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.     

Serial changes in serum VEGF and HGF in patients with acute myocardial infarction

The time course of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) release in patients with acute myocardial infarction (AMI) is unknown. Blood samples were obtained at the time of admission and 3, 7, 14 and 21 days later in 32 patients with AMI and 30 control patients. Serum VEGF and HGF, as well as C-reactive protein (CRP) and amyloid A protein (SAA), were determined. Both serum VEGF and HGF levels on admission in patients with AMI were higher than control values and peaked on day 7. VEGF levels in patients with preinfarction angina were higher than in patients with no preinfarction angina, whereas the HGF level did not differ. Both CRP and SAA levels peaked on day 3, and the CRP level on day 3 correlate with both VEGF and HGF levels on day 7. We hypothesized that the serum VEGF level is associated with preinfarction ischemia and the increase in VEGF and HGF on day 7 of AMI may represent a response to acute inflammation.     

Clinical evaluation of coronary lesion characteristics in acute myocardial infarction

Coronary lesion instability at the onset of acute myocardial infarction (AMI) was evaluated. The mechanism of AMI has been considered to be coronary lesion instability with occlusive thrombus, although more than one half of AMI occurs in clinically stable patients. A total of 313 AMI patients treated by primary percutaneous transluminal coronary angioplasty with provisional stenting (rate, 41%) were studied. They were divided into 2 groups: group 1A (n = 211), without unstable angina before AMI onset, and group 1B (n = 102), with unstable angina before onset. Moreover, angina patients treated similarly were studied: group 2A (n = 180), with stable angina, and group 2B (n = 204), with unstable angina. Coronary lesion instability at AMI onset was also predicted by C-reactive protein (CRP) levels within 6 hours after onset, before they were affected by myocardial damage. The incidence of repeated AMI and/or target vessel revascularization was 1.9% in group 1A, 7.8% in 1B (p=0.035), 1.7% in 2A, and 5.9% in 2B (p=0.043). Event-free survival curves were consistent with each other in groups 1A and 2A and in groups 1B and 2B. CRP levels on admission were 2.0 +/- 1.7 mg/L in group 1A, 3.3 +/- 4.8 mg/L in group 1B (p<0.001), 2.1 +/- 1.7 mg/L in group 2A, and 3.4 +/- 4.7 mg/L in group 2B (p<0.001). Thus coronary lesion characteristics at AMI onset appeared to be similar in groups 1A and 2A and in groups 1B and 2B. A substantial number of patients have stable culprit lesions at the onset of AMI.     

蛋白芯片法联检急性冠状动脉综合征患者血中细胞因子的意义

目的 探讨急性冠状动脉综合征(ACS)患者血中炎性细胞因子、炎性细胞相关因子及心肌损伤因子浓度的变化及临床意义.方法 运用蛋白芯片技术同步联检经冠状动脉造影及临床表现证实为ACS患者104例及对照者50例血清或血浆中10种细胞因子水平;同时对不稳定性心绞痛(UA)患者按Braunwald分级进行分析.结果 急性心肌梗死(AMI)组和UA组血清中C反应蛋白(CRP)、白介素(IL)-6、可溶性CD40L(sCD40L)、基质金属蛋白酶(MMP)-9、心脏型脂肪酸结合蛋白(H-FABP)、肌钙蛋白Ⅰ(cTnⅠ)及血浆中的IL-8、内皮素(ET)-1、可溶性血管细胞黏附分子(sVCAM)-1、氨基酸N末端脑钠肽原(NT-proBNP)浓度高于对照组,差异有统计学意义(P＜0.01);AMI组cTnⅠ[(11.08±10.49) μg/L]和H-FABP[(19.80±4.60)μg/L]浓度高于UA组[cTnⅠ:(0.69±0.18)μg/L,H-FABP:(4.12±2.45)μg/L,P＜0.01],而CRP、IL-6、MMP-9、sCD40L及ET-1浓度,两组比较差异无统计学意义;UA组MMP-9、sCD40L及H-FABP的浓度与Braunwald分级存在显著正相关(分别r=0.653,r=0.745,r=0.933,均P＜0.01).随着心绞痛严重程度的增加,MMP-9、sCD40L及H-FABP水平明显升高,心绞痛Ⅰ级＜心绞痛Ⅱ级＜心绞痛Ⅲ级(P＜0.01).结论 ACS患者血中存在多种细胞因子浓度异常,其中MMP-9、sCD40L、H-FASP的浓度与UA患者心绞痛严重程度存在良好的相关性.提示上述细胞因子参与和促使了ACS的发生、发展,为ACS的危险分层、预后判断提供了可能的分子标志物依据.     

Prognostic value of C-reactive protein,fibrinogen, interleukin-6, and macrophage colony stimulating factor in severe unstable angina

BACKGROUND: Inflammatory process plays an important role in the pathogenesis of acute coronary syndromes. HYPOTHESIS: The study was undertaken to evaluate whether admission levels of C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6). and macrophage colony stimulating factor (MCSF) can predict short-term prognosis in patients with unstable angina. METHODS: C-reactive protein, fibrinogen, IL-6, and MCSF were measured on admission in 141 consecutive patients, aged 59 +/- 10 years, with unstable angina (Braunwald class IIIb). Patients were divided into two groups according to their in-hospital outcome: Group 1 comprised 77 patients with a complicated course (2 died, 15 developed nonfatal myocardial infarction, and 60 had recurrence of angina), and Group 2 comprised 64 patients with an uneventful course. RESULTS: Admission median levels of CRP (8.8 vs. 3.1 mg/l, p = 0.0002). fibrinogen (392 vs. 340 mg/dl, p = 0.008), IL-6 (8.8 vs. 4.5 pg/ml, p = 0.03), and MCSF (434 vs. 307 pg/ml, p = 0.0001) were higher in Group I than in Group 2. The MCSF levels were an independent risk factor for in-hospital events, with an adjusted odds ratio for eventful in-hospital outcome of 3.3 (95% confidence interval 1-10.9, p = 0.04), and correlated with levels of IL-6 (r(s) = 0.52, p = 0.0001), CRP (r(s) = 0.43, p = 0.0001), and fibrinogen (r(s) = 0.25, p = 0.004). CONCLUSIONS: These findings suggest that among the studied inflammatory indices only increased admission levels of MCSF are strongly and independently related with adverse short-term prognosis in patients with severe unstable angina.     

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.     

Comparison of protective effects of preinfarction angina pectoris in acute myocardial infarction treated by thrombolysis versus by primary coronary angioplasty with stenting.

The protective effects of preinfarction angina were evaluated in acute myocardial infarction (AMI) treated by primary percutaneous transluminal coronary angioplasty (PTCA) and stenting. We studied 613 patients with AMI. Group 1 (n = 306) was treated by conventional medical therapies and coronary thrombolysis and group 2 (n = 307) was treated by primary PTCA supported by stenting. Each group was subdivided into those with and without preinfarction angina within 24 hours before the onset of AMI. There was no significant difference in clinical characteristics between the subgroups of groups 1 and 2. In group 1, there were differences between patients with preinfarction angina (n = 84) and those without (n = 222) in in-hospital mortality (11% vs 18%), pump failure (Killip classes 3 and 4) (11% vs 21%, p <0.05), left ventricular ejection fraction at discharge (52 +/- 13% vs 48 +/- 14%, p <0.05), and peak creatine kinase (2,106 +/- 1,637 vs 2,764 +/- 2,154 U/L, p <0.02). In group 2, however, there was no significant difference between those with preinfarction angina (n = 82) and those without (n = 225) in mortality (6% vs 6%), pump failure (12% vs 12%), left ventricular ejection fraction (50 +/- 13% vs 50 +/- 13%) and peak creatine kinase (3,285 +/- 2,306 vs 3,291 +/- 2,262 U/L). Multivariate analysis indicated that preinfarction angina was an independent determinant of in-hospital death and pump failure in group 1, but not in group 2. We conclude that the protective effects of preinfarction angina in AMI are not evident in those treated by primary PTCA and stenting, possibly because of the overwhelming protective effects of complete coronary revascularization provided by primary PTCA and stenting.     

Is inflammation related to the clinical severity of unstable angina?

The present study determined the white blood cell (WBC) count and the serum C-reactive protein (CRP) level in 27 patients with coronary spastic angina, 16 with Braunwald class IB unstable angina (UA) and 13 with Braunwald class IIIB. The relationship between the clinical presentation of UA and the requirement for emergency percutaneous transluminal coronary angioplasty (PTCA) was examined, and in patients with medically refractory angina, the determining factor among the clinical manifestations of angina was also investigated. In the acute phase, the WBC count and the serum CRP level were significantly higher in patients with Braunwald class IIIB than in those with coronary spastic angina or Braunwald class IB UA (p<0.001). In the Braunwald class IIIB group, a significantly higher rate of patients required emergency PTCA than that of the coronary spastic angina group (p<0.01). Patients with medically refractory angina had a significantly higher WBC count and higher serum CRP level on admission, and the WBC count on admission was independently associated with medically refractory angina by multivariate analysis (p<0.05). Inflammation may play a major pathological role in the rapid development of acute coronary syndrome.     

Enhanced inflammatory response in patients with preinfarction unstable angina

OBJECTIVES: We assessed the extent and the time course of the acute phase response following myocardial cell necrosis and its relationship with the presence of preinfarction unstable angina (UA). BACKGROUND: Elevated levels of acute phase proteins have been reported in patients with UA and in patients with acute myocardial infarction (MI). METHODS: C-Reactive Protein (CRP), serum amyloid A protein (SAA) and interleukin-6 (IL-6) were measured in 36 patients with MI admitted within 3 h from symptoms onset. All patients had normal levels of creatine kinase and of troponin T on admission, rising above diagnostic levels within 6 to 12 h. Blood samples for CRP, SAA and IL-6 measurements were taken on admission, at 6, 24, 48, 72 h and at discharge. RESULTS: Twenty of the 36 patients studied presented an unheralded MI (Group 1); the remaining 16 patients had symptoms of unstable angina in the preceding 7 days (Group 2). Group 2 patients have much higher levels of CRP and SAA on admission (median values 8.8 vs. 3 mg/L and 28 vs. 3.4 mg/L, respectively, all p<0.001). Following the necrotic insult, despite similar infarct size and clinical signs of reperfusion, Group 2 patients had strikingly higher peaks of IL-6 (median values 85.2 vs. 19 pg/ml, p<0.05), CRP (50 vs. 31.4 mg/L, p<0.05) and SAA (228 vs. 45 mg/L, p<0.001). CONCLUSIONS: Our data demonstrated that the acute phase response is greatly enhanced in patients with preinfarction UA compared with those presenting with an unheralded MI. The significant differences in acute phase response observed in these two clinical presentations of MI indicate a major difference in their underlying pathogenetic components.     

Increased soluble platelet/endothelial cell adhesion molecule-1 in the early stages of acute coronary syndromes

Specific molecules including inflammatory cell adhesion molecules mediate attachment of blood leukocyte and platelets to the endothelium and mononuclear cell migration into the arterial intima. However, the clinical significance of soluble cell adhesion molecules very early in the course of acute coronary syndrome is not known. We assayed platelet/endothelial cell adhesion molecule-1 (PECAM-1, CD31), intercellular adhesion molecule-1 (ICAM-1, CD54), and P-selectin (CD62P) in plasma obtained from 20 patients within 3 h after the onset of acute myocardial infarction (AMI); 16 patients with unstable angina pectoris; 20 patients with stable angina pectoris, and 28 controls. Blood samples were obtained on hospital admission and again 1 week after onset of AMI and unstable angina, and on admission in patients with stable angina and controls. Plasma PECAM-1 concentration (ng/ml) on admission was higher in patients with AMI (25.6±4.7) and unstable angina (24.7±4.4) than in stable angina (20.5±4.4) and control (18.8±3.8) groups. In both AMI and unstable angina, plasma PECAM-1 had decreased significantly by 1 week (AMI, 20.8±4.0; unstable angina, 21.0±4.1). Plasma ICAM-1 concentration (ng/ml) on admission was higher in patients with AMI (254±70), unstable angina (264±78), and stable angina (245±68) than in controls (201±56), but did not differ between the three coronary syndromes. Plasma P-selectin concentration did not differ between the four groups, including controls. Therefore, soluble PECAM-1 concentration may be a sensitive markers providing early diagnostic aid in acute coronary syndromes.     

Unstable angina: Relationship of clinical presentation,coronary artery pathology,and clinical outcome

Patients with unstable angina are heterogeneous with respect to presentation, coronary artery morphology, and clinical outcome. Subclassification of these patients based on clinical history has been proposed as a means of identifying individuals at increased cardiac risk. We applied such a classification system to 129 patients discharged from a coronary care unit with a diagnosis of acute myocardial ischemia. Patients were then assessed for cardiac events (recurrent angina requiring revascularization, myocardial infarction, death) 12 months following hospital discharge. Patients were classified as recent onset unstable angina preinfarction (n = 42), crescendo unstable angina preinfarction (n = 48), and unstable angina postinfarction (n = 39). Within each of these groups, the patients were further subclassified based on the occurrence of angina on effort, at rest, or both. No attempt was made to subset patients taking antiischemic drugs at the time of clinical presentation to the physician. Coronary angiographic pathology (morphology and number of vessels involved) was similar in the subgroups, but coronary artery thrombus was statistically more likely to be found in patients with crescendo rest angina preinfarction or with frequent anginal episodes at rest postinfarction. Mortality was significantly higher for patients with unstable angina postinfarction (7.7%) than preinfarction (1.1%). No statistical differences were noted between the subgroups with respect to the occurrence of myocardial infarction or recurrent unstable angina requiring revascularization. These data suggest that subclassification of unstable angina patients based on clinical characteristics at presentation is not useful to predict subsequent myocardial infarction or recurrent angina requiring revascularization. However, as one might expect, patients with recurrent angina postinfarction have a higher mortality rate than patients with unstable angina preinfarction, and patients with recurrent rest angina, either pre- or postinfarction, are more likely to have intracoronary thrombus than patients with new onset angina or crescendo effort angina; however, the presence of thrombus did not predict a poor clinical outcome.     

直接经皮冠状动脉介入治疗对有无梗死前心绞痛患者心肌存活性和心室收缩同步性的影响

目的　探讨直接经皮冠状动脉介入治疗 (PCI)对有无梗死前心绞痛的急性心肌梗死 (AMI)患者心肌存活性和心室收缩同步性的近期影响。方法　 87例首次 AMI患者 ,按梗死前有无心绞痛分为 3组 :A组 :无心绞痛史 30例。 B组 :梗死前 4 8h内有心绞痛史 39例。 C组 :仅在梗死前 >4 8h有心绞痛史 18例。所有患者均在发病 6 h内行直接 PCI术。术后 1周、4周行 99m　 Tc- MIBI心肌灌注断层显像 (SPECT)测定心肌存活性 ;术后 2周行 99m　 Tc心血池显像测定心室收缩同步性参数。结果　 (1) B组肌酸激酶同工酶 (CK- MB)峰值显著低于 A组 (P<0 .0 1)。 (2 ) B组放射性缺损面积 (MIA)小于 A组 (P<0 .0 5 ) ;AMI后 4周与 1周比较 ,B组 MIA显著缩小 (P<0 .0 1) ,病变区放射性计数显著增加 (P<0 .0 1) ;C组和 A组前后比较均无显著差异。 (3)心功能 :B组左心室射血分数 (L VEF)高于 A组 (P<0 .0 1) ;左心室收缩同步性 :B组左心室相角程 (L PS)低于 A组 (P<0 .0 5 ) ;以上各参数 ,C组和 A组比较均无显著差异。结论　 (1)首次急性心肌梗死前 4 8h内心绞痛发作可导致心肌缺血预适应 (ischemic preconditioning,IP)的产生 ,并可缩小心肌梗死面积 ,保护心功能。 (2 )直接 PCI可显著提高有 IP的急性心肌梗死患者的近期心肌存活性和     

Early and late mortality after surgery for unstable angina in relation to Braunwald class

BACKGROUND: The prognostic value of the preoperative Braunwald class of unstable angina to predict early and long-term outcome after urgent coronary artery bypass grafting (CABG) has not been studied previously. METHODS: Deaths were recorded after all primary isolated CABG performed for unstable (n = 992) and stable (n = 5376) angina pectoris during 1980-1995. Severity of symptoms in the unstable patients was classified according to Braunwald. RESULTS: Death within 30 days of surgery occurred in 4.6% of the patients having unstable angina and in 1.6% of those with stable angina. Early mortality was 2.5% in Braunwald class II, 4.9% in class IIIB, and 6. 2% in class IIIC unstable patients. The risk of early death, after adjustment for risk factors, was about four times higher in Braunwald class IIIB (odds ratio [OR] 4.3, 95% confidence interval [CI] 2.4-7.7) and IIIC (OR 4.7, 95% CI 2.2-10.3) patients than in stable patients. The risk of death during postoperative months 1 to 6 tended to be higher (relative risk 2.4, 95% CI 0.8-7.1) in Braunwald class IIIC patients than in stable patients. After the first 6 months up to 5 years, survival rates in all Braunwald classes were similar to those in patients operated on for stable angina. CONCLUSIONS: There was a higher risk of early death after urgent bypass surgery in patients with Braunwald class III unstable angina than after elective CABG. The long-term survival rates after the first 6 postoperative months was similar in stable and unstable patients, regardless of preoperative Braunwald class.     

Relation between the timing of the last preinfarction angina and microvascular reperfusion in patients with recanalized acute myocardial infarction

In patients with recanalized acute myocardial infarction (AMI), the relation between the timing of preinfarction angina (PA) and microvascular reperfusion remains unclear. A total of 186 patients (114 with anterior and 72 with inferior AMI) who had total occlusion and TIMI 3 recanalization < or = 6 hours from the onset of AMI were divided into 4 groups according to the time interval between the last episode of PA and the onset of AMI: < or = 2 hours (group A, n = 52); 2 to 48 hours (group B, n = 43), > or = 48 hours (group C, n = 33), and no PA (group D, n = 58). The angiographic myocardial blush grade, a marker of microvascular reperfusion, was retrospectively assessed immediately after recanalization. There were no differences in baseline characteristics, except for sex among the 4 groups. Myocardial blush grade 3 was more frequent (42% vs 21%, 9%, and 14%) and peak creatine kinase was lower (2659 vs 3455, 4422, and 4622 mU/mL) in group A than in groups B, C, and D (all P < 0.05). Multivariate analysis showed that PA occurring < or = 2 hours before AMI (OR 3.88, P < 0.05), a smaller summed ST-segment elevation before recanalization (OR 0.84, P < 0.01), earlier time to recanalization (OR 0.52, P < 0.05), and interior AMI (OR 4.87, P < 0.05) were independently associated with adequate microvascular reperfusion. We conclude that PA < or = 2 hours before the onset of AMI is independently associated with adequate microvascular reperfusion after recanalization in patients with AMI.     

Effect of preinfarction angina on heart rate variability in the early phase of the first anterior wall acute myocardial infarction.

The aim of this study was to clarify the effect of preinfarction angina on heart rate variability (HRV) in anterior wall acute myocardial infarction (AMI). A total of 36 patients experiencing their first anterior wall AMI were prospectively examined. The patients were divided into 2 groups according to the presence (group A, n=24) or absence (group B, n = 12) of preinfarction angina. HRV was assessed on 24-h Holter electrocardiograms recorded on day 3. Peak creatine kinase activity was significantly lower in group A than in group B (2,747+/-1,939 vs 4,891+/-2,639 IU/L, p<0.05). The SD of all RR intervals and ultra-low frequency, very low frequency, and low frequency powers was significantly less reduced in group A than in group B (86+/-24 vs 64+/-22 ms, p<0.05; 2,098+/-1,462 vs 867+/-502 ms2, p<0.01; 1,430+/-1,042 vs 546+/-344ms2, p<0.01; and 354+/-272 vs 186+/-136ms2, p<0.05; respectively). High frequency power, low frequency/high frequency, and pNN50 did not differ significantly between the 2 groups. In conclusion, preinfarction angina has a favorable influence on HRV in the early phase of anterior wall AMI.     

Prognostic value of C-reactive protein and troponin T level in patients with unstable angina pectoris

OBJECTIVES: The prognosis of unstable angina pectoris may be more accurately predicted by the combination of C-reactive protein (CRP), which is a known inflammation marker, and troponin T (TnT), which is used for risk assessment for the prognosis of acute coronary syndrome. The present study investigated the correlations between pathophysiology and prognosis of severe unstable angina pectoris and CRP and TnT levels. METHODS: The correlation between CRP at admission and the prognosis was studied in 367 patients with severe unstable angina pectoris (Braunwald type II and III) who were admitted to our hospital between January 1998 and December 2000. The in-hospital and long-term prognosis was investigated in TnT-positive patients. In-hospital cardiac events were defined as death, myocardial infarction, heart failure and angina attacks during hospitalization. Long-term cardiac events were defined as death, myocardial infarction, heart failure and recurrence of angina. RESULTS: The incidence of in-hospital cardiac events in all patients was 30.2%. The CRP levels were higher in patients with cardiac events (0.97 +/- 2.67 vs 0.53 +/- 1.29 mg/d/, p = 0.057), but there was no significant difference between the two groups. The incidence of long-term cardiac events was 26.8%. The mean CRP level was significantly higher in patients with cardiac events than in patients without cardiac events (1.17 +/- 1.86 vs 0.43 +/- 1.14 mg/dl, p = 0.098). In TnT-positive patients (TnT > 0.1 ng/ml, 23% of all patients), the incidence of in-hospital cardiac events was 47.6% (p < 0.0001), significantly higher than that in all patients. TnT-positive patients with CRP levels of 0.5 mg/dl or higher (8% of all patients) had a markedly higher incidence of in-hospital cardiac events of 56.7% (p = 0.001) and long-term cardiac events of 46.7% (p = 0.01). CONCLUSIONS: CRP levels were useful in prediction of the long-term prognosis. TnT levels were useful in prediction of in-hospital prognosis. The present study suggested the possibility that the combined use of these biological markers could predict the prognosis of patients with unstable angina at early stage and more accurately.     

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.     

Prognostic value of C-reactive protein levels within six hours after the onset of acute myocardial infarction

BACKGROUND: Inflammation is an important feature of atherosclerotic lesions, and the vulnerability of coronary lesions in acute myocardial infarction (AMI) at the time of onset may be related to blood levels of C-reactive protein (CRP) on admission, before CRP levels are affected by myocardial damage. METHODS: A total of 234 patients with AMI in whom plasma CRP was measured within 6 hours after onset were studied. They were divided into 2 groups: group 1 (n = 49) with elevated CRP (>/=0.3 mg/dL) on admission within 6 hours after onset and group 2 (n = 185) with normal CRP (<0.3 mg/dL) within 6 hours after onset. All were treated by primary percutaneous transluminal coronary angioplasty with provisional stenting. RESULTS: There were no significant differences in baseline characteristics between the 2 groups. In-hospital adverse coronary events, including coronary reocclusion, reinfarction, target vessel revascularization, and death, were significantly more frequent in group 1 (22.4%) than in group 2 (4.3%, P <.005), and bailout stenting was performed significantly more frequently in group 1 (61. 2%) than in group 2 (37.8%, P <.005). In contrast, there were no significant differences between the 2 groups in parameters that represent myocardial damage, including peak creatine kinase and left ventricular ejection fraction. CONCLUSION: CRP levels within 6 hours after the onset of AMI reflect the vulnerability of culprit coronary lesions and predict adverse coronary events after primary PTCA/stenting.     

Increased platelet reactivity in unstable angina patients is not related to C-reactive protein levels

Platelets are a major component of thrombi, and coronary thrombosis plays a key role in the pathogenesis of unstable angina (UA). Whether platelet aggregability is increased in UA patients however, is not known. Furthermore, no study has investigated the relationship between platelet reactivity and inflammation in UA patients In this study, venous blood samples were collected at admission in coronary care unit in 37 patients with unstable angina (Braunwald class IIIB) and in 37 sex- and age-matched patients with chronic stable angina (CSA). Patients taking thienopyridine or anticoagulant drugs were excluded from the study, as also were excluded patients with a history of acute myocardial infarction in the previous 12 months. Platelet aggregability was measured on flowing blood as time to occlude a ring coated with collagen-adenosine diphosphate (ADP), using the platelet function analyzer (PFA-100) system. By this method, the time to occlusion (closure time) is taken as a measure of platelet adhesion/aggregability, with shorter times indicating greater platelet reactivity.There were 23 men and 14 women in both groups, and age was 67.7 +/- 8 and 67.5 +/- 8 years in UA and SA, respectively (P = 0.93). Closure time was significantly reduced in UA patients (78.8 +/- 14 s), compared to SA patients (93.3 +/- 19 s, P < 0.001). Among UA patients, serum C-reactive protein (CRP) levels had a median value of 5.1 mg/l (bottom and top quartile levels, 1.50-7.95). There was no significant correlation between closure time and CRP levels (r = 0.22, P = 0.29). Our data show that, in patients with unstable angina there is an increase of platelet reactivity in response to ADP/collagen stimulation, which is not related to inflammation.     

Effect of preinfarction angina pectoris on outcome in patients with acute myocardial infarction treated with primary angioplasty (results from the Myocardial Infarction Registry

Preinfarction angina is associated with better clinical outcome in patients with acute myocardial infarction (AMI) who receive intravenous thrombolysis. This has not been proved in patients with AMI treated with primary angioplasty. We analyzed the data of the prospective multicenter Myocardial Infarction Registry (MIR). Of 14,440 patients with AMI, 774 with a prehospital delay of < or =12 hours were treated with primary angioplasty. Five hundred thirty-two patients (68.7%) had preinfarction angina. Patients with preinfarction angina were slightly older than patients without (63 vs 62 years, p = 0.042), prehospital delay was 1 hour longer (180 vs 120 minutes, p = 0.001), and arterial hypertension was more prevalent (47.6% vs 32.2%, odds ratio [OR] 1.91, 95% confidence intervals [CI] 1.39 to 2.62). There was no significant difference in hospital mortality (5.6% vs 3.3%, OR 1.75, 95% CI 0.79 to 3.87), reinfarction, stroke, or the combined end point of death, reinfarction, or stroke between the 2 groups. Logistic regression analysis showed no association of preinfarction angina with the occurrence of either death (OR 2.21, 95% CI 0.91 to 6.08) or the combined end points (OR 1.10, 95% CI 0.55 to 2.31). There was also no significant difference in mortality (6% vs 5.1%, OR 1.19, 95% CI 0.56 to 2.52), reinfarction, stroke, postinfarction angina, or the combined end points between patients with preinfarction angina within 48 hours compared with patients with preinfarction angina between 49 hours and 4 weeks before the AMI. Thus, the MIR data showed no protective effects of preinfarction angina in patients with AMI treated with primary angioplasty.