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Biomedical subjects

Marco A Costa

Publications and source records attributed to Marco A Costa.

At least 19 recordsLinked to original sources
PubMed2007

Relocation of minimal luminal diameter after bare metal and drug-eluting stent implantation: incidence and impact on angiographic late loss.

Late loss (LL) has been a fundamental angiographic end-point in drug-eluting stents (DES) clinical trials. However, calculation of LL may be affected by a mismatch between post-procedure (PO) and follow-up (FU) sites of the minimal lumen diameter (MLD). Our aims were to investigate the incidence and methodological implications of the relocation of MLD after bare metal (BMS), sirolimus-eluting (SES), and paclitaxel-eluting (PES) stent implantation. Data from DIABETES I and II trials, which involved diabetic patients treated with BMS, SES, and PES, were analyzed. Angiographic data with matched projections between PO and 9-month angiographic FU were included. In-stent, in-lesion, and in-segment analyses included conventional and customized sub-segmental (5-mm/subsegment) methodology. MLD relocation was considered when the sites of MLD shifted a distance >> the intrinsic variability of the method. Conventional LL, site matched LL, maximal LL (MaxLL), and average LL (AvgLL) were calculated. Relationships between various LL and 1-year target lesion revascularization (TLR) were investigated. Post MLD was located distally, outside the stent, in > or =65% of the analyses. At FU, MLD relocation occurred in 70.5% (BMS), 40% (SES), and 35% (PES). MLD shifted > or =11 mm on average, mainly towards the stented segment. MLD relocation still occurred in 42.8% (BMS), 33.7% (SES), and 36.4% (PES), when analysis was restricted to in-stent segment. Among LL measurements, MaxLL showed the best association with TLR rates. Relocation of the MLD is a frequent phenomenon after both BMS and DES, and should be taken into account when calculating LL. Comprehensive LL analyses, including MaxLL and AvgLL, provides a better appraisal of the biological and clinical effectiveness of DES.

Aged↗
PubMed2006

Influence of the CD14 C260T promoter polymorphism on C-reactive protein levels in patients with coronary artery disease.

The CD14 receptor is an important mediator of inflammatory reactions, and its expression is under genetic control. The allelic variant of the C260T polymorphism located in the promoter region of the CD14 gene is associated with receptor expression and ischemic risk. To date, most studies assessing the functional implications of the C260T polymorphism have been performed under proinflammatory conditions (e.g., acute coronary syndromes), and whether gene sequence variations of the CD14 receptor have any functional effect on systemic inflammation in patients in a stable phase of their atherosclerotic disease process is unknown. Eighty-two patients with stable coronary artery disease were studied. High-sensitivity C-reactive protein (hs-CRP) was used as a measurement of systemic inflammation. The genotype distribution of the C260T polymorphism of the CD14 gene was as follows: CC in 18 of 82 patients (22%), TC in 48 of 82 patients (58.5%), and TT in 16 of 82 patients (19.5%). TT subjects had increased hs-CRP levels compared with carriers of the C allele (p = 0.04). A higher percentage of T allele homozygotes had hs-CRP levels >0.3 mg/dl (p = 0.01). Homozygosis status of the T allele was independently associated with hs-CRP levels >0.3 mg/dl (p = 0.004). In conclusion, these observations may support the findings in large-scale studies that T homozygotes of this functional polymorphism are at increased ischemic risk.

Adult↗
PubMed2006

Characterization of plaque prolapse after drug-eluting stent implantation in diabetic patients: a three-dimensional volumetric intravascular ultrasound outcome study.

OBJECTIVES: The aim of this research was to evaluate the plaque prolapse (PP) phenomenon after bare-metal (BMS) and drug-eluting stent (DES) implantation in patients with diabetes mellitus using 3-dimensional volumetric intravascular ultrasound (IVUS). BACKGROUND: Plaque prolapse has been observed in up to 22% of patients treated with BMS. Diabetic patients have a larger atherothrombotic burden and may be more prone to have PP. However, the incidence of PP and its clinical impact after DES implantation is unknown. METHODS: Three-dimensional IVUS was performed after intervention and at 9-month follow-up in 168 patients with diabetes (205 lesions) treated with bare BX Velocity stents ((BX Velocity/Sonic, Cordis, Johnson & Johnson) (BMS, n = 65), sirolimus-eluting stents (Cypher, Cordis) (SES, n = 69), and paclitaxel-eluting stents (Taxus, Boston Scientific, Natick, Massachusetts) (PES, n = 71). Intravascular ultrasound data at the sites of PP were compared with stented segments without PP in each lesion. Outcomes were evaluated at 9- and 12-month follow-up. RESULTS: There were 42 sites of PP (BMS = 11, SES = 11, PES = 20, p = NS) in 34 stented segments of 205 (16.6%) lesions. Plaque prolapse was more frequent in the right coronary artery and in chronic total occlusion lesions. Post-procedure PP volume was 1.95 mm3 in BMS, 2.96 mm3 in SES, and 4.53 mm3 in PES. At follow-up, tissue volume increased at PP sites in both BMS and PES, but not after SES. Neointimal proliferation was similar between PP and non-PP sites. Stent thrombosis and restenosis rates were similar between PP and non-PP lesions. CONCLUSIONS: The incidence of PP after implantation of new generation tubular stents in patients with diabetes remains high. Drug-eluting stent implantation was not associated with increased risk of PP. Plaque prolapse was not associated with stent thrombosis or increased neointimal proliferation.

Aged↗
PubMed2006

Quantitative contrast enhanced magnetic resonance imaging for the evaluation of peripheral arterial disease: a comparative study versus standard digital angiography.

OBJECTIVE: The purpose of this study is to evaluate the accuracy of semiautomated analysis of contrast enhanced magnetic resonance angiography (MRA) in patients who have undergone standard angiographic evaluation for peripheral vascular disease (PVD). BACKGROUND: Magnetic resonance angiography is an important tool for evaluating PVD. Although this technique is both safe and noninvasive, the accuracy and reproducibility of quantitative measurements of disease severity using MRA in the clinical setting have not been fully investigated. METHODS: 43 lesions in 13 patients who underwent both MRA and digital subtraction angiography (DSA) of iliac and common femoral arteries within 6 months were analyzed using quantitative magnetic resonance angiography (QMRA) and quantitative vascular analysis (QVA). Analysis was repeated by a second operator and by the same operator in approximately 1 month time. RESULTS: QMRA underestimated percent diameter stenosis (%DS) compared to measurements made with QVA by 2.47%. Limits of agreement between the two methods were +/- 9.14%. Interobserver variability in measurements of %DS were +/- 12.58% for QMRA and +/- 10.04% for QVA. Intraobserver variability of %DS for QMRA was +/- 4.6% and for QVA was +/- 8.46%. CONCLUSIONS: QMRA displays a high level of agreement to QVA when used to determine stenosis severity in iliac and common femoral arteries. Similar levels of interobserver and intraobserver variability are present with each method. Overall, QMRA represents a useful method to quantify severity of PVD.

Algorithms↗
PubMed2006

Insulin therapy is associated with platelet dysfunction in patients with type 2 diabetes mellitus on dual oral antiplatelet treatment.

OBJECTIVES: This study sought to assess the influence of type 2 diabetes mellitus (T2DM) and the impact of hypoglycemic treatment (insulin vs. noninsulin) on platelet function profiles in patients treated with dual oral antiplatelet therapy. BACKGROUND: Insulin inhibits platelet aggregation by suppressing the P2Y12 pathway. However, T2DM patients have a loss of responsiveness to insulin that leads to upregulation of the P2Y12 pathway, increased platelet reactivity, and reduced responsiveness to antiplatelet agents. Patients with insulin-treated diabetes mellitus (ITDM) have a more advanced disease status and higher atherothrombotic risk compared with non-ITDM (NITDM). However, the impact of insulin therapy on platelet dysfunction in patients treated with P2Y12 antagonists is unknown. METHODS: A total of 201 T2DM and 65 nondiabetic patients with coronary artery disease in a steady phase of aspirin and clopidogrel treatment were studied. Platelet aggregation was assessed using agonists specific (6 and 20 microM adenosine diphosphate [ADP]) and nonspecific (6 microg/ml collagen and 20 microM epinephrine) for the P2Y12 pathway. High shear-induced platelet reactivity was assessed by means of the PFA-100 system (Dade-Behring International, Miami, Florida). RESULTS: The T2DM patients had platelet aggregation and shear-induced platelet function significantly increased compared with nondiabetic patients using all assays. Platelet aggregation was increased in ITDM (n = 68) compared with NITDM (n = 133) patients after P2Y12-specific stimuli. Insulin treatment was the strongest predictor of ADP-induced aggregation. Platelet function profiles were similar between ITDM and NITDM using assays nonspecific to the P2Y12 pathway. Platelet dysfunction was independent of glycemic control and inflammatory status. CONCLUSIONS: The P2Y12-dependent and -independent pathways of platelet reactivity are altered in T2DM compared with nondiabetic patients, and ITDM have greater ADP-induced platelet aggregation compared with NITDM.

Aged↗
PubMed2006

Vascular effects of sirolimus-eluting versus bare-metal stents in diabetic patients: three-dimensional ultrasound results of the Diabetes and Sirolimus-Eluting Stent (DIABETES) Trial.

OBJECTIVES: A predefined intravascular ultrasound (IVUS) substudy was performed to evaluate the vascular effects of sirolimus-eluting stent (SES) versus bare-metal stent (BMS). BACKGROUND: The Diabetes and Sirolimus-Eluting Stent (DIABETES) trial is a prospective, multicenter, randomized, controlled trial aimed at demonstrating the efficacy of the SES compared with BMS in diabetic patients. METHODS: Serial intravascular ultrasound analyses were performed in 140 lesions (SES = 75; BMS = 65) immediately after stent implantation and at nine-month follow-up. Vessel, luminal, and stent mean areas and volumes were evaluated at both edges and within the stented segment. Qualitative assessment of residual dissections and stent apposition were also performed. RESULTS: Baseline clinical and angiographic characteristics were similar between groups. At 9 months, in-stent neointimal hyperplasia (NIH) mean area and volume were significantly reduced in the SES group (median NIH area 0.01 mm2 [0.0 to 0.1] vs. 2.0 mm2 [1.0 to 2.9] and median NIH volume 0.11 mm3 [0 to 2.1] vs. 35.3 mm3 [16.6 to 62.6]; both p < 0.0001). In the SES group, stent edges evidenced significant increase in lumen dimensions mainly due to significant increase in vessel volume, whereas those of the BMS group presented vessel shrinkage leading to significant lumen reduction. Late acquired incomplete stent apposition was observed in 11 lesions (14.7%) in the SES group and 0 in the BMS group (p = 0.001). At one year, no stent thromboses occurred in malapposed stents. CONCLUSIONS: The SES implantation effectively inhibits NIH in diabetic patients. The antirestenotic effect of SES is also appreciated at the stent edges. Late acquired stent malapposition is a frequent phenomenon in diabetic patients treated with SES.

Aged↗
PubMed2006

Contribution of gene sequence variations of the hepatic cytochrome P450 3A4 enzyme to variability in individual responsiveness to clopidogrel.

OBJECTIVE: Metabolic activity of cytochrome P450 (CYP) 3A4 has been associated with clopidogrel response variability. Because metabolic activity of CYP3A4 is genetically regulated, we hypothesized that genetic variations of this enzyme may contribute to clopidogrel response variability. METHODS AND RESULTS: The CYP3A4*1B, CYP3A4*3, IVS7+258A>G, IVS7+894C>T, and IVS10+12G>A polymorphisms of the CYP3A4 gene were assessed in 82 patients in a steady phase of clopidogrel therapy. Glycoprotein (platelet glycoprotein (GP) IIb/IIIa receptor activation and platelet aggregation were assessed. A cohort of 45 clopidogrel-naïve patients was studied to determine the modulating effects of these polymorphisms after loading dose (300 mg) administration. Only the IVS7+258A>G, IVS7+894C>T, and IVS10+12G>A polymorphisms were sufficiently polymorphic. During the steady phase of clopidogrel treatment, IVS10+12A allele carriers had reduced GP IIb/IIIa activation (P=0.025) and better responsiveness (P=0.02); similarly, clopidogrel-naïve patients carriers of the IVS10+12A allele had reduced GP IIb/IIIa activation during the first 24 hours after a loading dose (P=0.025), increased platelet inhibition (P=0.006), and a more optimal drug response (P=0.003). This polymorphism did not influence platelet aggregation profiles. No association was observed between the other polymorphisms and clopidogrel responsiveness. CONCLUSIONS: The IVS10+12G>A polymorphism of the CYP3A4 gene modulates platelet activation in patients treated with clopidogrel and may therefore contribute to clopidogrel response variability.

Adenine↗
PubMed2006

"Head-to-head comparison between sirolimus-eluting and paclitaxel-eluting stents in patients with complex coronary artery disease: an intravascular ultrasound study".

BACKGROUND: The aim of this study was to assess neointimal hyperplasia following sirolimus-eluting (SES) and paclitaxel-eluting stents (PES) implantation in a patients with complex coronary disease. METHOD: Between January to December 2004, 70 patients were enrolled in this study (SES = 37; PES = 33. The primary objective was to assess the efficacy of SES and PES on neointimal proliferation inhibition in patients with complex coronary lesions by volumetric 3D intravascular ultrasound (IVUS) assessment at six-month follow-up. RESULTS: Baseline clinical, demographic or angiographic characteristics were well balanced in both groups. All procedures as well as hospitalisation were uneventful. The percentage of B2/C lesions in our study was > 90% in both groups. The IVUS-assessed in-stent mean neointimal hyperplasia volume was significantly lower in lesions treated with SES compared to PES (4.1 +/- 11 mm3 vs. 17.4 +/- 23 mm3, p < 0.002) at 6 month follow-up. No difference in both MACE (3.0 versus 6.0%, p = NS) and restenosis (5.4 versus 9.1%, p = NS) were found. The in-segment late loss at six month was 0.26 mm in the SES and 0.48 mm in the PES group (p = NS). CONCLUSIONS: The present study showed reduced neointimal proliferation after sirolimuseluting as compared to paclitaxel-eluting stents in patients with complex coronary artery disease. Both SES and PES were associated with low rate of angiographic restenosis or major adverse cardiovascular events.

Angioplasty, Balloon, Coronary↗
PubMed2006

Lack of association between gene sequence variations of platelet membrane receptors and aspirin responsiveness detected by the PFA-100 system in patients with coronary artery disease.

Platelet membrane receptors play a pivotal role in thrombus formation. Expression of platelet membrane receptors are under genetic control and gene sequence variations of receptors pivotal to thrombotic formation have been hypothesized to contribute to different degrees of individual response to aspirin. The aim of the present study was to investigate the impact of functional genetic polymorphisms of platelet membrane receptors on aspirin sensitivity assessed by means of the PFA-100 system in patients with coronary artery disease. Gene sequence variations of three platelet membrane receptors (GPIa/IIa, P2Y12, GPIIb/IIIa) pivotal to thrombus formation were assessed in 76 patients with coronary artery disease on chronic aspirin treatment. Patients with reduced sensitivity to aspirin were defined when closure-times of collagen/epinephrine cartridges < or =193 seconds and coined as PFA-100 non-responders. PFA-100 non-responders were observed in 33% of patients. Patients with diabetes mellitus were more frequently PFA-100 non-responders. Closure times of collagen/ADP coated cartridges were reduced in PFA-100 non-responders. The genotype distribution was similar in PFA-100 responder and non-responder patients for all three genotypes and did not vary in contemporaneous carriers of allelic variants. In conclusion, in vitro determined sensitivity to aspirin assessed using PFA-100 is not associated with gene sequence variations of platelet membrane receptors key to thrombus formation.

Aged↗
PubMed2006

[Efficacy of sirolimus-eluting stent implantation in diabetic patients with very small vessels (< or = 2.25 mm). Insights from the DIABETES trial].

INTRODUCTION AND OBJECTIVES: Diabetic patients frequently have small-diameter vessels, which increases their risk of restenosis. The aim of this study was to determine the efficacy of sirolimus-eluting stent implantation in these high-risk patients following percutaneous coronary intervention. METHODS: Our study population comprised a subset of 85 diabetic patients from the DIABETES (DIABETes and sirolimus Eluting Stent) trial who had very small vessels, defined as those with a reference diameter < or =2.25 mm. In the 100 lesions treated, 49 sirolimus-eluting stents and 51 bare-metal stents were used. Glycoprotein IIb/IIIa inhibitors were used as recommended by the protocol and dual antiplatelet therapy was administered for 1 year. RESULTS: Baseline clinical and angiographic characteristics were comparable in the two groups. The patients' mean age was 66 (9) years, 42% were women, and 37% were insulin-dependent. On average, the lesion length was 15.0 (9.0) mm and the reference diameter was 1.9 (0.2) mm. At 9-month follow-up, both late lumen loss and the restenosis rate were significantly lower in the sirolimus-eluting stent group than in the bare-metal stent group, at -0.03 (0.3) mm vs 0.44 (0.5) mm (P< .001), and 9.1% vs 39.1% (P=.001), respectively. These differences were also observed in the subgroup of insulin-dependent patients. At 1-year follow-up, the stent thrombosis rate was 0% in the sirolimus-eluting stent group, whereas two patients in the bare-metal stent group presented with stent thrombosis. CONCLUSIONS: Sirolimus-eluting stent implantation in diabetics with very small vessels is safe and effective, even in insulin-dependent patients.

Aged↗
PubMed2006

Clopidogrel withdrawal is associated with proinflammatory and prothrombotic effects in patients with diabetes and coronary artery disease.

Inhibition of the P2Y12 pathway by the platelet antagonist clopidogrel is associated with a marked reduction in platelet reactivity. Recent reports have shown that P2Y12 inhibition has anti-inflammatory effects as well. However, whether clopidogrel withdrawal is associated with proaggregatory and proinflammatory effects has not yet been explored. Since diabetic subjects are characterized by a prothrombotic and proinflammatory status, we hypothesize that these patients may be more vulnerable to these effects. A total 54 patients with diabetes on long-term (12 months) dual antiplatelet therapy (aspirin plus clopidogrel) were studied. Platelet aggregation (following 6 and 20 micromol/l ADP stimuli) and inflammatory markers (C-reactive protein and P-selectin expression) were assessed before and 1 month following clopidogrel withdrawal. Following clopidogrel withdrawal, aspirin responsiveness using platelet function analyzer-100 was determined as well. A significant increase in all the assessed platelet (P < 0.0001 for 6 and 20 micromol/l ADP-induced aggregation) and inflammatory (P < 0.05 for C-reactive protein, P < 0.001 for P-selectin expression in resting platelets, and P < 0.0001 for P-selectin expression in ADP-stimulated platelets) biomarkers was observed following clopidogrel withdrawal. Low responders to aspirin had increased platelet aggregation profiles (P < 0.05 for 6 and 20 micromol/l ADP-induced aggregation) but no differences in inflammatory markers. In conclusion, clopidogrel withdrawal is associated with an increase in platelet and inflammatory biomarkers in diabetic patients, supporting pleiotropic effects coupled with P2Y12 receptor antagonism.

Aged↗
PubMed2005

Intravascular ultrasound characterization of the "black hole" phenomenon after drug-eluting stent implantation.

An intraluminal echolucent tissue, dubbed "black hole," has been identified by intravascular ultrasonography after intracoronary brachytherapy. This study reports the characteristics and incidence of the black hole in patients treated with drug-eluting stent implantation using a sirolimus-eluting stent (SES). We included intravascular ultrasound data from the Compassionate Use of Sirolimus-Eluting Stent (SECURE, n = 61 lesions) registry, a study involving patients in whom previous brachytherapy had failed, and the DIABETES trial (n = 165 lesions), a multicenter, randomized study comparing SES versus bare metal stents in diabetic patients. Intravascular ultrasound follow-up was scheduled at 8 months (SECURE trial, post-brachytherapy population) and 9 months (DIABETES trial). In the SECURE population, a black hole was observed in 10 patients (19.6%). Seven black hole segments had significant intimal hyperplasia (> 10%). A black hole accounted for 27% of total intraluminal tissue. In the DIABETES trial, 2 patients (2.5%) in the SES group and none in the bare metal stent group showed echolucent intimal hyperplasia. In conclusion, a black hole occurred frequently after implantation of a SES in patients in whom intracoronary brachytherapy had previously failed. Black holes were also identified in a nonirradiated population, although the incidence was lower than in the post-brachytherapy patients. Bare metal stents were not associated with this phenomenon.

Adult↗
PubMed2005

Influence of aspirin resistance on platelet function profiles in patients on long-term aspirin and clopidogrel after percutaneous coronary intervention.

Increased platelet inhibition is achieved when clopidogrel is added to aspirin (acetylsalicylic acid [ASA]). A broad variability in platelet inhibition profiles during the early phases of treatment has been demonstrated and may be attributed to ASA resistance. However, the influence of ASA sensitivity on platelet function profiles of patients on long-term dual antiplatelet therapy has yet to be explored. A total of 135 patients who had previously undergone percutaneous coronary intervention on long-term (>1 month) ASA and clopidogrel therapy was included. The PFA-100 system was used to define ASA resistance. Platelet aggregation, after adenosine diphosphate (6 and 20 micromol/L) and collagen (6 microg/ml) stimuli, and platelet activation (glycoprotein IIb/IIIa activation and P-selectin expression), after adenosine diphosphate (2 micromol/L) and thrombin receptor-activating peptide (50 micromol/L) stimuli, were assessed by light transmittance aggregometry and flow cytometry, respectively. Patient variability in response to treatment was defined by the coefficient of variability. ASA resistance was found in 60 of 135 patients (44%). Patients with diabetes were more frequently ASA resistant. Collagen/epinephrine- and collagen/adenosine diphosphate-coated cartridges on the PFA-100 had shorter closure times in the ASA-resistant population compared with ASA-sensitive patients. Platelet aggregation and activation were significantly higher in ASA-resistant patients. A broad variability (coefficient of variation >0.25) in patient response to treatment was observed in ASA-resistant and -sensitive patients. In conclusion, ASA resistance is associated with increased platelet reactivity in patients on long-term dual antiplatelet treatment.

Adenosine Diphosphate↗
PubMed2005

Variability in platelet aggregation following sustained aspirin and clopidogrel treatment in patients with coronary heart disease and influence of the 807 C/T polymorphism of the glycoprotein Ia gene.

A broad variability in patient response to dual antiplatelet treatment has been described during the first month of treatment. Data on platelet function profiles in patients on dual antiplatelet therapy for a more sustained period are limited. Whether gene sequence variations of the glycoprotein Ia/IIa receptor influence platelet aggregation in these patients is also unknown. The aim of this study was to characterize platelet aggregation profiles in patients on dual antiplatelet treatment (aspirin plus clopidogrel) for >1 month and to assess whether these may be influenced by the C807T polymorphism of the glycoprotein Ia gene. We included 82 patients, who were divided into 2 groups: carriers (CT + TT genotypes; n = 51) and noncarriers (CC genotype; n = 31) of the mutant T allele. Platelet aggregation was assessed using light transmittance aggregometry after stimuli with adenosine diphosphate (20 micromol/L), collagen (6 microg/ml), and epinephrine (20 micromol/L). A significant variability in the distribution of platelet aggregation was observed in the overall study population, as well as in carriers and noncarriers of the T allele. T allele carriers had increased platelet aggregation compared with noncarriers after stimuli with adenosine diphosphate, collagen, and epinephrine (p <0.05 for all platelet aggregation assays). Thus, platelet aggregation varied significantly in patients on long-term dual antiplatelet treatment and was increased in T allele carriers of the 807C/T polymorphism of the glycoprotein Ia gene. These findings may contribute to the increased ischemic risk observed in these patients.

Adult↗
PubMed2005

Four-year angiographic and intravascular ultrasound follow-up of patients treated with sirolimus-eluting stents.

BACKGROUND: Despite the proven superiority of sirolimus-eluting stents (SESs) compared with bare stents in the first year after implantation, long-term outcomes of patients treated with these novel devices remain unknown. Our goal was to evaluate the clinical, angiographic, and intravascular ultrasound (IVUS) outcomes of patients treated with SESs 4 years after implantation. METHODS AND RESULTS: The study included 30 patients treated with sirolimus-eluting Bx Velocity stenting (slow release [SR; n=15] and fast release [FR; n=15]). Twenty-six patients underwent 4-year angiographic and IVUS follow-up and had matched assessments at all time points (index and 4-, 12-, 24-, and 48-month follow-up). One death occurred during the study period in a patient with a patent SES. There were no target-vessel revascularizations or thromboses between 2- and 4-year follow-up examinations. There was no stent thrombosis, target-lesion revascularization, death, or myocardial infarction in the SR group up to 4 years. Cumulative event-free survival rate was 87% for the total population (80% in the FR group and 93% in the SR group). In-stent late loss was slightly greater in the FR group (0.41+/-0.49 mm) than the SR group (0.09+/-0.23) after 4 years. One patient in the FR group had a 52% in-stent restenosis lesion. Percent neointimal hyperplasia volume, as detected by IVUS, remained minimal after 4 years (FR=9.1% and SR=5.7%). CONCLUSIONS: This study confirms the longevity of the optimal outcomes observed in patients treated with sirolimus-eluting Bx Velocity stents 4 years after implantation. In-stent lumen dimensions remained essentially unchanged at 4-year follow-up, particularly in the population treated with the currently available SES (SR formulation).

Cardiovascular Diseases↗
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↗