Increased Creatine Kinase MB Research Articles

Measuring Aspirin Resistance, Clopidogrel Responsiveness, and Postprocedural Markers of Myonecrosis in Patients Undergoing Percutaneous Coronary Intervention

Aspirin and clopidogrel are proven to prevent thromboembolic events during percutaneous coronary intervention (PCI). Enzyme release of creatine kinase-MB (CK-MB) enzyme during PCI has been associated with an increased risk of future adverse cardiac events. This study examined the correlation between measurements of aspirin resistance and the level of inhibition of the thienopyridine-specific P2Y12 platelet receptor and CK-MB release after PCI. We prospectively studied 330 patients with elective PCI treated with drug-eluting stents. Patients were pretreated with aspirin and clopidogrel. Patients with positive CK-MB or acute coronary syndrome and those on glycoprotein IIb/IIIa inhibitors were excluded. Serum assays of aspirin resistance (Ultegra Rapid Platelet Function Assay-ASA, Accumetrics) and clopidogrel resistance (Rapid Platelet Function Assay P2Y12, Accumetrics) were performed before PCI. Serum troponinI and CK-MB levels were measured at 8, 16, and 24 hours after PCI. Aspirin resistance unit (ARU) measurement > or =550 was detected in 12 patients (3.7%). Mean platelet reactivity unit (PRU; measurement of inhibition of P2Y12 activity) was 192.2 +/- 95.4 (lower PRU, more inhibition of P2Y12 receptor). There was no correlation between level of ARU or PRU and troponin I or CK-MB release after PCI at any time point. Only multivessel coronary disease was found to be a predictor of any increase in CK-MB in a multivariate analysis (odds ratio 2.2, 95% confidence interval 1.4 to 3.3, p = 0.0003). A positive correlation was found between levels of ARU and PRU. Target vessel revascularization/major adverse cardiac event rate at 6 months was 8.2% with no correlation between ARU or PRU and release of cardiac enzymes or occurrence of adverse cardiac events. In conclusion, this study does not support routine measurements of aspirin and clopidogrel resistance in stable patients undergoing PCI.

Predictors of Periprocedural Creatine Kinase-Myocardial Band Elevation Complicating Elective Percutaneous Coronary Intervention

Limited data are available regarding the predictors of periprocedural creatine kinase-MB (CK-MB) isoenzyme increase after elective percutaneous coronary intervention (PCI) in the stenting era. We explored the predictors of periprocedural CK-MB increase in 882 consecutive patients with normal preprocedural CK-MB who underwent 919 angiographically successful elective PCIs with (n = 814) or without (n = 105) stenting. Patients were categorized into 3 groups based on their peak CK-MB levels after PCI: (1) normal CK-MB (n = 761), (2) minor CK-MB increase (CK-MB 1 to 3 times normal, n = 112), and (3) major CK-MB increase (CK-MB >3 times normal, n = 46). By logistic regression analysis, independent predictors for minor CK-MB increase included thrombus (odds ratio [OR] 5.09, p = 0.001), platelet IIb/IIIa antagonist use (OR 0.53, p <0.01), number of lesions treated (per additional lesion, OR 1.54, p <0.01), maximum balloon size (per millimeter increase, OR 1.57, p <0.05), American College of Cardiology/American Heart Association type C lesion (OR 1.68, p <0.05), sustained chest pain during procedure (OR 1.94, p <0.05), dissection (OR 2.05, p <0.05), and transient side branch occlusion (OR 4.54, p <0.05). Independent predictors for major CK-MB increase were chest pain at end of procedure (OR 9.66, p <0.001), type C lesion (OR 2.42, p <0.05), Canadian Cardiovascular Society angina class III to IV (OR 3.32, p <0.05), thrombus (OR 5.09, p = 0.001), and abrupt closure (OR 5.30, p <0.05). In conclusion, baseline clinical and angiographic characteristics and procedural complications were associated with minor and major CK-MB increases. Patients with chest pain at the end of the procedure were at the highest risk for major CK-MB increase.

Comparison of Effectiveness of Bare Metal Stents Versus Drug-Eluting Stents in Large (≥3.5 mm) Coronary Arteries

Drug-eluting stents (DESs) are superior to bare metal stents (BMSs) in decreasing restenosis rates across a wide range of patient and lesion subsets. However, widespread utilization of DESs raises concerns with regard to risks of prolonged dual antiplatelet therapy, the potential for late adverse events such as late thrombosis, and cost. Vessel diameter and lesion length have been previously identified as predictors for restenosis for DESs and BMSs. This study compared the clinical outcomes of DESs versus BMSs in large coronary arteries (> or =3.5 mm). A cohort of 233 patients who underwent single-vessel angioplasty with DES implantation in large vessels was compared with 233 propensity-matched patients who received BMSs in vessels with similar reference vessel diameters. Clinical outcomes at 30 days, 6 months, and 1 year were compared between groups. Baseline clinical and procedural characteristics were similar. Target lesion revascularization and target vessel revascularization rates and the incidence of major adverse cardiac events were low and comparable between the 2 groups at all follow-up intervals. At 1 year, the primary outcome occurred in 8.5% of patients with DESs and 7.7% of patients with BMSs (p = 0.80). There were no episodes of subacute stent thrombosis or late thrombosis in either group. In conclusion, implantation of DESs in large coronary arteries confers no additional benefit compared with BMSs, and the 2 approaches are associated with equally favorable clinical outcomes at 1 year.

Hemodynamic Significance of Periprocedural Myocardial Injury Assessed With N-Terminal Pro-B-Type Natriuretic Peptide After Percutaneous Coronary Intervention in Patients With Stable and Unstable Coronary Artery Disease (from the JUMBO-TIMI 26 Trial)

The clinical relevance of periprocedural myocardial injury related to percutaneous coronary intervention (PCI) remains controversial. N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) is a sensitive indicator of hemodynamic stress and when increased is associated with higher mortality in patients with acute and chronic ischemic heart disease. We measured the serum level of NT-pro-BNP using the Elecsys 2010 proBNP assay at baseline, 4 to 6 hours, and 12 to 24 hours in 747 patients undergoing elective or urgent PCI and enrolled in the JUMBO-TIMI 26 trial. Periprocedural myocardial infarction (MI) was independently adjudicated and required a new increase in creatine kinase-MB >3 times the upper limit of normal distinct from MI as the indication for PCI. Patients with procedural MI had significantly higher levels of NT-pro-BNP at 12 to 24 hours (405 vs 146 pg/ml, p <0.001). Moreover, the greater increase in NT-pro-BNP in patients with periprocedural MI was independent of each clinical and other procedural correlates of NT-pro-BNP after PCI (p <0.001). In addition, the magnitude of increase in NT-pro-BNP correlated strongly with extent of myocardial injury, including in patients with evidence of injury (creatine kinase-MB 1 to 3 times upper limit of normal) not meeting criteria for MI (p = 0.001) or low-level increase in troponin T (p = 0.001). In conclusion, periprocedural myocardial injury, even at low levels, during PCI is associated with increased hemodynamic stress as measured by increasing NT-pro-BNP. This finding supports the physiologic relevance of procedural MI and the continued effort to define therapies that decrease the risk of this complication.

Comparison of the Effects of Nicorandil Versus Verapamil on the Incidence of Slow Flow/No Reflow During Rotational Atherectomy

In rotational atherectomy, the slow-flow/no-reflow phenomenon is a common complication, which usually results in myocardial injury. We prospectively randomized 111 patients with successful rotational atherectomy into a verapamil group (group V, n = 56) and a nicorandil group (group N, n = 55). We compared final burr size, total ablation time, maximum decrease in revolutions per minute, incidence of slow flow/no reflow, creatine kinase-MB increase, and cardiac troponin T increase between the 2 groups. Patient and procedural characteristics were not significantly different between groups. The incidence of no reflow/slow flow was significantly lower in group N than in group V (3.6% vs 17.9%, respectively, p <0.05). The incidence of a minor increase in cardiac markers was also significantly lower in group N than in group V (creatine kinase-MB 3.6% vs 16.1%, p <0.05; cardiac troponin T 5.5% vs 21.4%, p <0.05). In conclusion, our results showed that nicorandil decreases the incidence of slow flow/no reflow during rotational atherectomy.

Angiographic Adverse Events, Creatine Kinase-MB Elevation, and Ischemic End Points Complicating Percutaneous Coronary Intervention (a REPLACE-2 Substudy)

Several angiographic adverse events during coronary balloon angioplasty have been associated with increased creatine kinase-MB (CK-MB) enzymes and adverse clinical outcomes. The significance of angiographic adverse events in the stent era has not been widely studied. We analyzed 10 types of angiographic adverse events that were reported in the 6,010-patient Second Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events (REPLACE-2) trial to determine their relation to CK-MB elevation and clinical ischemic end points after percutaneous coronary intervention (PCI). Angiographic adverse events occurred in 9.1% of REPLACE-2 patients. Most (8 of 10) types of angiographic adverse events were associated with an increased risk of increased CK-MB (p <0.001 for each), and 47% of all patients with an angiographic adverse event developed increased CK-MB. Logistic regression analysis showed that the strongest predictor of death, myocardial infarction, or revascularization at 6 months was the occurrence of an angiographic adverse event during PCI (odds ratio 1.9, 95% confidence interval 1.6 to 2.4, p <0.001). Side branch closure, abrupt closure, any decreased flow during the procedure, angiographic distal embolization, and perforation or tamponade were individual predictors of the occurrence of the combined clinical ischemic end point at 6-month follow-up (p <0.005 for each). In conclusion, most angiographic adverse events during PCI are associated with increased CK-MB and are powerful predictors of adverse clinical events within 6 months.

Interleukin-6 Mediated Non-ischemic Injury To Cardiac Myocytes During Marathon Running

Since the fatal collapse of the legendary Pheidippides in 490 BC, mechanisms contributing to sudden cardiac death as shown to occur in 1 per 50,000 marathon runners during races are poorly understood. PURPOSE To explore the role of an acute inflammatory response to exertional rhabdomyolysis in the triggering of acute cardiac events. METHODS measurement of total creatine kinase, interleukin (IL)-6, C reactive protein (CRP), creatine kinase MB (CK-MB), cardiac troponin T (cTnT) and ischemia modified albumin (IMATM) by the albumin cobalt binding ACB ± TM Test in 46 asymptomatic middle-aged marathon runners before and sequentially after the 2001–02 Boston Marathons. RESULTS A 15-fold post-race rise in CK was accompanied by 40- and 20- fold increases in IL-6 and C-reactive protein respectively. There was a transient increase in cTnT to diagnostically indeterminate levels with no change in IMA by the ACB Test despite a 14-fold increase in CK-MB (Table 1).TableCONCLUSIONS These findings are consistent with non-ischemic injury to cardiomyocytes without necrosis perhaps due to IL-6 mediated leakage of cytosolic cTnT. Strategies for primary prevention of exertional cardiac events including the Pheidippides factor and the diagnostic assessment of such runners for acute coronary syndromes are considered. Supported by NIH Grants PO1- DA14528, K05-DA00101, K05-DA0064.

Interleukin-6 Mediated Non-ischemic Injury To Cardiac Myocytes During Marathon Running

Since the fatal collapse of the legendary Pheidippides in 490 BC, mechanisms contributing to sudden cardiac death as shown to occur in 1 per 50,000 marathon runners during races are poorly understood. PURPOSE To explore the role of an acute inflammatory response to exertional rhabdomyolysis in the triggering of acute cardiac events. METHODS measurement of total creatine kinase, interleukin (IL)-6, C reactive protein (CRP), creatine kinase MB (CK-MB), cardiac troponin T (cTnT) and ischemia modified albumin (IMATM) by the albumin cobalt binding ACB ± TM Test in 46 asymptomatic middle-aged marathon runners before and sequentially after the 2001–02 Boston Marathons. RESULTS A 15-fold post-race rise in CK was accompanied by 40- and 20- fold increases in IL-6 and C-reactive protein respectively. There was a transient increase in cTnT to diagnostically indeterminate levels with no change in IMA by the ACB Test despite a 14-fold increase in CK-MB (Table 1).TableCONCLUSIONS These findings are consistent with non-ischemic injury to cardiomyocytes without necrosis perhaps due to IL-6 mediated leakage of cytosolic cTnT. Strategies for primary prevention of exertional cardiac events including the Pheidippides factor and the diagnostic assessment of such runners for acute coronary syndromes are considered. Supported by NIH Grants PO1- DA14528, K05-DA00101, K05-DA0064.

Myocardial Stress After Ultra-Endurance Running In Extreme Heat

The effects of prolonged exercise on cardiac muscle integrity and function are still more controversial and less well investigated than skeletal muscle damage. The Badwater Ultra, a 216 km race through Death Valley, CA, USA, might serve as an excellent model to further research cardiac muscle integrity and function under the conditions of prolonged exercise in temperatures up to 54°C. PURPOSE To investigate possible negative effects of prolonged, exhaustive exercise in extreme heat on the heart based on creatine kinase MB (CKMB) and cardiac troponin (cTnT) reflecting myocardial damage and nt-pro-brain natriuretic peptide (nt-proBNP) indicating cardiac dysfunction in experienced ultra-endurance runners. METHODS Venous blood samples were obtained from eight highly-trained male endurance athletes (median (P25 /P75 percentile): 54.5 (44.0 /59.25) yrs, 176 (170 /181) cm, 74.8 (69.8 /80.9) kg) before and after termination of the race. Creatine kinase (CK), CKMB, cTnT and nt-proBNP were measured. RESULTS Six runners finished the race within the time limit of 60 hours. One runner dropped out after approx.194 km (57 h) and the other after approx.85 km (16 h). Due to the exercise both, CK (136 (97.25 /215.25) vs. 2868 (531.0 /6883.5)U/L) and CKMB (11.5 (10.0 /12.75) vs. 66.0 (22.75 /109.5)U/L) showed a clear increase (p =0.012). The percentage of CKMB on total CK was unsuspicious (3.0 (1.7 /5.2)%) and cTnT remained below detectable level, whereas the nt-proBNP showed a significant increase (17.49 (12.39/30.48) vs. 317.95 (79.23 /339.35)ng/L, p =0.012) after the run. CONCLUSIONS Since cTnT remained unchanged following the ultra-endurance exercise in extreme heat the clear increase in CK and CKMB seems to be mainly attributed to skeletal muscle damage. However, the rise in nt-pro BNP may reflect a temporal, reversible left ventricular dysfunction. Supported by Limbach Laboratory, Heidelberg, Germany.

Increased creatine kinase MB level predicts postoperative mortality after cardiac surgery independent of new Q waves

Recent consensus statements recommend cardiac enzyme release as the essential criterion for diagnosing myocardial infarction. However, the outcome implications of cardiac enzyme release in patients undergoing coronary artery bypass grafting are controversial. Eight hundred patients were followed for 30 days after elective on-pump coronary artery bypass grafting in a multicenter, prospective, randomized trial of the anti-C5 complement antibody pexelizumab. Data from centralized electrocardiography and creatine kinase MB analyses were examined for any association with death or severe left ventricular dysfunction. More than half of the 800 patients had peak creatine kinase MB levels of more than 5 times the upper limit of 5 ng/mL set by the core laboratory. The median peak value was 29 ng/mL. The incidence of the combined outcome (death or severe left ventricular dysfunction) was 1.7% if the peak creatine kinase MB level was less than 25 ng/mL and 18.0% if 100 ng/mL or greater (P < .01). Similarly, the incidence of new Q-wave myocardial infarction was 3.9% if the peak creatine kinase MB level was less than 25 ng/mL and 30.6% if 100 ng/mL or greater (P < .01). In a multivariate analysis that included preoperative and intraoperative factors, as well as peak enzyme release and Q-wave myocardial infarction, the strongest predictor of the combined outcome was a peak creatine kinase MB level of 100 ng/mL or greater. New Q-wave myocardial infarction did not significantly predict the combined outcome. Increased postoperative peak creatine kinase MB level, especially when 20 times or more of the upper limit of normal, indicates increased risk of severe postoperative left ventricular dysfunction and mortality within 30 days of coronary artery bypass grafting. High peak enzyme level is a stronger predictor of adverse outcomes than is postoperative Q-wave myocardial infarction in this population.

Preprocedural plasma C-reactive protein levels, postprocedural creatine kinase-MB release, and long-term prognosis after successful coronary stenting (four-year results from the GENERATION study)

Increased creatine kinase-MB isoenzymes after coronary stenting are common, and many studies have suggested an association of this increase with an adverse long-term prognosis. How such postprocedural creatine kinase-MB release affects long-term prognosis remains unclear. Whether any actual causal relation exists remains unanswered.

Causes of acute renal dysfunction after percutaneous coronary intervention and comparison of late mortality rates with postprocedure rise of creatine kinase-MB versus rise of serum creatinine

Increases in both serum creatinine and creatine kinase-MB (CK-MB) after percutaneous coronary intervention are associated with increased risk for late adverse cardiovascular events. In 5,397 patients, the strength of the association of each with late events and the risk factors for each of these markers were compared. A postprocedural increase in creatinine was a more powerful predictor of late mortality than an increase in CK-MB. Risk factors for an increase in creatinine are similar to those for contrast-induced nephropathy, suggesting that vulnerability to such injury may identify patients with increased risk for late mortality.

Creatine kinase-myocardial band isoenzyme elevation after percutaneous coronary interventions using sirolimus-eluting stents

We evaluated predictors of increased periprocedural creatine kinase-MB isoenzyme levels after implantation of sirolimus-eluting stents with an intent to fully cover the diseased segment. The total stent length per patient (predisposing factor) and elective use of glycoprotein IIb/IIIa (protective factor) were independent predictors of increased creatine kinase-MB isoenzyme levels.

Myocardial Stress after Competitive Exercise in Professional Road Cyclists

Based on the determination of cardiac troponin (cTnT), brain natriuretic peptide (BNP), and echocardiographic measurements, recent investigations have reported myocardial damage and reversible cardiac dysfunction after prolonged endurance exercise in apparently healthy subjects. In the present study, we investigated the myocardial stress reaction in professional endurance athletes after strenuous competitive physical exercise. Eleven highly trained male professional road cyclists (age 27 +/- 4 yr; .VO2peak 67 +/- 5 mL.kg-1.min-1; training workload 34,000 +/- 2,500 km.yr-1) were examined. The following parameters were determined before and after one stage of a 5-d professional cycling race: BNP, cTnT (third-generation assay that shows no cross reactivity with skeletal TnT), creatine kinase (CK), creatine kinase MB (CKMB), myoglobin (Myo), and urea. All participants were submitted to a careful cardiac examination including echocardiography and stress ECG. None of the athletes showed pathological findings in the cardiac examination. CK (P < 0.01), CKMB (P < 0.05), and Myo (P < 0.01) were increased after the race. Normal postexercise cTnT levels indicate that the increase in CK, CKMB, and Myo was of noncardiac origin. In contrast, BNP rose significantly from 47.5 +/- 37.5 to 75.3 +/- 55.3 pg.mL-1 (P < 0.01). Pre- and postexercise values of BNP as well as the individual exercise-induced increase in BNP were significantly correlated with age (R2 = 0.68, R2 = 0.66, and R2 = 0.58, respectively; P < 0.05). Strenuous endurance exercise in professional road cyclists does not result in structural myocardial damage. The rise in BNP in older athletes may reflect a reversible, mainly diastolic left ventricular dysfunction. This needs to be confirmed by larger trials including different intensities, sports, and age groups.

Clinical significance of elevated troponin I levels in patients with nontraumatic subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage (SAH) is associated with electrocardiographic abnormalities, regional or focal wall-motion abnormalities on echocardiograms, and/or increased creatine kinase MB isoenzyme (CK-MB) or cardiac troponin I (cTnI). The goal of this prospective study was to compare the sensitivity and specificity of cTnI with those of CK-MB in the prediction of left ventricular dysfunction on echocardiograms in patients with nontraumatic SAH. In addition, those patients with abnormal findings on their echocardiograms and elevated cTnI levels were further evaluated for the presence of coronary artery disease (CAD) by a cardiologist and to determine whether any left ventricular dysfunction that had been detected was reversible. The authors obtained electrocardiograms and echocardiograms, and measured serial levels of cardiac enzymes (CK-MB and cTnI) in 43 patients with nontraumatic SAH. Patients with known CAD were excluded. Those patients found to have elevated enzyme levels and abnormal findings on their echocardiograms underwent additional evaluation for CAD. The sensitivity and specificity of both cTnI and CK-MB for detecting left ventricular function were determined. Twenty-eight percent of patients with SAH in the study had elevated cTnI levels within the first 24 hours after hemorrhage. Seven of the 12 patients had evidence of left ventricular dysfunction on echocardiograms. In all these patients a return to baseline function was found during follow-up examinations. The authors found that cTnI is much more sensitive than CK-MB (100% compared with 29%) in the detection of left ventricular dysfunction in patients with SAH. An elevated level of cTnI is a good indicator of left ventricular dysfunction in patients with SAH. In this study cardiac dysfunction was reversible and should not necessarily preclude these patients from undergoing operative interventions or becoming heart donors. Clinical management may require more aggressive hemodynamic monitoring until cardiac function returns to normal.

Cardiac troponin T and myocardial injury during routine cardiac catheterisation in children

Background: This study aims to investigate whether intracardiac catheterization produces myocardial damage on pediatric heart. Methods: Five blood samples were collected (basal, immediate post procedure, at 4, 12 and 24 h after the procedure) for troponin T and creatine kinase MB (CKMB) from 48 consecutive patients (age: 5.34±6.03 years). The effect of age, duration of procedure, pulmonary hypertension, cyanosis, and medication taken for congestive heart failure on the levels of troponin T and CKMB were sought. Results: The increase in CKMB (basal CKMB: 3.93±3.70 ng/ml; peak CKMB: 8.68±10.89 ng/ml; P<0.0001) and troponin levels (basal troponin: 0.002±0.003 ng/ml; peak troponin: 0.11±0.23 ng/ml; P<0.0001) over time was significant in the study group. Additionally younger patients (≤1 year), patients with pulmonary hypertension (mean pulmonary artery pressure >25 mmHg), longer procedure time (>30 min), and patients taking anti-congestive heart failure therapy had significantly higher levels of CKMB and troponin ( P>0.05). Conclusion: All patients undergoing cardiac catheterization are under risk of myocardial injury, and younger patients with pulmonary hypertension and especially with compensated cardiac failure have increased risk of myocardial damage, and need to be handled carefully.

Myocyte and endothelial effects of preconditioning the jeopardized heart by inhibiting Na+/H+ exchange

Objectives: The preconditioning effects of the adjunctive, cardiac-specific sodium-hydrogen ion exchange inhibitor cariporide (cariporide mesilate, HOE 642) were studied in hearts subjected to 30 minutes of normothermic ischemia and reperfusion to assess myocardial and endothelial changes. Methods: Sixteen Yorkshire-Duroc pigs (27-34 kg) receiving cardiopulmonary bypass underwent either cardiopulmonary bypass alone (control, n = 4) or 30 minutes of normothermic ischemia, followed by 30 minutes of blood reperfusion (n = 12). Six hearts were treated with 5 mg/kg cariporide administered intravenously 15 minutes before ischemia. Results: Cardiopulmonary bypass alone caused no changes. Conversely, 30 minutes of global normothermic ischemia caused 33% mortality and, in survivors, depression of left ventricular function to 22% ± 6% of baseline preload recruitable stroke work and increased creatine kinase MB by 406% (88 ± 13 U/L), conjugated dienes by 17% (161 ± 0.2 AU/mL), and myeloperoxidase activity by 297% (0.036 ± 0.005 U/g). Myocardial edema developed (3.5% water gain). Coronary sinus endothelin 1 increased by 111% (2.05 ± 0.38 pg/mL), and nitric oxide production decreased by 10%. These adverse effects were limited by pretreatment with cariporide, which allowed complete survival and restored preload recruitable stroke work to 78% ± 11%. Measurements of creatine kinase MB, conjugated dienes, myeloperoxidase, water, and endothelin 1 returned to baseline values, and nitric oxide production was accentuated 3-fold. Conclusions: These observations show that adjunctive pretreatment with cariporide delays myocardial and endothelial injury during ischemia and reperfusion, limits oxygen-derived radical injury, restores function, reduces edema, and preserves endothelin and nitric oxide balance at normal values. The myeloperoxidase changes show that less white blood cell adherence supports reduced reperfusion endothelial damage.J Thorac Cardiovasc Surg 2002;124:1113-21

Cardiovascular News

Cardiovascular News

Heparin-coated Wiktor stents in human coronary arteries (MENTOR Trial)

The purpose of this study was to determine the feasibility, safety, and efficacy of elective stenting with heparin-coated Wiktor stents in patients with coronary artery disease. In experimental studies, heparin coating has been shown to prevent subacute thrombosis and restenosis. Recently, a new method of heparin coating was developed, resulting in a more stable and predictable heparin layer on stent devices. This trial constitutes the first in-human use of this coating procedure, applied on the well-known Wiktor stent device. Heparin-coated Wiktor stent implantation was performed in 132 consecutive patients (132 lesions) in a multicenter international trial from September 1996 to February 1997. Forty-three percent of patients had unstable angina, 33% had previous myocardial infarction, and 10% had diabetes mellitus. Patients were followed for 12 months for occurrence of major adverse cardiovascular events, and 96% of the eligible patients underwent quantitative angiographic control at 6 months. Stent deployment was successful in 95.5% of lesions. Minimal lumen diameter increased by 1.67 ± 0.48 mm (from 1.02 ± 0.38 mm before to 2.69 ± 0.37 mm after the stent implantation). Mean percent diameter stenosis decreased from 67.4 ± 11.3% before to 18.9 ± 7.7% after the intervention. A successful intervention (<50% diameter stenosis and no major adverse cardiac events within 30 days) occurred in 97% of the patients. The subacute thrombosis rate was 0.8%, which compares favorably with historical controls of this stent, and a low incidence of postprocedural increase in creatine kinase-MB was noted. At 6 months, event-free survival was 85% and angiographic restenosis rate was 22% with late loss of 0.78 ± 0.69 mm and a loss index of 0.48 ± 0.44. Heparin-coated Wiktor stents appeared to be an efficacious device to treat Benestent-like lesions, yielding angiographic and clinical results comparable to a heparin-coated Palmaz-Schatz stent. Despite its use in more complex lesions, the incidence of subacute thrombosis appeared to be lower than historical controls with a similar noncoated stent.

Response to “Increased Creatine Kinase MB and Cardiac Troponin T with Normal Cardiac Troponin I in Metastatic Alveolar Rhabdomyosarcoma”

We wish to comment on the case reported recently by Isotalo et al. (1). Two different cardiac troponin I (cTnI) assays were used: the AxSYM (Abbott) and the Opus Plus (Dade Behring). The title of the letter claimed that the cTnI value was normal. This is not consistent with the data presented. The AxSYM values for cTnI of 1.2 (day 1), 0.8 (day 2), and 1.1 μg/L (2 weeks) are not normal. The limit of detection for the AxSYM is 0.3 μg/L, with a quoted upper reference limit of 0.4 μg/L and an acute myocardial infarction cutoff of 2.0 μg/L (2). The patient’s values fall within the range for detectable and prognostically significant myocardial damage. The main conclusion that Isotalo et al. (1) make is that the increased cardiac troponin T (cTnT) and creatine kinase MB (CK-MB) concentrations are the result of release from a non-cardiac source related to abnormal expression of these proteins. They did not perform experiments to detect evidence of abnormal cTnT or CK-MB expression in the tumor biopsy. Therefore, we fully agree with the authors that their conclusions were “speculative”. However, we disagree with their discussion. The authors clearly state that the patient had no biochemical evidence of renal failure. However, they go on to describe, in detail, the findings of three conflicting studies that discuss the issue of skeletal muscle expression of cTnT in uremic patients. The reference to these studies in this case presentation implies that the authors are making an association with the issues of cTnT in patients with renal failure. We believe this to be a tenuous link between their limited study and the subject of skeletal muscle expression of cTnT in renal failure. In addition, we feel that they have either misread or misinterpreted two of the references dealing with this … [↵][1]bAddress correspondence to this author at: Division of Biochemistry, Department of Laboratory Medicine, Ottawa Hospital–Civic Campus, 1053 Carling Ave., Ottawa, Ontario, Canada K1Y 4E9. Fax 613-761-5361; e-mail jdonnelly{at}civich.ottawa.on.ca [1]: #xref-corresp-2-1