Abstract
Introduction: In experimental myocardial infarction (MI), a rise in cell counts of circulating monocyte subsets contributes to impaired myocardial healing, and to atherosclerotic plaque destabilization.The underlying pathophysiological mechanisms for the post-MI monocytosis and the prognostic role of monocyte subsets in patients suffering ST-elevation MI (STEMI) are still unclear. Hypothesis: The kinetics of the three monocyte subsets (classical CD14++CD16-, intermediate CD14++CD16+ and non-classical CD14+CD16++ monocytes) and gut microbial translocation are associated with cardiovascular outcomes after STEMI. Methods: In 100 STEMI patients treated with primary percutaneous coronary intervention (PCI), monocyte subsets and microbial translocation markers (lipopolysaccharide [LPS] and D-lactate) were measured on Days 1, 2, 3, 5 and 7 of STEMI onset, compared with 35 stable coronary heart disease patients and 35 healthy volunteers. All STEMI patients were prospectively followed for the first occurrence of an adverse cardiovascular event. Results: From Day 1 to Day 7, a parallel increase in CD14++CD16- cell counts, CD14++CD16+ cell counts, and gut permeability markers was observed, with peak levels on Day 2. During a median follow-up of 1.5 years, 25 events were recorded. Univariate Kaplan-Meier analysis revealed that Day 2 CD14++CD16- cell counts ( P =0.022), CD14++CD16+ cell counts ( P =0.024) and Δ LPS (Day 2 – Day 1; P =0.027) each predicted the primary endpoint when stratified by median values. After adjustment for confounders, Day 2 CD14++CD16+ monocyte counts showed the strongest predictive value (per SD increase: hazard ratio [HR]: 2.127; 95% CI 1.313 to 3.446; P =0.002) for cardiovascular events. Conclusions: The expansion of the CD14++CD16+ monocyte subset on Day 2, which is associated a transient increase in microbial translocation, independently predicts adverse cardiovascular outcome in STEMI patients treated with primary PCI.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.