Incidence Of Recurrent Ischemic Events Research Articles

Pharmacogenomic Polygenic Model of Clopidogrel Predicts Recurrent Ischemic Events in Chinese Patients With Coronary Artery Disease

Patients with coronary artery disease (CAD) need to take antiplatelet drugs regularly in order to prevent thrombosis; however, there is existing inter-individual variability in drug response. Pharmacogenomic studies indicate that drug response may also be influenced by genetic variants, and multiple genetic variants may work together. We assumed that patients carrying more risk alleles might have a worse clopidogrel drug response and that a polygenic model integrated different single variants might have the potential to explain clopidogrel drug response variability better. We aimed to investigate whether the polygenic model could be used to predict clopidogrel drug response. A total of 935 CAD patients were enrolled in the study. We investigated the association between 19 clopidogrel-related single-nucleotide polymorphisms (SNPs) and the incidence of recurrent ischemic events. Additionally, a polygenic model was constructed to assess the risk of ischemic events. There were only 2 SNPs of CYP2C8 gene (rs1934980 and rs17110453) that were nominally associated with incidence of recurrent ischemic events. We constructed a polygenic model integrated with 6 clopidogrel-related SNPs. When compared with patients carrying 6 or fewer risk alleles, patients with 7 or more risk alleles had a higher risk of ischemic events (hazard ratio = 1.87; P = 0.04). The polygenetic model may be useful for clopidogrel drug response prediction in patients with CAD.

Association between Red Blood Cell Distribution Width and Neutrophil-to-lymphocyte Ratio and the Incidence of Recurrent Ischemic Events in Patients with Transient Ischemic Attack

Association between Red Blood Cell Distribution Width and Neutrophil-to-lymphocyte Ratio and the Incidence of Recurrent Ischemic Events in Patients with Transient Ischemic Attack

Effect of pretreatment with a P2Y12 inhibitor in patients with non-ST-elevation acute coronary syndrome: a systematic review and network meta-analysis.

This study aimed to systematically evaluate the effects of different types and doses of pretreatment with P2Y12 inhibitors in patients with non-ST-elevation acute coronary syndrome (NSTE-ACS) undergoing percutaneous coronary intervention (PCI). Electronic databases were searched for studies comparing pretreatment with different types and doses of P2Y12 inhibitors or comparison between P2Y12 inhibitor pretreatment and nonpretreatment. Electronic databases included the Cochrane Library, PubMed, EMBASE, and Web of Science. Literature was obtained from the establishment of each database until June 2022. The patients included in the study had pretreatment with P2Y12 inhibitors with long-term oral or loading doses, or conventional aspirin treatment (non-pretreatment). The primary endpoint was major adverse cardiac and cerebrovascular events (MACCEs) during follow-up within 30 days after PCI, which included determining the composite endpoints of cardiac death, myocardial infarction, ischemia-driven revascularization, and stroke. The safety endpoint was a major bleeding event. A total of 119,014 patients from 21 studies were enrolled, including 13 RCTs and eight observational studies. A total of six types of interventions were included-nonpretreatment (placebo), clopidogrel pretreatment, ticagrelor pretreatment, prasugrel pretreatment, double loading pretreatment (double loading dose of clopidogrel, ticagrelor, prasugrel) and P2Y12 inhibitors pretreatment (the included studies did not distinguish the types of P2Y12 inhibitors, including clopidogrel, ticagrelor, and prasugrel). The network meta-analysis results showed that compared to patients without pretreatment, patients receiving clopidogrel pretreatment (RR = 0.78, 95% CI:0.66, 0.91, P < 0.05) and double-loading pretreatment (RR = 0.62, 95% CI:0.41, 0.95, P < 0.05) had a lower incidence of MACCEs. There was no statistically significant difference in the incidence of major bleeding events among the six pretreatments (P > 0.05). In patients with NSTE-ACS, pretreatment with P2Y12 inhibitors before percutaneous intervention reduced the incidence of recurrent ischemic events without increasing the risk of major bleeding after PCI compared with nonpretreatment. Clopidogrel or double loading dose P2Y12 inhibitors can be considered for the selection of pretreatment drugs.

Whether it is safe to start anticoagulation after intracranial hemorrhage within 2 weeks: A systematic review and meta-analysis.

Whether restarting anticoagulation (RA) treatment after intracranial hemorrhage (ICH) is still controversial. We performed a systematic review and meta-analysis to summarize the relationship between anticoagulation after ICH with the recurrence of hemorrhagic events, ischemic events, and long-term mortality. Medline, Embase, and the Cochrane Central Register of Controlled Trials, from inception to November 2020. We searched the published medical literature to ensure cohort studies involving ICH associated with anticoagulation in adults. Primary outcomes were long-term mortality, hemorrhagic events, and ischemic events (myocardial infarction, pulmonary embolism, ischemic stroke, or systemic embolization). We concluded seven retrospective cohorts, including 1876 intracranial hemorrhage patients with indications of anticoagulation. The ratio of the anticoagulant restart was 35.3% (664n). RA was associated with a significantly lower incidence of recurrent ischemic events (pooled odds ratio [OR] 0.29, 95% confidence interval [CI] 0.19% to 0.45%, p = 0.97) and death events (pooled OR 0.56, 95% CI 0.40%-0.79%, p = 0.27). There is no evidence that early recovery of anticoagulation (within 2 weeks or 1 month) is associated with the occurrence of hemorrhagic events (within 2 weeks: pooled OR 0.80, 95% CI 0.3-2.12, p = 0.52 vs. within 1 month: pooled OR 1.14, 95% CI 0.77-1.68, p = 0.82). Based on these, recovery of anticoagulation after ICH is beneficial for long-term mortality and recurrence of ischemic events. The meta-analysis showed a resumption of oral anticoagulation within 2 weeks or 1 month in patients who had a cerebral hemorrhage was beneficial and did not increase the risk of hemorrhagic events and reduced the occurrence of ischemic and fatal endpoint events.

Transcatheter Closure of Patent Foramen Ovale in Older Patients With Cryptogenic Thromboembolic Events.

The main randomized trials evaluating patent foramen ovale (PFO) closure after a presumed PFO-associated stroke excluded patients older than 60 years. We aimed to evaluate the early- and long-term clinical outcomes of transcatheter PFO closure in older (>60 years) patients with a cryptogenic ischemic event. This is a multicenter study including consecutive patients older than 60 years (mean age, 67±5 years) who had a PFO closure following a presumed PFO-related ischemic event. Patients ≤60 years old (mean age, 44±10 years) served as the control group. The primary end point was the occurrence of stroke, transient ischemic attack, or peripheral embolism over the follow-up period. New-onset atrial fibrillation was a secondary end point. A total of 388 and 883 patients >60 and ≤60 years old were included, respectively. Procedural success rate was high (99.9%), and procedural-related complications low (<2%) in both groups. After a median follow-up of 3 (1-8) years, older patients exhibited an incidence of stroke/transient ischemic attack/peripheral embolism of 1.6 events per 100 patient-years (stroke: 0.6 events per 100 patient-years), lower than that expected according to the risk of paradoxical embolism score (observed-to-expected ratio, 0.31 [95% CI, 0.11-0.91]). However, the event rate in older patients was higher than that observed in their younger counterparts (incidence rate ratio, 4.7 [95% CI, 2.36-9.8]). De novo atrial fibrillation after the procedure was more frequent in older patients (2.66 per 100 patient-years versus 0.49 per 100 patient-years, P<0.001). In patients older than 60 years with a presumed PFO-related ischemic event, PFO closure was safe and associated with a relatively low incidence of recurrent ischemic events after a median follow-up of 3 years compared with historical cohorts of patients who did not undergo PFO closure. However, a higher risk of recurrent cerebrovascular events was observed in older patients compared to their younger counterparts. Randomized trials are warranted in this population.

Gastro-Cardiology: A Novel Perspective for the Gastrocardiac Syndrome.

The gastrocardiac syndrome was coined originally at the beginning of the 19th century to describe an alleged gastric-cardiopathy with reflux heartburn mimicking cardiac chest pain. Today, a wider perspective of gastrocardiac syndrome has emerged. First, the cardiovascular risk factor chronic systemic inflammation may reflect gastroenterological inflammatory conditions, such as inflammatory bowel disease and gastrointestinal infections, in particular, chronic Helicobacter pylori infection. Furthermore, since contemporary treatment of cardiovascular disease commonly includes potent antithrombotic medications, the cardiovascular benefit in terms of a decrease in the incidence of recurrent ischemic events and death needs to be carefully balanced with an increased risk of gastrointestinal bleeding. Several strategies to target chronic gastrointestinal inflammation and to diagnose and treat Helicobacter pylori to reduce the risk of cardiovascular events and gastrointestinal bleeding are available but residual controversy remains and large-scale gastro-cardiology trials are needed to determine the optimal treatment approaches. In perspective, the centennial gastrocardiac syndrome is more relevant than ever in a contemporary gastroenterology and cardiology setting. A collaborative subspecialty, namely Gastro-cardiology, would introduce novel unique means to study, diagnose and treat gastrocardiac conditions with the aim to reduce the risk of cardiovascular and bleeding events to improve the prognosis for gastro-cardiology patients.

Results of Register in Patients with Acute Coronary Syndrome and Atrial Fibrillation Receiving Rivaroxaban.

Aim To evaluate outcomes in patients with acute coronary syndrome and atrial fibrillation who receive rivaroxaban and the patients' compliance with the antithrombotic therapy.Material and methods The study was performed from October 2017 through December 2019 and included 129 patients. Events between the discharge from the hospital and 12 months of follow-up were recorded. The primary endpoint was development of major, minor or requiring medical attention bleeding according to the TIMI scale. The secondary endpoint was a combination of recurrent myocardial infarction, nonfatal acute ischemic cerebrovascular disease, nonfatal systemic embolism, stent thrombosis, and cardiovascular mortality.Results 32 (24.8%) patients early terminated the antiplatelet treatment and 22 (17.1%) patients terminated the rivaroxaban treatment. 26 (20.2 %) patients had hemorrhagic complications. The highest incidence of hemorrhage was observed within the first 2 months after the discharge. None of the bleedings was fatal. Composite endpoint events were observed in 24 (18.6 %) patients, including 14 (10.9 %) who died from cardiovascular causes.Conclusion The compliance with the antiplatelet therapy was insufficient. The incidence of hemorrhagic complications was relatively high; minor and requiring medical attention hemorrhages mostly contributed to the structure of these complications. The observed incidence of recurrent ischemic events associated with a high mortality presents a more serious problem compared to hemorrhagic complications of the combination antiplatelet therapy and warrants a more aggressive tactics of the antiplatelet treatment in high-risk patients.

MicroRNA‐9 overexpression suppresses vulnerable atherosclerotic plaque and enhances vascular remodeling through negative regulation of the p38MAPK pathway via OLR1 in acute coronary syndrome

Acute coronary syndrome (ACS) is characterized by atherosclerotic plaque rupture with a high incidence of recurrent ischemic events. Several microRNAs are found to be aberrantly expressed in atherosclerotic plaques. This study aims to investigate the effects of microRNA-9 (miR-9) on vulnerable atherosclerotic plaque and vascular remodeling in ACS and underlying mechanisms. Microarray-based gene expression profiling was used to identify differentially expressed genes related to ACS and regulatory miRNAs. Oxidized low-density lipoprotein (lectin-like) receptor 1 (OLR1) was identified to be aberrantly activated in ACS and regulated by miR-9. OLR1 was verified as a target gene of miR-9 by bioinformatics prediction and dual luciferase reporter gene assay. The atherosclerotic models were induced in ApoE-/- mice, in which the agomir or antagomir of miR-9, or small interfering RNA (siRNA) against OLR1 were separately introduced. Serum lipid levels and expression of vascular remodeling and inflammatory response-related factors were determined, respectively. On the basis of the obtained results, in the atherosclerosis mice treated with theagomir of miR-9 and siRNA against OLR1, the p38-mitogen-activated protein kinase (p38MAPK) pathway was inhibited; levels of triglyceride, total cholesterol, low-density lipoprotein cholesterol, tumor necrosis factor-α, interleukin-6, and vascular endothelial growth factor were reduced, but the high-density lipoprotein cholesterol level was increased, along with decreased vulnerable atherosclerotic plaque area and enhanced vascular remodeling. Taken together, these findings suggested an inhibitory role miR-9 acts in the formation of vulnerable atherosclerotic plaques in ACS mice, along with a promoted vascular remodeling, via a negative feedback regulation of OLR1-mediated p38MAPK pathway.

Two-Year Clinical, Cerebral Hemodynamic, and Cognitive Outcomes of Adult Patients Undergoing Medication Alone for Symptomatically Ischemic Moyamoya Disease Without Cerebral Misery Perfusion: A Prospective Cohort Study.

In nonsurgical adult moyamoya disease (MMD) patients with ischemic onset and stable hemodynamics, the cerebral hemodynamic and cognitive course remains unclear. To clarify, through a prospective cohort study, 2-yr clinical, cerebral hemodynamic, and cognitive outcomes of adult patients receiving medication alone for symptomatically ischemic MMD without cerebral misery perfusion. Seventy patients without cerebral misery perfusion on the first 15O gas positron emission tomography (PET) were clinically followed up for 2 yr. The second PET was performed at the end of the 2-yr follow-up. Neuropsychological tests were also performed at the study entry and the end of the 2-yr follow-up. During the 2-yr follow-up period, 2 patients (3%) developed further cerebral ischemic symptoms and showed new cerebral misery perfusion on PET performed at recurrence. None of the 68 patients without further ischemic symptoms showed cerebral misery perfusion on second PET. All 66 patients who underwent the first and second neuropsychological tests displayed unchanged interval cognition at the 2-yr follow-up. Among adult patients receiving medication alone for symptomatically ischemic MMD without cerebral misery perfusion, the incidence of recurrent ischemic events was 3% per 2 yr. In patients without recurrent ischemic events, cerebral hemodynamics and cognitive function had not deteriorated by 2 yr after the last event.

The association between high on-treatment platelet reactivity and early recurrence of ischemic events after minor stroke or TIA

Objectives: To evaluate the role of HTPR in predicting early recurrence of ischemic events in patients with minor ischemic stroke or high-risk TIA.Methods: From January 2014 to September 2014, a single center continuously enrolled patients with minor ischemic stroke or high-risk TIA and gave them antiplatelet therapy consisting of aspirin with clopidogrel. HTPR was assessed by TEG after 7 days of antiplatelet therapy and detected CYP2C19 genotype. The incidence of recurrent ischemic events was assessed 3 months after onset. The incidence of recurrent ischemic events was compared between the HTPR and NTPR groups with the Kaplan-Meier method, and multivariate Cox proportional hazards models were used to determine the risk factors associated with recurrent ischemic events.Results: We enrolled 278 eligible patients with minor ischemic stroke or high-risk TIA. Through TEG testing, patients with HTPR were 22.7%, and carriers were not associated with HTPR to ADP by TEG-ADP(%) (p = 0.193). A total of 265 patients completed 3 months of follow-up, and Kaplan-Meier analysis showed that patients with HTPR had a higher percentage of recurrent ischemic events compared with patients with NTPR (p = 0.002). In multivariate Cox proportional hazards models, history of ischemic stroke or TIA (HR 4.45, 95% CI 1.77–11.16, p = 0.001) and HTPR (HR 3.34, 95% CI 1.41–7.91, p = 0.006) was independently associated with recurrent ischemic events.Discussion: In patients with minor stroke or TIA, the prevalence of HTPR was 22.7%, and HTPR was independently associated with recurrent ischemic events.

Anticoagulation Reversal and Treatment Strategies in Major Bleeding: Update 2016.

Anticoagulation is the mainstay of medical treatment, prevention and reduction of recurrent venous thromboembolism, stroke prevention in patients with non-valvular atrial fibrillation, and it reduces the incidence of recurrent ischemic events and death in patients with acute coronary syndrome. Options for anticoagulation have been steadily increasing. Physicians need to be aware of the clinical profile of anticoagulation agents, reversal agents and treatment strategies in the face of major bleeding.

Abstract WP168: The Impact of Intracardiac Thrombi on Recurrent Ischemic Events in Acute Ischemic Stroke Patients With Non-valvular Atrial Fibrillation the Samurai-nvaf Study

Objective: The intracardiac thrombus is associated with an increase in the risks of stroke and thromboembolism for primary prevention. However, it remains unclear in the setting of early management of patients with acute ischemic stroke/TIA. The purpose of this study was to clarify the impact of intracardiac thrombi on recurrent ischemic events in acute ischemic stroke/TIA patients with nonvalvular atrial fibrillation (NVAF). Methods: In the SAMURAI-NVAF study (an ongoing prospective, multicenter, observational study), 1192 acute ischemic stroke/TIA patients with NVAF were registered. Of these, the patients who underwent transesophageal echocardiography (TEE) and/or transthoracic echocardiography (TTE) during acute hospitalization were included. We evaluated the association between the prevalence of intracardiac thrombi and recurrent ischemic events (composite of ischemic stroke/TIA and systemic embolism) during hospital stay (median 29 days). Results: A total of 1091 patients (474 women, 77.6±9.9 y.o) were studied. Of these, 48 patients had intracardiac thrombus (4.4% [95% CI, 3.3-5.7%]). In acute hospital stay, 29 recurrent ischemic events (2.7% [1.9-3.8%]; 24 ischemic stroke, 3 TIA, and 2 systemic embolism) occurred. Patients with intracardiac thrombi had higher incidence of recurrent ischemic events than those without (12.5% versus 2.2%, p&lt;0.001). The thrombus was an independent predictor for ischemic events after adjusted for age, sex and platelet count (OR 6.5; 95% CI 2.28-16.36, p=0.002). Detectability of thrombi increased when only patients undergoing both TEE and TTE were studied (34/216, 16%). Conclusion: In acute ischemic stroke/TIA patients with NVAF, intracardiac thrombi are associated with risk of recurrent ischemic events. The evaluation of intracardiac thrombus should be considered in acute phase of ischemic stroke/TIA.

Solitaire stents for the treatment of complex symptomatic intracranial stenosis after antithrombotic failure: safety and efficacy evaluation

ObjectivesTo evaluate the feasibility, safety, and efficacy of Solitaire stent placement after balloon angioplasty for the treatment of complex symptomatic intracranial atherosclerotic stenosis (ICAS).MethodsWe retrospectively reviewed the clinical data from...

Early carotid angioplasty and stenting may offer non-inferior treatment for symptomatic cases of carotid artery stenosis

ObjectiveEarly intervention is desirable in patients presenting with stroke or transient ischemic attack (TIA) referable to carotid artery stenosis because of the high incidence of recurrent ischemic events within 48...

Nonculprit Plaques in Patients With Acute Coronary Syndromes Have More Vulnerable Features Compared With Those With Non–Acute Coronary Syndromes

Background— Patients with acute coronary syndrome (ACS) have a higher incidence of recurrent ischemic events. The aim of this study was to compare the plaque characteristics of nonculprit lesions between ACS and non-ACS patients using optical coherence tomography (OCT) imaging. Methods and Results— Patients who had 3-vessel OCT imaging were selected from the Massachusetts General Hospital (MGH) OCT Registry. MGH registry is a multicenter registry of patients undergoing OCT. The prevalence and characteristics of nonculprit plaques were compared between ACS and non-ACS patients. A total of 248 nonculprit plaques were found in 104 patients: 45 plaques in 17 ACS patients and 203 plaques in 87 non-ACS patients. Compared with plaques of non-ACS patients, plaques of ACS patients had a wider lipid arc (147.3 ± 29.5° versus 116.2 ± 33.7°, P &lt;0.001), a longer lipid length (10.7 ± 5.9 mm versus 7.0 ± 3.7 mm, P =0.002), a larger lipid volume index [averaged lipid arc×lipid length] (1605.5 ± 1013.1 versus 853.4 ± 570.8, P &lt;0.001), and a thinner fibrous cap (70.2 ± 20.2 µm versus 103.3 ± 46.8 µm, P &lt;0.001). Moreover, thin-cap fibroatheroma (64.7% versus 14.9%, P &lt;0.001), macrophage (82.4% versus 37.9%, P =0.001), and thrombus (29.4% versus 1.1%, P &lt;0.001) were more frequent in ACS patients. Although the prevalence of microchannel did not differ between the groups, the closest distance from the lumen to microchannel was shorter in ACS subjects than in non-ACS (104.6 ± 67.0 µm versus 198.3 ± 133.0 µm, P =0.027). Conclusions— Nonculprit lesions in patients with ACS have more vulnerable plaque characteristics compared with those with non-ACS. Neovascularization was more frequently located close to the lumen in patients with ACS.

Promises of PAR-1 Inhibition in Acute Coronary Syndrome

Platelet activation is a key process in the pathogenesis of acute coronary syndromes (ACS). Of the many triggers involved in this process, three are presumed to be critical: thromboxane A(2) (TBXA(2)) via the TBXA(2) receptor, adenosine diphosphate via the P2Y(12) receptor, and thrombin via the protease-activated receptor (PAR)-1. Despite the effective inhibition of the first two pathways with aspirin and an expanding family of P2Y(12) inhibitors, the incidence of recurrent ischemic events remains high after ACS. PAR-1 inhibitors are a novel class of antiplatelet agents that inhibit thrombin-mediated platelet activation. Preclinical data and phase 2 clinical trials in patients with stable and unstable coronary disease support the potential of these compounds to improve clinical outcome. In this review we discuss the rationale for developing this novel class of agents with a focus on the two compounds in most advanced clinical development, vorapaxar (SCH 530348) and atopaxar (E5555).

Standardized Bleeding Definitions for Cardiovascular Clinical Trials

Advances in antithrombotic therapy, along with an early invasive strategy, have reduced the incidence of recurrent ischemic events and death in patients with acute coronary syndromes (ACS; unstable angina, non–ST-segment–elevation myocardial infarction [MI], and ST-segment–elevation MI).1,–,4 However, the combination of multiple pharmacotherapies, including aspirin, platelet P2Y12 inhibitors, heparin plus glycoprotein IIb/IIIa inhibitors, direct thrombin inhibitors, and the increasing use of invasive procedures, has also been associated with an increased risk of bleeding. Editorial see p 2664 Bleeding complications have been associated with an increased risk of subsequent adverse outcomes, including MI, stroke, stent thrombosis, and death, in patients with ACS and in those undergoing percutaneous coronary intervention (PCI),5,–,10 as well as in the long-term antithrombotic setting.11,12 Thus, balancing the anti-ischemic benefits against the bleeding risk of antithrombotic agents and interventions is of paramount importance in assessing new therapies and in managing patients. Prior randomized trials comparing antithrombotic agents suggest that a reduction in bleeding events is associated with improved survival.13,14 Because prevention of major bleeding may represent an important step in improving outcomes by balancing safety and efficacy in the contemporary treatment of ACS, bleeding events have been systematically identified as a crucial end point for the assessment of the safety of drugs during the course of randomized clinical trials, and are an important aspect of the evaluation of new devices and interventional therapies.15 Unlike ischemic clinical events (eg, cardiac death, MI, stent thrombosis), for which there is now general consensus on end-point definitions,16,17 there is substantial heterogeneity among the many bleeding definitions currently in use. Lack of standardization makes it difficult to optimally organize key clinical trial processes such as adjudication, and even more difficult to interpret relative …

Atorvastatin Improves Myocardial Perfusion in a Patient With Hypercholesterolemia and Single-Vessel Coronary Disease

Lipid-lowering agents may improve the prognosis in patients with coronary artery disease (CAD) or with risk factors for atherosclerosis. A high dose of atorvastatin (80 mg/d) reduced the LDL cholesterol level in stable patients with CAD and was seen to be as effective as coronary angioplasty in reducing the incidence of ischemic events. In patients with acute coronary syndrome, high-dose atorvastatin (80 mg/d) has lowered the incidence of recurrent ischemic events and emergency rehospitalization. We demonstrated that long-term oral low-dose (10 mg/d) administration of atorvastatin improved myocardial uptake of Tc-99m tetrofosmin in a patient with single-vessel coronary artery disease normalizing the plasma level of LDL cholesterol. The normalization of the perfusion pattern was obtained using the same protocol and level of physical stress after 10 months of therapy.

Role of oral blockade of platelet glycoprotein IIb/IIIa on neutrophil activation in patients with acute coronary syndromes.

Orbofiban is a unique antiplatelet agent that inhibits the binding of fibrinogen to gycoprotein (GP) IIb/IIIa integrin receptors and thus prevents platelet aggregation induced by various agents. However, recent studies indicate that treatment with orbofiban does not reduce the incidence of recurrent ischemic events. The mechanisms underlying the lack of benefit of orbofiban in patients with acute coronary syndromes are not completely clear. The purpose of this study was to characterize the effects of orbofiban on cellular activation (neutrophil superoxide generation) and surface expression of adhesion molecules of circulating neutrophils (CD18, CD11b, and L-selectin) and platelets (P-selectin and GP IIb/IIIa) in patients with acute coronary syndromes. After 5-7 days, orbifiban (50 mg BID) did not reduce PMN adhesion molecule expression and ex vivo-stimulated PMN superoxide generation--as was observed in the placebo group, without orbofiban. In contrast, orbofiban induced marked reductions in GP IIb/IIIa and P-selectin expressions after 5-7 days of treatment. The sustained neutrophil activation observed with orbofiban may have a role on the recurrent thrombotic events observed with orbofiban treatment in the OPUS-TIMI 16 trial.

Influencia del volumen plaquetario medio sobre el pronóstico a corto plazo del infarto agudo de miocardio

The increase of mean platelet volume in the late phase of myocardial infarction is an independent predictor for recurrent myocardial infarction and death, but the association between this finding and the short-term prognosis after acute myocardial infarction is unknown. The goals of this study were to assess the influence of mean platelet volume on the risk of death, recurrent ischemic events or cardiac heart failure during the in-hospital phase of myocardial infarction and to analyse the relationship between mean platelet volume and several demographic and clinical variables registered on admission. A population of 1,082 patients with acute myocardial infarction were distributed in two groups according to the platelet volume measured on admission: group 1, mean platelet volume > 9 fl (n = 443) and group 2, mean platelet volume < or = 9 fl (n = 639). The difference between both groups on the end-point of this study were assessed by univariate and multivariate statistical methods. An univariate analysis was also applied to assess the relationship between platelet volume and the baseline variables. A mean platelet volume > 9 fl was associated with a significant increase of risk for the combined end-point considered (OR = 1.37; p = 0.026). By univariate analysis, an increased platelet volume was related to a higher risk of cardiac failure (OR = 1.46; p = 0.01) and a non-significant increase in the incidence of recurrent ischemic events (OR = 1.35; p = 0.07). In addition, a large platelet volume was also associated with a higher prevalence of prior myocardial infarction, arterial hypertension and diabetes mellitus. The results of this study suggest that the increase of mean platelet volume on admission is an independent risk factor for cardiac heart failure and is associated with a non significant higher rates of ischemic events during the recovery phase of acute myocardial infarction.