Clopidogrel In Acute Coronary Syndromes Research Articles

Optimum Utilisation of Novel Antiplatelet Agents in Clinical Practice.

Prasugrel and ticagrelor are two novel promising antiplatelet agents inhibiting the platelet activation via the adenosine diphosphate pathway. Both achieve a faster, more intense, and more consistent platelet inhibition than clopidogrel. Both novel antiplatelet agents have demonstrated superiority over clopidogrel in large, randomised controlled trials in patients with acute coronary syndrome (ACS). Prasugrel may be best suited for younger patients with planned percutaneous coronary intervention and large areas of myocardium at risk or diabetes mellitus who have a low risk of bleeding. The benefits of prasugrel relative to clopidogrel in ACS must be weighed against the increase in the risk of bleeding associated with its use. Ticagrelor may be the best option for patients with ACS without T elevations, elderly patients or patients managed conservatively. Vorapaxar, a new oral protease-activated-receptor 1 antagonist, may be a good option for secondary prevention in patients with stable atherosclerosis and no history of stroke.

Comparison of the Degree of Platelet Aggregation Inhibition With Prasugrel Versus Clopidogrel and Clinical Outcomes in Patients With Unprotected Left Main Disease Treated With Everolimus-Eluting Stents

The everolimus-eluting stent (EES) performs better than the first generation drug-eluting stent. Prasugrel compared with clopidogrel in acute coronary syndromes treated invasively is associated with improved clinical outcome and decreased risk of stent thrombosis. The aim of the study was to compare the clinical outcome and degree of platelet aggregation inhibition of patients treated with EES for unprotected left main disease (ULMD) and receiving clopidogrel or prasugrel. Patients receiving an EES for ULMD and with low residual platelet reactivity on clopidogrel or prasugrel treatment were included in the analysis. The primary end point of the study was the composite of cardiac mortality and myocardial infarction at 1 year. The secondary end point was the degree of platelet aggregation inhibition as assessed by light transmittance aggregometry. From January 2009 to December 2011, 252 patients with low residual platelet reactivity on thienopyridine treatment were treated with EES for ULMD. Of these, 104 patients received clopidogrel and 148 received prasugrel. The primary end point rate was lower in the prasugrel group compared with clopidogrel group: 1.3% and 9.6%, respectively (p= 0.002). Residual platelet reactivity was less in the prasugrel group compared with clopidogrel group (adenosine diphosphate 10μmol/L 37 ± 17% and 45 ± 15%, respectively, p <0.001). At multivariate analysis, prasugrel treatment was related to the primary end point (hazard ratio 0.17; 95% confidence interval 0.04 to 0.77, p= 0.022). In conclusion, in patients treated with EES for ULMD, prasugrel compared with clopidogrel is associated with increased platelet aggregation inhibition and a better clinical outcome.

GW24-e1802 Limited role of genotyping for the prediction of clopidogrel antiplatelet efficacy in Chinese patients with acute coronary syndrome

ObjectivesCytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogel absorption and bioactivation. Genotypes in these genes have been associated with the variability of responsiveness...

Genetic determinants of high on-treatment platelet reactivity in clopidogrel treated Chinese patients

IntroductionCytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogel absorption and bioactivation. Genetic polymorphisms in these genes have been associated with the variability of the response to clopidogrel, however their contribution to high on-treatment platelet reactivity (HPR) in clopidogrel treated Chinese patients is less known. Materials and methodsFive-hundred Chinese-Han patients treated with clopidogrel for acute coronary syndrome (ACS) were consecutively recruited from the Department of Geriatric Cardiology, General Hospital of Chinese People’s Liberation Army, from September 2010 to September 2012. We assessed the relations of CYP2C19*2 (rs4244285), CYP2C19*3 (rs4986893), CYP2C19*17 (rs12248560), PON1Q129R (rs662) and ABCB1C3435T (rs1045642) to the platelet aggregation after 5days maintenance dose of clopidogrel administration, and the risk for HPR. The cutoff of HPR was defined as 20μmol/L adenosine diphosphate (ADP)-induced platelet aggregation>50%. ResultsBoth CYP2C19*2 and *3 alleles were significantly associated with higher platelet aggregation after 5days maintenance dose of clopidogrel administration (P<0.00001and P=0.042, respectively). The platelet aggregation in carriers of at least one CYP2C19 loss-of-function allele (*2 or *3, accounted for 58% of the study population) was obviously higher than that in non-carriers (P<0.00001). Patients with the CYP2C19*2 allele had a higher risk of HPR than those with the CYP2C19 wild-type genotype [adjusted hazard ratio (HR), 1.56; 95% confidence interval(CI), 1.04–2.33, P=0.03]. The carriers of at least one CYP2C19 loss-of-function allele could also predict significantly greater risk of HPR compared with non-carriers (adjusted HR1.79,95% CI: 1.33–2.4,P=0.003). However, the carriage of CYP2C19*3 alone could not predict the risk of HPR significantly (adjusted HR, 1.5; 95% CI: 0.83–3, P=0.16). Significant relation of CYP2C19*17, PON1Q129R and ABCB1C3435T to the platelet aggregation was not found. ConclusionIn clopidogrel treated Chinese patients with ACS, carriers of at least one CYP2C19 loss-of-function allele could predict greater risk of HPR, with the impact mainly attributing to CYP2C19*2. Neither ABCB1 nor PON1 genotype could influence the antiplatelet response of clopidogrel in the cohort of Chinese patients.

Prasugrel versus Clopidogrel for Acute Coronary Syndromes without Revascularization

BackgroundThe effect of intensified platelet inhibition for patients with unstable angina or myocardial infarction without ST-segment elevation who do not undergo revascularization has not been delineated.MethodsIn this double-blind, randomized trial, in a primary analysis involving 7243 patients under the age of 75 years receiving aspirin, we evaluated up to 30 months of treatment with prasugrel (10 mg daily) versus clopidogrel (75 mg daily). In a secondary analysis involving 2083 patients 75 years of age or older, we evaluated 5 mg of prasugrel versus 75 mg of clopidogrel.ResultsAt a median follow-up of 17 months, the primary end point of death from cardiovascular causes, myocardial infarction, or stroke among patients under the age of 75 years occurred in 13.9% of the prasugrel group and 16.0% of the clopidogrel group (hazard ratio in the prasugrel group, 0.91; 95% confidence interval [CI], 0.79 to 1.05; P=0.21). Similar results were observed in the overall population. The prespecified analysis of multiple recurrent ischemic events (all components of the primary end point) suggested a lower risk for prasugrel among patients under the age of 75 years (hazard ratio, 0.85; 95% CI, 0.72 to 1.00; P=0.04). Rates of severe and intracranial bleeding were similar in the two groups in all age groups. There was no significant between-group difference in the frequency of nonhemorrhagic serious adverse events, except for a higher frequency of heart failure in the clopidogrel group.ConclusionsAmong patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.)

TCT-51 Comparison of Clopidogrel and Prasugrel in Patients with Unprotected Left main Disease Treated with Everolimus-Eluting Stents: Insight From the Florence Left Main-PCI Registry

Randomized trials and registries have shown that everolimus-eluting stent (EES) performs better than first generation drug-eluting stent (DES). Prasugrel as compared to clopidogrel in acute coronary syndromes treated invasively is associated with improved clinical outcome and decreased risk of stent

Prior smoking status, clinical outcomes, and the comparison of ticagrelor with clopidogrel in acute coronary syndromes—Insights from the PLATelet inhibition and patient Outcomes (PLATO) trial

Habitual smoking has been associated with increased platelet reactivity, increased risk of thrombotic complications and greater efficacy of clopidogrel therapy over placebo. In the PLATO trial, ticagrelor compared to clopidogrel in patients with acute coronary syndromes (ACS) reduced the primary composite end point of vascular death, myocardial infarction and stroke, without increasing overall rates of major bleeding. We evaluated the results in relation to smoking habits. Interactions between habitual smokers (n = 6678) and in ex/nonsmokers (n = 11,932) and the effects of randomized treatments on ischemic and bleeding outcomes were evaluated by Cox regression analyses. Habitual smokers had an overall lower risk profile and more often ST-elevation ACS. After adjustment for baseline imbalances, habitual smoking was associated with a higher incidence of definite stent thrombosis (adjusted HR, 1.44 [95% CI, 1.07-1.94]); there were no significant associations with other ischemic or bleeding end points. The effects of ticagrelor compared to clopidogrel were consistent for all outcomes regardless of smoking status. Thus, there was a similar reduction in the primary composite end point for habitual smokers (adjusted HR, 0.83 [95% CI, 0.68-1.00]) and ex/nonsmokers (adjusted HR, 0.89 [95% CI, 0.79-1.00]) (interaction P = .50), and in definite stent thrombosis for habitual smokers (adjusted HR, 0.59 [0.39-0.91]) and ex/nonsmokers (adjusted HR, 0.69 [95% CI, 0.45-1.07]) (interaction P = .61). In patients hospitalized with ACS, habitual smoking is associated with a greater risk of subsequent stent thrombosis. The reduction of vascular death, myocardial infarction, stroke, and stent thrombosis by ticagrelor compared to clopidogrel is consistent regardless of smoking habits.

Clopidogrel plus indobufen in acute coronary syndrome patients with hypersensitivity to aspirin undergoing percutaneous coronary intervention

The prescription of aspirin (acetylsalicylic acid (ASA)) to patients with a history of hypersensitivity to this drug could prove harmful. The aim of the study was to assess the antiplatelet activity and safety of a combined antiplatelet treatment with indobufen and clopidogrel in acute coronary syndrome (ACS) patients with hypersensitivity to aspirin, undergoing coronary stenting. Forty-two consecutive ACS patients treated with stent implantation were randomly assigned to receive clopidogrel 75 mg daily (loading dose 300 mg) plus indobufen 100 mg twice a day (group A), or clopidogrel 75 mg daily, after 300 mg of loading dose (group B). Platelet activity and safety were monitored in both groups at 1, 3, 6, 12, and 18 months with laboratory and clinical evaluation. A lower value of max % platelet aggregation to arachidonic acid and collagen was found in group A compared to group B (31.79 ± 27.33 vs. 73.67 ± 19.92; p < 0.0001 and 28.53 ± 21.32 vs. 73.58 ± 17.71; p < 0.0001, respectively). There was no difference in max % of platelet inhibition to adenosine diphosphate between the two groups (14.23 ± 18.92 vs. 10.30 ± 18.97; p = 0.23). In the population that was under indobufen treatment, the serum thromboxane B2 (TXB2) production at 1 week and 1 month was very low (2.6 ± 1.6 ng/ml and 3.0 ± 2.7 ng/ml, respectively; p = 0.82). The combined treatment was well tolerated in group A patients. This study suggests that the combined antiplatelet treatment with clopidogrel and indobufen could be a good option in ACS patients with hypersensitivity to aspirin undergoing coronary stenting.

GREATER EFFICACY OF TICAGRELOR COMPARED TO CLOPIDOGREL IN ACUTE CORONARY SYNDROME IS NOT DRIVEN BY OUTCOMES IN POOR METABOLIZERS OF CLOPIDOGREL

Greater efficacy of ticagrelor compared to clopidogrel in acute coronary syndrome is not driven by outcomes in poor metabolizers of clopidogrel

Use of Clopidogrel Post-Coronary Artery Bypass Surgery in Canadian Patients With Acute Coronary Syndromes

Background Randomized trials have established the efficacy of clopidogrel in acute coronary syndromes (ACS). The benefit of clopidogrel has also been observed in the subgroup of ACS patients who subsequently undergo coronary artery bypass surgery (CABG); however, this therapy is discontinued preoperatively and the frequency with which clopidogrel is restarted post-CABG is unknown. Methods We examined the pattern of clopidogrel use in the Canadian Global Registry of Acute Coronary Events (GRACE), GRACE2, and CANRACE (2003-2008) post-CABG ACS patients. We stratified the patients according to whether they underwent CABG during their index hospitalization for ACS and whether they were prescribed clopidogrel at discharge. Results Among those patients in whom clopidogrel status at discharge was known, 5904 (60%) of 9841 were discharged from hospital on clopidogrel. Use of clopidogrel at discharge was observed in 2222 (40.8%) of 5443 patients who were medically managed (ie, did not undergo percutaneous coronary intervention [PCI] or CABG) and in 3585 (90.1%) of 3980 patients who underwent in-hospital PCI. Overall, 455 (3.3%) of 13,776 patients underwent CABG during the index hospitalization; 255 (56%) patients were started on clopidogrel during the first 24 hours, and 66 of these patients (25.9%) were discharged on clopidogrel. In contrast, 5681 (61.3%) of the 9262 patients who did not undergo in-hospital CABG were discharged on clopidogrel. Conclusions Although current guidelines recommend the use of clopidogrel post-CABG in patients with ACS, our observations suggest that only 1 in 4 or 5 Canadian patients are discharged on this therapy.

Clopidogrel in acute coronary syndromes: Where are we now?

Acute coronary syndromes (ACS) are the most common cause of death worldwide. In the United States, over 1,500,000 patients with an ACS are discharged annually (1). ACS is caused by disruption of an atherosclerotic plaque with superimposed thrombotic occlusion of the coronary artery, resulting in myocardial ischaemia or infarction. Platelets play a central role in the initiation and propagation of this process. As a result, effective anti-platelet therapy has become a cornerstone of ACS treatment. The objective of this article is to review the evidence regarding clopidogrel and its impact on the treatment of ACS in contemporary practice.

Explaining the unexpected: Insights from the PLATelet inhibition and clinical Outcomes (PLATO) trial comparing ticagrelor and clopidogrel

Over the last several decades a number of cardiovascular trials have provided unexpected findings that did not fit the pharmacological effects of what is known for a particular compound. The scientific community finds this very unsettling and usually within a few months there are a plethora of “potential” reasons for these unexpected findings. Dr. Frank Harrell, a noted biostatistician, some 20 years ago stated that “medical scientists are programmed to provide a plausible scientific explanation for an observation even if there is none, while biostatisticians try to determine if the observation is real in statistical terms.” In this issue of Thrombosis and Haemostasis Dr. Serebruany (1) has attempted to provide plausible “scientific” answers for some unusual observations from the PLATelet inhibition and clinical Outcomes (PLATO) trial (2) published in 2009. In this trial there was a significant reduction in cardiovascular (CV) mortality as part of a composite clinical endpoint (death, stroke and myocardial infarction). Using a hierarchical statistical testing strategy for the primary endpoint, to preserve statistical power, they concluded that the ticagrelor was superior to clopidogrel in acute coronary syndrome (ACS) for the composite endpoint, and the individual components myocardial infarction (MI) and CV mortality, but not for stroke. All-cause mortality was numerically lower as well, but statistically could not be inferred for the primary endpoint, as then adjustments had to be made to account for the multiple statistical tests that were performed. Dr. Serebruany has focused on the all-cause mortality rate which he notes was higher in the PLATO trial compared with other ACS trials. There are several flaws with his arguments as will be pointed out. The argument that the all-cause mortality observed in the PLATO trial is not consistent with other ACS trials cannot be made for many reasons. First, none of the trials quoted have included the same type of ACS patients. The PLATO trial (2) enrolled 40% ST-segment elevation myocardial infarction (STEMI) patients (with known high early mortality), while CURE (3) and ACUITY (4) included none; CHARISMA (5) was a chronic prevention trial where stable patients were enrolled (about 30% up to one year after MI (not necessarily STEMI)) and CREDO (6) was a PCI trial with only a portion of ACS patients. It is therefore expected that the overall mortality rates should be substantially different in these trials, particularly as patients were enrolled in different countries over the last decade. Second, we do not believe it is appropriate to compare the conduct and, specifically, the monitoring of the PLATO trial with other trials and to suggest that problems with these processes contributed to the mortality rates observed in the PLATO trial. Experienced clinical trial researchers understand that the operational conduct of a large, global cardiovascular trial is very complex and cannot be adequately judged or evaluated by outside “experts” who have little experience in these matters, and specifically, no role in the operational conduct of the trial in quesCorrespondence to: Prof. Magnus Ohman, MB, FRCPI, FESC, FACC Duke University Medical Center Box 3126 DUMC Durham, NC 27710, USA Tel.: +1 919 681 2069, Fax: +1 919 681 6443 E-mail: ohman001@mc.duke.edu

Clinical Summaries

Clinical Summaries

This Month in Gastroenterology

This Month in Gastroenterology

Clopidogrel in acute coronary syndrome: implications of recent study findings

The platelet ADP receptor antagonist clopidogrel is recommended for the treatment of patients with acute coronary syndrome and/or percutaneous coronary intervention. Patients who received a coronary stent in particular should be protected by sufficient antiplatelet therapy to prevent stent thrombosis. Clopidogrel is a prodrug and has to undergo extensive metabolization before the active metabolite can irreversibly bind to platelets. This makes clopidogrel treatment susceptible to genetic and drug interactions. Recent study findings suggest that initial treatment with a higher dose of clopidogrel may be superior to the currently approved dose. It is not clear whether this approach will be sufficient to entirely overcome clopidogrel hyporesponsiveness, which worsens outcomes in up to one-third of patients. Newer antiplatelet agents are emerging but clopidogrel remains the best established treatment option, with more than 120,000 patients treated in randomized trials and 12 years of clinical postmarketing experience.

Ticagrelor Versus Clopidogrel in Acute Coronary Syndromes in Relation to Renal Function

Reduced renal function is associated with a poorer prognosis and increased bleeding risk in patients with acute coronary syndromes and may therefore alter the risk-benefit ratio with antiplatelet therapies. In the Platelet Inhibition and Patient Outcomes (PLATO) trial, ticagrelor compared with clopidogrel reduced the primary composite end point of cardiovascular death, myocardial infarction, and stroke at 12 months but with similar major bleeding rates. Central laboratory serum creatinine levels were available in 15 202 (81.9%) acute coronary syndrome patients at baseline, and creatinine clearance, estimated by the Cockcroft Gault equation, was calculated. In patients with chronic kidney disease (creatinine clearance <60 mL/min; n=3237), ticagrelor versus clopidogrel significantly reduced the primary end point to 17.3% from 22.0% (hazard ratio [HR], 0.77; 95% confidence interval [CI], 0.65 to 0.90) with an absolute risk reduction greater than that of patients with normal renal function (n=11 965): 7.9% versus 8.9% (HR, 0.90; 95% CI, 0.79 to 1.02). In patients with chronic kidney disease, ticagrelor reduced total mortality (10.0% versus 14.0%; HR, 0.72; 95% CI, 0.58 to 0.89). Major bleeding rates, fatal bleedings, and non-coronary bypass-related major bleedings were not significantly different between the 2 randomized groups (15.1% versus 14.3%; HR, 1.07; 95% CI, 0.88 to 1.30; 0.34% versus 0.77%; HR, 0.48; 95% CI, 0.15 to 1.54; and 8.5% versus 7.3%; HR, 1.28; 95% CI, 0.97 to 1.68). The interactions between creatinine clearance and randomized treatment on any of the outcome variables were nonsignificant. In acute coronary syndrome patients with chronic kidney disease, ticagrelor compared with clopidogrel significantly reduces ischemic end points and mortality without a significant increase in major bleeding but with numerically more non-procedure-related bleeding. URL:http://www.clinicatrials.gov. Unique identifier: NCT00391872.

Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial

In the PLATO trial of ticagrelor versus clopidogrel for treatment of acute coronary syndromes, ticagrelor reduced the composite outcome of cardiovascular death, myocardial infarction, and stroke, but increased events of major bleeding related to non-coronary artery bypass graft (CABG). CYP2C19 and ABCB1 genotypes are known to influence the effects of clopidogrel. In this substudy, we investigated the effects of these genotypes on outcomes between and within treatment groups. DNA samples obtained from patients in the PLATO trial were genotyped for CYP2C19 loss-of-function alleles (*2, *3, *4, *5, *6, *7, and *8), the CYP2C19 gain-of-function allele *17, and the ABCB1 single nucleotide polymorphism 3435C→T. For the CYP2C19 genotype, patients were stratified by the presence or absence of any loss-of-function allele, and for the ABCB1 genotype, patients were stratified by predicted gene expression (high, intermediate, or low). The primary efficacy endpoint was the composite of cardiovascular death, myocardial infarction, or stroke after up to 12 months' treatment with ticagrelor or clopidogrel. 10 285 patients provided samples for genetic analysis. The primary outcome occurred less often with ticagrelor versus clopidogrel, irrespective of CYP2C19 genotype: 8·6% versus 11·2% (hazard ratio 0·77, 95% CI 0·60-0·99, p=0·0380) in patients with any loss-of-function allele; and 8·8% versus 10·0% (0·86, 0·74-1·01, p=0·0608) in those without any loss-of-function allele (interaction p=0·46). For the ABCB1 genotype, event rates for the primary outcome were also consistently lower in the ticagrelor than in the clopidogrel group for all genotype groups (interaction p=0·39; 8·8%vs 11·9%; 0·71, 0·55-0·92 for the high-expression genotype). In the clopidogrel group, the event rate at 30 days was higher in patients with than in those without any loss-of-function CYP2C19 alleles (5·7%vs 3·8%, p=0·028), leading to earlier separation of event rates between treatment groups in patients with loss-of-function alleles. Patients on clopidogrel who had any gain-of-function CYP2C19 allele had a higher frequency of major bleeding (11·9%) than did those without any gain-of-function or loss-of-function alleles (9·5%; p=0·022), but interaction between treatment and genotype groups was not significant for any type of major bleeding. Ticagrelor is a more efficacious treatment for acute coronary syndromes than is clopidogrel, irrespective of CYP2C19 and ABCB1 polymorphisms. Use of ticagrelor instead of clopidogrel eliminates the need for presently recommended genetic testing before dual antiplatelet treatment. AstraZeneca.

Discontinuation of antiplatelet agents

Neurologists frequently lament that we are about a decade behind cardiologists: therapies initially pioneered in coronary artery disease, such as use of thrombolytics and statins, eventually filter down to the treatment of stroke. However, an opportunity presents itself by taking advantage of cardiology therapeutic advances or red flags raised in the treatment of coronary artery disease. Should neurologists be concerned about potential implications for our patients with stroke or TIAs if concerns arise in the context of cardiovascular disease? One concern that has been raised is the potential for adverse vascular events following the discontinuation of clopidogrel1 in those receiving dual antiplatelet therapy with aspirin and clopidogrel for acute coronary syndrome. In these patients, dual antiplatelet therapy is frequently administered for 3 to 12 months and subsequently aspirin monotherapy is continued indefinitely. A few …

Prasugrel vs. clopidogrel for cytochromeP450 2C19-genotyped subgroups: integration of the TRITON-TIMI38 trial data.

Prasugrel is a newly marketed antiplatelet drug with improved cardiac outcomes as compared with clopidogrel for acute coronary syndromes involving percutaneous coronary intervention (PCI). Analysis of a subset of the TRITON-TIMI 38 trial demonstrated that cytochrome P450 2C19 (CYP2C19) reduced-function genotypes are associated with differential clinical responses to clopidogrel, but not prasugrel. Whether the CYP2C19 genotype has the potential to influence clinical choice of these drugs prior to PCI for individuals with unstable angina or non-ST segment elevation myocardial infarction is currently uncertain. An exploratory, secondary analysis was undertaken to estimate the clinical benefit of prasugrel over clopidogrel in subgroups defined by CYP2C19 genotype, by integrating the published results of the genetic substudy and the overall TRITON-TIMI 38 trial. Individuals with a CYP2C19 reduced-metabolizer genotype were estimated to have a substantial reduction in the risk of the composite primary outcome (cardiovascular death, myocardial infarction, or stroke) with prasugrel as compared with clopidogrel [relative risk (RR) 0.57; 95% confidence interval (CI) 0.39-0.83]. For CYP2C19 extensive metabolizers (∼70% of the population), however, the composite outcome risks with prasugrel and clopidogrel were not substantially different (RR 0.98; 95% CI 0.80-1.20). Integration of the TRITON-TIMI 38 data suggests that the CYP2C19 genotype can discriminate between individuals who receive extensive benefit from using prasugrel instead of clopidogrel, and individuals with comparable clinical outcomes with prasugrel and clopidorel. Thus, CYP2C19 genotyping has the potential to guide the choice of antiplatelet therapy, and further research is warranted to validate this estimate.

Ticagrelor was more effective than clopidogrel in acute coronary syndromes with planned invasive treatment

Source Citation Cannon CP, Harrington RA, James S, et al. Comparison of ticagrelor with clopidogrel in patients with a planned invasive strategy for acute coronary syndromes (PLATO): a randomised d...