Patients with chronic obstructive pulmonary disease (COPD) show a poor prognosis after myocardial infarction (MI) and percutaneous coronary intervention (PCI). We evaluated on-treatment platelet reactivity (PR) and several gene polymorphisms related to PR in 130 patients undergoing PCI with and without COPD. Those with concomitant COPD showed higher on-treatment PR values both at the time of PCI and 1 month after. This finding may contribute to explain the poor prognosis of COPD patients after MI and PCI.
- COPD epidemiology
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Patients with myocardial infarction undergoing percutaneous coronary intervention (PCI) with concomitant chronic obstructive pulmonary disease (COPD) are at increased risk for death and hospital readmissions compared with those without COPD.1 Abnormalities in the on-treatment platelet reactivity (PR) values could be involved in this worse outcome.
In the Prolonging Dual Antiplatelet Treatment After Grading Stent-Induced Intimal Hyperplasia study we enrolled 1970 patients treated with PCI and stent implantation and all received dual antiplatelet therapy (aspirin+clopidogrel).2 In 723 patients (random sample), we assessed on-treatment PR at the time of PCI and after 1 month (by P2Y12 VerifyNow system and Multiplate Analyzer) together with the gene polymorphisms CYP2C19*2, *17, ABCB1 and Q192R PON1.3 ,4 Sixty-five (9%) patients had a documented COPD (cases). COPD was defined as a history or presence of physician-diagnosed COPD. The patients were required to be on chronic pharmacologic therapy and/or have an forced expiratory volume in the first second (FEV)1 <75% of predicted value. As control group, sixty-five patients without COPD matched for baseline characteristics were selected (propensity score analysis). Informed written consent was obtained from all patients, and the study was approved by the local ethics review board. All tests used for statistical analysis were reported in the online supplementary file.
At the time of PCI, on-treatment PR was significantly higher in patients with concomitant COPD as compared with those without (table 1). As expected, on-treatment PR values decreased from baseline to 1 month, both in patients with and without concomitant COPD (table 1). As for baseline values, 1 month on-treatment PR remained significantly higher in patients with concomitant COPD (table 1). These findings are consistent considering both platelet function assays and using different agonists (table 1). We did not observe differences in gene polymorphisms between the two groups (table 1).
It is known that on-treatment PR can be influenced by age, sex, smoking, diabetes and renal failure;5 however, the impact of COPD has been less investigated. This is probably due to different reasons: (i) exclusion of COPD patients from clinical studies; (ii) possible interaction between COPD therapy and on-treatment PR; (iii) poor compliance to antiplatelet drugs in COPD patients. For the first time, our post-hoc analysis showed a significantly higher on-treatment PR in COPD patients undergoing PCI independently from age, sex, cardiovascular risk factor and clinical presentation. This finding is consistent as it occurs at the time of PCI and 1 month after, both in acute coronary syndrome and stable patients. The underlying causes are not known. Genetic determinants were not involved. We may speculate that the proinflammatory nature of COPD could be involved, influencing both platelet function and drug responsiveness. Regardless of the cause, this heightened on-treatment PR may have an important clinical relevance and may influence the long-term outcome. COPD patients undergoing PCI could be candidates for the newer antiplatelet drugs (such as ticagrelor and prasugrel). Contemporaneously, they showed a higher bleeding risk.1 Further studies should be planned to confirm our suggestion and to select the best antiplatelet treatment in COPD patients.
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Files in this Data Supplement:
- Data supplement 1 - Online supplement
Contributors GC, RP: conception and design; GC, AP, MT: analysis and interpretation of data; GC, MT: drafting the article; RP, AP: revising the article critically for important intellectual content; RF: final approval of the version to be published.
Funding This work was supported by a grant from Fondazione Anna Maria Sechi per il Cuore (FASC), Italy. The funders had no role in the study design, data collection and analysis, decision to publish or the preparation of the manuscript.
Competing interests None.
Ethics approval Comitato Etico Della Provincia Di Ferrara.
Provenance and peer review Not commissioned; externally peer reviewed.