Acute Coronary Stent Thrombosis Research Articles

Influenza vaccination and cardiovascular events in patients with ischaemic heart disease and heart failure: A meta-analysis.

Randomized controlled trials (RCTs) enrolling patients at high cardiovascular risk have found that influenza vaccination may reduce the incidence of cardiovascular events. We performed an updated meta-analysis assessing the effect of influenza vaccination on the incidence of cardiovascular events in patients with ischaemic heart disease or heart failure. We searched PubMed, EMBASE and other sources to identify RCTs examining the effect of influenza vaccination on the incidence of cardiovascular events assessed as efficacy outcomes in patients with ischaemic heart disease or heart failure. Eligible studies followed patients for at least one influenza season, defined as a minimum duration of 6 months. The primary endpoint was a composite of cardiovascular death, acute coronary syndrome, stent thrombosis or coronary revascularization, stroke or heart failure hospitalization. The secondary endpoints were cardiovascular death and all-cause death. Two investigators independently identified and extracted data from studies. Results were compared using hazard ratios (HRs) in both random effects and fixed effects models. We included five peer-reviewed and one non peer-reviewed RCTs for a total of 9340 patients. Five trials included patients with ischaemic heart disease (n = 4211) and one trial included patients with heart failure (n = 5129). Influenza vaccination was associated with a reduced incidence of the primary composite endpoint (random effects HR [rHR] 0.74, 95% confidence interval [CI] 0.63-0.88, p < 0.001, I2 = 52%), cardiovascular death (rHR 0.63, 95% CI 0.42-0.95, p = 0.028, I2 = 58%) and all-cause death (rHR 0.72, 95% CI 0.54-0.95, p = 0.0227, I2 = 52%). Results were similar when non peer-reviewed data were excluded. In this meta-analysis of available RCTs in patients at high cardiovascular risk, influenza vaccination was associated with a reduced incidence of cardiovascular events, cardiovascular death and all-cause death as compared to placebo or no treatment.

Acute coronary artery stent thrombosis caused by a spasm: A case report

Acute coronary artery stent thrombosis caused by a spasm: A case report

Aspirin vs. Clopidogrel as a Chronic maintenance monotherapy after PCI in patients with high ischemic risk and high bleeding risk: Subgroup analysis of the HOST-EXAM trial

Abstract Funding Acknowledgements Type of funding sources: None. OnBehalf on behalf of the HOST-EXAM investigators Background The HOST-EXAM randomized clinical trial recently performed a comparison of clopidogrel monotherapy vs. aspirin monotherapy in patients requiring indefinite antiplatelet monotherapy after percutaneous coronary intervention (PCI). This study randomized 5,438 patients who maintained dual antiplatelet therapy without clinical events for 6–18 months after PCI with drug-eluting stents (DES) to receive a monotherapy agent of clopidogrel 75 mg once daily or aspirin 100 mg once daily for 24 months. During the 24-month follow-up, the primary outcome (a composite of all-cause death, non-fatal myocardial infarction, stroke, readmission due to acute coronary syndrome, and Bleeding Academic Research Consortium (BARC) bleeding type 3 or greater) rate was significantly lower in the clopidogrel group (hazard ratio [HR] 0.73 [95% CI 0.59–0.90]; p = 0.0035). However, it is uncertain whether the beneficial effect of clopidogrel will be consistent in patients with high ischemic risk or those with high bleeding risk. Methods This is a post-hoc analysis of the HOST-EXAM trial. A high ischemic risk was defined as those who had at least 1 of the following procedural features: 3 vessels treated, ≥3 stents implanted, ≥3 lesions treated, bifurcation PCI, total stent length &amp;gt;60 mm, or left main PCI. Patients with high bleeding risk were defined according to the Academic Research Consortium for High Bleeding Risk (ARC-HBR) criteria. The co-primary outcome were thrombotic endpoints (a composite of cardiac death, non-fatal myocardial infarction, ischemic stroke, readmission due to acute coronary syndrome, and definite or probable stent thrombosis) and bleeding endpoints (BARC type ≥2 bleeding events) at 24-month follow-up. Results Among the total population, 22.1% had high ischemic risk and 21.4% had high bleeding risk. Complex PCI was not associated with a higher risk of thrombotic endpoints, nor bleeding endpoints. For patients with a high bleeding risk, these patients had a higher risk of both thrombotic endpoints (HR 1.545, 95% CI 0.141-2.092, p = 0.005) and bleeding endpoints (HR 3.418, 95% CI 2.413-4.840, p &amp;lt; 0.001). The primary results focusing on the interaction between high ischemic risk, high bleeding and the antiplatelet regimen will be presented. Conclusion The current post-hoc analysis of the HOST-EXAM trial will evaluate the efficacy of clopidogrel monotherapy vs. aspirin monotherapy during the chronic maintenance period after PCI, in patients with high ischemic risk or those with high bleeding risk.

Abstract 14077: One-year Outcome After PCI in Patients Treated Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers - Subanalysis From Multicenter Registry -

Background: The prescription of inhibitors for renin-angiotensin-aldosterone system (RAAS) is associated with improved prognosis but have respectively different mechanisms of action in patients with coronary artery disease (CAD). We aimed to compare the clinical outcomes between angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) therapy in patients with CAD undergoing percutaneous coronary intervention (PCI). Methods: This study is a subanalysis from the TWINCRE registry that is a multicentral prospective cohort including patients who underwent PCI. After excluding 18 patients who received both ACEi and ARB from 2,896 registered patients, we ultimately evaluated 369 patients treated with ACEi, 492 with ARB and 541 without ACEi or ARB. The primary endpoint was a major adverse cardiovascular and cerebrovascular events (MACCE) including death from any cause, acute coronary syndrome, stent thrombosis, stroke and hospitalization for heart failure. The impact of RAAS inhibitors on all-cause mortality alone was also evaluated. Results: During the observation period with 366 days of a median follow-up, Kaplan-Meier analysis revealed that the ARB group had the lowest rate of MACCE than other two groups (Log-rank for trend, p&amp;lt; for &lt; 0.0001, Figure). Regarding all-cause mortality, the ARB group and ACEi group had comparable rates for MACCE, which were lower than the no-ACEi/ARB group (p&amp;lt; for &lt; 0.0001). In a Cox regression analysis, after adjusting with age, gender, comorbidities, multivessel disease, acute myocardial infarction, and medications at discharge including dual antiplatelet therapy and statins, ARB therapy was still had a superiority to ACEi therapy regarding with MACCE (hazard ratio: 0.54, 95% confidence interval: 0.30-0.98). Conclusion: In the multicenter cohort study, ARB therapy was associated with better one-year clinical outcomes compared to ACEi therapy in patients undergoing PCI.

Abstract 14931: Low-Dose Prasugrel Has Prognostic Superiority to Clopidogrel in High-Bleeding Risk Patients Undergoing Contemporary Percutaneous Coronary Intervention

Introduction: The combination of aspirin and P2Y12 receptor antagonist is the standard antiplatelet therapy after percutaneous coronary intervention (PCI). Previous trials reported that prasugrel reduced the risk of ischemic events, but increased bleeding events compared to clopidogrel. Hypothesis: The prognostic impact of low-dose prasugrel (3.75 mg/day), which the dose was determined by phase II trial, is different from that of clopidogrel, depending on patient’s bleeding risk. Methods: This study is a subanalysis from the TWINCRE registry that is a multicentral prospective cohort including patients who underwent PCI. We analyzed 1,001 patients who received the combination of aspirin and prasugrel or clopidogrel after PCI. The primary endpoint was a composite of major bleeding event and major adverse cardiovascular and cerebrovascular events (MACCE) including any death, acute coronary syndrome, stent thrombosis, stroke and heart failure hospitalization. Results: There were 490 patients with high bleeding risk (HBR) and 511 patients with low bleeding risk (LBR), based on ARC-HBR criteria. In HBR patients, the Low-dose prasugrel group had significantly lower rates of MACCE (Log-rank, p=0.003) and the composite endpoint than the Clopidogrel group (p=0.001). While, in LBR patients, there was no significant difference in rates of MACCE or the composite endpoint between the groups (p=0.76, p=0.15, respectively), and a higher rate of major bleeding event in the Low-dose prasugrel group (p=0.002). With Cox proportional hazards analysis, low-dose prasugrel has still retained the superiority to clopidogrel regarding with the composite endpoint in HBR patients, even after adjusting with diverse covariates (hazard ratio: 0.33, 95% confidence interval: 0.16-0.65). Conclusion: In the multicenter cohort study in Japan, low-dose prasugrel showed a long-term prognostic superiority to clopidogrel only in HBR patients undergoing contemporary PCI.

Allergic Acute Coronary Artery Stent Thrombosis After the Administration of Sugammadex in a Patient Undergoing General Anesthesia: A Case Report

In addition to cutaneous, gastrointestinal, hemodynamic, and respiratory symptoms, allergic reactions can induce an acute coronary syndrome in normal or atheromatous coronary arteries and can cause coronary stent thrombosis. Here, we report a case of coronary stent thrombosis due to allergic acute coronary syndrome during anaphylaxis induced by sugammadex in a female patient undergoing general anesthesia. She was emergently treated with percutaneous transluminal coronary balloon angioplasty with catecholamine, vasodilator, and intraaortic balloon support. Knowledge of perioperative allergy-triggered acute coronary syndrome is crucial for prompt and appropriate treatment.

Etiology of Acute Coronary Syndrome after Noncardiac Surgery.

The objective of this investigation was to determine the etiology of perioperative acute coronary syndrome with a particular emphasis on thrombosis versus demand ischemia. In this retrospective cohort study, adult patients were identified who underwent coronary angiography for acute coronary syndrome within 30 days of noncardiac surgery at a major tertiary hospital between January 2008 and July 2015. Angiograms were independently reviewed by two interventional cardiologists who were blinded to clinical data and outcomes. Acute coronary syndrome was classified as ST-elevation myocardial infarction, non-ST-elevation myocardial infarction, or unstable angina; myocardial infarctions were adjudicated as type 1 (plaque rupture), type 2 (demand ischemia), or type 4b (stent thrombosis). Among 215,077 patients screened, 146 patients were identified who developed acute coronary syndrome: 117 were classified as non-ST-elevation myocardial infarction (80.1%); 21 (14.4%) were classified as ST-elevation myocardial infarction, and 8 (5.5%) were classified as unstable angina. After coronary angiography, most events were adjudicated as demand ischemia (type 2 myocardial infarction, n = 106, 72.6%) compared to acute coronary thrombosis (type 1 myocardial infarction, n = 37, 25.3%) and stent thrombosis (type 4B, n = 3, 2.1%). Absent or only mild, nonobstructive coronary artery disease was found in 39 patients (26.7%). In 14 patients (9.6%), acute coronary syndrome was likely due to stress-induced cardiomyopathy. Aggregate 30-day and 1-yr mortality rates were 7 and 14%, respectively. The dominant mechanism of perioperative acute coronary syndrome in our cohort was demand ischemia. A subset of patients had no evidence of obstructive coronary artery disease, but findings were consistent with stress-induced cardiomyopathy.

Erythropoietin therapy after out-of-hospital cardiac arrest: A systematic review and meta-analysis.

AIMTo assess safety and efficacy of early erythropoietin (Epo) administration in patients with out-of-hospital cardiac arrest (OHCA).METHODSA systematic literature search was performed using PubMed, MEDLINE, EMBASE, EBSCO, CINAHL, Web of Science and Cochrane databases, of all studies published from the inception through October 10, 2016. Inclusion criteria included: (1) Adult humans with OHCA and successful sustained return of spontaneous circulation; and (2) studies including mortality/brain death, acute thrombotic events as their end points. Primary efficacy outcome was “brain death or Cerebral Performance Category (CPC) score of 5”. Secondary outcomes were “CPC score 1, and 2-4”, “overall thrombotic events” and “acute coronary stent thrombosis”.RESULTSWe analyzed a total of 606 participants (n = 276 received Epo and n = 330 with standard of care alone) who experienced OHCA enrolled in 3 clinical trials. No significant difference was observed between the Epo and no Epo group in brain death or CPC score 5 (OR = 0.77; 95%CI: 0.42-1.39), CPC score 1 (OR = 1.16, 95%CI: 0.82-1.64), and CPC score 2-4 (OR = 0.77, 95%CI: 0.44-1.36). Epo group was associated with increased thrombotic complications (OR = 2.41, 95%CI: 1.26-4.62) and acute coronary stent thrombosis (OR = 8.16, 95%CI: 1.39-47.99). No publication bias was observed.CONCLUSIONOur study demonstrates no improvement in neurological outcomes and increased incidence of thrombotic events and acute coronary stent thrombosis in OHCA patients who were treated with Epo in addition to standard therapy.

Efficacy and safety of triple versus dual antithrombotic therapy in atrial fibrillation and ischemic heart disease: a systematic review and meta-analysis.

The optimal antithrombotic regimen for patients with atrial fibrillation and ischemic heart disease remains unclear. Therefore, we aimed to compare the efficacy and safety of triple therapy (TT [an anticoagulant and 2 antiplatelet drugs]) with dual therapy (DAPT [2 antiplatelet drugs] or DT [an anticoagulant and a single antiplatelet drug]) in patients with atrial fibrillation and ischemic heart disease. We systematically searched the Cochrane Library, PubMed and Embase databases for all relevant studies up to August 2017. The overall risk estimates were calculated using the random-effects model. A total of 17 observational studies were included. Regarding the efficacy outcomes, no differences were observed between the triple therapy and the dual therapy for all-cause death, cardiovascular death, or thrombotic complications (i.e., acute coronary syndrome, stent thrombosis, thromboembolism/stroke, and major adverse cardiac and cerebrovascular events). Regarding the safety outcomes, compared with DAPT, TT was associated with increased risks of major bleeding (a relative risk of 1.96 [1.40–2.74]), minor bleeding (1.69 [1.06–2.71]) and overall bleeding (1.80 [1.23–2.64]). Compared wtih DT, TT was associated with a greater risk of major bleeding (1.65 [1.23–2.21]), but rates of minor bleeding (0.99 [0.56–1.77]) and overall bleeding (1.14 [0.76–1.71]) were similar. Overall, TT confers an increased hazard of major bleeding with no thromboembolic protection compared with dual therapy in patients with atrial fibrillation and ischemic heart disease.

Paraoxonase 1 (Q192R) gene polymorphism, coronary heart disease and the risk of a new acute coronary event

IntroductionParaoxonase 1 (PON1) plays a major role in the oxidation of low density lipoprotein and in the prevention of coronary atherogenesis. In this context, coding region polymorphisms of PON1 gene, responsible for the enzyme activity, has become of interest as a marker for atherogenesis. MethodsA study and follow-up was conducted on 529 patients with an acute coronary event in order to assess the association between the PON1 Q192R (rs662;A/G) polymorphism, the type of acute coronary syndrome, cardiovascular risk factors (arterial hypertension, diabetes mellitus, dyslipidaemia, and smoking), the extent and severity of coronary atherosclerosis, and the medium-term clinical follow-up. ResultsThe QQ genotype was found in 245 (46.3%) patients, with 218 (41.2%) patients showing the QR genotype, and 66 (14.5%) patients had the RR genotype. No significant differences were found between the QQ and QR/RR genotypes as regards the clinical characteristics, the analytical data, and the angiographic variables. Similarly, Kaplan–Meier survival analysis showed no significant differences in presenting with a new acute coronary event (p=0.598), cardiac mortality (p=0.701), stent thrombosis (p=0.508), or stent re-stenosis (p=0.598) between QQ and QR/RR genotypes during the follow-up period (3.3±2.2 years). ConclusionsIn patients with an acute coronary syndrome, the PON1 Q192R genotypes did not influence the risk of suffering a new acute coronary event during the medium-term follow-up.

Paraoxonase 1 (Q192R) gene polymorphism, coronary heart disease and the risk of a new acute coronary event

IntroductionParaoxonase 1 (PON1) plays a major role in the oxidation of low density lipoprotein and in the prevention of coronary atherogenesis. In this context, coding region polymorphisms of PON1 gene, responsible for the enzyme activity, has become of interest as a marker for atherogenesis. MethodsA study and follow-up was conducted on 529 patients with an acute coronary event in order to assess the association between the PON1 Q192R (rs662;A/G) polymorphism, the type of acute coronary syndrome, cardiovascular risk factors (arterial hypertension, diabetes mellitus, dyslipidaemia, and smoking), the extent and severity of coronary atherosclerosis, and the medium-term clinical follow-up. ResultsThe QQ genotype was found in 245 (46.3%) patients, with 218 (41.2%) patients showing the QR genotype, and 66 (14.5%) patients had the RR genotype. No significant differences were found between the QQ and QR/RR genotypes as regards the clinical characteristics, the analytical data, and the angiographic variables. Similarly, Kaplan–Meier survival analysis showed no significant differences in presenting with a new acute coronary event (p=0.598), cardiac mortality (p=0.701), stent thrombosis (p=0.508), or stent re-stenosis (p=0.598) between QQ and QR/RR genotypes during the follow-up period (3.3±2.2 years). ConclusionsIn patients with an acute coronary syndrome, the PON1 Q192R genotypes did not influence the risk of suffering a new acute coronary event during the medium-term follow-up.

Gene polymorphism of CYP2C19*2, *3 and CYP3A4*1B and early stent thrombosis: case reports and literature review.

We present two clinical cases of acute and subacute coronary artery stent thrombosis in patients treated at the Department of Interventional Cardiology in Aktobe, Kazakhstan. Our results draw attention to the impact of CYP3A4*1B on the clinical effect of clopidogrel during dual antiplatelet therapy after PCI. The genotyping performed at the Laboratory of Molecular Cardiology of Institute of Cardiology of Lithuanian University of Health Sciences in Lithuania revealed that both patients were homozygous carriers of CYP3A4*1B*1B. They also were carriers of CYP2C19 loss-of-function *2 or *3 alleles (*1*2 and *1*3, respectively).

First report of stent thrombosis after a switch therapy resulting from ticagrelor-related dyspnea

Keyword: Acute coronary syndrome Stent thrombosis Ticagrelor Balloon angioplasty and subsequent stenting (a 2.4 mm × 18 mm sirolimus-eluting stent, EXCEL, JW, China) of the right coronary artery (RCA) lesion was performed with good angiographic results (Fig. 1B). He was discharged from the hospital on a regimen of aspirin (100 mg once daily) and ticagrelor (90 mg twice daily). Ten days later, the patients still complained of dyspnea and went to his local clinic. Ticagrelor was switched to clopidogrel 75 mg daily without loading dose. Clopidogrel therapy was commenced at about 12 h after the last dose of ticagrelor. Dyspnea was alleviated by the

Monitoring Aspirin and Clopidogrel Response: Testing Controversies and Recommendations

Antiplatelet therapy is the cornerstone of the treatment for patients with coronary artery disease (CAD). Dual therapy with clopidogrel and aspirin is currently the standard treatment after percutaneous coronary interventions. However, despite the use of clopidogrel, a considerable number of patients continue to suffer major adverse cardiac events. There is a growing degree of evidence supporting high on-treatment platelet reactivity (HPR) as a predictive factor for recurrent ischemic complications. Numerous studies have shown an interindividual variability of responsiveness to clopidogrel and aspirin, which is one of the reasons for HPR. There is yet to be established an assay for antiplatelet drug response as the gold standard. This paper provides a background to the current controversies surrounding the issue of testing for the effectiveness of antiplatelet therapy and reviews the various genetic and phenotype-based laboratory tests to measure aspirin and clopidogrel response and their correlation with clinical outcomes. On the basis of the current evidence and trying to be cost-effective, testing should be considered on a case-by-case basis, especially in patients who present with an acute coronary syndrome or stent thrombosis. In the case of stable CAD, we think that testing might be helpful in particular risk groups of patients to avoid ischemic or bleeding complications.

Kounis syndrome: a monster for the atopic patient.

When anaphylactic or anaphylactoid and allergic or hypersensitivity reactions from causes such as insect stings, drugs and other environmental exposures combine with cardiovascular signs and symptoms, acute coronary events and stent thrombosis with thrombus infiltrated by eosinophils and/or mast cells, the result is the Kounis hypersensitivity associated syndrome (1).

Dual non-responsiveness to antiplatelet treatment is a stronger predictor of cardiac adverse events than isolated non-responsiveness to clopidogrel or aspirin

BackgroundHigh platelet reactivity (HPR) under treatment with clopidogrel or aspirin is associated with adverse outcome. We aimed to investigate whether high platelet reactivity (HPR) to both aspirin and clopidogrel is a stronger predictor of adverse events compared to isolated HPR to clopidogrel or aspirin. MethodsIn this prospective cohort study platelet reactivity to adenosine diphosphate (ADP) and arachidonic acid (AA) was assessed by Multiple Electrode Aggregometry (MEA) in 403 patients undergoing percutaneous coronary intervention. The rates of the composite of cardiac adverse events (acute coronary syndrome, stent thrombosis, stroke, death and revascularization) were recorded during 12-month follow-up. ResultsThe composite endpoint of cardiovascular adverse events occurred more often in patients with high platelet reactivity (HPR) to both agonists ADP and AA (37.5%) than in those with isolated HPR to ADP (33.3%), AA (25.6%) or without any HPR (18.6%; p=0.003). Classification tree analysis indicated that any HPR emerged as an independent predictor influencing outcome, which was associated with a 1.75 higher risk of cardiac adverse events (OR=1.75: 95%CI=1.1–2.9). Interestingly, the predictive value of HPR tended to be greater among patients with diabetes mellitus (OR=2.18; 95%CI=1.20–3.95). C-reactive protein and diabetes mellitus were independent predictors of high platelet reactivity to both agonists. ConclusionsDual low responsiveness to clopidogrel and aspirin is a strong predictor of cardiac adverse events, especially in patients with diabetes mellitus, which underlines the need for personalized antiplatelet treatment.

Acute Coronary Stent Thrombosis in Cancer Patients: A Case Series Report

There have been a growing numbers of patients diagnosed with malignancy and coronary artery disease simultaneously or serially. In the era of percutaneous coronary intervention (PCI), stent thrombosis has been a rare but challenging problem. Recently, we experienced two unique cases of acute stent thrombosis in patients with malignancy. The first case showed acute and subacute stent thrombosis after PCI. The second case revealed simultaneous thromboses in stent and non-treated native coronary artery. We believe that we need rigorous precautions in the treatment of patients with coronary artery disease and malignancy, especially with regards to deciding how and whether to revascularize, as well as which anti-platelet agents to select.

Disseminated Intravascular Coagulation as a Possible Cause of Acute Coronary Stent Thrombosis: A Case Report and Literature Review

Disseminated intravascular coagulation (DIC), as a cause of acute coronary stent thrombosis, has not yet been reported to our knowledge. We report a case of 64-year-old male, who presented with non-ST-segment elevation myocardial infarction (NSTEMI). Coronary angiography revealed right coronary artery (RCA) stenosis and a drug eluting stent was deployed. Fifteen hours following the intervention, the patient developed an inferior wall ST elevation myocardial infarction. Repeat cardiac catheterization showed an acute in-stent thrombosis. Following thrombectomy, another stent was placed. The patient noted to have an acute drop in platelet count following the second intervention. Two hours following repeat intervention, the patient again developed chest pain and EKG showed recurrent ST-segment elevations in leads II, III, and aVF. Prior to repeat cardiac catheterization, the patient became unresponsive and developed cardiogenic shock. The patient was resuscitated and intubated, and repeat catheterization showed complete stent thrombosis. Intracoronary tissue plasminogen activator (tPA) was given. The platelet count further dropped. Additional studies confirmed the diagnosis of DIC. No further cardiac catheterization was done at this point. The patient then later had a cardiac arrest and unfortunately cardiopulmonary resuscitation could not revive him. Amongst the etiologies of acute stent thrombosis, DIC was deemed a possible cause.

Extended-Infusion Eptifibatide to Prevent Stent Thrombosis in a Patient Undergoing Orthopedic Surgery

To report the use of extended-infusion eptifibatide in a patient who had undergone placement of a drug-eluting stent and required repeat intervention of a hip fracture following mechanical failure. An 82-year-old female with an extensive history of coronary disease who had undergone placement of a drug-eluting stent was admitted following continued problems with her surgically repaired right hip. Radiographic imaging of the area revealed mechanical failure of the surgically repaired hip, requiring intervention. Clopidogrel and aspirin therapy was discontinued and intravenous eptifibatide 1 μg/kg/min was initiated prior to surgery; the drugs were then discontinued 4 hours before the procedure. During this admission, the patient received a total of 155 hours of eptifibatide to prevent acute coronary stent thrombosis while awaiting surgical intervention. Postoperatively, the patient experienced anemia and severe thrombocytopenia and required 11 units of packed red blood cells, but displayed no signs of stent thrombosis. Use of eptifibatide in this patient minimized the potential risk for stent thrombosis by reducing the interruption in antiplatelet therapy from 5 days, as is recommended for use with clopidogrel, to 4 hours. While this patient required several transfusions and experienced severe thrombocytopenia postoperatively, she recovered and had no cardiac-related problems. It is unclear whether the use of eptifibatide contributed to these complications, given the chronology of events. Extended-infusion eptifibatide appears to be an option for prevention of stent thrombosis in patients who require an interruption in antiplatelet therapy and are scheduled to undergo major orthopedic procedures. Careful consideration should be given regarding the risks and benefits of extended infusions of eptifibatide, as the potential for significant hemorrhage is a concern. Further research is warranted in this area.

Life-threatening cardiac manifestations of primary antiphospholipid syndrome

We report a rare case of primary antiphospholipid syndrome (APS) in a 43-year-old man presenting as recurrent acute coronary stent thrombosis and complicated by three myocardial infarctions. As illustrated in this report, in APS patients recurrent life-threatening arterial thrombotic events may occur in spite of recommended anticoagulant therapy. We conclude that the APS should be considered as a potential cause of acute coronary syndrome, particularly in young individuals with a history of recurrent thrombotic events and/or with abnormal coagulation test results. Further studies are needed to determine the best therapeutic strategy for APS patients with acute coronary syndrome.