尼可地尔对经皮冠状动脉介入治疗心肌损伤的影响

目的观察经皮冠状动脉介入治疗（PCI）术前服用尼可地尔对心肌损伤的影响。方法纳入行择期PCI治疗的冠心病患者100例,随机分为尼可地尔组（n=52）和常规治疗组（n=48）。常规治疗组接受冠心病及PCI术常规药物治疗,尼可地尔组在PCI术前接受7天口服尼可地尔（5mg,tid）治疗,并在PCI术前5h加服尼可地尔5mg。比较两组患者PCI术前及术后6h、18h、24h的肌酸激酶同工酶（CK-MB）、肌钙蛋白I（cTnI）水平的变化。结果两组患者在PCI术前cTnI和CK-MB水平无差异（P〉0.05）;PCI术后6h、18h、24h,尼可地尔组cTnI和CK-MB水平均低于常规治疗组,差异均有统计学意义（P〈0.05）。结论冠心病患者择期PCI术前使用尼可地尔,对PCI术造成的心肌损伤有一定保护作用。     

Effects of persistent platelet reactivity despite aspirin therapy on cardiac troponin I and creatine kinase-MB levels after elective percutaneous coronary interventions

BACKGROUND: Creatinine kinase-MB (CK-MB) and cardiac troponin I (cTnI) elevations are highly specific for myonecrosis after percutaneous coronary intervention (PCI). Aspirin is used to prevent thrombotic complications. Several studies have shown that some individuals exhibit a reduced or completely missing antiplatelet response to aspirin. The aim of this study is to investigate the effects of platelet reactivity despite aspirin therapy on CK-MB and cTnI levels after elective percutaneous coronary interventions despite 600 mg loading dose of clopidogrel. METHODS: One hundred fourteen (mean age 61.2+/-9.3 years, 78.1% male) patients receiving 300 mg daily enteric coated aspirin for at least 7 days with documented coronary artery disease were included in the study. Platelet reactivity despite aspirin was measured by platelet function analyzer (PFA)-100 collagen/epinephrine cartridge. Blood samples for CK-MB and cTnI were obtained before and at 6, 24, and 36 h after the PCI. Persistent platelet reactivity was defined when collagen/epinephrine closure time<165 s. RESULTS: A total of 87 (76.4%) patients were noted to have normal platelet reactivity (Group A), and 27 (23.6%) had persistent platelet reactivity (Group B). The elevations of CK-MB and cTnI levels were statistically significant within the groups (both P<0.001). However, there were no significant differences in the CK-MB and cTnI levels of the groups at baseline and after PCI for all studied hours. CONCLUSION: Persistent platelet reactivity was not associated with increased risk of CK-MB, cTnI elevations in low-to-intermediate risk PCI patients.     

Patterns and diagnostic value of cardiac troponin I vs. troponin T and CKMB after OPCAB surgery.

BACKGROUND: Cardiac troponin I (cTnI) has been shown to be a specific marker for myocardial injury in cardiac surgery. The object of this prospective study was to determine the patterns and kinetic and diagnostic value of cTnI, cardiac troponin T (cTnT), and creatine kinase MB (CKMB) activity after minimally invasive coronary revascularization using an octopus device on the beating heart (OPCAB). METHODS: 48 patients (33 male/15 female, mean age 68.3 +/- 8.7 years) underwent their first elective OPCAB surgery with median sternotomy without mortality. The mean number of grafts was 2.0 +/- 0.8 per patient. Preoperative mean ejection fraction was 56.6 % +/- 14.9%. CTnI and T levels, total creatine kinase (CK) and CK-MB activity in the serum were measured before operation, at arrival at the ICU, and 6, 12, 24, 48 and 120 hours afterward. Serial 12-lead ECGs were recorded preoperatively and at days 1, 2 and 5. The relationship between perioperative data and postoperative cTnI and cTnT levels and CKMB were statistically identified for all variables. RESULTS: The best cutoff value for cTnI was 8.35 micrograms/l. The patients were grouped by the ECG findings and maximal slopes of cTnI postoperatively (group I: unchanged ECG and cTnI < 8.35 micrograms/l, n = 38; group II: unchanged ECG and cTnI > 8.35 micrograms/l n = 6; group III: Q-wave in ECG and cTnI > 8.35 micrograms/l, n = 4). Baseline serum concentrations of cTnI were in the normal range, and significantly increased after surgery with a peak 24h after the operation. Maximal slopes of cTnI ranged in group II between 9.1 and 18.0 micrograms/l, and in group III between 35.9 and 88.8 micrograms/l. There was strong concordance between maximum cTnI, cTnT (p < 0.0001) and CK-MB levels (p = 0.003). First cTnI levels immediately post-op correlated with the maximum cTnI levels during the postoperative course (p = 0.009). CONCLUSIONS: CTnI after minimal invasive surgery shows a characteristic pattern with a maximum at 24h after the operation. The measurement of postoperative biochemical marker concentrations, specially cTnI, reflects myocardial injury incurred during the procedure. It is an accurate method for confirming or excluding a perioperative myocardial injury diagnosis after OPCAB surgery.     

Comparison of Cardiac Troponin I versus T and Creatine Kinase MB after Coronary Artery Bypass Grafting in Patients with and without Perioperative Myocardial Infarction

BACKGROUND AND PURPOSE: Cardiac troponins have shown to be specific markers of myocardial injury. The aim of this prospective study was to compare patterns and kinetics of troponin I and T after coronary artery bypass grafting (CABG) with or without perioperative myocardial infarction (PMI). PATIENTS AND METHODS: 119 patients (male/female: 96/23, age 64 +/- 10 years) underwent first time elective CABG. Preoperative mean ejection fraction was 55.8% +/- 15.6%. The mean number of grafts was 3.1 +/- 1.1/patient, in 85.7% the internal mammary artery was used. Cardiac troponin I (cTnI) and T (cTnT) levels, total serum activities of creatine kinase (CK) and creatine kinase isoenzyme MB (CK-MB) were measured before operation, at arrival on the intensive care unit (ICU), and 6, 12, 24, 48, and 120 h after unclamping of the aorta. Twelve lead electrocardiograms (ECGs) were recorded preoperatively and at days 1, 2, and 5. Perioperative data and postoperative cTnI and cTnT levels were correlated statistically. RESULTS: Two patients died due to refractory myocardial failure in the early postoperative period. For further evaluation, patients were divided in two groups according to postoperative ECG changes (group I: patients without PMI, n = 107; group II: patients with PMI, n = 10: six of them with Q-wave and four of them with non-Q-wave PMI). Calculated best cutoff values for cTnI and cTnT were 8.35 microg/l and 0.768 microg/l in ROC (receiver-operator characteristic) analysis. Serum concentrations of cTnI, and cTnT were in the normal range preoperatively and increased significantly after surgery in both groups. In both groups, cTnI reached its medium peak level after 24 h (group I: 2.7 microg/l, 95% confidence interval [CI]: [2.1,3.2]); group II: 70.5 microg/l). CTnT reached its medium peak level in group I without PMI after 48 h (0.298 microg/l, 95% CI: [0.254,0.354]), in group II with PMI not until 120 h (3.0 microg/l) postoperatively. In group II serum level of both troponins remained considerably high at 120 h (cTnI median = 10.75 microg/l, cTnT median = 3 microg/l). CONCLUSION: Release patterns of cTnI and cTnT after CABG are different: cTnI reaches its postoperative peak value earlier and declines more quickly than cTnT. After uncomplicated CABG, serum levels of both cardiac troponins remain continuously low. Elevated concentrations reflect perioperative myocardial ischemia or infarction. CTnT shows a different release pattern in patients with or without myocardial infarction.     

Nicorandil reduces the incidence of minor cardiac marker elevation after coronary stenting

BACKGROUND: Minor cardiac marker elevation after percutaneous coronary intervention has long-term prognostic significance. We examined whether nicorandil, a nicotinamide-nitrate ester, reduces the incidence of minor cardiac marker elevation after coronary stenting. METHODS: Patients (n=192) undergoing coronary stenting were randomly assigned to receive nicorandil (nicorandil group, n=91) or vehicle (control group, n=101). Nicorandil (2 mug/kg/min, intravenously) was administered immediately after the patients were transferred into the catheterization laboratory and continued for 6 h. We measured the serum concentrations of creatine kinase isoenzyme MB (CK-MB) before, immediately after, and 6, 12, and 24 h after the procedure, and those of cardiac troponin T (cTnT) 24 h after the procedure. RESULTS: There was no significant difference in clinical background between the 2 groups. The nicorandil group showed a significantly lower incidence of CK-MB elevation (>1x upper limit of control range, 20 IU/l) than the control group (8.8% vs 21.8%, p<0.05). The levels of serum CK-MB in the nicorandil group were significantly lower than those in the control group (13.4+/-5.7 vs 16.5+/-9.7 IU/l, p<0.01). Similarly, the nicorandil group showed a significantly lower incidence of cTnT elevation [>1x (0.1 ng/ml) or >2x (0.2 ng/ml)] upper limit of control range than the control group (14.3% vs 26.7%, p<0.05, or 7.7% vs 17.8%, p<0.05). Serum cTnT levels were also significantly lower in the nicorandil group than in the control group (0.05+/-0.10 vs 0.15+/-0.36 ng/ml, p<0.05). CONCLUSIONS: The results demonstrated that nicorandil reduces minor cardiac marker elevation after coronary stenting.     

Effect of combined intracoronary adenosine and nicorandil on no-reflow phenomenon during percutaneous coronary intervention.

BACKGROUND: This study aimed to clarify the effect of intracoronary administration of combined adenosine and nicorandil on the no-reflow phenomenon. METHODS AND RESULTS: Fifty patients (67+/-10 years, 30 male) with acute myocardial infarction (AMI) who developed no-reflow phenomenon during primary percutaneous coronary intervention (PCI) between June 2001 and May 2003 comprised the study group, which was divided into 2 groups: group I [25 patients, 67+/-10 years, 13 male; adenosine (24 microg/ml) alone in addition to nitrate] and group II [25 patients, 66+/-9 years, 17 male; combined intracoronary administration of adenosine and nicorandil (2 mg/ml) in addition to nitrate]. In-hospital and 6-month major adverse cardiac events (MACE) after PCI were compared between the 2 groups. Risk factors of coronary disease, left ventricular ejection fraction and wall motion score were not significantly different between the 2 groups (p=NS). Time interval from the onset of chest pain to PCI, number of involved vessels, lesion type according to ACC/AHA classification and TIMI flow grade (TFG) were not significantly different in both groups (p=NS). Incidence of thrombosis or dissection after balloon angioplasty, diameter and length of stent, and use of Reopro during PCI were not significantly different. TFG after PCI (2.0+/-0.9 vs 2.6+/-0.6, p=0.024), DeltaTFG (1.5+/-1.1 vs 2.2+/-1.0, p=0.033) and difference in TIMI frame count (TFC) before and after PCI (DeltaTFC) were greater in group II than group I (45.2+/-24.5 vs 63.6+/-23.2, p=0.014). Myocardial blush score 3 was obtained more frequently in group II than group I (44% vs 76%, p=0.014). In-hospital death did not occur in any of group II, but 4 patients of group I died (p=0.043). Two cases of MACE developed in each group and heart failure occurred in 3 (12%) of group I and 1 (4%) of group II patients during the 6-month follow-up (p=NS). CONCLUSIONS: Intracoronary administration of adenosine combined with nicorandil may improve both the occurrence of no-reflow in patients during PCI for AMI and short-term clinical outcome, compared with adenosine alone.     

Timing of peak troponin T and creatine kinase-MB elevations after percutaneous coronary intervention

STUDY OBJECTIVE: The prognostic significance of elevations in creatine kinase-MB and troponin T (cTnT), which have been conventionally measured 6 to 8 h after percutaneous coronary intervention (PCI), has been established. However, the time to peak biomarker appearance in the circulation has not been defined and is the purpose of this pilot study. DESIGN: Nonrandomized, nonconsecutive patient cohort. SETTING: Clinical practice, Mayo Clinic, Rochester, MN. PATIENTS: Cohort (n = 57) undergoing elective PCI. INTERVENTIONS: cTnT and creatine kinase (CK)-MB measured at baseline, 2 h, 4 h, 8 h, and > or = 2 h (mean +/- SEM, 18 +/- 5 h) after PCI. Measurements and results: Postprocedure cTnT elevations were detected in 30 of 57 patients (53%). Of these, 4 of 30 patients (13%) had peak cTnT at 4 h (0.80 +/- 0.40 ng/mL), 5 of 30 patients (17%) had peak cTnT at 8 h (1.07 +/- 0.48 ng/mL), and 21 of 30 patients (70%) had peak cTnT at > or = 12 h (0.21 +/- 0.06 ng/mL); 22 of 30 patients received abciximab. Elevations in CK-MB occurred in 14 of 57 patients (25%). Of these, 3 of 14 patients (21%) demonstrated peak CK-MB at 2 h (18.5 +/- 7.9 ng/mL) and the remainder (11 of 14 patients, 79%) during the 12- to 20-h interval (20.2 +/- 4.4 ng/mL); 12 of 14 patients received abciximab. CONCLUSION: More cTnT than CK-MB elevations occur after PCI; however, both biomarkers demonstrate a longer time to peak value than anticipated in clinical practice. Early surveillance monitoring (< 12 h) does not detect peak biomarker levels, especially in patients with normal baseline values. If peak levels are to be used to determine prognosis, then longer time intervals should be used for post-PCI surveillance. The timing of peak elevations appears to be influenced by baselines values as well. Early elevations may reflect the conjoint effects of injury associated with the disease process and the intervention itself. These data suggest that a re-evaluation of surveillance monitoring to account for the variability reported and the influence of baseline elevations of biomarkers may improve the prognostic power of the measurements.     

Isolated elevation in troponin T after percutaneous coronary intervention is associated with higher long-term mortality.

OBJECTIVES: The aim of this study was to evaluate whether, in patients with normal post-procedure CK-MB, an isolated elevation in cardiac troponin T (cTnT) predicts long-term survival. BACKGROUND: Cardiac troponin T is a sensitive and specific marker of myonecrosis. There is little known about the incidence and prognostic significance of an isolated elevation of cTnT without a rise in creatine kinase (CK)-MB following PCI. METHODS: We evaluated the outcomes of 1,949 patients from the Mayo Clinic registry who had normal pre-procedure cTnT and CK-MB, required nonemergency percutaneous coronary intervention (PCI), and had normal CK-MB after the procedure. RESULTS: An elevation in cTnT (cTnT+) was observed in 383 patients (19.6%) (median 0.04 ng/ml, interquartile range 0.03 to 0.06 ng/ml). The TnT+ status was associated with adverse clinical and angiographic characteristics, and multivessel PCI. Over the median follow-up duration of 26 months, mortality (p < 0.001) and the combined rate of death and myocardial infarction (p = 0.004) were significantly higher in cTnT+ patients. Estimated 3-year survival for those with and without cTnT elevation was 86.9% and 93.2%, respectively. By multivariate analysis, an elevation in cTnT after PCI was an independent predictor of increased long-term mortality. A doubling in the post-PCI cTnT was associated with a partial hazard ratio of 1.20 (95% confidence interval 1.02 to 1.40; p = 0.023). CONCLUSIONS: An isolated minor elevation in cTnT after PCI provides long-term prognostic information regarding mortality and myocardial infarction.     

Randomized comparison of upstream tirofiban versus downstream high bolus dose tirofiban or abciximab on tissue-level perfusion and troponin release in high-risk acute coronary syndromes treated with percutaneous coronary interventions: the EVEREST trial.

OBJECTIVES: We aimed to compare the effects of upstream tirofiban versus downstream high-dose bolus (HDB) tirofiban and abciximab on tissue level perfusion and troponin I release in high-risk non-ST-segment elevation acute coronary syndrome (ACS) patients treated with percutaneous coronary intervention (PCI). BACKGROUND: Optimal timing and dosage of glycoprotein IIb/IIIa inhibitors for ACS remain to be explored. METHODS: We randomized 93 high-risk ACS patients undergoing PCI to receive upstream (in the coronary care unit) tirofiban, downstream (just prior to PCI) HDB tirofiban, and downstream abciximab. We evaluated the effects of the three drug regimens on tissue-level perfusion using the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count, the TIMI myocardial perfusion grade (TMPG), and intracoronary myocardial contrast echocardiography (MCE) before and immediately after PCI and after cardiac troponin I (cTnI). RESULTS: The TMPG 0/1 perfusion was significantly less frequent with upstream tirofiban compared with HDB tirofiban and abciximab both before (28.1% vs. 66.7% vs. 71%, respectively; p = 0.0009) and after PCI (6.2% vs. 20% vs. 35.5%, respectively; p = 0.015). Upstream tirofiban was also associated with a significantly higher MCE score index (0.88 +/- 0.18 vs. 0.77 +/- 0.32 vs. 0.71 +/- 0.30, respectively; p < 0.05). Post-procedural cTnI elevation was significantly less frequent among patients in the upstream tirofiban group compared with the HDB tirofiban and abciximab groups (9.4% vs. 30% vs. 38.7%, respectively; p = 0.018). The cTnI levels after PCI were significantly lower with upstream tirofiban compared with HDB tirofiban (3.8 +/- 4.1 vs. 7.2 +/- 12; p = 0.015) and abciximab (3.8 +/- 4.1 vs. 9 +/- 13.8; p = 0.0002) CONCLUSIONS: Among high-risk non-ST-segment-elevation ACS patients treated with an early invasive strategy, upstream tirofiban is associated with improved tissue-level perfusion and attenuated myocardial damage.     

Cardiac troponins T and I in patients with end-stage renal disease: the relation with left ventricular mass and their prognostic value

BACKGROUND: Cardiac troponins are frequently elevated in patients with end-stage renal disease (ESRD) in the absence of acute myocardial ischemia. The cause and prognostic value of cardiac troponin elevations in such patients are controversial. HYPOTHESIS: The aims of this study were (1) to define the incidence of cTnT and cTnI elevations in patients with ESRD, (2) to evaluate the relationship between troponin elevations and left ventricular mass index (LVMI), and (3) to evaluate the prognostic value of elevations in cTnT and cTnI prospectively. METHODS: We included 129 patients with ESRD (71 men, age 44 +/- 16 years) with no clinical evidence of coronary artery disease. All patients underwent cardiac examinations, including medical history, physical examination, electrocardiogram, and transthoracic echocardiography. Left ventricular mass index was calculated and all patients were followed for 2 years. RESULTS: The cTnT concentration was > 0.03-0.1 ng/ml in 27 (20.9%) and > 0.1 ng/ml in 27 (20.9%) of the 129 patients. The cTnI concentration was > 0.5 ng/ml in 31 (24%) of 129 patients. Multiple logistic regression analysis identified LVMI (p < 0.001), diabetes (p = 0.001), and serum albumin level (p = 0.009) as a significant independent predictor for elevated cTnT. Left ventricular mass index was the only significant independent predictor for elevated cTnI (p = 0.002). There were 25 (19.4%) deaths during follow-up. Multivariable analysis showed that elevation of cTnT and cTnI did not emerge as an independent predictor for death. Serum albumin level (p < 0.001) was the strongest predictor of mortality, followed by age (p = 0.002) and LVMI (p = 0.005). CONCLUSIONS: Cardiac troponin T and I related significantly to the LVMI. The increased serum concentration of cardiac troponins probably originates from the heart; however, they are not independent predictors for prognosis.     

Detection of myocardial injury during radiofrequency catheter ablation by measuring serum cardiac troponin I levels: procedural correlates.

OBJECTIVES: In the present prospective controlled study, we measured blood levels of cardiac troponin I (cTnI) in patients undergoing radiofrequency (RF) catheter ablation (RFA), and we sought to investigate the degree of myocardial injury incurred by the application of RF energy and determine its procedural correlates. BACKGROUND: Measurement of serum creatine kinase (CK) levels after RFA may underestimate the degree of myocardial injury due to its thermal inactivation by RFA. Cardiac troponin I is a newer, more specific marker of myocardial injury, which may circumvent this limitation; its use in this setting has rarely been studied. METHODS: In 118 consecutive patients, 67 men and 51 women aged 38 +/- 19 years undergoing RFA for a variety of arrhythmias, cTnI and creatine kinase isoenzyme (CK-MB) levels were measured before, immediately after and 4 to 24 h after RFA. Cardiac troponin I was also measured in 39 patients (control group) having only electrophysiologic studies (EPS) without RFA. RESULTS: All RFA procedures were uncomplicated, lasted 3.2 +/- 2.0 h and included delivery of 16 +/- 22 (median: 9) RF current applications. Baseline cTnI levels averaged 0.17 +/- 0.18 ng/ml, rose to 0.88 +/- 1.12 at the end of RFA and to 2.19 +/- 2.46 at 4-24 h later. Creatine kinase isoenzyme was found to be elevated (>6 microg/l) in 32 patients (27%), while cTnI levels were increased (> or =1 ng/ml) in 80 patients (68%) (p = 0.0001). Cardiac troponin I levels correlated with the number of RF lesions applied (r = 0.53, p < 0.0001), the site of RFA, being higher with ventricular > atrial > annular lesions (p = 0.012) and the approach to the mitral annulus (transaortic > transseptal, p = 0.004). In a control group of 39 patients undergoing EPS, all but one patient had normal cTnI or CK-MB. CONCLUSIONS: The degree of myocardial injury incurred by RFA is far more accurately assessed by cTnI levels rather than by CK-MB measurements. Cardiac troponin I levels correlate with the number of RF lesions applied, the site of RFA and the approach to the mitral annulus.     

Baseline troponin level: key to understanding the importance of post-PCI troponin elevations.

AIMS: The adverse prognostic significance of biomarker elevations after percutaneous coronary intervention (PCI) is well established. However, often baseline troponin values are not included in the analysis or sensitive criteria are not employed. Accordingly, we assessed the timing and magnitude of post-PCI troponin T (cTnT) levels and their relationships to outcomes in patients with and without pre-PCI baseline cTnT elevations using a sensitive assay and sensitive cut-off values. METHODS AND RESULTS: cTnT was measured at baseline (pre-PCI), 8 and 16 h post-PCI in 2352 patients. A cTnT elevation was defined as > or =0.03 ng/mL. No baseline cTnT elevations were detected in 1619 patients undergoing mostly (97%) non-urgent procedures (cTnT = 0.01 +/- 0.002 ng/mL; mean +/- SD). 733 patients had baseline cTnT elevations. Only the baseline troponin value had prognostic importance. Patients with elevated cTnT baseline levels had a higher overall cumulative 12-month death/MI rate of 11.1% compared with those without elevated baseline levels of 4.7% (P < 0.05). Neither the timing nor the magnitude of the post-procedure cTnT elevations was predictive of long-term death/MI rates when baseline elevations were included in the analysis. Similar findings were observed for baseline creatine kinase-MB (CK-MB) levels. Late increases in cTnT levels (16 h post-PCI) presaged in-hospital events only. CONCLUSION: Long-term prognosis is most often related to the baseline pre-PCI troponin value and not the biomarker response to the PCI. These results support a re-evaluation of the use of biomarker data in relation to PCI.     

Prognostic significance of elevated troponin I after percutaneous coronary intervention

OBJECTIVES: We sought to assess the incidence and clinical significance of elevated cardiac troponin I (cTnI) after percutaneous coronary intervention (PCI). BACKGROUND: Elevated creatine kinase-MB (CK-MB) is prognostically important after PCI, but the prognostic significance of elevated cTnI after PCI is uncertain. METHODS: In a prospective substudy of the Sibrafiban Versus Aspirin to Yield Maximum Protection From Ischemic Heart Events Post-acute Coronary Syndromes (SYMPHONY) trials, which randomized patients with acute coronary syndromes (ACS) to receive aspirin or sibrafiban, we measured cTnI (positive, > or =1.5 ng/ml) and CK-MB (positive, > or =7 ng/ml) in 481 patients with PCI. Samples were collected immediately before and at 0, 8 and 16 h after PCI and analyzed by a core laboratory. The primary end point was the Kaplan-Meier estimate of death, myocardial infarction or severe, recurrent ischemia at 90 days. RESULTS: Overall, 230 patients (48%) had elevated cTnI after PCI. Such patients underwent PCI sooner and were more likely to have coronary stenting. Elevated cTnI was associated with nonsignificantly higher risks of the primary end point (11.5% vs. 8.7%; p = 0.15) and of death (1.8% vs. 0.4%; p = 0.4) and a significantly higher risk of death or infarction (10.6% vs. 4.2%; p = 0.005). This pattern was more pronounced for patients who became positive only after PCI: primary end point, 20.7% vs. 10.1% for patients who remained negative after PCI (p = 0.05); death, 5.2% vs. 0% (p = 0.02); death or infarction, 18.1% vs. 4.1% (p = 0.007). CONCLUSIONS: Elevated cTnI, often observed after PCI in patients with ACS, is associated with worse 90-day clinical outcomes. This marker, therefore, is a useful prognostic indicator in such patients.     

Correlation of postpercutaneous coronary intervention creatine kinase-MB and troponin I elevation in predicting mid-term mortality

Creatine kinase-MB (CK-MB) and troponin I elevations after successful percutaneous coronary intervention (PCI) are common, and different gradations have been correlated with mortality. To establish which of these 2 markers of myonecrosis, CK-MB and troponin I, accurately predicts mortality after successful PCI, we analyzed 2,873 patients without acute myocardial infarction who underwent PCI for in-hospital events and mid-term mortality. Patients were stratified into 4 groups based on peak post-PCI cardiac markers values: group I: normal CK-MB (<16 U/L) or troponin I (<2 ng/ml); group II: CK-MB or troponin I levels 1 to 3 times normal; group III: >3 to 5 times normal; and group IV: >5 times normal. CK-MB elevation occurred in 16.1% of patients, with 12.2%, 2.3%, and 1.6% in groups II to IV, respectively. Troponin I elevation was detected in 38.9% of patients, with 16.4%, 8.4%, and 14.1% in groups II to IV, respectively. There was poor correlation between postprocedural CK-MB and troponin I values (r = 0.10) and in their individual subgroups. Kaplan-Meier estimates of death for postprocedure CK-MB were 2.1%, 2.7%, 1.7%, and 10.3% (p = 0.002) for groups I to IV, respectively; for troponin I, these estimates were 2.2%, 2.3%, 2.9%, and 2.1% for groups I to IV, respectively (p = 0.58). A Cox proportional hazards model showed that CK-MB >5 times normal was the strongest predictor of mortality (hazard ratio 6.7, 95% confidence interval 1.9 to 22.9; p = 0.002), although heart failure, peripheral vascular disease, pre-PCI digoxin therapy, and post-PCI renal failure also predicted mortality. However, neither troponin I peak elevation nor any subgroup predicted mortality. Troponin I is frequently elevated after PCI, but does not predict mortality. Periprocedural CK-MB elevation >5 times normal remains an independent predictor of mid-term mortality and a valuable marker for PCI prognosis in low-to-medium risk patients.     

Minor myocardial injury after elective uncomplicated successful PTCA with or without stenting: detection by cardiac troponins.

Cardiac troponins are sensitive and specific markers for the detection of minor myocardial injury. However, they have been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels after elective uncomplicated successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare their results with serum creatinine kinase MB isoenzyme (CKMB). CTnI and cTnT levels were compared with those of CK or CKMB in 98 consecutive patients with stable angina undergoing elective uncomplicated successful PTCA with stenting (n = 71) or without stenting (n = 27). Markers were measured before and 6, 12, 24, and 48 hr after the procedure. Peak postprocedural levels for each marker were compared and related to angiographic and procedural characteristics as well as to the occurrence of side-branch occlusion. None of the patients had abnormal markers before the procedure. Abnormal postprocedural values of one or more markers were observed in 28 patients (29%), 23 after stenting and 5 after PTCA alone. The frequencies of abnormal cTnI and cTnT levels were significantly higher than that of CKMB after coronary intervention (26% and 18% vs. 7%; P = 0.00016 and 0.015, respectively), with cTnI being the most significant. When compared with troponin-negative patients, abnormal cardiac troponin values were significantly related to total time of inflation (223 +/- 128 vs. 170 +/- 105 sec; P = 0.008) and inflation maximal pressure (12.9 +/- 2.3 vs. 12.0 +/- 2.7 atm; P = 0.04). Small side-branch occlusion was noticed in 36% of the troponin-positive patients and in 6% of the troponin-negative group (P = 0.00047). In conclusion, minor myocardial injury is not uncommon after elective uncomplicated successful PTCA with or without stenting. Cardiac troponins, especially cTnI, are more sensitive than CKMB for the detection of this minor myocardial injury. Total time of inflation and inflation maximal pressure are predictors of postprocedural elevation of cardiac troponins. Side-branch occlusion may account for some, but not all, periprocedural minor myocardial injury.     

The long-term clinical outcomes after rescue percutaneous coronary intervention in patients with acute myocardial infarction

Rescue percutaneous coronary intervention (PCI) has been used to treat patients after failed thrombolysis in acute myocardial infarction. However, the short- and long-term benefits of rescue PCI have not been known exactly. The goal of this study was to examine the clinical and angiographic outcomes, the success rate of the procedure, and the long-term survival rate after rescue PCI. The clinical and angiographic outcomes of 31 patients (Group I; 59.7 +/- 11.4 years, 80.6% male), who underwent rescue PCI were compared with those of 177 patients (Group II; 59.7 +/- 9.7 years, 79.7% male), who underwent primary PCI at Chonnam National University Hospital between January 1997 and December 1999. There were no significant differences in the risk factors for coronary artery diseases except for smoking (Group I; 24/31, 77.4% vs. Group II; 76/177, 42.9%, P = 0.011). The incidence of cardiogenic shock was higher in Group I than in Group II (Group I; 7/31, 22.6% vs. Group II; 11/177, 6.2%, P = 0.021). The coronary angiographic findings were not different between two groups, except for Thrombolysis in Myocardial Infarction (TIMI) flow of Group I was lower than in Group II (Group I; 1.14 +/- 0.93 vs. Group II; 1.61 +/- 1.14, P = 0.001). The primary success rate was 93.6% (29/31) in Group I and 94.9% (168/177) in Group II (P = 0.578). The baseline ejection fraction was lower in Group I than in Group II (Group I; 44.2 +/- 8.9% vs. Group II; 50.8 +/- 11.7, P = 0.023), which improved in both groups (Group I; 51.7 +/- 7.9% vs. Group II; 60.7 +/- 13.4%, P = 0.001 respectively) at 6 months after the procedures. The survival rates of Group I were 93.5%, 93.5%, and 90.3% and those of Group II were 94.5%, 93.7%, and 91% at 1, 6, and 12 months, respectively. Rescue PCI is associated with the risk factor of smoking. The indication for rescue PCI was more common in patents with cardiogenic shock. The success rate of rescue PCI was comparable to that of primary PCI, and left ventricular function is improved after rescue PCI on long-term clinical follow-up with relatively high survival rate.     

Prognostic value of cardiac troponin I elevation after percutaneous coronary intervention in patients with chronic renal insufficiency: a 12-month outcome analysis.

Serum cardiac troponin I (cTnI) is a highly specific marker for myocardial damage in patients with chronic renal insufficiency (CRI), unlike creatine kinase myocardial band fraction (CK-MB), which may be elevated in the absence of myocardial injury in patients with CRI. We studied 116 consecutive CRI patients (serum creatinine +/- 1.8 mg/dL, not on dialysis) with normal baseline cTnI levels who underwent successful percutaneous coronary intervention (PCI). Patients were divided into two groups: group 1, elevated postprocedural cTnI (n = 50), and group 2, normal cTnI (n = 66). Patients with elevated cTnI were older and had a higher incidence of postinfarction angina and lower creatinine clearance compared to patients who did not have cTnI elevation. Atheroablative devices (rotational and directional atherectomy and excimer laser coronary angioplasty) were more frequently used in group 1 patients (27.1% vs. 18.5%; P = 0.04). In-hospital mortality, cardiac mortality, and Q-wave myocardial infarction rates did not differ between the two groups. At 12-month follow-up, total mortality rates were significantly higher in group 1 (28.0% vs. 9.9%; P = 0.002). Multivariate analysis showed that cTnI was an independent predictor of late mortality (OR = 2.26; CI = 1.07-4.77; P = 0.03). Thus, in patients with CRI, elevated cTnI levels after successful PCI is an important predictor of poor long-term outcome. Our data suggest that patients with cTnI elevation > 3 times above normal values are particularly at higher risk.     

Cardiac troponin T and I and creatine kinase-MB as markers of myocardial injury and predictors of outcome following percutaneous coronary intervention

AIMS: This study was performed to determine the most sensitive biochemical marker for the detection of cardiac myocyte damage potentially sustained during percutaneous coronary intervention (PCI) and to assess whether such a marker can be used to identify patients at increased risk of poor subsequent clinical outcome. METHODS AND RESULTS: We studied 109 consecutive patients presenting with clinical stable and unstable angina and undergoing PCI at our institution. Blood was sampled for creatine kinase-MB (CK-MB), cardiac Troponin T (cTnT) and I (cTnI) immediately before and at 6, 14 and 24 h post-PCI. Five patients with raised cardiac markers pre-PCI were excluded from further analysis. The occurrence of major adverse cardiac events (MACE) was documented in-hospital, at 30 days and at long-term clinical follow up of up to 20 months. MACE occurred in 26/109 (24%) patients: death=1, QWMI=4, NQWMI=5, repeat PCI=16 (nine target vessel revascularisations and seven de-novo lesions), CABG=5. cTnI had the highest detection rate for myocardial damage, with 58 cTnI-positive patients, 38 cTnT-positive patients and 28 CK-MB-positive patients in the 24 h following PCI (Pearson's Chi square test, P<0.01). The type of interventional strategy per se was not significantly associated with post-procedural cardiac marker concentrations (Kruskal-Wallis ANOVA, P>0.05). There was a significant association between post-procedural cardiac marker concentrations of CK-MB, cTnT and cTnI and the occurrence of procedural angiographic complications (P=0.0003, 0.0002, 0.001, respectively). All three markers, at each sampling time point between 6 and 24 h post-PCI, showed a significant predictive relationship with MACE in-hospital and at long-term follow up (ROC curve AUC analysis, P<0.05). All three markers provided equally predictive information at each of the three post-procedural sampling time points between 6 and 24 h following PCI. All levels of cardiac marker elevation above the clinically discriminant cut-off values were significantly predictive of outcome at long-term follow up. CONCLUSIONS: cTnI proved to be the most sensitive marker in detecting myocardial necrosis following PCI. CK-MB, cTnT and cTnI all provided similarly reliable prognostic information, with cTnT and cTnI being marginally superior in predicting MACE at follow up.     

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.     

Coronary revascularization: off-pump versus on-pump--a comparison of behavior of biochemical cardiac ischemia markers

BACKGROUND: Recently, coronary artery bypass grafting (CABG) on the beating heart with avoidance of extracorporeal circulation (off-pump CABG technique) has been gaining increasing importance in modern cardiac surgery. The object of this prospective study was to compare postoperative kinetic and patterns of cardiac troponin I (cTnI), T (cTnT), and creatine kinase MB (CKMB) activities after off-pump CABG versus conventional on-pump CABG. METHODS: We studied 106 patients who underwent first-time elective on-pump (group I, n = 69, 56 male, 13 female, mean age: 64.3 +/- 9.9 years, mean ejection fraction: 56 +/- 15%) or off-pump (group II, n = 37, 24 male, 13 female, mean age: 68.4 +/- 9.1 years, mean ejection fraction: 57 +/- 13%) CABG surgery via median sternotomy. CTn I and cTnT levels, total creatine kinase (CK) and CK-MB activities in the serum were measured before operation, up on arrival at the ICU and 6, 12, 24, 48 and 120 hours later. Serial 12-lead ECGs were recorded preoperatively and on days 1, 2 and 5. RESULTS: Serum concentrations of cardiac troponins in all patients were preoperatively either not detectable or in the normal range and significantly increased after surgery. In group I, one patient developed a Q wave myocardial infarction, one patient a non-Q wave infarction and two patients a new left bundle branch block on the ECG. One patient of group II developed a new Q-wave myocardial infarction and another patient permanent atrial fibrillation associated with a continuous arrhythmia. All patients with a myocardial infarction in the ECG showed significant elevation of concentrations or activities of these biochemical markers. The median postoperative peak values for cTnI were measured at 24 h in both groups (2.7 micrograms/l, 95%-CI: [2.2, 3.2] in group I and 1.1 micrograms/l, 95%-CI: [0.5, 1.3] in group II). CTnT postoperatively presented an earlier median peak of 0.128 microgram/l at 12 h in group II (95%-CI: [0.041, 0.146]) than in group I at 48 h (0.298 microgram/l, 95%-CI: [0.254, 0.335]). CONCLUSIONS: All patients undergoing CABG surgery with or without extracorporeal circulation postoperatively showed an increase of cardiac troponin levels. After uncomplicated coronary revascularization, patients with the off-pump CABG technique continuously presented lower serum cardiac troponin concentrations than those with the on-pump CABG technique. CTnI showed the same patterns of release in both groups with different median postoperative peak values at 24 h. The patterns off cTnT release following CABC surgery with or without extracorporal circulation were different: CTnT reaches its postoperative peak value in patients with the off-pump CABG technique earlier than those with the on-pump CABG technique (12 h postoperatively versus 48 h).