2 weeks of hospital stay was related to occurrence of death but as predictor was inferior to NT-proBNP measured at the same time point.     

Usefulness of serum cardiac myosin light chain I for the estimation of acute myocardial infarction size]

To evaluate the usefulness of serum level of cardiac myosin light chain I (LC I) for the estimation of the extent of acute myocardial infarction (AMI), peak LC I level was compared with myocardial infarction weight (AMI weight) which was obtained by myocardial emission tomography with Tc-99m pyrophosphate (PYP). In 11 patients with AMI, serum LC I levels were measured once a day in most cases, and plasma CPK levels were measured serially (every 4 hours at least 48 hours after admission). Tc-99m PYP imagings were performed at second or third day of AMI, and AMI weight was calculated from the voxel numbers of myocardial hot spot in which Tc-99m PYP had accumulated. Peak LC I level correlated well with AMI weight (r = 0.72, p less than 0.02). As well as peak LC I level, peak CPK level correlated well with AMI weight (r = 0.68, p less than 0.05). But the estimation of the infarct size from peak LC I level had the following advantages over the estimation from peak CPK level. 1) We could compare peak LC I level with AMI weight in all 11 patients, but peak CPK level was able to compared with AMI weight in only 9 of them. This was because CPK level changed rapidly and reached maximum within 24 hours after the onset of AMI, while LC I level peaked after 3 to 5 days. 2) A good correlation between LC I and AMI weight was obtained by the determination of serum LC I level once a day.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heart-type fatty acid binding protein--a reliable marker of myocardial necrosis in a heterogeneous group of patients with acute coronary syndrome without persistent ST elevation

BACKGROUND: Myocardial infarction (MI) is one of the most serious challenges of contemporary cardiology. Among biochemical markers, heart-type specific fatty acid binding protein (h-FABP) has a high potential as a marker for the early diagnosis of acute MI. The h-FABP is released early to the bloodstream and may be useful for both rapid confirmation and exclusion of infarction. As opposed to patients with ST segment elevation MI (STEMI), patients with unstable angina (UA)/non-ST segment elevation MI (NSTEMI) present a heterogeneous group in which the confirmation of MI often meets diagnostic difficulties. A rapid, qualitative immunoenzymatic 'point of care' type test, revealing h-FABP in blood, has recently been made available (CardioDetect med). AIM: To evaluate diagnostic value of early measurements of h-FABP and other markers of necrosis (cTnT, CK-MB, CK-MB mass) in a group of 100 patients with an acute coronary syndrome (ACS) without persistent ST segment elevation (NSTE ACS). METHODS: We studied 100 consecutive patients (34 women, 66 men; mean age 61.6 years) with strong suspicion of NSTE ACS and chest pain lasting <24 h before admission. During admission and after 3 and 6 hours patients had measured a panel of conventional biomarkers as well as quantitative measurements of h-FABP (on admission and 3 hours later) using CardioDetect med. The ultimate diagnosis of infarction (NSTEMI) was confirmed in case of a second (6 h after admission) positive quantitative result of cardiac troponin. Non-ST segment elevation MI was finally diagnosed in 56 patients. RESULTS: The comparison of diagnostic utility of all analysed biomarkers of necrosis revealed that h-FABP was superior to other parameters, when measured on admission, and was characterised by 94.7% sensitivity, 100% specificity, 100% positive predictive value, 93.4% negative predictive value and 97% accuracy. Other biomarkers had on admission lower sensitivity - 70.1% for CK-MB mass, 66.7% for CK-MB, 64.9% for cTnT, whereas their specificity was 97.6% for CK-MB mass, 93% for CK-MB and 100% for cTnT. CONCLUSIONS: Qualitative h-FABP test (CardioDetect med) showed excellent sensitivity, higher than measurements of CK-MB mass, CK-MB, and cTnT on hospital admission, and high specificity in the patient group with NSTE ACS. The h-FABP seems to be an excellent biochemical cardiac marker for diagnosing NSTEMI, especially in its early phase, allowing exclusion of myocardial necrosis.     

Increased plasma level of soluble E-selectin in acute myocardial infarction

BACKGROUND: E-selectin, also known as endothelial cell leukocyte adhesion molecule-1, is a member of the selectin family of adhesion molecules and is expressed on vascular endothelial cells in inflammatory reactions. The induction of surface E-selectin expression by endothelial cells is considered a marker of activation. METHODS AND RESULTS: We examined the plasma soluble E-selectin (sE-selectin) level in 41 patients within 6 hours after the onset of acute myocardial infarction (AMI) and in 37 patients with stable exertional angina and 27 control patients. Blood samples were obtained on admission, after reperfusion therapy, and at 4 hours, 8 hours, 12 hours, 24 hours, 48 hours, 3 days, 5 days, 1 week, and 2 weeks after admission in the AMI group. In this group, 21 patients had a history of prodromal unstable angina before infarction and 20 had sudden onset of infarction. The plasma sE-selectin level (ng/mL) on admission was higher in the AMI group than in the stable exertional angina group and control group (38.5 +/- 3.1 vs 28.5 +/- 1.5, P <.01, 26.0 +/- 1.8, P <.01, respectively). In addition, plasma sE-selectin levels were higher in the patients with AMI with prodromal unstable angina than in those with a sudden onset of infarction on admission (44.7 +/- 5.4 vs 32.0 +/- 2.1, P <.05). The plasma sE-selectin level decreased slowly during the chronic phase both in patients with AMI with prodromal unstable angina (from 44.7 +/- 5.4 to 33.8 +/- 3.4, P <.01) and those with a sudden onset of infarction (from 32.0 +/- 2.1 to 24.9 +/- 2.4, P <.01). CONCLUSIONS: These results suggest that an increase of sE-selectin may reflect enhanced endothelial cell activation in patients with AMI. The higher sE-selectin level in patients with AMI with prodromal unstable angina may have been associated with repeated episodes of myocardial ischemia and reperfusion.     

心肌型脂肪酸结合蛋白(H-FABP)与cTnI、CK-MB组合在诊断早期AMI中的比较

目的研究血清心肌型脂肪酸结合蛋白（H—FABP）在早期急性心肌梗死（AMI）诊断中的价值,比较不同心肌损伤标志物组合诊断早期AMI的价值。方法选择疑似急性冠脉综合征患者102例,采用酶联免疫吸附法（Elisa）测定AMI患者发病1h、2h、3h、4～6h、7～12h时血清H—FABP浓度变化,并与心肌肌钙蛋白I（cTnI）、肌酸激酶同工酶（CK—MB）的检测结果进行比较,分析3种心肌损伤标志物及不同心肌标志物组合H—FABP＋cTnI与H—FABP＋CK—MB在诊断不同发病时间段AMI的敏感性和特异性。结果①在AMI发病3h内,H—FABP的诊断敏感性（66．7％）优于cTnI（0％）和CK—MB（0％）,差异有统计学意义（P〈0．05）。在AMI发病4～6h内,H—FABP的敏感性（94．4％）仍高于cTnI（61．1％）和CK—MB（50％）,差异有统计学意义（P〈0．05）。②H—FABP＋cTnI组合对AMI的诊断敏感度最高（95．8％）,特异度亦最高（100％）。H-FABP＋cTnI组合次之,分别为93．75％和97．2％。这两种组合对AMI的诊断敏感度与单个H—FABP、cTnI和CK—MB比较,差异有统计学意义（P〈0．05）,诊断特异度亦明显升高。结论在AMI发病6h内,H—FABP是最为敏感的心脏标志物,尤以发病3h内最敏感。H—FABP与不同心肌损伤标志物cTnI和CK—MB的组合均具有较高的敏感性和特异性,可提高早期诊断AMI的准确率。     

Heart fatty acid binding protein in patients with ST-elevation acute coronary syndrome hospitalized within 6 hours after onset of pain

AIM: To compare diagnostic value of a novel marker of myocardial necrosis heart fatty acid binding protein (FABP) with that of troponin I (TnI) and total creatine kinase (CK) in patients admitted early after onset of ST-elevation acute coronary syndrome. MATERIAL: Fifty seven patients with ST-segment elevations justifying thrombolytic therapy admitted within 6 hours (29/57 within 3 and 12/57 - 2 hours) after onset of chest pain. In all patients myocardial infarction (MI) was eventually confirmed by development of Q waves and/or diagnostic increase of CK. METHODS: Samples of blood were taken at admission to coronary care unit. Cut-off values for an elevated level of FABP was 12 ng/ml, TnI - 1.2 and 0.4 ng/ml, CK - 400 IU/l. RESULTS: Overall FABP was elevated in 47 (83%), TnI - in 16 (28.1%), CK in 7 (12.3%) patients. Among patients admitted within first 3 and 2 hours FABP was elevated in 23/29 (79.3%) and 11/12 (91%), TnI - in 9/29 (31%) and 5/12 (41.7%), CK in 3/29 (10.3%) and 1/12 (8.3%) patients, respectively. The use of lower cut-off of abnormality (0.4 ng/ml) increased proportion of patients with elevated TnI up to 56.1% in the group as a whole, to 48.3% and 50% among patients admitted within first 3 and 2 hours, respectively. Nevertheless proportion of patients with elevated FABP remained higher with difference being significant for the whole group and patients admitted within first 3 hours (p=0.004 and 0.016, respectively). CONCLUSION: Most patients with ST-elevation acute coronary syndrome hospitalized within 2-6 hours after onset of pain had elevated levels of heart FABP.     

Value of the assay of serum myoglobin in recent myocardial infarction

The serum myoglobin (MG) was assayed by the radio-immunological method in 30 patients, all victims of a recent myocardial infarction (MI) and in 30 tests subjects suffering (21 cases) or not (9 cases) from heart diseases, but none from myocardial infarction (MI). The blood samples have been collected on hospital admission of the patient, then every four hours during the first 48 hours and finally, every 12 hours from the 48th to 72nd hour. The normal value is less than 85 micrograms/l. The creatine-kinase (CK), the aspartate aminotransferase (ASAT), the alanine aminotransferase (ALAT) and the lactate dehydrogenase (LDH) were also assayed each time. In MI, there is a significant increase in the serum MG level (731 +/- 323 micrograms/l against 174 +/- 198 micrograms/l in the test subjects; p less than 0.001). The sensitivity of this assay reaches 97%, its specificity 80%, its positive predictive value 83% and its negative predictive value 96%. Starting from the beginning of the characteristic pain of infarction, the MG level exceeds the normal values after 3.3 +/- 1.6 hours, reaches its maximum after 9.3 +/- 3.7 hours and comes back to normal after 38 +/- 8.1 hours. On the other hand, the MG level does not enable any conclusion regarding either the transmural/not transmural nature, or the site, or the acuteness of the MI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early recanalization and plasma brain natriuretic peptide as an indicator of left ventricular function after acute myocardial infarction

Background Although plasma brain natriuretic peptide (BNP) levels have been widely measured in patients with acute myocardial infarction (AMI), it is still uncertain whether the early recanalization modulates the levels and whether the levels can predict chronic stage left ventricular function. This study was designed to elucidate these issues. Methods In 80 consecutive patients with AMI, plasma BNP levels were measured at admission and at 4 hours, 24 hours, 48 hours, and 1 month after admission. Results In 35 of the 80 patients, the infarct-related artery was patent within 6 hours from the onset of MI (6-hour patency group), and in 27 patients, the artery was still occluded after 6 hours (6-hour occlusion group). The remaining 18 patients in whom it was unclear whether recanalization of the infarct-related artery had occurred within 6 hours or not were excluded from the analyses. In the 6-hour patency group, the BNP level gradually increased and reached a maximum value at 24 hours after admission. In the 6-hour occlusion group, the level increased more, with the values at 4 hours, 24 hours, and 48 hours significantly higher than those in the 6-hour patency group (86 ± 18 pmol/L versus 35 ± 8 pmol/L; P < .01; 112 ± 13 pmol/L versus 74 ± 9 pmol/L; P < .05; 102 ± 15 pmol/L versus 53 ± 11 pmol/L; P < .01). Chronic stage left ventricular function was correlated with not only the BNP level at same stage but also that at 24 hours and that at 48 hours after admission. Multiple regression analysis indicated that the BNP level at 24 hours was the most powerful predictor of chronic stage left ventricular function. Conclusion Plasma BNP levels can predict subsequent cardiac function. In addition, the importance of early recanalization may also be supported with BNP kinetics. (Am Heart J 2002;143:790-6.)     

Usefulness of electrocardiographic findings and creatine kinase levels on admission in predicting the accuracy of the interval between onset of chest pain of acute myocardial infarction and initiation of thrombolytic therapy

Patients with chest pain lasting greater than 6 hours and suggesting acute myocardial infarction (AMI) are often excluded from thrombolytic therapy, because myocardial necrosis is believed to be largely irreversible beyond that time. To evaluate the relation between time of onset of chest pain and enzymatic evidence of myocardial necrosis, enzymes on admission were analyzed in 221 consecutive patients with greater than or equal to 2 mm ST-segment elevation by electrocardiography on admission and no contraindications to thrombolytic therapy. Patients with symptoms within 6 hours (n = 170, early) received thrombolytic therapy, but those with symptoms after 6 hours did not (n = 51, late). Eventually, 219 (168 early, 51 late) patients had enzymatically proven AMI within 24 hours. Creatine kinase levels on admission less than twice the upper normal limit were found in 155 (91%) early patients, but surprisingly, also in 30 (59%) late patients. By electrocardiography on admission, ST-segment elevation per lead was 2.1 +/- 1.1 mm in late patients with low initial enzymes versus 1.1 +/- 0.3 mm in those with elevated initial enzymes (p less than 0.0001). Concomitantly, Q waves in leads with ST-segment elevation were present in 17 (57%) late patients with low enzymes on admission versus 17 (81%) with elevated enzymes on admission (p = 0.06). Eventually, maximal creatine kinase levels were similar in all late patients irrespective of enzyme levels on admission. Therefore, many patients with symptoms of AMI after 6 hours have low enzymes on admission and may still be eligible for thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

The serial changes in plasma homocysteine levels and it's relationship with acute phase reactants in early postmyocardial infarction period.

OBJECTIVE: We aimed to study the change in the plasma homocysteine concentration in the early stage of acute myocardial infarction and its relationship with the acute phase reactants. METHODS: We included into the study 33 patients who were admitted to the hospital with acute myocardial infarction within the first three hours after the onset of symptoms. The plasma samples were obtained on admission (within 3 hours onset of symptom) and at 6, 12, 24 hours and 2, 4, 7, 30 and 90th day after admission. RESULTS: The serial homocysteine measurements were as following: 11.87+/-0.71 micromol/L, 11.89+/-0.62 micromol/L, 11.37+/-0.83 micromol/L, 10.96+/-0.93 micromol/L, 11.37+/-0.89 micromol/L, 11.24+/-0.66 micromol/L, 13.09+/-0.64 micromol/L, 12.85+/-0.71 micromol/L, and 12.19+/-0.91 micromol/L, respectively (p=0.05). Statistically significant difference was found only between the hour 24 and the day 7 (p=0.04). However, there was no statistically significant difference between the admission level and none of the other time points. No correlation was identified between acute phase reactants and lipid parameters that were measured serially at the same time periods and homocysteine levels. CONCLUSION: Although homocysteine plasma values obtained during the sixth and twelfth hours of acute myocardial infarction provide reliable results as a risk markers, timing of blood sampling during the myocardial infarction does not have significant role since plasma values of homocysteine did not affect acute phase reactants.     

The roles of serum myoglobin,total CPK,and CK-MB isoenzyme in the acute phase of myocardial infarction

Frequent blood samples were drawn for determination of serum myoglobin, creatine phosphokinase (CPK), and the MB isoenzyme of CPK (CPK-MB) in patients with acute myocardial infarction (AMI). Significantly elevated levels of myoglobin were present 1.5 hours following onset of chest pain and predated elevations of CPK and CPK-MB by 3 hours. No evidence of the previously described “staccato” phenomenon was found. Due to very frequent blood sampling, a detailed picture of the evolution over time of the above indices was obtained. Significant differences were found in the biochemical profile of anterior wall infarction and diaphragmatic wall MI. A time-sensitivity curve (showing sensitivity of the assay at each time following onset of symptoms) was obtained for myoglobin, CPK, and CPK-MB. It appears that myoglobin is the most sensitive biochemical indicator of AMI in its early phase and since it decreases rapidly back to normal values, it can serve as an invaluable aid in the diagnosis of reinfarction and infarct extension. CPK-MB is a less sensitive indicator of MI but has the advantage of greater specificity.     

Hepatocyte growth factor production may be related to the inflammatory response in patients with acute myocardial infarction.

Hepatocyte growth factor (HGF) is a well-known powerful proliferative factor of vascular endothelial cells and it has been reported that plasma HGF concentrations are increased in acute myocardial infarction (AMI), although the mechanisms are not yet well delineated. Serum HGF levels and C-reactive protein (CRP) were measured in 22 patients with unstable angina pectoris (UAP) (15 males, 7 females; class IIb or IIIb of the Braunwald classification), 60 patients with AMI (37 males, 23 females; average time from the onset of symptoms to admission 4.6+/-0.7h, range, 0.5-12h), and 20 normal subjects. Immediate angioplasties were performed in 51 patients with AMI, and the time course of the HGF levels were measured in 31 patients among them. Heparin dramatically increased the HGF level and it declined to the normal range 18h after heparin injection. Blood samples were taken before heparin treatment, or at least 24h after. Serum HGF levels on admission was significantly increased in UAP (mean+/-SE: 0.30+/-0.03ng/ml, p<0.01), and AMI (0.27+/-0.02ng/ml, p<0.01) compared with the normal subjects (0.19+/-0.01 ng/ml). Even in the early stage (within 3 h of onset of symptoms to admission, average time was 1.8+/-0.1 h), serum HGF levels were already elevated (0.25+/-0.02 ng/ml, p<0.05). There was no significant difference between the HGF levels in UAP and AMI. Fifty-one of the 60 patients with AMI underwent immediate percutaneous transluminal coronary angioplasty and blood samples were obtained from 31 of them on days 7, 14, and 21 after MI. Serum HGF levels peaked on day 7 (0.34+/-0.04ng/ml, p<0.01) and there was a weak relationship between peak creatine kinase and serum HGF levels at that time. A statistically significant correlation was found between peak CRP and serum HGF levels on day 7 (r=0.62: p<0.001). Serum HGF levels decreased to nearly normal by day 21 (0.22+/-0.01 ng/ml). The study shows that serum HGF levels during the early stage of AMI increased significantly and peaked by day 7 after the onset, at which time there was a strong correlation with peak CRP levels. These data suggest that HGF production may be related to the inflammatory response in AMI.     

心肌脂肪酸结合蛋白对早期急性心肌梗死的诊断

目的研究血浆心肌脂肪酸结合蛋白(HFABP)在早期急性心肌梗死(AMI)诊断中的价值。方法选择93例发病6h内的胸痛患者,其中AMI组32例,非AMI组61例[含不稳定型心绞痛(UAP)24例,稳定型心绞痛(SAP)者22例,非心源性胸痛者15例];正常对照组选择69例正常人。采用双抗体夹心酶联免疫一步法检测正常人和患者发病0～3h或3～6h血浆的HFABP含量,并与心肌肌钙蛋白I(cTnI)、肌酸激酶同工酶(CKMB)和肌红蛋白(MYO)的检测结果进行比较,分析4种生化标志物诊断发病3h内和6h内AMI的敏感性、特异性和准确性。结果在0～3h、0～6h时间段,HFABP诊断AMI的敏感性(64.29%、84.38%)显著高于cTnI(28.57%、53.13%)和CKMB(21.43%、56.25%),与MYO(71.43%、78.13%)比较差异无统计学意义;在诊断特异性上,4种生化标志物差异无统计学意义;在诊断准确性上,HFABP的ROC曲线下面积(0.979、0.958)显著高于cTnI(0.800、0.878)、CKMB(0.575、0.782)和MYO(0.796、0.882)。结论HFABP对于诊断早期AMI具有较高的敏感性和良好的特异性,其诊断准确性优于cTnI、CKMB、MYO。     

血清TpP、hs-CRP、CKMB、cTnI在急性心肌梗死中的诊断意义

目的探讨血栓前体蛋白(TpP)、高敏C反应蛋白(hs-CRP)、肌酸激酶同工酶(CKMB)及心肌肌钙蛋白I(cTnI)联合检测在急性心肌梗死(AMI)中的诊断价值。方法 测定26例急性心肌梗死患者胸痛发作6小时内及24小时TpP、hs-CRP、CKMB及cTnI。结果AMI胸痛发作6小时内TpP的敏感性最高,发病6小时后hs-CRP、CKMB及cTnI显著升高,cTnI阳性持续时间长,而hs-CRP在AMI时可出现明显升高。结论TpP对于AMI具有早期诊断价值,cTnI与hs-CRP、CKMB一起相互补充,具有重要的临床诊断及判断预后的意义。     

Fibrin formation and platelet aggregation in patients with acute myocardial infarction: effects of intravenous and subcutaneous low-dose heparin

Fibrinopeptide A (FPA) and beta thromboglobulin (BTG) were measured in 42 patients with acute myocardial infarction (AMI) allocated on admission to one of three groups: 14 patients received a heparin bolus injection of 5000 IU intravenously followed by a 2-hour intravenous infusion (830 IU/hr) (group 1), 14 patients received a heparin bolus of 5000 IU subcutaneously (group 2), and the remaining 14 patients received no anticoagulant treatment (group 3). In group 1 the initially elevated FPA level of 5.8 +/- 1.8 ng/ml dropped to 2.0 +/- 1.5 ng/ml 30 minutes after the intravenous heparin bolus injection of 5000 IU (p less than 0.001) and returned to normal (1.9 +/- 0.8 ng/ml) in 8 of 14 patients. The initially elevated BTG level of 64 +/- 21 ng/ml did not change significantly during intravenous heparin treatment, whereas there was a rapid but only transitory increase in platelet factor 4, (PF4) from 25 +/- 9 to 74 +/- 16 ng/ml (p less than 0.01) after the intravenous heparin bolus. In group 2 the initial FPA of 5.0 +/- 2.3 ng/ml was similarly elevated as in group 1 and dropped to 2.7 +/- 1.7 and 3.3 +/- 1.5 ng/ml 2 and 4 hours after 5000 IU subcutaneously (p less than 0.05), whereas 6 and 8 hours after subcutaneous heparin bolus the mean FPA levels were 4.2 +/- 1.7 and 5.5 +/- 2.0 ng/ml and no more significantly different from the initial FPA values. BTG and PF4 did not change significantly after the subcutaneous heparin bolus. In group 3 the initially elevated mean FPA level of 4.9 +/- 2.4 ng/ml did not change significantly during the first 8 hours after admission, whereas the FPA level 24 hours after admission was 8.4 +/- 3.9 ng/ml and higher than the initial value (p less than 0.01). We conclude that heparin may reduce the elevated FPA level in plasma found in patients with AMI; however, neither subcutaneous nor intravenous heparin in a dosage frequently used is sufficient to consistently normalize the elevated rate of fibrin formation found in these patients.