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PubMed2005

Dual-isotope myocardial SPECT in patients with redefined myocardial infarction.

BACKGROUND: According to the redefinition of myocardial infarction (MI) by the ESC/ACC Committee, patients with unstable angina (UA) without significant elevation of creatine kinase (CK) but with elevation of troponin T should be diagnosed as MI. METHODS: One hundred and forty-six consecutive patients formerly diagnosed as UA, with peak CK levels 0.10 ng/ml). Dual SPECT findings were analyzed qualitatively and quantitatively in blinded manner. RESULTS: Forty-seven patients (32%) were redefined as MI and 99 patients (68%) were redefined as UA. On admission, there were small but statistically significant elevations in laboratory parameters such as white blood cell count, C-reactive protein, CK and CK-MB in the redefined MI group compared with the redefined UA group. The proportion of patients with perfusion and metabolic abnormalities was significantly higher in the redefined MI group (Tl defect 36% vs. 4%, odds ratio: 13.5, p<0.001; BMIPP defect 64% vs. 23%, odds ratio: 5.8, p<0.001). Semi-quantitative evaluation revealed that the total Tl and BMIPP scores were significantly higher in the redefined MI patients (p<0.001). CONCLUSIONS: In the redefined MI patients, perfusion and metabolic abnormalities occurred frequently and more extensively. However, Tl/BMIPP dual SPECT had limited ability to detect minor myocardial infarcts classified as redefined MI. A more sensitive stratification combined with troponin T directed assignment should be established to incorporate the ongoing minor infarcts which could not be assessed by serial dual-scintigraphic evaluations.

Aged↗
PubMed2006

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.

Aged↗
PubMed2006

Impact of redefining acute myocardial infarction on incidence, management and reimbursement rate of acute coronary syndromes.

BACKGROUND: Although redefinition for acute myocardial infarction (AMI) has been proposed few years ago, to date it has not been universally adopted by many institutions. The purpose of this study is to evaluate the diagnostic, prognostic and economical impact of the new diagnostic criteria for AMI. METHODS: Patients consecutively admitted to the emergency department with suspected acute coronary syndromes were enrolled in this study. Troponin T (cTnT) was measured in samples collected for routine CK-MB analyses and results were not available to physicians. Patients without AMI by traditional criteria and cTnT > or = 0.035 ng/mL were coded as redefined AMI. Clinical outcomes were hospital death, major cardiac events and revascularization procedures. In-hospital management and reimbursement rates were also analyzed. RESULTS: Among 363 patients, 59 (16%) patients had AMI by conventional criteria, whereas additional 75 (21%) had redefined AMI, an increase of 127% in the incidence. Patients with redefined AMI were significantly older, more frequently male, with atypical chest pain and more risk factors. In multivariate analysis, redefined AMI was associated with 3.1 fold higher hospital death (95% CI: 0.6-14) and a 5.6 fold more cardiac events (95% CI: 2.1-15) compared to those without AMI. From hospital perspective, based on DRGs payment system, adoption of AMI redefinition would increase 12% the reimbursement rate [3552 Int dollars per 100 patients evaluated]. CONCLUSIONS: The redefined criteria result in a substantial increase in AMI cases, and allow identification of high-risk patients. Efforts should be made to reinforce the adoption of AMI redefinition, which may result in more qualified and efficient management of ACS.

Acute Disease↗
PubMed2005

C-reactive protein in patients with acute coronary syndrome: correlation with diagnosis, myocardial damage, ejection fraction and angiographic findings.

BACKGROUND: C-reactive protein (CRP) plasmatic levels increase in patients with acute coronary syndromes (ACS). Correlations between CRP levels, myocardial functional damage and cardiomyocyte lysis remain to be defined. METHODS: 192 consecutive patients with acute coronary syndromes (64.97 +/- 11.08 mean age, 71.35% male gender) were included in the study; 138 patients (71.87%) were discharged with an acute myocardial infarction (AMI) diagnosis (28 with non Q-wave AMI) and 54 with an unstable angina (UA) diagnosis (28.13%). In all patients CRP, CK, LDH, CK-MB and troponin I plasmatic concentrations were evaluated every 6 h for 48 h and every 24 h for the following 2 days from the onset of symptoms. Ejection fraction was estimated by bidimensional echocardiography and extension of myocardial lysis by cardiac enzymes plasmatic release. 92 patients (67 with AMI, 25 with UA) underwent coronary-angiography. Incidence of adverse cardiac events was recorded in a 6 months follow up. RESULTS: Mean CRP levels in Q-wave MI showed a statistically significant increase in the different blood samples with baseline. Mean CRP levels of the three groups were not statistically different at baseline and after 6, 12, and 18 h. Q-wave AMI CRP levels showed a statistically significant difference as against non Q-wave AMI at 36 (p < 0.05), 48 (p < 0.05) and 72 h (p < 0.05) and UA at 24 (p < 0.01), 30 (p < 0.01), 48 (p < 0.0001), 72 (p = 0.0001) and 96 h (p = 0.0003); non Q-wave AMI CPR levels showed a statistically significant difference as against UA at 48 h (p < 0.01). CRP peak mean levels were significantly different when comparing Q-wave AMI patients with UA patients (8.21 +/- 7.85 vs. 2.75 +/- 3.33 mg/dl, p < 0.001). In patients with Q-wave AMI there was a correlation between CRP peak concentrations and CK (r = 0.264, p = 0.008) and LDH (r = 0.32, p = 0.001), while correlation with CK-MB peak concentrations was not statistically significant (r = 0.196, p = 0.051). In the same patient group, there was also a correlation between CRP plasmatic concentrations and troponin I plasmatic concentrations from the 30th to 96th h after the onset of symptoms (r = 0.38-0.53, p < 0.05). No correlation was found between CRP levels and ejection fraction and angio-coronarography findings (number of stenotic vessels, culprit lesions, ruptured plaques). Peak CRP levels were associated in a 6 months follow up with an increased incidence of major adverse cardiac events (MACEs) in patients with Q-wave AMI (HR 1.1649, 95% C.I. 1.0197-1.3307, p < 0.05). CONCLUSIONS: CRP plasmatic concentrations showed a different release curve in patients with Q-wave AMI in comparison with patients with non Q-wave AMI and with patients with UA. CRP peak concentrations did not correlate with ejection fraction and angiographic findings, but correlate with incidence of MACE. The increase in CRP levels during Q-wave MI seems to be linked to the extension of myocardial damage rather than pre-existing inflammation.

Acute Disease↗
PubMed2005

Comparison of clinical and angiographic features and longterm follow-up events between patients with variant angina and patients with ST elevation myocardial infarction.

We investigated to what extent patients with variant angina and significant coronary stenosis (>or=70%) present a clinical and angiographic profile similar to patients with ST elevation myocardial infarction. Thus, the clinical and angiographic features as well as follow-up events of 200 patients were prospectively analyzed and were compared with those of 422 patients with a first ST elevation myocardial infarction survivors of the early phase (3 days) and those of 70 patients with variant angina and non significant stenosis. Age and incidence of smoking, systemic hypertension, diabetes and maximum ST elevation were similar in the 2 groups. Furthermore, among patients with significant coronary stenosis, stenosis severity and the proportion of eccentric lesions were also comparable. Incidence of recent-within 30 days prior to admission-angina at rest was higher in variant angina patients with significant stenosis (67% vs. 27%, p<0.001) than in those with myocardial infarction but long standing angina at rest (>30 days) was low and comparable in these 2 groups (15% vs. 11%, ns). Also, in a 5-year follow-up most patients from these 2 groups were free from angina at rest (86% vs. 84%) which in variant angina patients was largely attributable to a high revascularization rate (72%). Moreover, the rate of myocardial infarction/cardiac death (20% vs. 19%) was also similar. Patients with variant angina and non-significant stenosis, however, had longer antecedent angina, more frequent follow-up angina and a lower incidence of cardiac events than the other 2 groups. Thus, these findings suggest that patients with variant angina and significant coronary stenosis generally behave as an acute coronary syndrome-likely associated with an acutely complicated plaque-rather than as recurrent vasospastic angina, and should be managed accordingly.

Angina Pectoris↗
PubMed2006

Soluble CD40 ligand and interleukin-6 in the coronary circulation after acute myocardial infarction.

BACKGROUND: Inflammation, operated by blood, vascular and immune cells interaction, is implicated in plaque disruption and CD40 ligand (CD40L) was identified on activated T cells and platelets. We sought to investigate the roles of local inflammation in acute myocardial infarction (AMI). METHODS: Coronary sinus (CS) and arterial (A) levels of interleukin (IL)-6 and soluble CD40L (sCD40L) and matrix metalloproteinase (MMP)-9 activity in serial blood samples obtained until 48 h after percutaneous coronary intervention (PCI) were determined. In tissue specimens obtained by aspirating thrombectomy and directional coronary atherectomy, CD40L was immunohistochemically stained. RESULTS: Trans-cardiac gradient (CS-A) of IL-6, indicating cardiac release into the coronary circulation, significantly increased at 24 h after PCI in patients with AMI (group MI, n=17) in contrast with angina pectoris (n=10). Soluble CD40L levels in CS showed earlier peak, yielding trans-cardiac gradient, at 9 h in both groups. The maximum (max) release of IL-6 in MI, but not sCD40L, positively correlated with end-diastolic volume index (R=0.84) and negatively with ejection fraction (R=-0.66) by contrast ventriculography at 6-month follow up. Immunohistological study revealed the expression of CD40L in intra-coronary occlusive and mural thrombi. Aspirating thrombectomy significantly reduced the increase in both sCD40L levels and MMP-9 activity, but not max IL-6 release in MI. CONCLUSIONS: In contrast with myocardial injury represented by IL-6 release, acute rise in sCD40L levels with the MMP-9 activation in the coronary circulation may possibly reflect local inflammation with platelet activation and be a novel marker of plaque damage by PCI.

Aged↗
PubMed2006

Evaluation of post-radiofrequency myocardial injury by measuring cardiac troponin I levels.

BACKGROUND: The aim of this study was to investigate the extent of myocardial injury created by radiofrequency (RF) ablation. We assessed the changes in levels of cardiac biochemical markers in patients who underwent RF ablation and we sought to evaluate the utility of cardiac troponin I (cTnI) in detecting minor myocardial injury following RF ablation and determine its procedural correlates. METHODS: We analyzed the data of 115 consecutive patients who underwent RF ablation. The target sites of RF ablation were slow pathway in 56, left atrioventricular (AV) annulus in 31, right AV annulus in 14, atrial wall in 3, ventricular wall in 6 and AV node in 3 patients. The levels of creatine kinase (CK), CK-MB, cTnI and myoglobin were compared with procedural data and targeted arrhythmia. RESULTS: Post-RF ablation the concentration of cTnI, CM-MB, CK and myoglobin were significantly different than those of the initial sample. The mean and peak cTnI levels were raised above normal in 63 patients (54.8%). Mean levels of cTnI correlated with the site of RF ablation, being significant for slow pathway ablation, ventricular tachycardia and left AV annulus. We also found a significant association of mean CK-MB, CK levels and left AV annulus. CONCLUSION: Our results indicate that radiofrequency ablation results in only minor injury. This marker is effective for detection of RF current induced myocardial injury. Lesions applied to the mitral annulus at the ventricular endocardium are associated with significantly greater myocardial damage.

Adolescent↗
PubMed2006

Combination of electrocardiographic and angiographic markers of reperfusion in the prediction of infarct size in patients with ST-segment elevation myocardial infarction undergoing successful primary angioplasty.

BACKGROUND: Optimal epicardial recanalization does not guarantee optimal myocardial perfusion. The aim of the current study was to evaluate angiographic and electrocardiographic markers of reperfusion in the prediction of infarct size in patients with STEMI undergoing successful primary angioplasty. METHODS: Our population is represented by 270 STEMI patients with ST successful primary angioplasty (postprocedural TIMI 3 flow and residual stenosis <50%) with available corrected TIMI frame count (cTFC), myocardial blush grade (MBG), ST-segment resolution and enzymatic infarct size (peak CK-MB) analyses. RESULTS: A significant linear relationship with enzymatic infarct size was observed for all markers of reperfusion, except for ST-segment resolution. These data were confirmed even when analyzed as continuous variables in case of cTFC (r=0.13, p=0.035), postprocedural residual cumulative ST-segment elevation (r=0.41, p<0.0001) and deviation (r=0.45, p<0.0001). At multivariate analysis applied to postprocedural angiographic and electrocardiographic markers of reperfusion, cumulative residual ST-segment deviation, myocardial blush grade, and corrected TIMI frame count were independent predictors of enzymatic infarct size. CONCLUSIONS: This study showed that, among patients with STEMI treated by primary angioplasty, cTFC, MBG and cumulative residual ST-segment deviation are independent predictors of infarct size. Therefore, angiography and electrocardiography may provide complementary information in the evaluation of myocardial perfusion.

Aged↗
PubMed2006

A study comparing the incidence and predictors of creatine kinase MB and troponin T release after coronary angioplasty. Does Clopidogrel preloading reduce myocardial necrosis following elective percutaneous coronary intervention?

BACKGROUND: To investigate the incidence and associated factors for enzyme release following percutaneous coronary intervention comparing assessment with creatine kinase MB (CK-MB) and troponin T (TnT). METHOD: TnT and CK-MB were measured post procedure in a consecutive series of 933 patients undergoing elective percutaneous coronary intervention between 1/4/2003 and 1/5/2004 at a single regional cardiac centre. RESULTS: CK-MB level significantly correlated to TnT levels (R=0.747, p<0.001) and a CK-MB level of above 3 times the upper limit of the local reference range (>3 x ULN) was predicted with 95% sensitivity (48% specificity) at a TnT level of 0.11. Multivariate predictors of >3 x ULN CK-MB release for uncomplicated percutaneous coronary intervention (n=898) were multi-vessel angioplasty (OR=2.51, 95% CI=1.57 to 4.01; p<0.001), saphenous venous graft angioplasty (OR=5.5, 95% CI=1.94 to 13.00; p=0.005) and lack of Clopidogrel preloading (OR=2.02, 95% CI=1.30 to 4.38; p=0.027). CONCLUSIONS: TnT was found to be a sensitive although not a highly specific marker of CK-MB release. In this study a TnT level above a threshold of 0.11 would identify 95% of the prognostically important 3-fold CK-MB releases. Replacing the >3 x ULN CK-MB threshold with a TnT level of 0.1 ng/l following percutaneous coronary intervention would increase the apparent rate of myocardial infarction from 11% to 20%. Lack of Clopidogrel preloading was independently associated with a >3 x ULN CK-MB release following uncomplicated elective percutaneous coronary intervention.

Angioplasty, Balloon, Coronary↗
PubMed2006

Pre-hospital detection of acute myocardial infarction with ultra-rapid human fatty acid-binding protein (H-FABP) immunoassay.

AIMS: To evaluate the diagnostic performance of a portable semi-quantitative whole blood immunoassay measuring soluble human fatty acid-binding protein [H-FABP] (CardioDetect) for the pre-hospital detection of myocardial infarction (MI). METHODS AND RESULTS: We enrolled prospectively 108 consecutive patients with acute ischemic type chest pain in whom the first medical care was delivered by a mobile intensive care unit (MICU). CTnI, myoglobin, CK-MB and CardioDetect were first assessed in the MICU before hospital admission using point-of-care assays and then cTnI was serially measured during the hospital stay. MI was defined as a positive cTnI in any sample over the first 24 h. The vast majority of the patients (77/108) were admitted <3 h of symptoms onset. Pre-hospital cTnI sample was normal in 96 patients (88.9%) of whom 43 had subsequent cTnI elevation. A positive H-FABP using the CardioDetect assay had a significantly better sensitivity than cTnI, myoglobin and CK-MB (87.3% vs 21.8%, 64.2% and 41.5%, respectively) to identify MI. The significant better sensitivity of the CardioDetect assay was also observed among patients who presented <3 h of symptom onset. The specificity of the CardioDetect assay was significantly better than that of myoglobin, irrespective of the time delay from symptom onset to measurement. In patients with normal pre-hospital cTnI and no ST-elevation (n=63), assessment based only on a positive H-FABP had 83.3% sensitivity, 93.3% specificity for the diagnosis of an evolving MI. CONCLUSION: Early assessment of H-FABP in patients presenting with chest pain improves the diagnosis of ongoing MI.

Aged↗
PubMed2003

Cardiac troponin I in acute pericarditis.

OBJECTIVES: This study was designed to investigate the prognostic value of cardiac troponin I (cTnI) in viral or idiopathic pericarditis. BACKGROUND: Idiopathic acute pericarditis has been recently reported as a possible cause of nonischemic release of cTnI. The prognostic value of this observation remains unknown. METHODS: We enrolled 118 consecutive cases (age 49.2 +/- 18.4 years; 61 men) within 24 h of symptoms onset. A highly sensitive enzymoimmunofluorometric method was used to measure cTnI (acute myocardial infarction [AMI] threshold was 1.5 ng/ml). RESULTS: A cTnI rise was detectable in 38 patients (32.2%). The following characteristics were more frequently associated with a positive cTnI test: younger age (p < 0.001), male gender (p = 0.007), ST-segment elevation (p < 0.001), and pericardial effusion (p = 0.007) at presentation. An increase beyond AMI threshold was present in nine cases (7.6%), with an associated creatine kinase-MB elevation, a release pattern similar to AMI, and echocardiographic diffuse or localized abnormal left ventricular wall motion without detectable coronary artery disease. After a mean follow-up of 24 months a similar rate of complications was found in patients with a positive or a negative cTnI test (recurrent pericarditis: 18.4 vs. 18.8%; constrictive pericarditis: 0 vs. 1.3%, for all p = NS; no cases of cardiac tamponade or residual left ventricular dysfunction were detected). CONCLUSIONS: In viral or idiopathic acute pericarditis cTnI elevation is frequently observed and commonly associated with young age, male gender, ST-segment elevation, and pericardial effusion at presentation. cTnI increase is roughly related to the extent of myocardial inflammatory involvement and, unlike acute coronary syndromes, is not a negative prognostic marker.

Acute Disease↗
PubMed2003

Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery.

OBJECTIVES: The aim of this study was to determine the long-term prognosis with postoperative markers of myocardial ischemia and infarction. BACKGROUND: Cardiac troponins (cTn) are superior to creatine kinase-MB fraction (CK-MB) in detecting perioperative myocardial infarction (PMI). However, their threshold levels signifying PMI and their long-term prognostic value are not yet determined. METHODS: A cohort of 447 consecutive patients who underwent 501 major vascular procedures was prospectively studied. Perioperative continuous 12-lead electrocardiogram monitoring, cardiac troponin-I (cTn-I) and/or cardiac troponin-T (cTn-T), and CK-MB levels on the first three postoperative days, and long-term survival were determined. The association of different cutoff levels of CK-MB, troponin, and ischemia duration with long-term survival was investigated. RESULTS: Between 14 (2.9%) and 107 (23.9%) of the patients sustained PMI, depending on the biochemical criteria used. Elevated postoperative CK-MB, cTn, and prolonged (>30 min) ischemia, at all cutoff levels examined, predicted long-term mortality independent of the preoperative predictors: patient's age, type of vascular surgery, previous myocardial infarction, and renal failure (Cox multivariate analysis). Both CK-MB >10% and cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml independently predicted a 3.75-fold and 2.06-fold increase in long-term mortality (p = 0.006 and 0.012, respectively). Similarly, both CK-MB >5% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml independently predicted a 2.15-fold and 1.89-fold increase in mortality (p = 0.018 and 0.01, respectively). Patients with both these markers elevated had a 4.19-fold increase in mortality (p < 0.001). CONCLUSIONS: Postoperative CK-MB and troponin, even at low cutoff levels, are independent and complementary predictors of long-term mortality after major vascular surgery.

Adult↗
PubMed2003

Increased CK-MB release is a "trade-off" for optimal stent implantation: an intravascular ultrasound study.

OBJECTIVES: We sought to determine the impact of aggressive stent expansion on creatine kinase-MB isoenzyme (CK-MB) release and clinical restenosis. BACKGROUND: Elevation of CK-MB after percutaneous coronary interventions has been associated with late mortality. METHODS: We identified 989 consecutive patients who underwent intravascular ultrasound-guided stenting of 1,015 coronary lesions. Patients were divided into three groups according to stent expansion, defined as the ratio of final lumen over the reference lumen cross-sectional areas: Group 1 (ratio <70%, n = 117 patients with 126 lesions); Group 2 (ratio 70% to 100%, n = 551 patients with 562 lesions); Group 3 (ratio >100%, n = 321 patients with 327 lesions). RESULTS: The peak CK-MB values increased significantly with increasing stent expansion: CK-MB = 3 to 5x normal occurred 16%, 18%, and 25% in Groups 1, 2, and 3, respectively, p = 0.02; CK-MB >5 times normal occurred 9%, 13%, and 16% respectively, p = 0.02. Conversely, at one year follow-up there was a stepwise decrease in target lesion revascularization (11% vs. 19% and 17%, respectively, p = 0.04) and major adverse cardiac events with increasing stent expansion. In addition, there was a trend toward lower mortality in Group 3 (9% vs. 4.4% vs. 4.0%, p = 0.07). CONCLUSIONS: Intravascular ultrasound-guided stent overexpansion (final lumen greater than reference lumen cross-sectional area) is accompanied by a higher periprocedural CK-MB release but a lower target lesion revascularization and a trend toward lower mortality at one year. Increased periprocedural CK-MB release appears as a trade-off for optimal stent implantation and lower clinical restenosis.

Cineangiography↗
PubMed2004

Treatment of multivessel coronary artery disease with sirolimus-eluting stent implantation: immediate and mid-term results.

OBJECTIVES: This study evaluated clinical outcome after multivessel stenting with sirolimus-eluting stents (SES) in unselected lesions. BACKGROUND: Safety and effectiveness of multivessel SES implantation is currently unknown. METHODS: Major adverse cardiac events (MACE) (death, myocardial infarction [MI], and repeat revascularization) were analyzed at 30 days and at 6 months after multivessel SES implantation. RESULTS: In 155 consecutive patients, 573 SES were implanted in 3.3 +/- 1.3 lesions per patient. At 30 days, the cumulative MACE rate was 10.3%: 7.1% patients developed a non-Q-wave MI, 1.9% developed a Q-wave MI, 0.6% died for non-cardiac reasons, and 0.6% had a repeat revascularization. Clinical follow-up was obtained in all 112 eligible patients treated for 359 lesions at a mean time of 6.5 +/- 2.2 months. The cumulative MACE rate was 22.3%: 3 (2.7%) deaths (1 for cardiac reasons), 4 (3.6%) MIs, target lesion revascularization (TLR) in 16 (14.3%) patients with 24 (6.7%) lesions. Target vessel revascularization was required in 18 (16.1%) patients due to TLR of lesions treated with SES or to disease progression (1.8% of patients). Cox regression analysis revealed total stent length per patient as the most powerful independent predictor of MACE. Overall stent thrombosis occurred in three (1.9%) patients. CONCLUSIONS: Multivessel SES implantation can be safely performed on patients with complex coronary artery disease. The need for revascularization increases because of the cumulative effect of TLR on patients with multiple lesions.

Aged↗
PubMed2004

Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment.

OBJECTIVES: We sought to investigate the effect of aspirin resistance on the incidence of myonecrosis after non-urgent percutaneous coronary intervention (PCI) among patients pretreated with clopidogrel. BACKGROUND: Oral antiplatelet therapy using aspirin and a thienopyridine is the standard of care for preventing thrombotic complications of PCI. The effect of aspirin resistance on the outcomes of patients undergoing PCI is unknown. METHODS: We used the Ultegra Rapid Platelet Function Assay-ASA (Accumetrics Inc., San Diego, California) to determine aspirin responsiveness of 151 patients scheduled for non-urgent PCI. All patients received a 300-mg loading dose of clopidogrel >12 h before and a 75-mg maintenance dose in the morning of the PCI. The incidence of myonecrosis was measured by creatine kinase-myocardial band (CK-MB) and by troponin I (TnI) elevations after PCI. RESULTS: A total of 29 (19.2%) patients were noted to be aspirin-resistant. There was a significantly higher incidence of female subjects in the aspirin-resistant versus aspirin-sensitive groups. The incidence of any CK-MB elevation was 51.7% in aspirin-resistant patients and 24.6% in aspirin-sensitive patients (p = 0.006). Elevation of TnI was observed in 65.5% of aspirin-resistant patients and 38.5% of aspirin-sensitive patients (p = 0.012). Multivariate analysis revealed aspirin resistance (odds ratio [OR] 2.9; 95% confidence interval [CI] 1.2 to 6.9; p = 0.015) and bifurcation lesion (OR 2.8; 95% CI 1.3 to 6.0; p = 0.007) to be independent predictors of CK-MB elevation after PCI. CONCLUSIONS: Despite adequate pretreatment with clopidogrel, patients with aspirin resistance as measured by a point-of-care assay have an increased risk of myonecrosis following non-urgent PCI.

Aged↗