Serum amyloid A predicts early mortality in acute coronary syndromes: A TIMI 11A substudy

OBJECTIVES: We evaluated the ability of serum amyloid A (SAA), alone and in combination with a rapid qualitative assay for cardiac-specific troponin T (cTnT), to predict 14-day mortality in patients with unstable angina or non-Q wave myocardial infarction (NQMI). BACKGROUND: Elevated C-reactive protein (CRP) has been associated with adverse outcomes in unstable coronary syndromes but data regarding its acute phase counterpart, SAA, are conflicting. METHODS: Serum amyloid A measurement and a rapid cTnT assay were performed on blood obtained at enrollment into Thrombolysis in Myocardial Infarction 11A, a dose-ranging trial of enoxaparin for unstable angina and NQMI. RESULTS: Serum amyloid A was higher in patients who died compared with survivors (6.28 vs. 0.75 mg/dL, p = 0.002). Among patients with a negative rapid cTnT, mortality was higher for those in the top quintile of SAA (6.1 vs. 0.7%, p = 0.003). Patients with both an early positive rapid cTnT (< or =10 min until assay positive) and SAA in the fifth quintile had the highest mortality followed by those with either markedly elevated SAA or an early positive rapid cTnT, while patients with both a negative rapid cTnT and SAA in quintiles 1-4 were at very low risk, (9.1 vs. 3.6 vs. 0.7%, p <0.002). CONCLUSIONS: Similar to CRP, baseline elevation of SAA identifies patients hospitalized with unstable angina and NQMI at higher risk for early mortality, even among those with a negative rapid assay for cTnT. These data support further investigation of inflammatory markers used alone and in combination with cardiac troponins for risk assessment in unstable coronary syndromes.     

Independent prognostic value of C-reactive protein and troponin I in patients with unstable angina or non-Q-wave myocardial infarction.

OBJECTIVES: Elevated concentrations of C-reactive protein (CRP), a non-specific acute phase reactant, and troponin I (TnI), a cardiac-specific marker of myocardial damage, have been found to be associated with a higher risk for cardiac events in patients with an acute coronary syndrome. We evaluated CRP alone and in combination with TnI for predicting the incidence of major cardiac complications within 6 months in patients with unstable angina or non-Q-wave infarction (NQMI). METHODS: CRP and TnI was measured on admission in patients with unstable angina or NQMI, but results were kept blinded. Patients were treated according to a conservative management strategy, and the incidence of major cardiac events within 6 months was assessed. RESULTS: An abnormal CRP (> 5 mg/l) and an abnormal TnI (> 0.4 microgram/l) were more frequent in patients that suffered a major cardiac event (CRP: 93 vs. 35%, P < 0.0001; TnI: 73 vs. 26%, P < 0.001). The incidence of major cardiac events was higher in patients with an abnormal CRP than in patients with a normal CRP, both when TnI was abnormal (42 vs. 4.5%, P = 0.003) and when TnI was normal (11 vs. 0%, P = 0.014). Mean event-free survival was excellent in patients with both a normal CRP and TnI, whereas survival was poorest in patients with both an abnormal CRP and TnI (121 +/- 16 vs. 180 days, P < 0.0001). CONCLUSIONS: An abnormal CRP on admission in patients with unstable angina or NQMI is associated with increased incidence of major cardiac events within 6 months, both in patients with normal and abnormal TnI. CRP and TnI have independent and additive prognostic value in this patient group, and the combination may be useful for early risk stratification.     

C-reactive protein is a marker for a complex culprit lesion anatomy in unstable angina.

BACKGROUND: The putative theory is that the clinical syndrome of unstable angina is caused by rupture of the atherosclerotic plaque with superimposed thrombus formation. It is characterized by angiographically complex coronary lesions in the majority of patients. HYPOTHESIS: This study aimed at assessing the correlation between C-reactive protein (CRP) and the complexity of culprit coronary lesions in unstable angina. METHODS: We identified culprit lesion complexity in 96 patients with unstable angina and normal creatine kinase (CK) and CK-MB mass. Serum concentrations of CRP (N < 5.0 mg/l) and cardiac troponin T (cTnT; N < 0.1 ng/ml) were measured on admission. RESULTS: There was a trend toward a higher grade of anatomical complexity of the culprit lesion in patients with elevated CRP (p = 0.007) and cTnT levels (p = 0.027). Patients who had intermediate- or high-grade lesion severity had a higher level of CRP (8.5 +/- 5.7 mg/l) and cTnT (0.118 +/- 0.205 ng/ml) on admission than those who had normal or low-grade lesions (5.7 +/- 4.0 mg/l, 0.017 +/- 0.021 ng/ml, respectively); Mann-Whitney U, p = 0.002 and p < 0.001, respectively. Furthermore, the likelihood of having intermediate- or high-grade complexity of the culprit lesion was higher when CRP levels were elevated in all patients (p = 0.007, odds ratio [OR] = 4.286; 95% confidence interval [CI] 1.492-12.310) and in those with normal cTnT levels (p = 0.025, OR = 3.876; 95% CI 1.185-12.678). Also, higher CRP levels strongly correlated with the need for revascularization interventions (p < 0.0005). CONCLUSION: Elevated CRP level on admission is a marker for anatomic complexity of culprit lesions and need for revascularization interventions in unstable angina.     

Dose-Ranging Trial of Enoxaparin for Unstable Angina: Results of TIMI 11A

Objectives. The Thrombolysis in Myocardial Infarction (TIMI) 11A trial compared the safety and tolerability of two weight-adjusted regimens of subcutaneous injections of enoxaparin, a low molecular weight heparin, in patients with unstable angina/non–Q wave myocardial infarction (NQMI).

Background. The optimal dose of enoxaparin in patients with arterial disorders has not been established.

Methods. Patients with unstable angina/NQMI were treated over a 14-day period in an open label dose-ranging trial. During the in-hospital phase, patients received either 1.25 mg/kg body weight (dose tier 1) or 1.0 mg/kg (dose tier 2) of enoxaparin subcutaneously every 12 h. A fixed dose of either 60 mg (body weight ≥65 kg) or 40 mg (body weight <65 kg) was administered subcutaneously every 12 h after hospital discharge.

Results. In an initial cohort of 321 patients (dose tier 1), the rate of major bleeding through 14 days was 6.5% and occurred predominantly at instrumented sites. In a second cohort of 309 patients (dose tier 2), the rate of major hemorrhage was reduced to 1.9%. In both dose tiers, only 3% to 5% of patients withdrew consent for subcutaneous injections during the home treatment phase. Through 14 days, the incidence of death, recurrent myocardial infarction or recurrent ischemia requiring revascularization was 5.6% in dose tier 1 and 5.2% in dose tier 2.

Conclusions. An acute phase regimen of enoxaparin (1.0 mg/kg every 12 h) is associated with an acceptable rate of major hemorrhage during the in-hospital phase. There is a high rate of patient compliance during the home treatment phase. A Phase III trial is now underway to test the benefits of uninterrupted treatment with enoxaparin during both the in-hospital and outpatient treatment phases.

(J Am Coll Cardiol 1997;29:1474–82)     

C-reactive protein and the stress tests for the risk stratification of patients recovering from unstable angina pectoris

We assessed the 90-day prognostic value of stress tests and C-reactive protein (CRP) after medical stabilization of unstable angina. We included 139 consecutive patients with unstable angina who were free of complications or did not undergo revascularization during hospitalization. Blinded CRP assays and a stress test (95 exercise electrocardiograms, 44 dobutamine echocardiograms) were performed within the first week after discharge. Of 139 participants, 44 (31.6%) had an ischemic stress test response. CRP was elevated (> 1.5 mg/dl) in 40 patients (28.7%). CRP >1.5 mg/dl was more frequently observed among patients who experienced death or myocardial infarction at 90 days (88.2% vs 20.5%, p <0.0001). Compared with the stress tests, CRP showed greater sensitivity (88% vs 47%) and specificity (81% vs 70%) for increased risk, and higher positive (37.5% vs 18.2%) and negative (98% vs 90%) predictive values. The area under the receiver operating curve of the relation with the 90-day outcome increased from 0.58 +/- 0.07 to 0.83 +/- 0.05 when the CRP data were added to the stress tests results (p <0.001). Elevation of CRP differentiated stress tests negative patients with increased risk of major events during follow-up. In patients who respond to medical treatment for unstable angina, CRP elevation may be a better parameter than the stress test in identifying the presence of persistent plaque instability.     

Comparison of C-reactive protein and terminal complement complex in patients with unstable angina pectoris versus stable angina pectoris

Elevated C-reactive protein (CRP) can identify patients with coronary artery disease who are prone to future acute events. We investigated whether elevated CRP is related to the activation of the terminal complement cascade in 66 patients with unstable angina pectoris (UAP), in 45 patients with stable angina pectoris, and in 42 controls. CRP, additional acute phase reactants, the terminal complement complex (sC5b-9), leukocytes, and troponin T were measured. In 47 patients with UAP the CRP values were regarded as elevated (>0.3 mg/dl). In patients with UAP and elevated CRP, the plasma levels of sC5b-9 were markedly higher than in patients with UAP and lower CRP (245 +/- 14 vs 188 +/- 19 ng/ml, p <0.02) and in patients with stable angina pectoris with slightly (0.4 +/- 0.1 mg/dl) increased CRP (sC5b-9 173 +/- 21 vs 130 +/- 7 ng/ml [controls; p <0.05]). A further acute phase reaction was present only in patients with UAP and elevated CRP already on admission (p <0.01). sC5b-9 was not related to troponin release. Thus, elevated CRP levels are associated with activation of the plaque destabilizating terminal complement system in patients with UAP during the acute phase reaction. This may explain the prognostic value of CRP in acute coronary syndromes (ACS).     

Elevation of C-reactive protein in "active" coronary artery disease

Unstable angina occurs most commonly in the setting of atherosclerotic coronary artery disease (CAD), but there is little information concerning the mechanisms responsible for the transition from clinically stable to unstable coronary atherosclerotic plaque. Recently, increased focal infiltration of inflammatory cells into the adventitia of coronary arteries of patients dying suddenly from CAD and activation of circulating neutrophils in patients with unstable angina have been observed. To characterize the presence of inflammation in "active" atherosclerotic lesions, the acute phase reactant C-reactive protein (CRP) was measured in 37 patients admitted to the coronary care unit with unstable angina, 30 patients admitted to the coronary care unit with nonischemic illnesses and 32 patients with stable CAD. CRP levels were significantly elevated (normal less than 0.6 mg/dl) in 90% of the unstable angina group compared to 20% of the coronary care unit group and 13% of the stable angina group. The average CRP values were significantly different (p = 0.001) for the unstable angina group (2.2 +/- 2.9 mg/dl) compared to the coronary care (0.9 +/- 0.7 mg/dl) and stable angina (0.7 +/- 0.2 mg/dl) groups. There was a trend for unstable angina patients with ischemic ST-T-wave abnormalities to have higher CRP values (2.6 +/- 3.4) than those without electrocardiographic changes (1.3 +/- 0.9, p = 0.1). The data demonstrate increased levels of an acute phase reactant in unstable angina. These findings suggest that an inflammatory component in "active" angina may contribute to the susceptibility of these patients to vasospasm and thrombosis.     

Cardiac troponin T in chest pain unit patients without ischemic electrocardiographic changes: angiographic correlates and long-term clinical outcomes

OBJECTIVES

We prospectively evaluated the relation between cardiac troponin T (cTnT) level, the presence and severity of coronary artery disease (CAD) and long-term prognosis in patients with chest pain but no ischemic electrocardiographic (ECG) changes who had short-term observation.

BACKGROUND

Cardiac TnT is a powerful predictor of future myocardial infarction (MI) and death in patients with ECG evidence of an acute coronary syndrome. However, for patients with chest pain with normal ECGs, it has not been determined whether cTnT elevation is predictive of CAD and a poor long-term prognosis.

METHODS

In 414 consecutive patients with no ischemic ECG changes who were triaged to a chest pain unit, cTnT and creatine kinase, MB fraction (CK-MB) were evaluated ≥10 h after symptom onset. Patients with adverse cardiac events, including death, MI, unstable angina and heart failure were followed for as long as one year.

RESULTS

A positive (>0.1 ng/ml) cTnT test was detected in 37 patients (8.9%). Coronary artery disease was found in 90% of 30 cTnT-positive patients versus 23% of 144 cTnT-negative patients who underwent angiography (p < 0.001), with multivessel disease in 63% versus 13% (p < 0.001). The cTnT-positive patients had a significantly (p < 0.05) higher percent diameter stenosis and a greater frequency of calcified, complex and occlusive lesions. Follow-up was available in 405 patients (98%). By one year, 59 patients (14.6%) had adverse cardiac events. The cumulative adverse event rate was 32.4% in cTnT-positive patients versus 12.8% in cTnT-negative patients (p = 0.001). After adjustment for baseline clinical characteristics, positive cTnT was a stronger predictor of events (chi-square = 23.56, p = 0.0003) than positive CK-MB (>5 ng/ml) (chi-square = 21.08, p = 0.0008). In a model including both biochemical markers, CK-MB added no predictive information as compared with cTnT alone (chi-square = 23.57, p = 0.0006).

CONCLUSIONS

In a group of patients with chest pain anticipated to have a low prevalence of CAD and a good prognosis, cTnT identifies a subgroup with a high prevalence of extensive and complex CAD and increased risk for long-term adverse outcomes.     

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.     

Predictive value of C-reactive protein and troponin T in patients with unstable angina: a comparative analysis. CAPTURE Investigators. Chimeric c7E3 AntiPlatelet Therapy in Unstable angina REfractory to standard treatment trial

OBJECTIVES: We evaluated C-reactive protein (CRP) and troponin T (TnT) for predicting six-month cardiac risk in patients with unstable angina. BACKGROUND: Troponin T is predictive of cardiac risk in patients with unstable angina. The clinical implications of elevated CRP in such patients remains controversial. METHODS: Baseline TnT and CRP values were determined in 447 patients with unstable angina enrolled in the placebo group of the Chimeric c7E3 AntiPlatelet Therapy in Unstable angina REfractory to standard treatment trial (CAPTURE) trial. All patients underwent a coronary intervention and were followed for a six month period in which 13 deaths and 47 myocardial infarctions were documented (MIs). RESULTS: Troponin T was >0.1 microg/liter in 30% and CRP was >10 mg/L in 41% of the patients. For the initial 72-h period (including coronary intervention), TnT (17.4% vs. 4.2%; p < 0.001) but not CRP (10.3% vs. 8%; p = 0.41) was predictive of mortality and MI. The TnT-positive patients displayed more frequent recurrent instability before the planned intervention (44.8% vs. 16.9%; p < 0.001), but in the CRP-positive patients, no such increase was observed (25.9% vs. 24.8%; p = 0.92). In contrast, for the six month follow-up period, CRP was predictive of cardiac risk (mortality, MI) (18.9% vs. 9.5%; p = 0.003). Using multivariate analysis, both CRP and TnT emerged as independent predictors of mortality and MI at six-month follow-up. Furthermore, the incidence of coronary restenosis during six-month follow-up was not related to TnT status (3% vs. 4.5%; p = 0.49); however, it was significantly related to CRP status (7% vs. 2.3%; p = 0.03). CONCLUSIONS: Troponin T, but not CRP, was predictive of cardiac risk during the initial 72-h period, whereas CRP was an independent predictor of both cardiac risk and repeated coronary revascularization (coronary artery bypass graft surgery and percutaneous transluminal coronary angioplasty) during six month follow-up.     

Non-Q wave myocardial infarction. Recurrent myocardial infarction, unstable angina and arrhythmia in 8-year observation

The contradictory views on long term clinical course of patients after non-Q wave myocardial infarction (NQMI) as compared with those after Q wave myocardial infarction (QMI)--induced us to undertake a comparative study of both types of myocardial infarction during a 8 year follow-up. The study was carried out in 400 patients (pts) with NQMI (mean age 51) and 485 pts with QMI (mean age 53). Both groups were compared. We have analysed the following parameters: the dynamics of ischaemic heart disease (unstable angina, reinfarction, arrhythmias, mortality) and coronary arteriography. During 8 year observation unstable angina and arrhythmias, were statistically more frequent in pts after NQMI. Recurrent myocardial infarction occurred in 196 (49%) of pts after NQMI and only in 87 pts (18%) after QMI (p less than 0.001). However, the difference in mortality between both groups was not significant (37% vs 39% respectively). Coronary angiography was performed at 1-6 months after myocardial infarction. In 65% of pts after NQMI detected lesions were limited to proximal part of one or two coronary arteries. Conclusion: NQMI is characterized by unstable long-term clinical course, and that is why pts with NQMI should be recommended for early coronary angiography and revascularization.     

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.     

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The clinical spectrum and outcome of 119 patients with acute non-Q wave myocardial infarction (NQMI) were studied, in comparison with those of 354 patients with acute Q wave myocardial infarction (QMI). The patients with NQMI had a significantly higher incidence of preinfarction angina (73% vs 63%), previous myocardial infarction (43% vs 22%), multivessel disease (73% vs 51%), postinfarction angina (55% vs 21%), and recurrent myocardial infarction during follow-up for an average of 25 months (17% vs 8%). NQMI patients also had a lower rate of complication of pump failure and smaller infarct size estimated by peak creating phosphokinase (CPK) levels (1361 +/- 1243 vs 2711 +/- 1684 IU/L) than those with QMI. There was no difference in in-hospital mortality between the two groups (17% vs 17%). However, death due to cardiac rupture was exclusively noted in the QMI group. The present study suggests that NQMI is more unstable than QMI in the clinical course.     

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.     

C反应蛋白与肌钙蛋白测定对于不稳定性心绞痛的诊断价值

目的:观察不稳定性心绞痛(UAP)与C反应蛋白(CRP)、肌钙蛋白(cTnT)的关系。方法;测定38例UAP患者(UAP组),35例稳定性心绞痛患者(SAP组)及32例健康对照组的CRP、cTnT和血脂水平,并进行比较,测定比较UAP组治疗前、后的CRP、cTnT水平。结果;UAP组与SAP组、对照组比较,其CRP、cTnT水平显著升高(P<0.05～0.01);UAP组的CRP、cTnT阳性率分别是42.8％、28.5％,两者比较有显著差异(P<0.05)。UAP组、SAP组血脂水平无显著差异(P>0.05),而与对照组相比均有显著差异(P<0.05);UAP组治疗后CRP、cTnT值显著下降(P分别<0.05,<0.01)。结论:UAP的触发因素可能与感染有关,CRP在UAP诊断中的敏感性比cTnT的高。动态观察CRP及cTnT有助于UAP疗效、预后的判断。     

The importance of lipoprotein(a) in pathogenesis of the high risk unstable angina]

OBJECTIVE: The aim of this study is to compare lipoprotein (a) [Lp(a)] levels in patients with low and high risk unstable angina pectoris, which is defined according to the cardiac troponin-I (Tn-I) levels and to investigate their relation with myocardial damage. METHODS: From patients with chest pain; venous blood samples were collected for measuring serum Lp(a) and C-reactive protein (CRP) levels on admission and serum cTn-I levels 12 and 24 hours after admission. Fifty-nine patients with serum cTn-I levels <1.0 ng/ml were assigned as negative unstable angina group and 53 patients with serum cTn-I levels >or=1.0 ng/ml were assigned as positive unstable angina groups, respectively. Severity of coronary artery disease was determined by angiography in all patients. RESULTS: Compared with cTn-I negative group, Lp(a) levels were significantly higher in cTn-I positive group (52.9+/-6.0 mg/dl vs 15.7+/-2.5 mg/dl, p<0.0001). There was a significant correlation between Lp(a) and cTn-I levels (r=0.870, p=0.0001). We could not establish any correlation between Lp(a) levels and Gensini score or between multiple vessel disease and low density lipoprotein cholesterol levels (p>0.05). Also, there was no significant difference between cTn-I positive and negative groups with respect to Gensini score (p>0.05). CONCLUSION: Increased Lp(a) levels and significant relation between Lp(a) and cTn-I levels support the opinion that Lp(a) can be a risk factor for plaque destabilization and thrombosis rather than severity of coronary artery disease in patients with high risk unstable angina. Furthermore, high levels of Lp(a) may be related with myocardial injury in patients with unstable angina.     

Usefulness of ST-segment changes in ≥2 leads on the emergency room electrocardiogram in either unstable angina pectoris or non-Q-wave myocardial infarction in predicting outcome

To determine the reliability of the admission electrocardiogram in predicting outcome in patients hospitalized for chest pain at rest, 90 patients were randomized into a trial of aspirin versus heparin in unstable angina or non-Q-wave myocardial infarction, and prospectively followed for 3 months. The emergency room admission electrocardiogram was analyzed for ST-segment deviation ≥1 mm/lead and T-wave changes. Unfavorable outcomes were recurrent ischemic pain, myocardial infarction and coronary revascularization with angioplasty or surgery. In patients who underwent coronary arteriography, a myocardium in jeopardy score ranging from 0 to 10 was assigned, based on the number of vessels with a diameter stenosis ≥70% and the location of the stenoses. Considering all 90 patients, an admission electrocardiogram with ST-segment deviation in ≥2 leads had a positive predictive value for adverse clinical events of 79% and a negative predictive value of 64%. In the subset of patients without left ventricular hypertrophy and whose admission electrocardiograms were recorded during chest pain (62 of 90), the positive predictive value of ST deviation in ≥2 leads improved to 89% and the negative value to 72%. Of the 62 patients, 53 underwent coronary arteriography. There was a positive linear correlation between the total number of leads with ST-segment deviation and the myocardium in jeopardy score (r = 0.80, p < 0.001). In patients with unstable angina or non-Q-wave myocardial infarction, an admission electrocardiogram recorded during pain and revealing ST-segment changes in ≥2 leads is by itself a reliable predictor of major clinical events. The total number of leads with ST changes predicts the extent of myocardium in jeopardy.     

心绞痛患者纤溶活性变化的研究

目的探讨不同类型心绞痛患者纤溶活性变化。方法将92例心绞痛患者分为三组,稳定型心绞痛组20例,cTnT阴性的不稳定型心绞痛组47例,cTnT阳性的不稳定型心绞痛组25例。另选20例同年龄组的健康体检者为对照组。测定并比较各组血浆D-二聚体(D-dimer)和组织型纤溶酶原激活剂(t-PA)及其抑制物(PAI-1)水平。结果cTnT阴性和阳性的不稳定型心绞痛组PAI-1和D-dimer水平均较对照组升高(P<0.01),各组心绞痛患者t-PA/PAI-1较对照组降低(P<0.01)。稳定型心绞痛、cTnT阴性的不稳定型心绞痛和cTnT阳性的不稳定型心绞痛PAI-1、t-PA/PAI-1和D-dimer差异有统计学意义(P<0.01),以cTnT阳性的不稳定型心绞痛患者变化最明显,稳定型心绞痛患者变化较小。结论稳定型和不稳定型心绞痛患者纤溶活性均存在异常,cTnT阳性的不稳定型心绞痛患者变化最明显。     

Elevated homocysteine levels are associated with increased ischemic myocardial injury in acute coronary syndromes

OBJECTIVES: This study was conducted to determine whether the amount of myocardial damage during acute coronary syndromes (ACS) is related to the admission plasma homocysteine concentration. BACKGROUND: Elevated homocysteine levels are associated with increased thrombosis in patients presenting with ACS. It is not known whether this association is reflected in the degree of myocardial injury in those patients. METHODS: We studied consecutive patients presenting with acute myocardial infarction (MI) (n = 205) and unstable angina pectoris (UAP) (n = 185). Plasma samples were collected on admission and prior to clinical intervention and were assayed for homocysteine by high performance liquid chromatography (HPLC). Myocardial necrosis was assessed by measurements of cardiac troponin T (cTnT) on admission and 12 h after admission (peak cTnT). The patients were studied by quintiles of homocysteine concentration. RESULTS: There was a significant increase in peak cTnT in the 5th homocysteine quintile in MI (analysis of variance [ANOVA], p = 0.005), the levels being 4.10, 3.86, 4.13, 6.20 and 7.85 microg/liter for quintiles 1 to 5, respectively (p < 0.0001, for top vs. bottom quintile). Similarly, there was a step-up in peak cTnT levels in the top homocysteine quintile in UAP (ANOVA, p < 0.0001), the levels being 0.03, 0.03, 0.02, 0.04 and 0.15 microg/liter, (p < 0.0001 for top vs. bottom quintile). In a multivariate regression model, the association between peak cTnT and the top homocysteine quintile remained strong after adjustment of other confounders including age, gender, final diagnosis and thrombolysis treatment (odds ratio [OR]: 2.92 (1.75-4.87) p < 0.0001). The patients with UAP were further examined according to peak cTnT levels below (cTnT negative) or above (cTnT positive) 0.1 microg/liter. Homocysteine levels were significantly higher in cTnT positive than cTnT negative patients; 13.8 (11.7-15.3) vs. 10.3 (9.4-11.3) micromol/liter, respectively, p = 0.002. CONCLUSIONS: Elevated homocysteine levels are associated with a higher risk of ischemic myocardial injury in patients presenting with ACS.     

Prognostic significance of serum creatinine concentration for in-hospital mortality in patients with acute myocardial infarction who underwent successful primary percutaneous coronary intervention (from the Heart Institute of Japan Acute Myocardial Infarction [HIJAMI] Registry)

This study evaluated the impact of serum creatinine levels on in-hospital mortality in 1,359 consecutive patients with acute myocardial infarction (from a Japanese prospective multicenter registry) who underwent successful primary percutaneous coronary intervention (PCI). Even in the patients who underwent successful primary PCI, the in-hospital mortality of patients with mild (1.2 ≤ creatinine < 2.0 mg/dl) and severe (creatinine ≥2.0 mg/dl) renal dysfunction was greater (17.1% and 34.5%, respectively) than that of patients without renal dysfunction (3.9%) (relative risk [RR] 1.72, 95% confidence interval [CI] 0.94 to 3.14, P = 0.080; and RR 4.26, 95% CI 1.48 to 12.27, p <0.0001, respectively).