Serum C-reactive protein elevation in left ventricular remodeling after acute myocardial infarction--role of neurohormones and cytokines

BACKGROUND: We previously reported that increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of cardiac rupture and long-term outcome. The aim of this study was to clarify the role of serum CRP elevation as a possible marker of left ventricular (LV) remodeling after AMI. METHODS: We prospectively studied 31 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Peak serum CRP level was determined by serial measurements after admission. LV volume and the plasma levels of various neurohormones and cytokines were measured on admission, and 2 weeks and 6 months after AMI. RESULTS: Patients with higher peak CRP levels (above the median) had a greater increase in LV end-diastolic volume during 2 weeks after AMI (+21+/-14 vs. +5+/-6 ml/m(2), P=0.001) and a lower ejection fraction (45+/-11 vs. 53+/-7%, P=0.02) than those with lower CRP levels, associated with a higher incidence of pump failure, atrial fibrillation, and LV aneurysm. Plasma levels of norepinephrine, brain natriuretic peptide, and interleukin-6 2 weeks after AMI were higher in the high CRP group than in the low CRP group. CONCLUSIONS: Increased peak serum CRP level was associated with a greater increase in LV volume after anterior AMI. Plasma norepinephrine and interleukin-6 levels were increased in patients with higher CRP levels, suggesting a possible role of sympathetic activation and enhanced immune response in the development of LV remodeling after AMI.     

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.     

Association between serum C-reactive protein elevation and left ventricular thrombus formation after first anterior myocardial infarction

STUDY OBJECTIVES: Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI. DESIGN: We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI. RESULTS: LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (+/- SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 +/- 12.6 vs 9.4 +/- 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of > or =20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (> or =60 years old), peak CK level (> or =3,000 IU/L), and peak WBC count (> or =12,000 cells/ microL). CONCLUSION: A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.     

Aging adversely affects postinfarction inflammatory response and early left ventricular remodeling after reperfused acute anterior myocardial infarction

BACKGROUND AND AIMS: We have demonstrated that an increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of left ventricular (LV) remodeling. We sought to clarify the effect of aging on the postinfarction inflammatory response and LV remodeling. METHODS: We studied 102 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Serum CRP levels, plasma neurohormones and interleukin-6 (IL-6) levels, and LV volume by left ventriculography were serially measured. Patients were divided into two groups according to their age (>or=70 years, n=33; <70 years, n=69). RESULTS: There was no difference in use of cardiovascular drugs and coronary angiographic findings. Older patients had a greater increase in LV end-diastolic volume during 2 weeks after AMI (p=0.0007) and a higher peak CRP level (12.4+/-7.3 vs. 5.5+/-4.2 mg/dl, p<0.0001), although peak CK level was comparable between the two groups. Plasma atrial natriuretic peptide, brain natriuretic peptide and IL-6 levels were higher in older patients at 2 weeks and 6 months after AMI. CONCLUSIONS: Augmented and prolonged activation of the inflammatory system after AMI was observed in older patients, in association with exaggerated LV remodeling. Aging may adversely affect LV remodeling through modification of the inflammatory response after AMI.     

C-reactive protein increase in acute myocardial infarction

OBJECTIVE: Considering acute myocardial infarctions (AMI), data demonstrate that C-reactive protein (CRP) levels reflect the severity of myocardial damage and that high CRP level is associated with a worse outcome. This study evaluates the prognostic value of CRP and the determinants of its increase during AMI. METHODS AND RESULTS: A retrospective observational study of 126 patients with a ST-segment elevation myocardial infarction (STEMI); 101 patients had reperfusion therapy (93 thrombolysis, 8 PTCA). Peak CRP (median: 3.5 mg/dl) was achieved the third day. A correlation existed between this peak and age (r = 0.1838; p = 0.0408). Diabetic patients not requiring insulin showed peaks double those of other patients (10.4 versus 6.1 mg/dl; p = 0.0165). The peak was higher in anterior infarctions (anterior: 8.4, lateral: 6.9, inferior: 6.4, posterior: 3.9 mg/dl; p = 0.0206) and for those showing a Q-wave (7.5 versus 3.9 mg/dl; p = 0.0020). It was correlated with the CK (r = 0.246; p = 0.0188) and troponin Ic (r = 0.242; p = 0.0224) peaks among thrombolysed patients. There was an increasing relationship between the occurrence of cardiac failure and the magnitude of the CRP peak. An inverse linear relationship existed between the ejection fraction of the left ventricle and the CRP peak (r = -0.4187; p = 0.0000). CRP peak was lower with statins (3.8 versus 7.0 mg/dl; p = 0.0446). Fibrates were only associated with lower CRP levels at admission (0.6 versus 0.9 mg/dl; p = 0.0010). CONCLUSIONS: CRP is an indicator of the severity of STEMI. It is also an indicator for the occurrence of complications during hospitalization. The effect of statins and fibrates on CRP levels in AMI should be studied further.     

C-Reactive protein as a risk factor for left ventricular thrombus in patients with acute myocardial infarction

BACKGROUND: Elevated C-reactive protein (CRP) has been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that CRP may be involved in initiation process of coagulation; however, the role of CRP level in the formation of left ventricular (LV) thrombus has not been studied. HYPOTHESIS: This study investigated whether CRP is a risk factor for LV thrombus in patients with AMI. METHODS: Clinical, echocardiographic, and biochemical data were analyzed in 141 consecutive patients (aged 57 +/- 13 years; 33 women) with first anterior AMI. Two-dimensional and Doppler echocardiographic examinations were performed on Days 1, 3, 7, 15, and 30. Blood samples were obtained every day during hospitalization. Serum CRP concentrations were measured by an ultrasensitive immunonephelometry method. RESULTS: Left ventricular thrombus was detected in 33 (23.4%) patients. Univariate analysis showed that patients with LV thrombus had a higher peak creatine kinase (CK) level (2,879 +/- 742 vs. 1,693 +/- 1,210 I/U, p = 0.001), higher peak CRP level (14.9 +/- 7.1 vs. 9.2 +/- 6.8 mg/dl, p = 0.001), higher wall motion score index (1.8 +/- 0.2 vs. 1.5 +/- 0.3, p = 0.002), higher apical wall motion score index (2.35 +/- 0.72 vs. 2.07 +/- 0.70, p = 0.001), larger end-diastolic volume (145.2 +/- 43.7 vs. 116.5 +/- 44.2 ml, p = 0.002), larger end-systolic volume (85.4 +/- 37.2 vs. 62.9 +/- 31.6 ml, p = 0.003), and lower ejection fraction (42.1 +/- 12 vs. 47.3 +/- 13, p = 0.04). In multivariate analyses, only peak CK level (p = 0.0001), LV apical wall motion score index (p = 0.001), and CRP levels (p = 0.001) were independent predictors of LV thrombus formation. CONCLUSIONS: These results suggest that CRP is a risk factor for LV thrombus in patients with AMI.     

Frequency and significance of late evolution of Q waves in patients with initial non-Q-wave acute myocardial infarction. Diltiazem Reinfarction Study Group

Serial 12-lead electrocardiogram and plasma creatine kinase (CK)-MB values from 544 patients with confirmed non-Q-wave acute myocardial infarction (AMI) were analyzed to define the rate of progression of non-Q-wave AMI to Q-wave AMI and to examine its relation to CK-MB evidence of extension. The baseline electrocardiogram was obtained 50 +/- 10 hours after AMI and compared with subsequent electrocardiograms at 48 and 72 hours after baseline record and at discharge. Plasma CK-MB was assayed every 12 hours after baseline. A total of 76 patients (14%) progressed to Q-wave AMI. Compared to the 468 patients who retained non-Q-wave AMI, those patients who evolved Q-wave AMI were more likely to exhibit ST elevation greater than or equal to 1.0 mm in greater than or equal to 2 infarct-related leads (49 vs 32%, p less than 0.005), higher peak CK values with the index AMI (754 +/- 625 vs 611 +/- 604 IU; p = 0.0018) and a greater incidence of CK-MB-confirmed extensions (18.5 vs 5.5%, p less than 0.0001). For those patients progressing to Q-wave AMI within 48 hours of baseline electrocardiogram, CK-MB extension occurred in 9.5% (4 of 42) versus 29.4% (10 of 34) of those who progressed after 48 hours (p = 0.0262). A distinct minority (14%) of patients with non-Q-wave AMI will develop Q waves before discharge. The progression to Q-wave AMI after initial non-Q-wave AMI appears to involve 2 different mechanisms: temporal lag in the electrocardiogram, and actual extension by quantitative CK-MB criteria.     

Levels and values of serum high-sensitivity C-reactive protein within 6 hours after the onset of acute myocardial infarction

BACKGROUND: C-reactive protein (CRP), which has been suggested to directly enhance inflammation in plaques, is rapidly synthesized and secreted in the liver 6 h after an acute inflammatory stimulus. Therefore, serum levels of CRP within 6 h after the onset of acute myocardial infarction (AMI) merely reflect a chronic and persistent inflammatory process and are not due to acute myocardial damage. We hypothesized that the serum CRP level, which would abnormally elevate thereafter, is followed by a plaque rupture in the clinical setting of AMI. METHODS AND RESULTS: CRP was prospectively measured by high-sensitivity CRP assay (hs-CRP) in 157 consecutive patients (106 patients within 6 h, and 51 patients >/= 6 h but < 12 h after the onset of AMI) with ST-segment elevation AMI undergoing primary percutaneous coronary intervention (PCI). Serum levels of hs-CRP were also measured in 30 patients with stable angina undergoing elective PCI and in 30 healthy control subjects. The serum level of hs-CRP was significantly higher in patients with an onset of AMI < 6 h than in patients with angina pectoris (2.7 +/- 2.3 mg/L vs 1.4 +/- 0.7 mg/L, p < 0.0001 [mean +/- SD]) and in healthy subjects (2.7 +/- 2.3 mg/L vs 1.0 +/- 0.6 mg/L, p < 0.0001). There were no significant differences in serum levels of hs-CRP in patients with an onset of AMI 3 h but < 6 h (2.7 +/- 2.5 mg/L vs 2.7 +/- 2.2 mg/L, p = 0.87). However, the serum level of hs-CRP was significantly higher in patients with an onset >/= 6 h than in patients with an onset < 6 h (14.1 +/- 16.5 mg/L vs 2.7 +/- 2.3 mg/L, p < 0.0001). CONCLUSIONS: Serum levels of hs-CRP were significantly higher in patients with an onset of AMI < 6 h than in healthy subjects and in patients with angina pectoris undergoing PCI. The inflammatory process has been proved as one of the mechanisms causing plaque rupture. Elevated serum hs-CRP levels in patients with AMI < 6 h may portend vulnerable plaque rupture.     

Prognostic significance of a low peak serum creatine kinase level in acute myocardial infarction

To assess the prognostic significance of a low peak creatine kinase (CK) level, 723 consecutive patients admitted with acute myocardial infarction (AMI) within 16 hours after onset of symptoms were studied. Thrombolytic therapy was not attempted during the study. Patients were dichotomized according to their peak CK levels, determined from a cluster analysis of peak CK distribution among the population of patients who died within 3 years after hospital discharge. The 139 patients with low peak CK (less than or equal to 650 IU/liter) (group 1) were compared to the 584 patients with high peak CK (greater than 650 IU/liter) (group 2). Patients in group 1 were older and had a higher incidence of previous AMI, angina pectoris before AMI and non-Q-wave AMI. Despite a lower incidence of in-hospital complications and a nonsignificantly lower hospital mortality rate (4 vs 9%) the group 1 three-year posthospital mortality rate was higher (26 vs 17%; p less than 0.02), especially in the subgroup of patients with a Q-wave infarct (mortality 31% in group 1 vs 16% in group 2; p less than 0.001). Among the 491 patients who had a first Q-wave AMI, 55 had a peak CK less than or equal to 650 IU/liter. Compared to the 436 patients with a higher peak CK, these 55 patients had a higher incidence of early postinfarction angina (31 vs 14%; p less than 0.01), a similar hospital mortality (4 vs 7%) but a higher 3-year posthospital mortality (23 vs 12%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Early use of beta-blockers attenuates systemic inflammatory response and lung oxygenation impairment after distal type acute aortic dissection

We have reported that serum C-reactive protein (CRP) elevation is an independent predictor of lung oxygenation impairment (LOI) after distal type acute aortic dissection (AAD). Systemic activation of the inflammatory system after aortic injury may play a role in the development of LOI. The aim of this study is to clarify the effect of beta-blockers on systemic inflammation and the development of LOI after distal type AAD. A total of 49 patients, who were admitted with distal type AAD and treated conservatively, were examined. White blood cell (WBC) count, serum CRP level, and arterial blood gases were measured serially. Forty patients received beta-blocker treatment within 24 h of the onset, while 9 patients received no beta-blocker treatment. Maximum WBC count, maximum CRP level, lowest PaO(2)/FiO(2) (P/F) ratio, and patient background were compared between the two groups. There was no difference between the groups according to age, sex, coronary risk factors, blood pressure, serum level of CRP, WBC count, and oxygenation index on admission. Beta-blocker treatment was associated with lower maximum WBC count (P = 0.0028) and lower maximum serum CRP level (P = 0.0004). The minimum P/F ratio was higher in patients with beta-blocker treatment than in those without (P = 0.0076). Multivariate analysis revealed that administration of a beta-blocker was an independent negative determinant of LOI (P/F ratio 相似文献   

Impact of intravenous beta-blockade before primary angioplasty on survival in patients undergoing mechanical reperfusion therapy for acute myocardial infarction

OBJECTIVES: We sought to examine the effect of intravenous beta-blockers administered before primary percutaneous coronary intervention (PCI) on survival and myocardial recovery after acute myocardial infarction (AMI). BACKGROUND: Studies of primary PCI but not thrombolysis have suggested that beta-blocker administration before reperfusion may enhance survival. Whether oral beta-blocker use before admission modulates this effect is unknown. METHODS: The Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) trial randomized 2082 AMI patients to either stenting or balloon angioplasty, each +/- abciximab. In accordance with the protocol, intravenous beta-blockers were administered before PCI in the absence of contraindications. RESULTS: A total of 1136 patients (54.5%, BB+ group) received beta-blockers before PCI, whereas 946 (45.5%, BB- group) did not. The 30-day mortality was significantly lower in the BB+ group than in the BB- group (1.5% vs. 2.8%, p = 0.03), an effect entirely limited to patients who had not been receiving beta-blockers before admission (1.2% vs. 2.9%, p = 0.007). In contrast, no survival benefit with pre-procedural beta-blockers was observed in patients receiving beta-blockers at home (3.3% vs. 1.9%, respectively, p = 0.47). By multivariate analysis, pre-procedural beta-blocker use was an independent predictor of lower 30-day mortality among patients without previous beta-blocker therapy (relative risk = 0.38 [95% confidence interval 0.17 to 0.87], p = 0.02). The improvement in left ventricular ejection fraction from baseline to seven months was also greater after intravenous beta-blockers (3.8% vs. 1.3%, p = 0.01), an effect limited to patients not receiving oral beta-blockers before admission. CONCLUSIONS: In patients with AMI undergoing primary PCI, myocardial recovery is enhanced and 30-day mortality is reduced with pre-procedural intravenous beta-blockade, effects confined to patients untreated with oral beta-blocker medication before admission.     

Prognostic implications of creatine kinase elevation after primary percutaneous coronary intervention for acute myocardial infarction.

OBJECTIVES: We examined the prognostic implications of the absolute level and rate of increase of creatine kinase (CK) elevation after primary percutaneous coronary intervention (PCI). BACKGROUND: Peak creatine kinase (CK(peak)) and the rate of CK increase are related to reperfusion success and clinical outcomes after thrombolytic therapy for acute myocardial infarction (AMI). The utility of routine serial CK monitoring after primary PCI, in which normal antegrade blood flow is restored in most patients, is unknown. METHODS: In the Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) trial, 1,529 patients with AMI randomized to either stenting or balloon angioplasty, each with or without abciximab, had CK levels determined at baseline and at 8 +/- 1 h, 16 +/- 1 h, and 24 +/- 1 h after PCI. RESULTS: The CK(peak) occurred at baseline in 3.9% of patients, at 8 +/- 1 h in 69.6%, at 16 +/- 1 h in 20.0%, and at 24 +/- 1 h in 6.5%. The CK levels at all post-procedural time points were significantly higher in patients who died compared with the one-year survivors, as was CK(peak) (mean, 2,865 U/l vs. 1,885 U/l, respectively, p < or = 0.001). By multivariate analysis, CK(peak) was a significant predictor of one-year mortality (hazard ratio = 2.15, p = 0.0002), independent from post-PCI Thrombolysis In Myocardial Infarction (TIMI) flow. Both the improvement in left ventricular ejection fraction from baseline to seven months and its absolute level were inversely correlated with CK(peak) (p < 0.001 for both). In contrast, the time to CK(peak) was not an independent predictor of mortality or myocardial recovery. CONCLUSIONS: The CK(peak) after primary PCI is a powerful predictor of one-year mortality independent of other clinical and angiographic measures.     

心肌梗死心脏破裂患者血浆C反应蛋白和D-二聚体水平的变化

目的:探讨测定血浆C反应蛋白(CRP)和D-二聚体水平在冠心病急性心肌梗死(AMI)心脏破裂患者中的临床意义。方法:观察50例AMI心脏破裂(心室游离壁破裂)患者血浆CRP和D-二聚体水平,并与50例AMI但未发生心脏破裂的患者进行对照比较。结果:心脏破裂患者组(实验组)CRP和D-二聚体水平较未破裂组(对照组)明显升高,CRP和D-二聚体水平高低与心脏破裂的发生率呈正相关(P<0.05)。从风险比看,高CRP患者的破裂风险是低的4.125倍,高D-二聚体患者的破裂风险是低的2.471倍。结论:AMI患者的血浆CRP和D-二聚体水平,作为一种敏感性指标,对预测心肌梗死患者发生心脏破裂有一定的价值。     

Relationship between myocardial damage and C-reactive protein levels immediately after onset of acute myocardial infarction

The present study investigated the relationship between myocardial damage and C-reactive protein (CRP) levels, with no increase in creatine kinase (CK) activity, immediately after the onset of acute myocardial infarction (AMI) in 85 patients with their first reperfused anterior AMI without CK elevation on admission and no ischemic events during hospitalization. Patients were classified into those with low levels (<0.3 mg/dl) of CRP (Group L; n=67) and those with high levels (> or =0.3 mg/dl) of CRP (Group H; n=18). Group H had a higher proportion of patients with a history of preinfarction angina (89 vs 55%, p<0.01), especially unstable angina. SigmaST in leads V1-6 on admission ECG was lower in Group H than in Group L (14+/-7 vs 21+/-13 mm, p<0.05). Predischarge left ventriculography showed that the left ventricular global ejection fraction (55+/-11 vs 48+/-10%, p<0.01) and SD/chord at the left anterior descending artery lesion (-1.7+/-0.9 vs -2.3+/-0.9, p<0.01) were better in Group H. Multivariate analysis demonstrated that both CRP on admission (p=0.011) and preinfarction angina (p=0.002) were independently associated with better regional wall motion (SD/chord >-2.0) before discharge. These results suggest that the clinical situation of elevated CRP immediately after onset is associated with less myocardial damage and better left ventricular function in reperfused anterior AMI.     

Early estimation of acute myocardial infarct size soon after coronary reperfusion using emission computed tomography with technetium-99m pyrophosphate

Early appearance of positive findings on a technetium-99m pyrophosphate scan has been shown to be associated with the presence of a reperfused acute myocardial infarction (AMI). Early technetium-99m pyrophosphate imaging was performed by emission computed tomography to evaluate reperfusion and to test the feasibility of estimating infarct size soon after coronary reperfusion based on acute positive tomographic findings. Twenty-seven patients with transmural AMI who were treated with intracoronary urokinase infusion followed by percutaneous transluminal coronary angioplasty underwent pyrophosphate imaging 8.7 +/- 2.1 hours after the onset of AMI. None of the 8 patients in whom reperfusion was unsuccessful had acute positive findings. Of 19 patients in whom reperfusion was successful, 17 had acute positive findings (p less than 0.001). In these 17, tomographic infarct volumes were determined from reconstructed transaxial images. The threshold for areas of increased pyrophosphate uptake within the infarct was set at 60% of peak activity by the computerized edge-detection algorithm. The total number of pixels in all transaxial sections showing increased tracer uptake were added and multiplied by a size factor and 1.05 g/cm3 muscle to determine infarct volume. The correlations of tomographic infarct volumes with peak serum creatine kinase (CK) levels (r = 0.82) and with cumulative release of CK-MB isoenzyme (r = 0.89) were good. Moreover, the time to positive imaging was significantly shorter than that to peak CK level (8.5 +/- 2.3 vs 10.4 +/- 2.2 hours, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Body temperature - a marker of infarct size in the era of early reperfusion

We measured body temperature in 40 consecutive patients treated for a first ST elevation acute myocardial infarction (AMI) with primary percutaneous coronary interventions. Left ventricular function was assessed by echocardiography, and blood samples were drawn for highly sensitive C-reactive protein (hs-CRP), white blood cell (WBC) count, fibrinogen, creatine kinase (CK), and cardiac troponin I levels (cTnI). The median (25th, 75th quartiles) peak 24-hour temperature was 37.4 degrees C (36.9 degrees C, 37.6 degrees C). Variables significantly associated with peak 24-hour temperature were CK (p = 0.01, r = 0.42), wall motion index (p = 0.01, r = 0.41), hs-CRP (p = 0.01, r = 0.41), and cTnI (p = 0.03, r = 0.35). There was no significant correlation between peak 24-hour temperature and WBC count (p = 0.39, r = 0.14) and fibrinogen (p = 0.12, r = 0.21). Thus, peak 24-hour body temperature after ST elevation AMI probably reflects infarct size rather than a nonspecific inflammatory response.     

Prognostic importance of delayed Q-wave evolution 3 to 24 hours after initiation of thrombolytic therapy for acute myocardial infarction

The timing of Q-wave evolution and its prognostic significance was studied in 201 patients who received thrombolytic therapy for a first acute myocardial infarction (AMI). One hundred forty-one patients (70%) had evidence of a Q-wave AMI within 3 hours of the initiation of thrombolytic therapy, 31 (16%) developed Q waves after 3 hours but before hospital discharge, and 29 (14%) were discharged with a non-Q-wave AMI. Laboratory indicators of myocardial damage and in-hospital morbidity and mortality were greater among patients with Q-wave AMIs than with non-Q-wave AMIs. When these indexes were examined with respect to the timing of Q-wave evolution, the prognosis of patients with delayed Q-wave development was similar to that of patients with non-Q-wave AMIs. Thus, compared to patients with early (less than or equal to 3 hours) Q-wave evolution, patients with delayed Q-wave evolution or with a non-Q-wave AMI had a smaller creatine kinase peak (mean 661 to 1,081 vs 1,251 to 1,541 IU; p = 0.005), better preservation of left ventricular function as measured by radionuclide ventriculography before discharge (mean +/- standard deviation 54 +/- 11% vs 47 +/- 13%; p less than 0.01), and a lower incidence of congestive heart failure at discharge (3 vs 15%; p = 0.02). In-hospital mortality was lower among patients with delayed Q-wave evolution or with a non-Q-wave AMI (5 of 141 vs 0 of 60; difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)     

Diabetes mellitus prevents ischemic preconditioning in patients with a first acute anterior wall myocardial infarction

OBJECTIVES: This study was undertaken to assess whether prodromal angina could have beneficial effects in diabetic patients with acute myocardial infarction (AMI). BACKGROUND: Prodromal angina occurring shortly before the onset of AMI is associated with favorable outcomes by the mechanism of ischemic preconditioning. However, little is known about the impact of diabetes on ischemic preconditioning. METHODS: We studied 611 patients with a first anterior wall AMI who underwent emergency catheterization within 12 h after the onset of chest pain: 490 patients without diabetes and 121 patients with non-insulin treated diabetes. Prodromal angina was defined as angina episode(s) occurring within 24 h before the onset of AMI. Serial contrast left ventriculograms were obtained in 424 patients at the time of acute and predischarge catheterization. RESULTS: In non-diabetic patients, prodromal angina was associated with lower peak creatine kinase (CK) value (3,068 +/- 2,647 IU/l vs. 3,601 +/- 2,462 IU/l, p = 0.037), larger increase in left ventricular ejection fraction (LVEF) (10.1 +/- 13.0% vs. 5.8 +/- 13.4%, p = 0.004) and lower in-hospital mortality (3.4% vs. 9.3%, p = 0.015). On the contrary, in diabetic patients, there was no significant difference in peak CK value (3,382 +/- 2,520 IU/l vs. 3,233 +/- 2,412 IU/l, p = NS), the change in LVEF (6.7 +/- 13.8% vs. 7.1 +/- 12.4%, p = NS) and in-hospital mortality (8.8% vs. 11.0%, p = NS) between patients with and patients without prodromal angina. CONCLUSIONS: Prodromal angina limited infarct size, enhanced recovery of LV function and improved survival in non-diabetic patients with AMI. However, such beneficial effects of prodromal angina were not observed in diabetic patients, suggesting that diabetes might prevent ischemic preconditioning.     

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.     

Long-term prognosis after myocardial infarction in patients with previous coronary artery bypass surgery

A group of 205 patients hospitalized with myocardial infarction 2 to 162 months (mean 66) after bypass surgery and 205 control patients with myocardial infarction were compared and followed up for 34 +/- 25 months after hospital discharge. At baseline the postbypass group contained more men (p less than 0.03) and more patients with previous myocardial infarction (p less than 0.06), but the groups were otherwise comparable. Indexes of infarct size were lower in postbypass patients: sum of ST elevation, QRS score, peak serum creatine kinase (CK) (1,115 +/- 994 versus 1,780 +/- 1,647 IU/liter) and peak MB CK (all p less than or equal to 0.001). Postmyocardial infarction ejection fraction was 45 +/- 15% in the postbypass group and 43 +/- 15% in the control group (p = NS); in-hospital mortality rate was 4 and 5%, respectively (p = NS). When patent grafts were taken into account, the two groups were comparable in extent of coronary artery disease. At 5 years after discharge, cumulative mortality was similar in the postbypass and control groups (30 versus 25%, respectively, p = NS). However, postbypass patients had more reinfarctions (40 versus 23%, p = 0.007), more admissions for unstable angina (23 versus 18%, p = 0.04) and more revascularization procedures (34 versus 20%, p = 0.04) than did control patients. The total for these events at 5 years was 70% in the postbypass group and 49% in the control group (p = 0.001). Thus, although patients with previous bypass surgery who develop acute myocardial infarction have a smaller infarct, their subsequent survival is no better than that of other patients with acute myocardial infarction. They experience more reinfarctions and unstable angina. Previous bypass surgery is an important clinical marker for recurrent cardiac events after myocardial infarction.