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Manel Sabaté

Publications and source records attributed to Manel Sabaté.

At least 37 records · Page 2Linked to original sources
PubMed2005

Lack of association between the P2Y12 receptor gene polymorphism and platelet response to clopidogrel in patients with coronary artery disease.

INTRODUCTION: Clopidogrel inhibits the ADP subtype P2Y(12) receptor. Recently, polymorphisms of this receptor have been associated with different degrees of platelet aggregation in healthy volunteers and have been suggested to modulate clopidogrel response. However, the role of gene sequence variations of the P2Y(12) receptor in patients treated with clopidogrel has not yet been assessed. MATERIALS AND METHODS: The T744C polymorphism of the P2Y(12) receptor gene was assessed in 119 patients: 36 undergoing coronary stenting receiving a 300 mg loading dose (Group A) and 83 on long-term clopidogrel (75 mg/day) treatment (Group B). Patients were divided into 2 subgroups according to the presence or absence of the C allele: carriers (CT heterozygotes and CC homozygotes) and non-carriers (TT homozygotes). Platelet aggregation, assessed by light transmittance aggregometry following ADP, collagen, TRAP and epinephrine stimuli, and platelet activation (GP IIb/IIIa activation and P-selectin expression), assessed by whole blood flow cytometry in ADP and TRAP-stimulated platelets, were performed. Platelet function was assessed at baseline and 4 and 24 h following clopidogrel loading dose in Group A and when patients where on clopidogrel treatment for at least 1 month in Group B. RESULTS: The genotype distribution of Group A was: 22/36 (61.1%) non-carriers and 14/36 (38.9%) carriers of the C allele; Group B: 57/83 (68.7%) non-carriers and 26/83 (31.3%) carriers of the C allele. There were no differences between groups for all the assessed platelet function assays. CONCLUSIONS: The T744C polymorphism of the P2Y(12) receptor gene does not modulate platelet response to clopidogrel either in the early or long-term phases of treatment. This specific gene polymorphism alone is therefore unlikely to be the cause of variability in individual response to antiplatelet therapy.

Aged↗
PubMed2005

Drug-eluting stent thrombosis: results from a pooled analysis including 10 randomized studies.

OBJECTIVES: We compared the risk of stent thrombosis (ST) after drug-eluting stents (DES) versus bare-metal stents (BMS), and tested the hypothesis that the risk of DES thrombosis is related to stent length. BACKGROUND: Whether DES increase the risk of ST remains unclear. Given the very low restenosis rate after drug-eluting stenting, longer stents are frequently implanted for the same lesion length in comparison to BMS. METHODS: We included in a meta-analysis 10 randomized studies comparing DES and BMS. Overall, 5,030 patients were included (2,602 were allocated to DES and 2,428 to BMS). The risk of thrombosis after DES versus BMS was compared, and the relationship between the rate of DES thrombosis and stent length was evaluated. RESULTS: Incidence of ST was not increased in patients receiving DES (0.58% vs. 0.54% for BMS; odds ratio: 1.05; 95% confidence interval [CI]: 0.51 to 2.15; p = 1.000). The overall rate of ST did not differ significantly between patients receiving sirolimus- or paclitaxel-eluting stents (0.57% vs. 0.58%; p = 1.000). We found a significant relation between the rate of ST and the stented length (Y = -1.455 + 0.121 X; 95% CI for beta: 0.014 to 0.227; R = 0.716; p = 0.031). In patients with DES, mean stented length was longer in those suffering ST (23.4 +/- 8.1 mm vs. 21.3 +/- 4.1 mm, p = 0.025). CONCLUSIONS: Drug-eluting stents do not increase the risk of ST, at least under appropriate anti-platelet therapy. The risk of ST after DES implantation is related to stent length.

Antibiotics, Antineoplastic↗
PubMed2005

Repeat stenting for the prevention of the early lumen loss phenomenon in patients with in-stent restenosis. Angiographic and intravascular ultrasound findings of a randomized study.

BACKGROUND: Early lumen loss (ELL) may be detected in patients undergoing coronary interventions for in-stent restenosis. This phenomenon may contribute to recurrences. This prospective, randomized study was designed to determine if repeat stent implantation may prevent ELL in patients with in-stent restenosis. METHODS: Forty patients were randomized: 20 were allocated to elective stent implantation and 20 to conventional balloon angioplasty. Quantitative coronary angiography and intravascular ultrasound (IVUS) volumetric studies were systematically performed (1) before the procedure, (2) immediately after intervention, and (3) 30 to 60 minutes later. RESULTS: Baseline characteristics were similar in both groups. After the delay time interval (46 +/- 8 minutes), quantitative coronary angiography revealed a significant reduction in minimal lumen diameter (2.2 +/- 0.5 mm vs 1.7 +/- 0.5 mm, P < .001) in the balloon angioplasty arm. Likewise, in this group, IVUS demonstrated a reduction in mean lumen area (7.1 +/- 2 mm2 vs 6.2 +/- 2 mm2 , P < .001) and lumen volume (144 +/- 59 mm3 vs 126 +/- 54 mm3 , P < .001). In 4 of these patients, ELL was severe enough to require further intervention. In the stent arm, however, angiographic data and IVUS mean lumen area (7.7 +/- 3 mm2 vs 7.7 +/- 3 mm2) and lumen volume (161 +/- 72 mm3 vs 160 +/- 69 mm3) remained unchanged after the delay time interval. On multivariate analysis, stent implantation was an independent predictor of the absence of ELL by quantitative coronary angiography and by IVUS. In addition, patients with a larger ELL on IVUS had a lower event-free survival at 1 year (40% vs 79%, log rank P = .003). CONCLUSIONS: This randomized study demonstrates that (1) ELL is frequently detected after treatment of in-stent restenosis with balloon angioplasty, that (2) ELL influences the long-term clinical outcome of these patients, and that (3) repeat stent implantation prevents ELL.

Aged↗
PubMed2005

Identification of low responders to a 300-mg clopidogrel loading dose in patients undergoing coronary stenting.

BACKGROUND: Although patients undergoing coronary stenting routinely receive dual antiplatelet treatment to reduce the risk of stent thrombosis, this undesired event still occurs. A suboptimal response to clopidogrel treatment (low responders) has been suggested to contribute to stent thrombosis. In the present study, platelet function profiles were assessed in patients undergoing coronary stenting receiving a standard 300-mg clopidogrel loading dose with the aim to identify low clopidogrel responders. MATERIALS AND METHODS: Platelet aggregation was assessed by light transmittance aggregometry following 6 microM ADP stimuli in 48 patients before and 10 min, 4 and 24 h after receiving clopidogrel front-loading. Patients having > or =40% inhibition of platelet aggregation 24 h after clopidogrel administration were defined as normal responders, whereas those having <40% inhibition were low responders. Glycoprotein (GP) IIb/IIIa activation and P-selectin expression were assessed by whole blood flow cytometry following 2 microM ADP stimuli at the same time points. Platelet function profiles were compared between normal and low clopidogrel responders. RESULTS: Twenty-seven patients (56%) were normal responders and 21 (44%) low responders. Baseline GP IIb/IIIa activation was higher in low responders (74.6+/-16.6% vs. 58.2+/-24.5%, p=0.03). Although GP IIb/IIIa activation reduced following clopidogrel front-loading in both groups, it remained increased among low responders at 24 h (58.6+/-21.3% vs. 40.2+/-28.7%, p=0.05) and during the overall study time course (p=0.02). There were no differences in P-selectin expression. CONCLUSIONS: A considerable proportion of patients have an early suboptimal response to a 300-mg clopidogrel loading dose. An increased GP IIb/IIIa activation before intervention may identify this group of patients suggesting the use of a more aggressive antithrombotic treatment in these individuals.

Aged↗
PubMed2005

Percutaneous coronary revascularization in diabetics: from balloon angioplasty to drug-eluting stents.

Diabetic patients may have aggressive coronary disease with an excessive rate of restenosis and accelerated atherosclerotic progression. This article reviews the different modalities of percutaneous treatment and their results in the diabetic population, from the early days of balloon angioplasty to the current implementation of drug-eluting stents. As restenosis may be virtually eradicated in the near future, plaque progression remains the cornerstone for interventional cardiologists and the medical community. In this regard, attempts to modify life habits, and a more accurate control of the components of the metabolic syndrome should be the main therapeutic objective.

Angioplasty, Balloon, Coronary↗
PubMed2005

Platelet function profiles in patients with type 2 diabetes and coronary artery disease on combined aspirin and clopidogrel treatment.

To assess platelet function profiles in diabetic and nondiabetic patients on aspirin and clopidogrel therapy, two patient populations were included to investigate the 1) acute effects of a 300-mg clopidogrel loading dose (group 1, n = 52) and 2) long-term effects of clopidogrel (group 2, n = 120) on platelet function in diabetic compared with nondiabetic patients already on aspirin treatment. Patients were stratified according to the presence of type 2 diabetes. Platelet aggregation was assessed using light transmittance aggregometry (groups 1 and 2). Platelet activation (P-selectin expression and PAC-1 binding) was determined using whole-blood flow cytometry (group 2). Clopidogrel response was also assessed. In group 1, platelet aggregation was significantly increased in diabetic (n = 16) compared with nondiabetic (n = 36) patients at baseline and up to 24 h following a 300-mg loading dose (P = 0.005). In group 2, platelet aggregation and activation were increased in diabetic (n = 60) compared with nondiabetic (n = 60) subjects (P < 0.05 for all platelet function assays). Diabetic subjects had a higher number of clopidogrel nonresponders (P = 0.04). Diabetic patients have increased platelet reactivity compared with nondiabetic subjects on combined aspirin and clopidogrel treatment. Reduced sensitivity to antiplatelet drugs may contribute to the increased atherothombotic risk in diabetic patients.

Aged↗
PubMed2005

Long-term outcome of patients with proximal left anterior descending coronary artery in-stent restenosis treated with a second percutaneous procedure.

Patients with in-stent restenosis involving the proximal segment of the left anterior descending coronary artery are frequently sent for surgical revascularization. We studied the long-term (3.3 +/- 2.8 years) outcome of 123 patients with in-stent restenosis involving the proximal left anterior descending coronary artery who were treated with a second percutaneous procedure. Cumulative survival rate, probability of being alive and free from surgical revascularization, and probability of being alive and free from new revascularization procedures was 98.3 +/- 1.2%, 92.8 +/- 2.5%, and 82.2 +/- 3.6% at 1 year, and 95.2 +/- 2.5%, 88.5 +/- 3.4%, and 76.9 +/- 4.3% at 3 years, respectively. Thus, in patients with in-stent restenosis involving the proximal left anterior descending artery, a second percutaneous procedure is a feasible and safe long-term strategy, with few patients ultimately requiring surgical revascularization.

Adult↗
PubMed2004

Effectiveness of percutaneous coronary interventions in nonagenarians.

Data on percutaneous coronary intervention (PCI) in nonagenarians are very scarce. The investigators present a series of 26 nonagenarians who underwent PCI (29 lesions, 1.1 +/- 0.3 per patient). Most (96%) had acute coronary syndrome at presentation, 27% underwent primary PCI for acute myocardial infarctions, and 54% had multivessel disease. Angiographically successful results were obtained in 24 patients (92%), and coronary stents were used in 81%. Five patients (19%) died during hospitalization. In-hospital mortality was significantly greater in patients with Killip class III or IV at presentation (100% vs 9%, p = 0.001), in those in whom the procedure was a primary PCI for acute myocardial infarction (57% vs 5%, p = 0.010), and in the presence of angiographic failure (100% vs 13%, p = 0.031). In-hospital mortality was 0% after excluding patients in cardiogenic shock and those with primary PCI. Thus, most nonagenarians who undergo PCI have a high-risk profile. However, PCI achieves a successful angiographic result in most patients. Mortality is high but concentrated in patients in cardiogenic shock and with primary angioplasty as PCI.

Aged↗
PubMed2004

Intracoronary brachytherapy after stenting de novo lesions in diabetic patients: results of a randomized intravascular ultrasound study.

OBJECTIVES: We studied the efficacy of intracoronary brachytherapy (ICB) after successful coronary stenting in diabetic patients with de novo lesions. BACKGROUND: Intracoronary brachytherapy has proven effective in preventing recurrences in patients with in-stent restenosis. However, the role of ICB for the treatment of de novo coronary stenoses remains controversial. METHODS: Ninety-two patients were randomized to either ICB or no radiation after stenting. Primary end points were in-stent mean neointimal area (primary end point of efficacy) and minimal luminal area of the entire vessel segment (primary end point of effectiveness), as assessed by intravascular ultrasound at six-month follow-up. Quantitative coronary angiography analysis was performed at the target, injured, irradiated, and entire vessel segments. RESULTS: At follow-up, the in-stent mean neointimal area was 52% smaller in the ICB group (p < 0.0001). However, there was no difference in the minimal luminal area of the vessel segment (4.5 +/- 2.4 mm2 vs. 4.4 +/- 2.1 mm2). Restenosis rates increased progressively by the analyzed segment in the ICB group: target (7.1% vs. 20.9%, p = 0.07), injured (9.5% vs. 20.9%, p = NS), irradiated (14.3% vs. 20.9%, p = NS), and vessel segment (23.8% vs. 25.6%, p = NS). At one year, 1 cardiac death, 6 myocardial infarctions (MIs) (3 due to late stent thrombosis), and 10 target vessel revascularizations (TVRs) (6 due to the edge effect) occurred in the ICB group, whereas in the nonradiation group, there were 11 TVRs and no deaths or MIs. CONCLUSIONS: Intracoronary brachytherapy significantly inhibited in-stent neointimal hyperplasia after stenting in diabetic patients. However, clinically this was counteracted by the occurrence of the edge effect and late stent thrombosis.

Aged↗
PubMed2004

Coronary stenting versus balloon angioplasty in small vessels: a meta-analysis from 11 randomized studies.

OBJECTIVES: A meta-analysis of 11 randomized trials was done to compare stenting versus balloon angioplasty (BA) in small coronary vessels. BACKGROUND: Randomized studies on coronary stenting (CS) in small vessels have yielded controversial results. METHODS: Eleven randomized trials on CS versus BA in small vessels, including angiographic re-evaluation at six months, were analyzed. RESULTS: The BeStent (Medtronic Instent, Minneapolis, Minnesota) was used in four studies, the Multi-Link (Guidant, Advanced Cardiovascular Systems Inc., Santa Clara, California) in three trials, and the NIR (Boston Scientific Corp., Boston, Massachusetts), JoStent (Jomed International AB, Helsingborg, Sweden), Tenax (Biotronik, Berlin, Germany), and BioDivysio (Abbott Vascular Devices, Redwood City, California) in the remaining four trials. Overall, 3,541 patients were included (1,672 allocated to BA and 1,869 to stent). The rate of cross-over from balloon to stent in the pooled population was 19%, and unsuccessful stent deployment occurred in 2% of the patients allocated to stent. The pooled rates of restenosis were 25.8% and 34.2% in patients allocated to stent and balloon, respectively (p = 0.003) (risk ratio [RR] 0.77; 95% confidence interval [CI] 0.65 to 0.92). A smaller reference vessel diameter at baseline was associated with a higher risk reduction in the restenosis rate (y = -3.551 + 1.826 [x]; p = 0.012). Patients allocated to stent had lower rates of major adverse cardiac events (15.0% vs. 21.8%, p = 0.002; RR 0.70; 95% CI 0.57 to 0.87) and new target vessel revascularizations (12.5% vs. 17.0%, p = 0.004; RR 0.75, 95% CI 0.61 to 0.91). CONCLUSIONS: Elective stenting is superior to provisional stenting in small coronary arteries. This benefit is more evident in smaller coronary arteries.

Angioplasty, Balloon↗
PubMed2004

Late stent thrombosis (> 1 year) following clopidogrel withdrawal after brachytherapy treatment: need to assess aspirin resistance?

We report on a patient presenting with late thrombosis of a stent 15 months after being treated with intracoronary brachytherapy. It occurred 17 days after clopidogrel withdrawal while maintaining treatment with aspirin. At the time of stent thrombosis, evaluation of platelet aggregation was performed, revealing a suboptimal response to aspirin. Pathophysiological insights of aspirin resistance and clinical implications are reviewed.

Adult↗
PubMed2004

Therapeutic implications of in-stent restenosis located at the stent edge. Insights from the restenosis intra-stent balloon angioplasty versus elective stenting (RIBS) randomized trial.

AIMS: In patients with in-stent restenosis (ISR) several anatomic subgroups have been identified. ISR affecting the stent edge (EDG) is a poorly characterised subgroup with undefined therapeutic implications. We sought to determine the implications of ISR affecting the stent EDG. METHODS AND RESULTS: 450 patients included in the "Restenosis Intra-stent: Balloon angioplasty vs elective Stenting" (RIBS) randomized study, were analysed. EDG ISR was predefined in the protocol and the pattern of ISR analysed in a centralized core-lab. Fifty-two patients (12%) had EDG ISR (29 stent group, 23 balloon arm). Patients with EDG ISR had less severe [minimal lumen diameter (MLD) (0.78+/-0.3 vs 0.66+/-0.3 mm, p=0.05)] and shorter lesions (lesion length 10.2+/-6 vs 13.2+/-7 mm, p=0.003). Patients with EDG ISR more frequently required crossover (12% vs 3%, p=0.006) but eventually the immediate angiographic result and the long-term clinical and angiographic outcome was similar to that found in patients without EDG ISR. Patients with EDG ISR treated in the balloon and stent arms had similar baseline characteristics. However, after intervention, the immediate angiographic result was better in the stent arm (MLD 2.79+/-0.4 vs 2.35+/-0.3 mm, p=0.001). This difference persisted at late follow-up: MLD (1.93+/-0.7 vs 1.39+/-0.7 mm, p=0.01), recurrent restenosis (20% vs 50%, p=0.03). In addition, the 1-year event-free survival was significantly better (83% vs 52%, log rank p=0.01; Cox HR 0.28, 95%CI 0.09-0.79) in the stent arm. Moreover, stent implantation was an independent predictor of freedom from target vessel revascularization (HR 0.15, 95%CI 0.03-0.67, p=0.003). CONCLUSIONS: EDG ISR constitutes a specific subgroup with relevant therapeutic implications. In patients with EDG ISR, repeat stent implantation provides better clinical and angiographic outcome than conventional balloon angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed2004

High clopidogrel loading dose during coronary stenting: effects on drug response and interindividual variability.

AIM: To assess platelet inhibitory effects, interindividual variability in platelet inhibition as well as response to a 600 mg, compared to a standard 300 mg, clopidogrel loading dose (LD) after coronary stenting METHODS AND RESULTS: Platelet function profiles were assessed in 50 patients undergoing coronary stenting receiving either a 300 mg (n=27) or 600 mg clopidogrel LD. ADP (6 microM) and collagen (6 microg/mL) induced platelet aggregation, as well as ADP (2 microM) induced glycoprotein (GP) IIb/IIIa activation and P-selectin expression were assessed at baseline and 4, 24, and 48 h following clopidogrel front-loading. A more intense and rapid inhibition of platelet activation (both GP IIb/IIIa activation and P-selectin expression) were achieved using a 600 mg, compared to a 300 mg, LD throughout the entire 48 hours (p<0.001). Although there were no differences in platelet aggregation, overall a 600 mg LD increased the number of clopidogrel responders and this was also achieved earlier compared to a 300 mg LD. A 600 mg LD did not reduce interindividual variability of platelet response. CONCLUSION: The use of a 600 mg clopidogrel LD in patients undergoing coronary stenting optimises platelet inhibitory effects early after intervention and may provide a more effective protection against early thrombotic complications.

Blood Platelets↗
PubMed2004

PlA polymorphism and platelet reactivity following clopidogrel loading dose in patients undergoing coronary stent implantation.

The PlA polymorphism (Leu33Pro) of the platelet glycoprotein (GP) IIIa gene has been suggested to play an important role in coronary thrombosis. In vitro studies have shown differences for this polymorphism in platelet sensitivity towards antiplatelet drugs (aspirin and abciximab), suggesting a pharmacogenetic modulation. The aim of the study was to assess the modulatory effect of the PlA polymorphism on clopidogrel-induced antiplatelet effects in 38 patients undergoing coronary stent implantation receiving a 300 mg clopidogrel loading-dose. Platelet reactivity was assessed as GPIIb/IIIa activation and P-selectin expression in platelets stimulated with 2 micromol/l adenosine diphosphate using whole blood flow cytometry. The distribution of the homozygous PlA1/A1 and heterozygous PlA1/A2 genotypes were 74 and 26%, respectively. PlA2 carriers had a higher degree of GPIIb/IIIa activation (P = 0.05) and P-selectin expression (P = 0.02) during the overall study time course and a lower antiplatelet effect to a 300 mg clopidogrel loading-dose up to 24 h following intervention (P < 0.05). In conclusion, the Pl polymorphism of the GPIIIa gene modulates platelet reactivity towards clopidogrel front loading in patients undergoing coronary stenting. This suggests the need for individualized antithrombotic regimens to optimally inhibit platelet reactivity.

Abciximab↗
PubMed2004

807 C/T Polymorphism of the glycoprotein Ia gene and pharmacogenetic modulation of platelet response to dual antiplatelet treatment.

Glycoprotein (GP) Ia/IIa is a major platelet-collagen receptor playing a key role in thrombosis following collagen exposure. The 807 C/T polymorphism of the GP Ia gene (ITGA2) has been associated with platelet GP Ia/IIa receptor expression, having T-allele carriers, increased receptor density and thrombotic risk. The aim of the study was to assess the role of the 807 C/T polymorphism on modulating platelet function in patients undergoing coronary stenting receiving a 300 mg clopidogrel loading dose. Platelet aggregation was assessed in 44 patients by light transmittance aggregometry following adenosine diphosphate and collagen stimuli at baseline, and 10 min, 4 h and 24 h after clopidogrel front loading. The T allele was found in 73% of patients. Clopidogrel reduced adenosine diphosphate-induced platelet aggregation (P < 0.01), which was similar in carriers and non-carriers of the T allele throughout the study (P = 0.73). Clopidogrel reduced collagen-induced platelet aggregation only in non-carriers of the T allele (P = 0.03), which resulted in an increase in T allele carriers during the overall study (P = 0.04). In conclusion, the T allele of the GP Ia gene modulates platelet aggregation and clopidogrel antiplatelet effects, suggesting an enhanced reactivity to fibrillar collagens (exposed during coronary stenting) in T allele carriers and might contribute to an increased thrombotic risk in these patients.

Adenosine Diphosphate↗
PubMed2004

Platelet aggregation according to body mass index in patients undergoing coronary stenting: should clopidogrel loading-dose be weight adjusted?

BACKGROUND: A 300 mg clopidogrel loading-dose (LD) is widely used as an adjunct antithrombotic treatment to reduce the risk of thrombotic events early after coronary stenting (CS). Antithrombotic drugs commonly used during percutaneous coronary interventions, such as heparin and platelet glycoprotein IIb/IIIa inhibitors, but not clopidogrel LD, are weight-adjusted, and few data are available on which is the most effective clopidogrel LD regimen. The aim of this study was to assess whether body mass index (BMI) influenced platelet response to clopidogrel LD in patients undergoing CS. METHODS: Adenosine diphosphate (ADP)-induced platelet aggregation (PA) was assessed by light transmittance aggregometry in 48 patients on aspirin treatment undergoing CS receiving a 300 mg clopidogrel LD at intervention time. PA was assessed at baseline and up to 24 hours after intervention. Patients were divided into 2 groups according to BMI: overweight (BMI greater than or equal to 25 kg/m2; 29 patients) and normal weight (BMI<25 kg/m2; 19 patients). PA was significantly higher in overweight than in normal weight patients at baseline (60.1+/-18.6%; versus 47.6+/-13.5%; p=0.01), at 24 hours (42.3+/-18.4% versus 38.5+/-18.3%; p=0.02) and during the overall study time (p=0.025). Percentage of inhibition of PA 24 hours following clopidogrel LD was suboptimal (<40%) in 59% and 26% of overweight and normal weight patients, respectively (p=0.04). An elevated BMI was the only independent predictor of suboptimal platelet response. CONCLUSION: These data suggest that overweight patients may need a higher loading-dose of clopidogrel and/or an adjunct antithrombotic treatment to adequately inhibit platelet aggregation early after CS.

Aged↗
PubMed2004

Is a 300 mg clopidogrel loading dose sufficient to inhibit platelet function early after coronary stenting? A platelet function profile study.

BACKGROUND: Clopidogrel combined to aspirin reduces the early risk of stent thrombosis and a clopidogrel pre-treatment strategy is associated with a better outcome. However, in clinical practice such pre-treatment strategy is not always feasible and clopidogrel is frequently not administered until the time of intervention. Aim of the study was to compare platelet function profiles in patients undergoing coronary stenting receiving clopidogrel pre-treatment (75 mg x 2 daily at least 48 hours before intervention) compared to that of patients receiving a 300 mg loading dose at intervention time. METHODS: A total of 50 patients were included in whom patients' platelet aggregation (using light transmittance aggregometry) and platelet activation (P-selectin and PAC-1 expression by whole blood flow cytometry) were assessed following ADP stimuli at baseline, and 4 hours and 24 hours following coronary stenting. RESULTS: In the overall study population, 16/50 (32%) patients were pre-treated with clopidogrel and 34/50 (68%) received clopidogrel loading dose at intervention time. Platelet aggregation, as well as P-selectin and PAC-1 expression were significantly lower in clopidogrel pre-treated patients at baseline (p<0.001) and at 4 hours (p<0.01), while they were similarly inhibited 24 hours after intervention. In conclusion, platelet reactivity of patients treated with clopidogrel front loading at intervention time remains significantly higher than that of pre-treated patients in the early hours after coronary stenting. A higher loading dose at intervention time may be warranted to overcome the early risk of thrombotic complications.

Adenosine Diphosphate↗