Brain amygdalar activity (TBR 0.65 vs 0.60; P=0.004), arterial inflammation, and macrophage haematopoiesis were significantly higher in AMI patients compared with controls.
Observational (n=62)
Is stress-associated neurobiological activity linked with acute plaque instability and macrophage activity in patients with acute myocardial infarction?
Brain amygdalar activity, arterial inflammation, and macrophage haematopoiesis are concordantly enhanced in patients with acute myocardial infarction, suggesting a neurobiological link to acute plaque instability.
Absolute Event Rate: 0.65% vs 0.6%
p-value: p=0.004
AIMS: Emotional stress is associated with future cardiovascular events. However, the mechanistic linkage of brain emotional neural activity with acute plaque instability is not fully elucidated. We aimed to prospectively estimate the relationship between brain amygdalar activity (AmygA), arterial inflammation (AI), and macrophage haematopoiesis (HEMA) in acute myocardial infarction (AMI) as compared with controls. METHODS AND RESULTS: 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) imaging was performed within 45 days of the index episode in 62 patients (45 with AMI, mean 60.0 years, 84.4% male; 17 controls, mean 59.6 years, 76.4% male). In 10 patients of the AMI group, serial 18F-FDG-PET/CT imaging was performed after 6 months to estimate the temporal changes. The signals were compared using a customized 3D-rendered PET reconstruction. AmygA target-to-background ratio (TBR), mean ± standard deviation: 0.65 ± 0.05 vs. 0.60 ± 0.05; P = 0.004, carotid AI (TBR: 2.04 ± 0.39 vs. 1.81 ± 0.25; P = 0.026), and HEMA (TBR: 2.60 ± 0.38 vs. 2.22 ± 0.28; P < 0.001) were significantly higher in AMI patients compared with controls. AmygA correlated significantly with those of the carotid artery (r = 0.350; P = 0.005), aorta (r = 0.471; P < 0.001), and bone marrow (r = 0.356; P = 0.005). Psychological stress scales (PHQ-9 and PSS-10) and AmygA assessed by PET/CT imaging correlated well (P < 0.001). Six-month after AMI, AmygA, carotid AI, and HEMA decreased to a level comparable with the controls. CONCLUSION: AmygA, AI, and HEMA were concordantly enhanced in patients with AMI, showing concurrent dynamic changes over time. These results raise the possibility that stress-associated neurobiological activity is linked with acute plaque instability via augmented macrophage activity and could be a potential therapeutic target for plaque inflammation in AMI.
Kang et al. (2020) conducted an observational in Acute myocardial infarction (n=62). 18F-FDG-PET/CT imaging vs. Controls was evaluated on Brain amygdalar activity (target-to-background ratio) (p=0.004). Brain amygdalar activity (TBR 0.65 vs 0.60; P=0.004), arterial inflammation, and macrophage haematopoiesis were significantly higher in AMI patients compared with controls.