Are glycoprotein inhibitors safe during percutaneous coronary intervention in patients on chronic warfarin treatment?

2009 ◽  
Vol 102 (12) ◽  
pp. 1227-1233 ◽  
Author(s):  
Heli Lahtela ◽  
Pasi Karjalainen ◽  
Matti Niemelä ◽  
Saila Vikman ◽  
Kari Kervinen ◽  
...  

SummaryThe aim of this study was to evaluate the safety of glycoprotein IIb/IIIa inhibitors (GPIs) during percutaneous coronary intervention (PCI) in patients on chronic warfarin therapy due to atrial fibrillation (AF).We analysed all consecutive AF patients (N = 377, mean age 70 years, male 71%) on warfarin therapy referred for PCI in seven centres. Major bleeding, access site complications and major adverse cardiovascular events were recorded during hospitalisation. A total of 111 patients (29%) received periprocedural GPIs with a wide inter-hospital variation in their use (range 3–68%).The use of GPIs increased with the severity of the disease presentation and 49% of patients with ST-elevation myocardial infarction received GPIs. Mean periprocedural international normalised ratio (INR) of patients who received GPIs was 1.89 (range 1.1–3.3). Major bleeding was more common in the patients treated with GPIs (9.0% vs. 1.5%, p = 0.001) than in those without GPIs, but there was no difference in major adverse cardiovascular events between the groups. In multivariable analysis, use of GPIs (odds ratio [OR]???????????5.1, 95% confidence interval [CI]???????????1.3–20.6, p = 0.02) and old age (OR 1.2, 95% CI 1.0–1.3, p = 0.02) remained as the only independent predictors of major bleeding. Also after adjusting for propensity score, GPIs remained as a significant predictor of major bleeding (OR 3.8, 95% CI 1.03–14.1, p = 0.045). In the GPI group, major bleeding was not predicted by INR level or warfarin pause. GPIs increase the risk of major bleeding events irrespective of periprocedural INR levels and should be used with caution in this fragile patient group.

Angiology ◽  
2020 ◽  
Vol 71 (7) ◽  
pp. 602-608
Author(s):  
Jayant Bagai ◽  
Azad R. Bhuiyan ◽  
Christopher J. White ◽  
Debabrata Mukherjee ◽  
Timir K. Paul

Transradial coronary intervention (TRI) lowers bleeding and mortality compared with transfemoral coronary intervention (TFI). There are limited data on outcomes as TFI operators transition to a default TRI practice. The aim of this study was to assess TFI and TRI outcomes before, during, and after the year TRI was first learned by femoral operators. Patients undergoing percutaneous coronary intervention (PCI) at a Veterans Affairs Medical Center from 2006 to 2012 were included. In 2009, TRI was learned by all operators and then used as the default PCI approach from 2010 to 2012. Baseline characteristics and outcomes were collected. Predictors of major bleeding, major adverse cardiovascular events (MACE), and mortality were determined by multivariable analysis; 1192 veterans were included. TRI rates were 9% (2006-2008), 65% (2009), and 90% (2010-2012). Incidence of 1-year MACE and mortality was 5.4% and 3.9%, respectively, in 2009, and 5.6% and 3%, respectively, during 2010 to 2012. Major bleeding remained at <1%. Age, glycoprotein IIb/IIIa inhibitors, and ST-elevation myocardial infarction were independently associated with major bleeding, whereas TRI was protective. Transition to default TRI is feasible over a short time period and associated with low rates of MACE and mortality and very low rate of major bleeding.


Author(s):  
Hendra Wana Nur’amin ◽  
Iwan Dwiprahasto ◽  
Erna Kristin

Objective: Antiplatelet therapy is recommended in patients with coronary heart disease (CHD) who had the percutaneous coronary intervention (PCI) procedure to reduce major adverse cardiovascular events (MACE). There has been a lack of population-based studies that showed the superior effectiveness of ticagrelor over clopidogrel and similar studies have not been conducted in Indonesia yet. The aim of the study was to investigate the effectiveness of ticagrelor compared to clopidogrel in reducing the risk of MACE in patients with CHD after PCI.Methods: A retrospective cohort study with 1-year follow-up was conducted. 361 patients consisted of 111 patients with ticagrelor exposure and 250 patients with clopidogrel exposure. The primary outcome was MACE, defined as a composite of repeat revascularization, myocardial infarction, or all-cause death. The association between antiplatelet exposure and the MACE was analyzed with Cox proportional hazard regression, adjusted for sex, age, comorbid, PCI procedures and concomitant therapy.Results: MACE occurred in 22.7% of the subjects. Clopidogrel had a significantly higher risk of MACE compared with ticagrelor (28.8%, vs 9.0%, hazard ratio (HR): 1.96 (95% CI 1.01 to 3.81, p=0.047). There were no significant differences in risk of repeat revascularization (20.40% vs 5.40%, HR: 2.32, 95% CI 0.99 to 5.42, p = 0.05), myocardial infarction (11.60% vs 3.60%, HR: 2.08, 95% CI, 0.73 to 5.93, p = 0.17), and death (1.60% vs 1.80%, HR: 0.77, 95% CI, 0.14 to 4.25, p = 0.77).Conclusion: Clopidogrel had a higher risk of MACE compared to clopidogrel in patients with CHD after PCI, but there were no significant differences in the risk of repeat revascularization, myocardial infarction, and all-cause death. 


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Kazuhiro Fujiyoshi ◽  
Yoshiyasu Minami ◽  
Kohki Ishida ◽  
Miwa Ishida ◽  
Ken-ichiro Wakabayashi ◽  
...  

Introduction: Sleep apnea syndrome (SAS) is a risk factor of cardiovascular disease. However, the impact of SAS on the clinical course after percutaneous coronary intervention (PCI) remains to be elucidated. Methods: A total of 206 consecutive patients who underwent PCI were included. The incidence of major adverse cardiovascular events (MACE) at 3-year was compared among patients with untreated SAS (untreated SAS group; n=60), those with SAS treated by continuous positive alveolar pressure (CPAP group; n=20) and those without SAS (non-SAS group; n=96). MACE included cardiac death, non-fatal myocardial infarction, target vessel revascularization (TVR), and non-TVR (NTVR). Results: There was no significant difference in baseline clinical characteristics among the untreated SAS group, the CPAP group and the non-SAS groups, other than in age (74.1 ± 9.6 vs. 71.2 ± 0.33 vs. 68.2 ± 10.7, p = 0.002) and hemoglobin A1c levels (6.54 ± 0.87 vs. 6.61 ± 0.58 vs. 6.09 ± 0.70 %, p < 0.001). The incidence of MACE, TLR and TVR was significantly higher in the untreated SAS group than in the CPAP group and the Non-SAS group although there was no significant difference in the incidence of NTVR among the three groups (Figure). The untreated SAS was independently associated with the incidence of 3-year MACE (odds ratio 3.24, 95% confidence interval 1.36-8.20, p = 0.008). Conclusions: The incidence of MACE was significantly higher in patients with untreated SAS than in those treated with CPAP and those without SAS after PCI. The present findings may highlight the importance of SAS management in patients requiring PCI.


Circulation ◽  
2019 ◽  
Vol 140 (9) ◽  
pp. 751-764 ◽  
Author(s):  
Yulin Li ◽  
Boya Chen ◽  
Xinying Yang ◽  
Congcong Zhang ◽  
Yao Jiao ◽  
...  

Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515


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