Monocyte-platelet aggregates with Mon2 are increased in patients with diffuse CAD and therefore could represent an important contributor to accelerated coronary atherosclerotic progression by a mechanism involving microvascular endothelial dysfunction.
We explored how dynamic changes in monocyte subset counts (as opposed to static values to specific time points), and their phagocytic and NFκB activity relate to major adverse cardiovascular events (MACE) and left ventricular ejection fraction (LVEF) in patients with ST-elevation myocardial infarction (STEMI). Changes in counts, phagocytic activity and intracellular levels of inhibitory κB kinase β (IKKβ) (a marker of NFκB activity) of monocyte subsets (CD14<sup>++</sup>CD16<sup>-</sup>CCR2<sup>+</sup> [Mon1], CD14<sup>++</sup>CD16<sup>+</sup>CCR2<sup>+</sup> [Mon2] and CD14<sup>+</sup>CD16<sup>++</sup>CCR2<sup>-</sup> [Mon3]) were measured by flow cytometry in patients with STEMI at baseline, and again after one week, two weeks, and one month. LVEF was measured by echocardiography at baseline and six months after STEMI. Baseline data included 245 patients (mean ± SD age 60 ± 12 years; 22% female), who were followed for a median of 46 (19-61) months. Multivariate Cox regression demonstrated that more prominent dynamic reduction in Mon2 by week 1 (n = 37) was independently associated with fewer MACE (HR 0.06, 95% CI 0.01-0.55, p = 0.01). Also, less prominent reduction in Mon2 at month 1 (n = 24) was independently predictive of 6-month LVEF. None of the other dynamic changes in monocyte subsets were associated with changes in survival from MACE. Neither phagocytic activity nor IKKβ were associated with survival for each monocyte subset. We showed how distinct pattern of dynamic changes in Mon2 are related to both MACE risk and recovery of cardiac contractility. Further research is needed to understand the mechanism of the monocyte effect and possibilities of their pharmacological manipulation.
Atrial fibrillation (AF) is considered a risk factor for dementia, especially in the elderly. However, the association between the two diseases is not well identified in different age subgroups. The association of incident AF with the development of dementia was assessed from 1 January 2005, to 31 December 2013, in 428,262 participants from a longitudinal cohort (the Korea National Health Insurance Service-Health Screening cohort). In total, 10,983 participants were diagnosed with incident AF during the follow-up period. The incidence of dementia was 11.3 and 3.0 per 1000 person-years in the incident-AF and without-AF groups, respectively. After adjustment for clinical variables, the risk of dementia was significantly elevated by incident AF, with a hazard ratio (HR) of 1.98 (95% confidence interval [CI]: 1.80-2.17, <i>p</i> < 0.001), even after censoring for stroke (HR: 1.74, 95% CI: 1.55-1.94, <i>p</i> < 0.001). The HRs of incident AF for dementia onset before the age of 65 (early-onset dementia) and for onset after the age of 65 (late-onset dementia) were 2.91 (95% CI: 1.93-4.41) and 1.67 (95% CI: 1.49-1.87), respectively. Younger participants with AF were more prone to dementia development than older participants with AF (<i>p</i> for trend < 0.001). AF was associated with an increased risk of both early- and late-onset dementia, independent of clinical stroke.