Prognostic implications of C-reactive protein and troponin following percutaneous coronary intervention

BACKGROUND:

C-reactive protein (CRP), a marker of inflammation, plays a role in the pathophysiology of atherosclerotic events. The relationship between CRP levels and myocardial necrosis assessed by troponin T (TnT) in patients undergoing percutaneous coronary intervention (PCI) has not been established. In addition, the long-term significance of TnT rise following PCI is not clear.

OBJECTIVES:

To examine the relationship between CRP and the rise in TnT levels, and evaluate the long-term prognostic implications of TnT rise following PCI.

METHODS:

A total of 1208 patients underwent successful nonemergent PCI. Baseline demographic characteristics, CRP and TnT levels were prospectively collected before and 12 h to 18 h following PCI. Long-term follow-up data over two years were available.

RESULTS:

Among the patients studied (mean age 62 years), 64% presented with acute coronary syndrome. A PCI procedure was associated with a significant increase in TnT levels (higher than 0.1 μg/L) in 238 patients (20%). Multivariate logistic regression identified presentation with acute coronary syndrome or myocardial infarction, no statin use at the time of the procedure, increased CRP and increasing length of stent as independent predictors of TnT rise following PCI. Periprocedural TnT rise was not associated with adverse events in follow-up examinations (OR 1.09, 95% CI 0.73 to 1.65).

CONCLUSIONS:

Myocardial necrosis commonly occurred in otherwise successful PCI and was particularly prevalent in the proinflammatory milieu of a recent myocardial infarction. This response was blunted with statin therapy. However, there was no long-term adverse sequelae of these troponin rises following otherwise uncomplicated PCI.     

Pretreatment with intracoronary adenosine reduces the incidence of myonecrosis after non-urgent percutaneous coronary intervention: a prospective randomized study.

AIMS: We sought to investigate the effect of adenosine pretreatment on the incidence of myonecrosis after non-urgent percutaneous coronary intervention (PCI). METHODS AND RESULTS: This was a prospective, randomized, open-label study. Patients who were scheduled for non-urgent PCI in de novo native coronary arteries were eligible. All patients were pretreated with aspirin and clopidogrel. Myonecrosis was measured by creatine kinase-myocardial band (CK-MB) elevation after PCI. A total of 62 patients were randomized into the adenosine (n = 31) or standard (n = 31) group. The adenosine group received 50 microg adenosine bolus before wiring of each lesion, whereas the standard group did not. Post-PCI myonecrosis occurred more frequently in the standard group (39 vs. 13%, OR 0.23, 95% CI 0.05-0.95, P = 0.020). After adjustment for drug-eluting stent implantation, multi-vessel stenting, and elevated baseline troponin, the OR was 0.19 (95% CI 0.05-0.72, P = 0.017). The median peak values of CK-MB in the adenosine and standard groups were 2 and 4 microg/L, respectively (P = 0.033). The adjusted difference was 1.95 microg/L (95% CI 0.13-3.77, P = 0.037). The incidences of myocardial infarction (>3 x CK-MB) were 6 and 16% in the adenosine and standard groups, respectively (OR 0.36; 95% CI 0.03-2.46, P = 0.229). CONCLUSION: Pretreatment with 50 microg of adenosine decreases the incidence of myonecrosis after non-urgent PCI compared with that without pretreatment.     

NT-proBNP on admission for early risk stratification in STEMI patients submitted to PCI. Relation with extension of STEMI and inflammatory markers

The prognostic implications of NT-proBNP measured on admission in patients with the ST-elevation myocardial infarction (STEMI) are not so far well elucidated. The present investigation, performed in 198 STEMI patients submitted to percutaneous coronary intervention (PCI), was aimed at assessing the prognostic value of NT-proBNP measured on admission to Intensive Cardiac Care Unit (ICCU) and its relation with the extension of myocardial infarction (indicated by cardiac biomarkers and ejection fraction) and inflammatory markers (C-reactive protein - CRP, erythrocyte sedimentation rate - ESR, leucocytes, fibrinogen). All patients who died during ICCU stay had increased values of NT-proBNP. Each quartile of NT-proBNP resulted directly correlated with age, heart rate, peak Tn I, admission creatinine serum levels, ESR, fibrinogen, and inversely correlated with ejection fraction. At backward logistic regression analysis, NT-proBNP values showed a significative correlation with peak Tn I (OR 1.013; 95% CI 1.001-1.025; p=0.036), and CRP positive (OR 6.450; 95% CI 1.714-24.272; p=0.006); age was close to reaching statistical significance (OR 1.043; 95% CI 0.999-1.089; p=0.055). At long term-follow-up NT-proBNP lacks any prognostic role in predicting adverse events such as hospitalization for rePCI, re-infarction and heart failure. Kaplan-Meier curves showed that all patients dead at follow-up were in the highest NT-proBNP quartiles.     

Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction.

AIMS: Peri-procedural non-Q-wave myocardial infarction is a frequent and prognostically important complication of percutaneous coronary intervention (PCI). It has been postulated that statins may reduce the rate of myocardial injury after PCI. METHODS AND RESULTS: Four hundred and fifty-one patients scheduled for elective PCI and not on statins were randomly assigned to either no treatment or to statin treatment. Statin administration was started at least 3 days before the procedure.Incidence of peri-procedural myocardial injury was assessed by analysis of creatinine kinase myocardial isoenzyme (CK-MB: upper limit of normal [ULN] 3.5 ng/ml) and cardiac troponin I (cTn I, ULN 0.10 ng/ml) before, 6 and 12 h after the intervention. A large non-Q-wave myocardial infarction was defined as a CK-MB elevation >5 times ULN alone or associated with chest pain or ST segment or T wave abnormalities. Median CK-MB peak after PCI was 1.70 (interquartile ranges 1.10-3.70) ng/ml in the Statin group and 2.20 (1.30-5.60) ng/ml in the Control group (p=0.015). Median peak of cTnI after PCI was 0.13 (0.05-0.45) ng/ml in the Statin group and 0.21 (0.06-0.85) ng/ml in the Control group (p=0.033). The incidence of a large non-Q-wave myocardial infarction was 8.0% in the Statin group and 15.6% in the Control group (p=0.012: OR=0.47; 95% CI=0.26-0.86). The incidence of cTnI elevation >5 times ULN was 23.5% in the Statin group and 32% in the Control group (p=0.043: OR=0.65; 95% CI=0.42-0.98). By logistic regression analysis, the independent predictors of CK-MB elevation >5 times ULN after PCI were intra-procedural angiographic complications (OR=9.36; 95% CI=3.06-28.64; p<0.001), statin pre-treatment (OR=0.33; 95% CI=0.13-0.86; p=0.023) and age >65 years (OR=2.58; 95% CI=1.09-6.11; p=0.031). CONCLUSIONS: Pre-procedural statin therapy reduces the incidence of large non-Q-wave myocardial infarction after PCI.     

Plasma N-terminal pro-B-type natriuretic peptide for prediction of death or nonfatal myocardial infarction following percutaneous coronary intervention

B-type natriuretic peptide (BNP) and the N-terminus of pro-BNP (NT-pro-BNP) have prognostic value in patients with heart failure and patients with acute coronary syndromes. Little is known about the prognostic value of baseline NT-pro-BNP alone or in combination with C-reactive protein (CRP) for clinical outcome after percutaneous coronary intervention (PCI). Within a single center registry of contemporaneous PCI, we investigated the prognostic value of baseline plasma NT-pro-BNP and CRP concentrations for the prediction of death or nonfatal myocardial infarction (MI) during 12 to 14 months of follow-up. Among 1,172 consecutive patients, the occurrence of death or MI increased significantly with baseline NT-pro-BNP before PCI (first quartile 0 of 294, second quartile 6 of 291 [2.1%], third quartile 4 of 294 [1.4%], fourth quartile 22 of 293 [7.5%)]; p <0.0001). NT-pro-BNP in the top quartile significantly predicted death (odds ratio [OR] 13.37, 95% confidence interval [CI] 4.50 to 40.38, p <0.0001) and was associated with nonfatal MI (OR 2.53, 95% CI 0.77 to 8.34, p = 0.22) An abnormal CRP was significantly associated with death (OR 3.47, 95% CI 1.26 to 9.54, p = 0.019). Stepwise multivariate logistic regression analysis identified age >65 years and NT-pro-BNP as independent significant predictors of death/MI (age OR 3.18, 95% CI 1.32 to 7.67, p = 0.01; NT-pro-BNP OR 4.57, 95% CI 2.07 to 10.10, p = 0.0001). Baseline NT-pro-BNP before PCI provides important, independent prognostic information for the occurrence of death or nonfatal MI during long-term follow-up.     

Stent thrombosis following bare-metal stent implantation: success of emergency percutaneous coronary intervention and predictors of adverse outcome.

AIMS: To investigate the efficacy and outcome of emergency percutaneous coronary interventions (PCI) in patients with stent thrombosis. METHODS AND RESULTS: Between 1995 and 2003, 6058 patients underwent bare-metal stent implantation, of which 95 (1.6%) patients suffered from stent thrombosis. The timing of stent thrombosis was acute in 10 (11%), subacute in 61 (64%), and late in 24 (25%) patients. Procedural and clinical outcomes of emergency PCI for treatment of stent thrombosis were investigated. Emergency PCI was successful in 86 (91%), complicated by death in 2 (2%), and coronary artery bypass grafting in 2 (2%) patients. Myocardial infarction occurred in 77 (81%) patients with a peak creatine kinase level of 1466+/-1570 U/L. Left ventricular ejection fraction declined from 0.54+/-0.19 prior to 0.48+/-0.16 (P<0.05) at the time of stent thrombosis after emergency PCI. A 6 month major adverse clinical events comprised death (11%), reinfarction (16%), and recurrent stent thrombosis (12%) after emergency PCI. Multivariable logistic regression analysis identified the achievement of TIMI 3 flow (OR=0.1, CI 95% 0.01-0.54, P<0.001) and diameter stenosis <50% (OR=0.06, CI 95% 0.01-0.32, P<0.001) during emergency PCI to be independently associated with a reduced risk of cardiac death. Recurrent stent thrombosis was independently predicted by the omission of abciximab (OR=4.3, CI 95% 1.1-17.5). CONCLUSION: Emergency PCI for treatment of stent thrombosis effectively restores vessel patency and flow. Patients presenting with stent thrombosis are at risk for recurrent myocardial infarction and recurrent stent thrombosis.     

A serum amyloid A and LDL complex as a new prognostic marker in stable coronary artery disease

BACKGROUND: Although some reports have indicated that acute phase proteins such as C-reactive protein (CRP) and serum amyloid A (SAA) can predict the prognosis in patients with acute coronary syndrome, the value of these markers in patients with stable coronary artery disease (CAD) still remains obscure. Therefore, our aim was to determine the prognostic value of inflammatory markers in patients with stable coronary artery disease. METHODS AND RESULTS: We conducted a prospective cohort study in 140 consecutive patients with stable coronary artery disease who had at least one coronary stenosis more than 50% in diameter seen on diagnostic coronary angiography (CAG). We determined serum levels of the SAA/LDL complex as a new marker in addition to CRP and SAA. Serum levels of the SAA/LDL complex were measured by a sandwich enzyme-linked immunosorbent assay (ELISA). End-points were defined as cardiac death, myocardial infarction, cerebral infarction, and coronary revascularization. End-point events occurred in 21 patients (2 death from myocardial infarction, 2 cerebral infarction, and 17 revascularization). Age (year) (OR = 1.14, CI: 1.05-1.25), diabetes mellitus (OR = 3.50, CI: 1.08-11.40), triglyceride (10mg/dl) (OR = 1.12, CI: 1.01-1.23) and SAA/LDL complex (10 microg/ml) (OR = 2.32, CI: 1.05-4.70) were independently related to the events. A reconstitution experiment suggested that the SAA/LDL complex is derived by oxidative interaction between SAA and lipoproteins. CONCLUSIONS: The SAA/LDL complex reflects intravascular inflammation directly and can be a new marker more sensitive than CRP or SAA for prediction of prognosis in patients with stable coronary artery disease.     

The impact of admission C-reactive protein levels on the development of poor myocardial perfusion after primary percutaneous intervention in patients with acute myocardial infarction

BACKGROUND: Increased preprocedural C-reactive protein (CRP) levels in patients with acute myocardial infarction (MI) undergoing primary percutaneous coronary intervention (PCI) may affect myocardial perfusion. Accordingly, this study was designed to investigate the impact of admission CRP levels on the development of poor myocardial perfusion after PCI in patients with acute MI. METHODS: The study population consisted of 75 patients (62 men, mean age, 61.6+/-6.68 years), who were admitted to our hospital with acute anterior MI and who underwent primary PCI in the left anterior descending coronary artery. All patients underwent stenting following balloon angioplasty. Myocardial perfusion was evaluated by using Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade (TMPG). Patients were divided into two groups according to TMPG after PCI. Group 1 consisted of 25 patients with TMPG 0-1 and group 2 comprised 50 patients with TMPG 2-3. Admission serum high sensitive CRP (hs-CRP) levels were analysed by using nephelometric method. RESULTS: Admission hs-CRP levels, pain to balloon time and white blood cell count (WBC) of patients in group 1 were significantly higher than those of the patients in group 2 (P<0.001; P<0.001; P=0.002, respectively). Univariate analysis identified ejection fraction, pain to balloon time, WBC and hs-CRP levels as the predictors of poor myocardial perfusion. In multivariate logistic regression analysis, hs-CRP levels and pain to balloon time were found to have statistically significant independent association with poor myocardial perfusion. Adjusted odds ratios were calculated as 1.85 for hs-CRP [P=0.003; 95% confidence interval (CI), 1.23-2.80] and 5.49 for pain to balloon time (P=0.04; 95% CI, 1.08-27.84). CONCLUSIONS: On admission, high CRP level in patients with acute MI undergoing primary PCI is likely to be in the causal pathway leading to the development of poor myocardial perfusion, especially when combined with prolonged pain to balloon time.     

Relation of C-reactive protein level and long-term risk of death or myocardial infarction following percutaneous coronary intervention with a sirolimus-eluting stent

Previous observations in the bare metal stent (BMS) era have demonstrated an association between a high preprocedural C-reactive protein (CRP) level and an increased incidence of death or myocardial infarction after percutaneous coronary intervention (PCI). We hypothesized that PCI with sirolimus-eluting stents (SESs) would result in a smaller increase in CRP compared with BMSs and that a high CRP level before PCI would be associated with a higher incidence of death or myocardial infarction at 12 months, regardless of the type of stent implanted. We analyzed patients who underwent PCI with stenting at the Cleveland Clinic Foundation. Patients who received BMSs and SESs were analyzed separately by categorizing them into low and high CRP groups based on whether their CRP level before PCI was above or below the median for each group. The increase in CRP that occurred with PCI was termed DeltaCRP. In total, 652 patients were included in the analysis. Median DeltaCRP was smaller in the SES group than in the BMS group (1.5 vs 0.7 mg/L, p = 0.009). In the BMS group, patients with a CRP level above the median before PCI had a higher incidence of 12-month death or myocardial infarction compared with patients with a CRP level below the median (11.3% vs 1.6%, p = 0.002). The same relation was present in the SES group, i.e., patients with a higher CRP level had a higher incidence of 12-month death or myocardial infarction compared with patients with a low CRP level (6.3% vs 1.0%, p = 0.005) and a higher 12-month mortality (5.2% vs 0%, p = 0.001). Multivariate logistic regression analysis demonstrated that the CRP level above the median before PCI was associated with a higher 12-month incidence of death or myocardial infarction, independent of the type of stent used, or DeltaCRP. In conclusion, PCI in the SES era causes a smaller increase in CRP compared with the BMS era. A high CRP level before PCI is independently associated with a higher risk of long-term death or myocardial infarction. This finding was present in the BMS and SES groups and highlights the need for aggressive risk-factor modification after PCI.     

Predictive value of preintervention C-reactive protein on clinical outcome after directional coronary atherectomy followed by stent implantation.

BACKGROUND: Preprocedural C-reactive protein (CRP) serum levels have been shown to predict the recurrence of angina or major adverse cardiac events after percutaneous coronary intervention. Directional coronary atherectomy (DCA), by reducing residual plaque burden and restenosis, has been shown to improve clinical outcome after coronary stenting. Thus, we assessed the influence of preprocedural CRP serum levels on the recurrence of cardiac events after DCA followed by bare metal stent implantation. METHODS: We enrolled 40 consecutive patients (34 males; 61+/-10 years old) with single-vessel disease who were undergoing DCA. In all patients, preprocedural CRP serum levels were measured by an ultrasensitive nephelometric method. The endpoint of the study was defined as the composite incidence of death, myocardial infarction, and recurrence of angina requiring repeat revascularization at 6-month follow-up. RESULTS: CRP serum levels were a significant independent predictor of the composite endpoint at multiple regression analysis [odds ratio=1.69; 95% confidence interval (95% CI)=1.04-2.75; P=.033]. Patients with recurrence of cardiac events had CRP serum levels higher than those of patients not having events on follow-up [3.95 (2.2-5.7) vs. 2 (1.3-3.3); P=.05]. CONCLUSION: In conclusion, our study shows that baseline CRP serum levels predict cardiac events after coronary bare metal stenting despite plaque debulking with directional atherectomy.     

Association of C-reactive protein and myocardial perfusion in patients with ST-elevation acute myocardial infarction

This study sought to evaluate the relation between C-reactive protein (CRP) on admission of patients with acute myocardial infarction (AMI) and myocardial perfusion as defined by postintervention angiographic myocardial blush grade (MBG) and their impact on subsequent mortality. The patient population comprised 191 consecutive patients with AMI undergoing PTCA within 12h of symptom onset on a native vessel. Patients were divided based on the CRP level on admission (Rolf Greiner BioChemica, Germany, cutpoint for the assay CRP: 5mg/l) into a group with elevated CRP (>or=5mg/l) and a group with normal CRP. Angiographic myocardial blush grade (MBG) after revascularization of the infarct-related artery was determined to evaluate myocardial reperfusion. Revascularization of the infarct-related artery was successful in 176 (92.6%) patients. The frequency of impaired perfusion (MBG 0-2) was higher in the elevated CRP group than in the normal CRP group (74.5% versus 59.7%, respectively, p=0.046). Elevated CRP on admission was an independent predictor of impaired myocardial perfusion (MBG 0-2, OR 1.92, 95% CI 1.02-4.01, p=0.042) in addition to age >70 years. Elevated CRP (OR 2.64, 95% CI 1.26-5.53, p=0.009) and MBG 0-2 (OR 4.58; 95% 1.73-12.20, p=0.002) were independent predictors of mortality during a 22.4+/-15.3 months follow-up in addition to heart rate on admission >100 beats/min (OR 3.07; 95% CI 1.30-7.25, p=0.009). In sequential Cox models, the predictive power of clinical data and MBG for mortality (model chi-squared 18.3) was strengthened by the inclusion of CRP levels (model chi-squared 24.3). In conclusion, there is a relation between elevated admission CRP and impaired reperfusion in the myocardium subtended to the infarct-related artery. The combination of clinical data, myocardial reperfusion levels after primary angioplasty for AMI and admission CRP increases the predictive value for subsequent survival.     

C-reactive protein in offspring is associated with the occurrence of myocardial infarction in first-degree relatives

The relevance of elevated levels of C-reactive protein (CRP) in cardiovascular disease is gaining increasing recognition. A family history of coronary artery disease is a major determinant of coronary artery disease in the offspring. In a cohort of 1048 individuals without clinical evidence of atherosclerosis, we investigated the relationships between CRP levels and a family history of myocardial infarction. We measured CRP, fibrinogen, plasminogen activator inhibitor-1, total cholesterol, triglycerides, and some genetic polymorphisms: plasminogen activator inhibitor-1 (4G/5G), fibrinogen (Bbeta-chain G-->A(-455)), and angiotensin-converting enzyme insertion/deletion (I/D). Clinical data were collected by a World Health Organization-modified questionnaire for cardiovascular disease. When compared with subjects without first-degree relatives who had suffered a myocardial infarction (n=867), subjects with such first-degree relatives (n=181) were older (P=0.001), more often hypertensive (P<0. 001), and homozygous for the 4G allele (4G/4G) of the plasminogen activator inhibitor-1 gene (P=0.003). In addition, they had a higher body mass index (P=0.036), raised plasma fibrinogen (P<0.007) and total cholesterol (P<0.001) concentrations, and CRP levels >0.33 mg/L (P=0.005). In a multiple logistic regression analysis, age (odds ratio [OR] 1.03, 95% confidence interval [95% CI] 1.01 to 1. 05), total cholesterol (OR 1.35, 95% CI 1.11 to 1.65), plasminogen activator inhibitor-1 4G/4G (OR 1.72, 95% CI 1.20 to 2.45), and CRP levels >0.33 mg/L (OR 1.75, 95% CI 1.05 to 2.91) were all independently associated with a positive family history of myocardial infarction. We therefore conclude that raised levels of CRP independently identify the offspring of patients with a myocardial infarction.     

Prognostic value of troponin T in hospitalized patients with angina or non-ST-segment elevation myocardial infarction

INTRODUCTION AND OBJECTIVES: Cardiac troponins are highly specific and sensitive for detecting minimal myocardial damage. The aim of our study was to determine the prognostic value of troponin T levels in patients hospitalized for suspected angina or myocardial infarction without ST-segment elevation. PATIENTS AND METHOD: We recorded the frequency of death, acute myocardial infarction, heart failure, or need for coronary revascularization in the three months after the onset of symptoms in 346 consecutive patients admitted for suspected acute coronary syndrome, excluding those who developed myocardial infarction with persistent ST-segment elevation. RESULT:. Serum troponin T levels were > or = 0.1 ng/ml in 133 patients (troponin T positive group) and lower in 213 patients (troponin T negative group). The relative risk (RR) and 95 percent confidence intervals (95% CI) of individual and grouped events for the troponin T positive group were 3.2 (95% CI, 1.4-7.3; p = 0.006) for death; 2.8 (95% CI, 1.43-5.51; p = 0.003) for death or myocardial infarction; and 2.8 (95% CI, 1.6-5.0; p < 0.001) for death, myocardial infarction or heart failure. Diabetes mellitus and troponin T levels > or = 0.1 ng/ml had independent prognostic value after adjusting for age, sex, and electrocardiographic changes; with RR 2.5 (95% CI, 1.01-5.9) for death, myocardial infarction or heart failure. CONCLUSIONS: The prognosis of patients hospitalized for chest pain who do not immediately develop transmural necrosis depends on serum troponin T levels at hospital admission. Troponin T levels > or = 0.1 ng/ml almost triple the risk of major events in the three months after the acute episode. The prognostic value of troponin T is independent of age, sex, presence of diabetes mellitus, and electrocardiographic changes.     

持续炎症状态对冠状动脉支架内再狭窄的影响和预测分析

目的探讨PCI前后持续炎症状态对PCI后支架内再狭窄的影响和预测作用。方法选择成功行支架置入术并于3个月后至1年内复查冠状动脉造影的患者431例,分为支架内再狭窄组(再狭窄组)124例和无支架内再狭窄组(无再狭窄组)307例。患者于PCI前及复查冠状动脉造影时均检测C反应蛋白(CRP)、高敏CRP(hs-CRP)。结果与无再狭窄组比较,再狭窄组患者PCI前CRP和hs-CRP以及PCI后CRP均明显升高,差异有统计学意义(P0.05,P0.01)。将PCI前hs-CRP分为2 mg/L和≤2 mg/L2个等级,hs-CRP增高的患者支架内再狭窄的发生率明显升高(χ~2=5.03,P0.05)。logistic回归分析显示,hs-CRP高的患者发生支架内再狭窄的风险明显增加(OR=1.840,95% CI:1.076～3.157,P0.05)。结论 PCI前后持续的炎症状态是发生支架内再狭窄的危险因素和预测指标,应积极加强抗炎以改善PCI后患者的临床预后。     

Intensity of statin therapy in relation to myocardial ischemia, troponin T release, and clinical cardiac outcome in patients undergoing major vascular surgery.

OBJECTIVES: This study sought to examine whether higher statin doses and lower low-density lipoprotein (LDL) cholesterol are associated with improved cardiac outcome in vascular surgery patients. BACKGROUND: Statins may have cardioprotective effects during major vascular surgery. METHODS: In a prospective study of 359 vascular surgery patients, statin dose and cholesterol levels were recorded preoperatively. Myocardial ischemia and heart rate variability were assessed by 72-h 12-lead electrocardiography starting 1 day before to 2 days after surgery. Troponin T was measured on postoperative day 1, 3, 7, and before discharge. Cardiac events included cardiac death or nonfatal Q-wave myocardial infarction at 30 days and follow-up (mean 2.3 years). RESULTS: Perioperative myocardial ischemia, troponin T release, 30-day events, and late cardiac events occurred in 29%, 23%, 4%, and 18%, respectively. In multivariate analysis, lower LDL cholesterol (per 10 mg/dl) correlated with lower myocardial ischemia (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.80 to 0.95), troponin T release (OR 0.89, 95% CI 0.82 to 0.96), and 30-day (OR 0.89, 95% CI 0.78 to 1.00) and late cardiac events (hazard ratio 0.91, 95% CI 0.84 to 0.96). Higher statin doses (per 10% of maximum recommended dose) correlated with lower myocardial ischemia (OR 0.85, 95% CI 0.76 to 0.93), troponin T release (OR 0.84, 95% CI 0.76 to 0.93), and 30-day (OR 0.62, 95% CI 0.40 to 0.96) and late cardiac events (hazard ratio 0.76, 95% CI 0.65 to 0.89), even after adjusting for LDL cholesterol. Significantly higher perioperative heart rate variability was observed in patients with higher statin doses. CONCLUSIONS: Higher statin doses and lower LDL cholesterol correlate with lower perioperative myocardial ischemia, perioperative troponin T release, and 30-day and late cardiac events in major vascular surgery.     

Outcomes 1 year after thrombus aspiration for myocardial infarction

Background Routine intracoronary thrombus aspiration before primary percutaneous coronary intervention(PCI) in patients with ST-segment elevation myocardial infarction(STEMI) has not been proved to reduce short-term mortality. We evaluated clinical outcomes at 1 year after thrombus aspiration.Methods We randomly assigned 7244 patients with STEMI to undergo manual thrombus aspiration followed by PCI or to undergo PCI alone, in a registry-based, randomized clinical trial. The primary end point of all-cause mortality at 30 days has been reported previously. Death from any cause at 1 year was a prespecified secondary end point of the trial.Results No patients were lost to follow-up. Death from any cause occurred in 5.3% of the patients(191 of 3621 patients) in the thrombus-aspiration group, as compared with 5.6%(202 of 3623) in the PCI-only group(hazard ratio, 0.94; 95% confidence interval [CI], 0.78 to 1.15; P = 0.57). Rehospitalization for myocardial infarction at 1 year occurred in 2.7% and 2.7% of the patients, respectively(hazard ratio, 0.97; 95% CI, 0.73 to1.28; P = 0.81), and stent thrombosis in 0.7% and 0.9%, respectively(hazard ratio, 0.84; 95% CI, 0.50 to1.40; P = 0.51). The composite of death from any cause, rehospitalization for myocardial infarction, or stent thrombosis occurred in 8.0% and 8.5% of the patients, respectively(hazard ratio, 0.94; 95% CI, 0.80 to1.11; P = 0.48). The results were consistent across all the major subgroups, including grade of thrombus burden and coronary flow before PCI.Conclusion Routine thrombus aspiration before PCI in patients with STEMI did not reduce the rate of death from any cause or the composite of death from any cause, rehospitalization for myocardial infarction, or stent thrombosis at 1 year.(From: N Engl J Med 2014; 371:1111-1120 September 18, 2014DOI: 10.1056 / NEJMoa1405707)     

Elevated cardiac troponin T in predialysis patients is associated with inflammation and predicts mortality

OBJECTIVES: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of myocardial damage. It has been shown that elevated serum concentrations of cTnT in haemodialysis (HD) patients are associated with poor prognostic outcome. The aim of the present study was to investigate the predictive value of cTnT in samples from predialysis patients and to investigate associations between cTnT and inflammatory markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6). DESIGN: Cohort, follow-up study. SETTING: Huddinge University Hospital, Sweden. SUBJECTS: A total of 115 (62% males, 28% diabetic patients) end-stage renal disease (ESRD) patients (52 +/- 1 years), of which 29% had cardiovascular disease (CVD), were studied shortly before the onset of dialysis therapy. Sixty-four patients started peritoneal dialysis (PD) as renal replacement therapy, whilst 49 started HD during the follow-up. MAIN OUTCOME MEASURES: The cTnT was analysed with the third generation TnT assay on Elecsys 2010. The prognostic value was calculated for cTnT, IL-6, age, CVD, malnutrition, diabetes mellitus (DM) and gender. Survival analyses were made with Kaplan-Meier and Cox regression analyses, with all-cause mortality as the clinical end point (mean follow-up period 2.7 +/- 0.1 years). RESULTS: Significant correlations were found between cTnT and CKMB (rho = 0.52, P < 0.0001), IL-6 (rho = 0.23, P < 0.05), CRP (rho = 0.30, P < 0.05), and serum albumin (rho = -0.31, P < 0.001), respectively. Diabetic patients had higher median serum cTnT level (0.09 microg L-1; range <0.01-0.51 vs. 0.04 microg L-1; range <0.01-0.67 microg L-1; P < 0.005) compared with nondiabetic patients. Likewise, patients with CVD had a significantly higher median level (0.08 microg L-1; range <0.01-0.67 microg L-1 vs. 0.04 microg L-1; range <0.01-0.61 microg L-1; P < 0.01) of cTnT compared with patients without CVD. Patients with cTnT > or =0.10 microg L-1 had a higher cumulative mortality rate than patients with cTnT < 0.10 microg L-1 (chi2 = 7.04; P < 0.01). Whilst age, CVD, malnutrition, DM, IL-6, cTnT and male gender were associated with poor outcome in the univariate analysis, only DM (P < 0.05) and cTnT (P < 0.05) were independently associated with mortality in a multivariate analysis. CONCLUSIONS: The present study demonstrates that serum concentrations of cTnT > or =0.10 microg L-1 is a significant predictor of mortality in patients starting dialysis. Moreover, the positive correlations between cTnT and IL-6, and CRP, respectively, suggest an association between inflammation and cTnT levels. Finally, the results of the present study suggest that cTnT is an independent predictor of mortality in ESRD patients starting dialysis.     

Usefulness of preprocedural serum N-terminal pro-brain natriuretic peptide levels to predict long-term outcome after percutaneous coronary intervention in patients with normal troponin T levels

Our objective was to evaluate the prognostic information of preprocedural serum N-terminus pro-brain natriuretic peptide (NT-pro-BNP) levels to predict the long-term outcome after percutaneous coronary intervention (PCI). A total of 891 consecutive patients with stable or unstable angina pectoris with normal serum troponin T levels (< or =0.03 microg/L) undergoing PCI were investigated. For each patient with a cardiovascular event (death or nonfatal myocardial infarction), 2 event-free patients were used as controls. The procedure was successful in all patients, and follow-up was complete. By the end of the follow-up period (mean 2.6 years), 75 patients had had a cardiovascular event (41 deaths and 34 nonfatal myocardial infarctions). On multivariate analysis, lesion severity, diabetes mellitus, and NT-pro-BNP levels in the highest quartile (>490 mg/L) were identified as independent factors for death or nonfatal myocardial infarction after PCI. In conclusion, preprocedural NT-pro-BNP levels are associated with long-term outcome after PCI. The use of NT-pro-BNP can be of value in risk stratification in patients undergoing PCI.     

生长停滞特异性基因6蛋白可预测老年急性ST段抬高型心肌梗死患者PCI术后发生心力衰竭

摘要 目的：探讨血清生长停滞特异性基因6（GAS6）蛋白对老年急性ST段抬高型心肌梗死（STEMI）患者经皮冠状动脉介入（PCI）术后住院期间发生心力衰竭的预测价值。方法：回顾性分析168例行急诊PCI治疗的老年STEMI患者的临床资料，根据患者PCI术后住院期间是否发生心力衰竭，分为无心力衰竭组（127例）和心力衰竭组（41例），比较2组患者一般资料。用酶联免疫吸附试验（ELISA）检测患者急诊入院时血清GAS6蛋白、血清B-型脑钠肽前体(BNP)、心肌肌钙蛋白 I（cTnI）、C反应蛋白（CRP）表达水平。用Pearson相关性分析、Logistic回归分析心力衰竭发生的影响因素；绘制受试者工作特征（ROC）曲线分析血清GAS6蛋白预测心力衰竭的价值，计算曲线下面积（AUC）。结果：心力衰竭组PCI术后TIMI血流3级患者比例和术前左室射血分数（LVEF）低于同时点无心力衰竭组（P均＜0.05）。心力衰竭组患者PCI术前BNP、cTnI和CRP水平高于无心力衰竭组（P均＜0.05）。心力衰竭组患者PCI术前血清GAS6蛋白水平与BNP、cTnI和CRP呈正相关，与LVEF呈负相关（P均＜0.05）。多因素分析显示，PCI术前血清GAS6蛋白、BNP、cTnI、CRP、LVEF和PCI术后TIMI血流3级是STEMI患者PCI术后发生心力衰竭的独立影响因素（P均＜0.05）。PCI术前血清GAS6蛋白水平预测STEMI患者PCI术后发生心力衰竭的AUC为0.832（P＜0.001）。当血清GAS6蛋白水平为26.09ng/mL时，约登指数最大（0.509），预测价值最高，此时灵敏度和特异性分别为70.65%和80.33%。结论：血清GAS6蛋白水平与患者心功能密切相关，血清GAS6蛋白表达水平的上升可能意味着心功能的下降，PCI术前血清GAS6蛋白水平对预测老年STEMI患者PCI术后发生心力衰竭有一定价值。.     

Contemporary outcome trends in the elderly undergoing percutaneous coronary interventions: results in 7,472 octogenarians. National Cardiovascular Network Collaboration

OBJECTIVES: We sought to define the risks facing octogenarians undergoing contemporary percutaneous coronary interventions (PCIs). BACKGROUND: The procedural risks of PCI for octogenarians have not been well established. METHODS: We compared the clinical characteristics and in-hospital outcomes of 7,472 octogenarians (mean age 83 years) with those of 102,236 younger patients (mean age 62 years) who underwent PCI at 22 National Cardiovascular Network (NCN) hospitals from 1994 through 1997. RESULTS: Octogenarians had more comorbidities, more extensive coronary disease and a two- to fourfold increased risk of complications, including death (3.8% vs. 1.1%), Qwave myocardial infarction (1.9% vs. 1.3%), stroke (0.58% vs. 0.23%), renal failure (3.2% vs. 1.0%) and vascular complications (6.7% vs. 3.3%) (p < 0.001 for all comparisons). Independent predictors of procedural mortality in octogenarians included shock (odds ratio [OR] 5.4, 95% confidence interval [CI] 3.3 to 8.8), acute myocardial infarction (OR 3.2, 95% CI 2.3 to 4.4), left ventricular ejection fraction (LVEF) <35% (OR 2.9, 95% CI 2.1 to 3.9), renal insufficiency (OR 2.8, 95% CI 2.0 to 3.8), first PCI (OR 2.3, 95% CI 1.7 to 3.3), age >85 years (OR 2.1, 95% CI 1.5 to 2.7) and diabetes mellitus (OR 1.5, 95% CI 1.1 to 2.0). For elective procedures, octogenarian mortality varied nearly 10-fold, and was strongly influenced by comorbidities (0.79% mortality with no risk factors vs. 7.2% with renal insufficiency or LVEF <35%). Despite similar case-mix, PCI outcomes in octogenarians improved significantly over the four years of observation (OR of 0.61 for death/myocardial infarction/stroke in 1997 vs. 1994; 95% CI 0.45 to 0.85). CONCLUSIONS: Risks to octogenarians undergoing PCI are two- to fourfold higher than those of younger patients, strongly influenced by comorbidities, and have decreased in the stent era.