Complexity of enzyme release during acute myocardial infarction in a controlled study with early nifedipine treatment

Fifty-seven consecutive patients with acute myocardial infarction(AMI), admitted to a coronary care unit (CCU) within 6 h fromonset of symptoms were included in the study and randomly allocatedto nifedipine treatment or placebo. The 23 patients in the treatmentgroup received 10 mg nifedipine orally at the onset the study,after 30 min, and then every 6 h. Placebo was given to the 34patients in the control group. The study was double blind. Serumtime-activity curves for creatine-kinase-MB (CK–MB) andmyoglobin (MG) were established from frequent determinations.Thetwo patient groups did not differ significantly regarding averagecumulative MG and CK–MB release. In both groups the rangewas wide, with the largest maximal individual release about30 times larger than smallest. In most patients the enzyme releaseoccurred stepwise, resulting in two or more separate peaks.In the treatment group significantly fewer patients had multiplepeaks of MG (P<0.05) and CK–MB (P<0.025) release.The initial peaks had a longer duration in the treatment groupand total release tended to stop earlier. In the control groupa highly significant correlation between cumulative MG and CK–MBrelease was obtained, while in the treatment group no such correlationwas observed. In conclusion, oral administration of nifedipine during acutemyocardial infarction appears to influence pattern of enzymerelease, although no effect on the total cumulative releasecould be demonstrated.     

The importance of creatine kinase determination in identifying acute myocardial infarction among patients complaining of chest pain in an emergency room

The contribution of serum creatine kinase (CK) levels to the diagnosis of acute myocardial infarction (AMI) in an emergency room was studied in 252 patients presenting with chest pain. Thirty percent were ultimately diagnosed as having AMI. The electrocardiogram (ECG) identified 66% of patients with AMI who were evaluated within 4 h of onset of symptoms; while CK serum levels were elevated in only 9%. Among patients evaluated more than 4 h after the onset of symptoms, the ECG was helpful in diagnosing AMI in only 36.6%, while serum CK levels were high in 63.4%. CK testing added significantly to the diagnosis of AMI in patients already studied by ECG. We suggest that determination of serum CK levels in the emergency room is of value in the evaluation of patients complaining of chest pain 4 or more hours after the onset of symptoms.     

C-reactive protein in patients with acute coronary syndrome: correlation with diagnosis, myocardial damage, ejection fraction and angiographic findings

BACKGROUND: C-reactive protein (CRP) plasmatic levels increase in patients with acute coronary syndromes (ACS). Correlations between CRP levels, myocardial functional damage and cardiomyocyte lysis remain to be defined. METHODS: 192 consecutive patients with acute coronary syndromes (64.97 +/- 11.08 mean age, 71.35% male gender) were included in the study; 138 patients (71.87%) were discharged with an acute myocardial infarction (AMI) diagnosis (28 with non Q-wave AMI) and 54 with an unstable angina (UA) diagnosis (28.13%). In all patients CRP, CK, LDH, CK-MB and troponin I plasmatic concentrations were evaluated every 6 h for 48 h and every 24 h for the following 2 days from the onset of symptoms. Ejection fraction was estimated by bidimensional echocardiography and extension of myocardial lysis by cardiac enzymes plasmatic release. 92 patients (67 with AMI, 25 with UA) underwent coronary-angiography. Incidence of adverse cardiac events was recorded in a 6 months follow up. RESULTS: Mean CRP levels in Q-wave MI showed a statistically significant increase in the different blood samples with baseline. Mean CRP levels of the three groups were not statistically different at baseline and after 6, 12, and 18 h. Q-wave AMI CRP levels showed a statistically significant difference as against non Q-wave AMI at 36 (p < 0.05), 48 (p < 0.05) and 72 h (p < 0.05) and UA at 24 (p < 0.01), 30 (p < 0.01), 48 (p < 0.0001), 72 (p = 0.0001) and 96 h (p = 0.0003); non Q-wave AMI CPR levels showed a statistically significant difference as against UA at 48 h (p < 0.01). CRP peak mean levels were significantly different when comparing Q-wave AMI patients with UA patients (8.21 +/- 7.85 vs. 2.75 +/- 3.33 mg/dl, p < 0.001). In patients with Q-wave AMI there was a correlation between CRP peak concentrations and CK (r = 0.264, p = 0.008) and LDH (r = 0.32, p = 0.001), while correlation with CK-MB peak concentrations was not statistically significant (r = 0.196, p = 0.051). In the same patient group, there was also a correlation between CRP plasmatic concentrations and troponin I plasmatic concentrations from the 30th to 96th h after the onset of symptoms (r = 0.38-0.53, p < 0.05). No correlation was found between CRP levels and ejection fraction and angio-coronarography findings (number of stenotic vessels, culprit lesions, ruptured plaques). Peak CRP levels were associated in a 6 months follow up with an increased incidence of major adverse cardiac events (MACEs) in patients with Q-wave AMI (HR 1.1649, 95% C.I. 1.0197-1.3307, p < 0.05). CONCLUSIONS: CRP plasmatic concentrations showed a different release curve in patients with Q-wave AMI in comparison with patients with non Q-wave AMI and with patients with UA. CRP peak concentrations did not correlate with ejection fraction and angiographic findings, but correlate with incidence of MACE. The increase in CRP levels during Q-wave MI seems to be linked to the extension of myocardial damage rather than pre-existing inflammation.     

急性心肌梗塞患者中性粒细胞氧化代谢的动态变化

以鲁米诺依赖的化学发光法观察１９例急性心肌梗塞（ＡＭＩ）患者中性粒细胞氧化代谢的动态变化，发现ＡＭＩ发病后２４ｈ中性粒细胞氧化代谢达到高峰，以后逐渐下降。同时观察了其中５例患者血清肌酸激酶（ＣＫ）活性的动态变化，发现ＡＭＩ发病后１８ｈＣＫ活性达到高峰，对比观察５例患者中性粒细胞化学发光峰值与同时期ＣＫ活性的相关关系，发现两者呈高度正相关（ｒ＝０．７１，Ｐ＜０．０５）。     

Procalcitonin in acute myocardial infarction

Objective: Procalcitonin (PCT) is released in severe bacterial infections, sepsis and in infection independent cases such as major surgery, multiple trauma, cardiogenic shock, burns, resuscitation, and after cardiac surgery. The aim of this study was to determine the levels and the kinetics of PCT in AMI and to investigate their possible correlation with the release of IL‐6 and CRP. Design‐Patients: The study included 60 patients (47 men, 63.2±14.8 years) with the diagnosis of AMI at admission. In all patients, serum levels of PCT, IL‐6, CK‐MB, TnI and CRP were measured at admission, at 3, 6, 12, 24, 48 and 72?h and at the seventh day. Results: PCT was elevated in all patients with AMI. It was initially detected in serum approximately 2–3?h after the onset of the symptoms. The median value at admission was 1.3?ng/ml (95% CI: 0.89 to 1.80). The value of PCT showed an increase and reached a plateau after 12–24?h. The median value at 24?h was 3.57?ng/ml (95% CI: 2.89 to 4.55). PCT values fell to baseline (<0.5?ng/ml) by the seventh day. PCT was detected in serum earlier than CK‐MB or TnI in 56 of the 60 patients (93.3%). The kinetics of PCT was similar to those of CK‐MB and TnI. The maximal values of PCT were positively correlated with the maximal values of IL‐6 (r = 0.59, P = 0.00) and of CRP (r = 0.65, P = 0.001). The maximal values of IL‐6 were positively correlated with max CRP (r = 0.35, P = 0.045). Conclusions: PCT could be considered as a novel sensitive myocardial index. Its release in AMI is probably due to the inflammatory process that occurs during AMI.     

Plasma mitochondrial coupling factor 6 in patients with acute myocardial infarction.

Previous studies have shown that mitochondrial coupling factor 6 (CF6) is an endogenous peptide that inhibits prostacyclin (PGI2) synthesis in vascular endothelial cells. In this study, we measured the plasma CF6 level of patients with acute myocardial infarction (AMI) to observe dynamic changes of CF6. All patients showed elevated plasma CF6 levels upon admission for treatment of AMI. Their CF6 levels peaked approximately 72 h after the onset of AMI and remained high for 7 days. At 7 days, their CF6 levels decreased to the level seen upon admission, but not to within a normal range. Hyperlipidemic patients had significantly greater CF6 levels at 24 h after onset of AMI than patients with a normal lipid profile. On admission, the plasma CF6 level in patients with a cardiac function of Killip class > or =II was higher than that in patients with a Killip class I cardiac function. At 3 days after the onset of AMI, the plasma CF6 levels of patients with a creatinine kinase (CK) peak value > or =1,500 units/l were significantly higher than those of patients with a CK peak value <1,500 units/l (p =0.05). At 7 days after the onset of AMI, the plasma CF6 levels of patients who received no reperfusion were significantly higher than those of patients who received a successful reperfusion. The plasma CF6 levels of AMI patients at admission, at 24 h, and at 3 days after onset of symptoms correlated positively with the cardiac function by Killip classification, respectively. At 24 h after onset of AMI, the plasma CF6 levels correlated positively with plasma total cholesterol levels and low-density lipoprotein levels. At 3 days, the plasma level of CF6 correlated positively with the plasma CK peak value and correlated negatively with left ventricular ejection fraction. These results suggest that the plasma CF6 level was elevated in patients with AMI.     

Relation between ST and QRS vector changes and myoglobin release in acute myocardial infarction

We analysed serum time activity curves for myoglobin (MG) and changes in the ST and QRS vectors for 18 consecutive patients with acute myocardial infarction admitted within 4 h of the onset of pain. The MG release was completed 16 +/- 7 (7 to 36) h after onset of symptoms, and the QRS vector changes were completed after 14 +/- 5 (4 to 23) h. the ST vector decline ceased after 11 +/- 5 h. The temporal correlation between completion of: a) ST vectors and MG release was r = 0.78 (P less than 0.001); b) QRS vectors and MG release was r = 0.85 (P less than 0.001). Stepwise release of MG and changes in ST and QRS vectors were often related. Seventeen additional ST-peaks were followed by further MG-release in 13 instances and for 10 additional changes of the QRS vector eight were associated with further MG-release. We conclude that VCG changes and MG-release show a close temporal relationship. Additional events are often simultaneously reflected by these independent markers of myocardial ischaemia and necrosis.     

Late estimation of myocardial infarct size by total creatine kinase nomogram

We studied the possibility of enzymatic estimation of myocardial infarct size in patients late (between days 2 and 6) after the onset of acute myocardial infarction (AMI), in whom estimation of infarct size was difficult by analysis of time-activity curves of serum creatine kinase (CK) because of the lack of the enzymatic information during the initial 48 hours. Serial determinations of serum enzymes were performed in 32 patients within 6 hours after the onset of AMI and significantly close correlations were observed between cumulative total CK release and the cardiac fraction of lactate dehydrogenase isoenzyme (LDH1) activities from day 2 to day 6 after the onset of AMI (r = 0.863 to 0.870; p less than 0.001). We developed a nomogram to estimate cumulative total CK release by serum LDH1 activities obtained between days 2 and 6 after AMI and evaluated the reliability of the nomogram. Cumulative total CK release obtained from serial serum CK activities correlated closely with total CK release obtained from the nomogram in the second group of patients with AMI (r = 0.923 to 0.946; n = 24; p less than 0.001). Our total CK nomogram requiring few blood samples was useful in late estimation of infarct size in patients who were admitted to the hospital between days 2 and 6 after the onset of AMI.     

Continuous ST- and QRS-vector changes and myoglobin release during streptokinase-treated acute myocardial infarction.

Twenty-two consecutive patients with a first myocardial infarction treated with streptokinase (SK) were compared to a group of 33 consecutive patients who did not receive SK. Age, infarct localization, duration of symptoms and infarct size, as estimated by cumulative creatine kinase (CK) release, did not differ between the two groups. Myoglobin (MG) release stopped after 5.5 +/- 3.3 h in SK-treated patients, which was 11 h earlier than in the controls (P less than 0.0001). CK release ceased after 15 +/- 7.8 h, about 13 h earlier than in the controls (P less than 0.0001). ST and QRS vector changes, registered by continuous vectorcardiography, were completed after 2.9 +/- 2.0 and 4.4 +/- 2.5 h respectively, about 2 and 4 earlier than in the controls (P less than 0.005 and P less than 0.0001 respectively). With SK, the termination of ST and QRS vector changes occurred more uniformly than corresponding vector changes in the controls, in whom a longer time interval between the termination of ST and the end of QRS vector changes was observed. With SK, the difference between the end of ST and QRS vectors decreased by about 3 h to 1.6 +/- 1.5 h (P less than 0.0001). Temporal relations between MG release and ST and QRS vector changes were similar but more uniform than in those of the reference group. In conclusion, we found that SK resulted in an accelerated and more uniform development of the infarct process, ending about 10 h after onset of therapy, compared with 20-30 h in the reference group.     

Nitric oxide production by neutrophils obtained from patients during acute coronary syndromes: expression of the nitric oxide synthase isoforms

OBJECTIVES: To analyze the differences in the nitric oxide (NO) forming system between neutrophils obtained from patients during unstable angina (UA) and during acute myocardial infarction (AMI). BACKGROUND: Neutrophils are involved in the regulation of thrombus formation through the release of active substances such as NO. Acute myocardial infarction is the result of an occlusive thrombus; unstable angina is attributed to intermittent thrombus formation. METHODS: We studied 49 patients admitted to hospital within 24 h after the onset of chest pain: 31 experienced AMI and 18 experienced UA. Acute myocardial infarction was defined as CK greater than two-fold the upper limit of normal value of biochemical laboratory, with CK-MB >10% total CK. Unstable angina was defined as transient ST segment changes without significant increases in CK and CK-MB. RESULTS: The amount of NO generated by neutrophils from AMI patients was significantly higher than that generated by neutrophils from UA patients. Neutrophils from UA and AMI patients showed low levels of endothelial-like NO synthase protein expression and a marked expression of the inducible NO synthase (iNOS) isoform. Although neutrophils from patients during acute coronary syndromes generated high amounts of NO, they did not demonstrate an increased ability to stimulate cyclic guanosine monophosphate (cGMP) synthesis in platelets. This lack of activity to release NO by neutrophils from patients during AMI was unrelated to a defect in the platelet cGMP-forming system; sodium nitroprusside, an exogenous NO donor, similarly increased cGMP levels in platelets from AMI patients and healthy donors. CONCLUSIONS: Neutrophils from patients during AMI and UA showed an increased production of NO and a marked expression of the iNOS isoform. However, NO released from these neutrophils showed a deficient functionality. These findings could have clinical implications because they show differences in thrombus growth in patients with UA versus patients with AMI.     

Tumour necrosis factor-alpha and interleukin-6 release during primary percutaneous coronary intervention for acute myocardial infarction is related to coronary collateral flow

OBJECTIVES: We tested the hypothesis that there was an association between tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) release and measured coronary collateral flow in patients undergoing primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). BACKGROUND: Tumour necrosis factor-alpha and IL-6 increase during acute myocardial infarction (AMI). However, their relation to coronary collateral flow is unknown. METHODS: Twelve patients with AMI due to complete thrombotic coronary occlusion underwent primary PCI within 12 h of symptom onset. Doppler-derived collateral flow index (CFI) was measured during first balloon inflation. TNF-alpha, IL-6, creatine kinase (CK), CK-MB fraction were measured from venous plasma samples serially for 24 h. Area at risk was determined off-line by coronary arteriography. Ejection fraction (EF) was measured using biplane left ventricular angiography. RESULTS: Maximal CK release varied between 569 and 6276 U/l and area at risk varied between 7 and 47% of myocardium. Tumour necrosis factor-alpha (peak 4.4+/-0.5 pg/ml) and IL-6 (peak 35.5+/-3.0 pg/ml) increased in all patients. Peak TNF-alpha and IL-6 release was independent of CK, CKMB. No minimal threshold of myocardial necrosis for cytokine expression could be detected. Similarly, TNF-alpha and IL-6 release was also independent of time to reperfusion, area at risk or EF. Using univariate regression analysis, peak TNF-alpha inversely correlated with CFI (r = 0.67, P = 0.017) whereas IL-6 positively correlated with CFI (r = 0.76, P = 0.004). CONCLUSIONS: Acute myocardial infarction is associated with a significant rise in TNF-alpha and IL-6 levels independent of infarct size or myonecrosis. Tumour necrosis factor-alpha and IL-6 correlate dichotomously with CFI indicating differing roles in reperfused AMI.     

血清促红细胞生成素水平与急性心肌梗死患者梗死面积有关

目的观察血清促红细胞生成素（EPO）水平与急性心肌梗死（AMI）直接经皮冠状动脉介入（PCI）治疗后梗死面积的关系。方法初次急性ST段抬高型心肌梗死86例,在发病12 h内成功地接受了PCI的患者测定血清EPO和肌酸肌酶（CK）,并计算其CK累积释放量。以EPO中间值（19.6 U/L）分为高EPO组[（39±17）U/L]和低EPO组[（14±4）U/L],对两组CK累计释放量进行比较,并对CK累积释放量的可能影响因素做多元逐步回归分析。结果CK累积释放量在血清高EPO组明显低于低EPO组[（1 150±226）μkat/（L.h）vs（1 740±210）μkat/（L.h）,P<0.05)]。多元逐步回归分析显示,血清EPO水平、PCI术后TIMI血流等级和梗死前心绞痛是CK累积释放量的独立预测因子。结论内源性EPO水平高者AMI成功地直接PCI术后梗死面积较少,两者呈负相关。     

Importance of coronary collateral circulation for kinetics of serum creatine kinase in acute myocardial infarction

The effect of coronary collateral perfusion on the kinetics of creatine kinase (CK) was examined in 32 patients undergoing intracoronary thrombolysis within 6 hours after the onset of a first acute myocardial infarction (AMI). Blood sampling for CK was performed every 2 to 4 hours for a period of 72 hours after AMI. The cumulative CK release was determined using the integrated appearance function curve with the individual disappearance rate. In 19 patients in whom thrombolysis was successful (group A), time to peak CK level was 11 +/- 1 (standard error of the mean) hours after AMI and cumulative CK release was 2,599 +/- 424 U/liter. In 6 patients who had a significant collateral circulation to the infarct-related coronary artery and unsuccessful reperfusion (group B), the time to peak CK was 16 +/- 1 hours (p less than 0.05 compared with group A) and cumulative CK release was 1,897 +/- 478 U/liter (difference not significant compared with group A). In the remaining 7 patients, with neither recanalization nor significant collateral perfusion group C, time to peak CK was 21 +/- 1 hours and significantly (p less than 0.05) longer than groups A and B. Cumulative CK release (2,707 +/- 776 U/liter) was not significantly different from groups A and B. Thus, collateral perfusion is an important determinant of the CK time-activity curve during AMI. Early peaking of CK levels does not reliably identify spontaneous or drug-induced recanalization of the infarct-related coronary artery.     

急性心肌梗死患者早期干预过程中血浆P选择素水平的动态变化

目的观察急性心肌梗死(AMI)患者早期干预过程中血浆P选择素、TNF-α以及细胞间黏附分子-1(ICAM-1)水平的动态变化和早期再灌注治疗对其水平的影响。方法AMI患者31例(AMI组),经冠状动脉造影证实的稳定性心绞痛(SAP)患者17例(SAP组),冠状动脉造影正常者19例(对照组)。分别于发病6、12、24、487、2 h抽取静脉血。使用ELISA法测定血浆P选择素、TNF-α及ICAM-1水平。结果AMI组患者发病6 h内P选择素的浓度显著高于SAP组和对照组(P<0.01);12 h P选择素浓度进一步升高;24 h P选择素明显下降,但仍高于SAP组和对照组(P<0.05);48、72 h P选择素浓度与对照组比较无统计学差异。AMI组患者发病6 hTNF-α与ICAM-1即升高,24 h达高峰,72 h后仍高于正常。直线相关分析,AMI患者发病6 h的P选择素与TNF-α、ICAM-1水平呈正相关(r=0.76,P<0.01;r=0.69,P<0.01)。结论早期成功干预治疗使P选择素很快达峰值,然后迅速下降,但对TNF-α和ICAM-1水平变化的影响则不显著。     

Time course of serum cardiac enzymes after intracoronary thrombolytic therapy. Creatine kinase, creatine kinase MB isozyme, lactate dehydrogenase, and serum glutamic-oxaloacetic transaminase

We analyzed the time course of serum creatine kinase (CK), the CK MB isozyme, lactate dehydrogenase (LDH), and serum glutamic-oxaloacetic transaminase (SGOT) activity and calculated rates of increase and decline for CK in 24 consecutive patients with acute myocardial infarction (AMI) who received intracoronary thrombolytic therapy. In 19 patients with successfully reperfused infarcts, peak CK activity occurred at 14.1 +/- 1.1 hours after onset of symptoms, the maximal rate of CK rise was 595 +/- 102 IU/L/hr, and the fractional disappearance rate (Kd) was (86 +/- 6) X 10(-5)/min. The peak CK MB activity occurred at 12.9 +/- 0.8 hours and the MB Kd was (223 +/- 39) X 10(-5)/min. In five patients in the nonreperfused group the peak CK (24.9 +/- 4.5 hours) and CK MB (22.7 +/- 3.3 hours) activity occurred later, the maximal rate of CK rise (281 +/- 37 IU/L/hr) was less, and the CK Kd [(68 +/- 5) X 10(-5)/min] and MB Kd [(116 +/- 28) X 10(-5)/min] were lower. The peak CK, CK MB, cumulative CK release, and area under the curve were not different. Except for a shortened time to peak SGOT in the reperfused (17.1 +/- 1.3 hours) compared with the nonreperfused (29.1 +/- 5.6 hours) groups, the time course of LDH and SGOT were not different. Thus, the initial serum CK kinetics and time to peak SGOT may be useful in assessing the reperfusion status in patients with AMI receiving thrombolytic therapy without coronary angiography or in those who may have spontaneous recanalization.     

Liver damage as a potential source of error in the estimation of myocardial infarct size from plasma creatine kinase activity

The occurrence of liver damage was investigated in patients with uncomplicated acute myocardial infarction (AMI). Cumulative plasma release of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) was compared with release of alanine aminotransferase (ALT). Up to 48 h after AMI, the appearance of ALT could be fully explained by myocardial ALT release. Thereafter additional release of ALT occurred, indicating liver damage. A possible effect of liver function on the rate of elimination of CK from plasma was studied in the dog. Complete temporary arrest of hepatic blood supply was obtained after previous implantation of a portacaval shunt, ligation of secondary inflows and blockade of retrograde perfusion. Neither these preliminary haemodynamic interventions nor the acute arrest of hepatic blood flow had any effect on the disappearance rate of CK from plasma. It is concluded that some liver damage commonly occurs in patients after AMI. However, this phenomenon does not interfere with the estimation of infarct size because the elimination of CK from plasma is unaltered during total hepatic ischaemia.     

Procalcitonin in acute myocardial infarction

OBJECTIVE: Procalcitonin (PCT) is released in severe bacterial infections, sepsis and in infection independent cases such as major surgery, multiple trauma, cardiogenic shock, burns, resuscitation, and after cardiac surgery. The aim of this study was to determine the levels and the kinetics of PCT in AMI and to investigate their possible correlation with the release of IL-6 and CRP. DESIGN-PATIENTS: The study included 60 patients (47 men, 63.2+/-14.8 years) with the diagnosis of AMI at admission. In all patients, serum levels of PCT, IL-6, CK-MB, TnI and CRP were measured at admission, at 3, 6, 12, 24, 48 and 72 h and at the seventh day. RESULTS: PCT was elevated in all patients with AMI. It was initially detected in serum approximately 2-3 h after the onset of the symptoms. The median value at admission was 1.3 ng/ml (95% CI: 0.89 to 1.80). The value of PCT showed an increase and reached a plateau after 12-24 h. The median value at 24 h was 3.57 ng/ml (95% CI: 2.89 to 4.55). PCT values fell to baseline (<0.5 ng/ml) by the seventh day. PCT was detected in serum earlier than CK-MB or TnI in 56 of the 60 patients (93.3%). The kinetics of PCT was similar to those of CK-MB and TnI. The maximal values of PCT were positively correlated with the maximal values of IL-6 (r = 0.59, P = 0.00) and of CRP (r = 0.65, P = 0.001). The maximal values of IL-6 were positively correlated with max CRP (r = 0.35, P = 0.045). CONCLUSIONS: PCT could be considered as a novel sensitive myocardial index. Its release in AMI is probably due to the inflammatory process that occurs during AMI.     

Myoglobin or enzymes for a rapid evaluation of infarction diagnosis?

Recently published clinical studies on patients with acute myocardial infarction (AMI) have documented that radioimmunologically determined serum peak concentrations of myoglobin (Mb) precede enzyme peak values. It has, therefore, been concluded that Mb (molecular weight 17,600) is liberated earlier from damaged myocardium than, for example, creatine kinase (CK, molecular weight 80,000). As rapid diagnosis is essential in the management of patients suffering from AMI, we have studied the liberation of cardiac enzymes and Mb using a nonrecirculating perfusion system. The release of malate dehydrogenase (MDH), lactate dehydrogenase (LDH), CK, and Mb from isolated guinea pig heart preparations was induced by anaerobic coronary perfusion at a constant flow rate. Thirty minutes after onset of anoxia there was a simultaneous increase in MDH, LDH, and Mb release. Maximum levels were reached between 120 and 180 min. The release curves for enzymes and Mb were approximately parallel. Close correlations exist between LDH/MDH (r = 0.94), CK/MDH (r = 0.98), LDH/Mb (r = 0.89), and MDH/Mb (r = 0.91). Based on these results and on calculations related to invasion and elimination kinetics, we suggest that the early peak of serum Mb in patients with AMI does not reflect a prior Mb release but depends on the more rapid rate of elimination of Mb from serum in comparison to enzymes.     

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.     

心脏肌钙蛋白I诊断急性心肌梗死的价值

目的 :探讨血清心脏肌钙蛋白 I（c Tn I）在急性心肌梗死 （AMI）中的诊断价值。方法 :急性心肌梗死 （AMI）组患者 2 0例 ,不稳定型心绞痛 （U A）组 31例 ,陈旧性心肌梗死 （OMI）组 11例 ,危重病患者 87例 （非心血管疾病 ）。AMI组患者系列采血测定血清 c Tn I和 CK- MB,U A与 OMI组、危重患者组均入院后次日晨取血 1次。结果 :c Tn I与CK- MB诊断 AMI的敏感性均为 10 0 % ,c Tn I诊断 AMI的特异性高于 CK- MB（P<0 .0 5 ） ;AMI时 c Tn I浓度高峰时间与 CK- MB平行 ,持续时间明显延长 （P<0 .0 1） ,溶栓患者高峰时间明显前移 （P<0 .0 1）。结论 :c Tn I诊断 AMI敏感性高 ,其特异性高于 CK- MB。且在血清中出现早且持续时间长。其峰值时间改变可用于判定 AMI的溶栓疗效