Background—: Atherosclerosis is considered to be an inflammatory disease associated with the activation of hematopoietic and immune-related organs such as the bone marrow (BM) and spleen. We evaluated the metabolic activity of those organs and of the carotid artery with ¹⁸ F-fluorodeoxyglucose positron emission tomography in patients with coronary artery disease, including acute myocardial infarction. Methods and Results—: Whole-body combined ¹⁸ F-fluorodeoxyglucose positron emission tomography/computed tomography was performed in 32 patients with acute myocardial infarction, 33 patients with chronic stable angina, and 25 control subjects. The mean standard uptake value was calculated in the regions of interest in the spleen and the BM of lumbar vertebrae. The target-to-background ratio of the standard uptake values of the carotid artery and jugular vein was also calculated. In patients with acute myocardial infarction, the standard uptake values of the BM (1.67±0.16) and spleen (2.57±0.39), as well as the target-to-background ratio of the carotid artery (2.13±0.42), were significantly higher than the corresponding values of patients with angina (1.22±0.62; 2.03±0.35; 1.36±0.37; all P <0.001) and controls (0.80±0.44; 1.54±0.26; 1.22±0.22; all P <0.001), independent of traditional cardiovascular risk factors and high-sensitivity C-reactive protein. In all groups combined, the target-to-background ratio of the carotid artery was significantly associated with the standard uptake values of the BM ( r =0.535; P <0.001), spleen ( r =0.663; P <0.001), and high-sensitivity C-reactive protein ( r =0.465; P <0.001). Conclusions—: The metabolic activity of the BM and spleen, as well as of the carotid artery, was highest in patients with acute myocardial infarction, intermediate in patients with angina, and lowest in control subjects. The activation of the BM and spleen was significantly associated with inflammatory activity of the carotid artery.

The impact of sarcopenia on atherosclerotic cardiovascular disease remains unclear. We aimed to investigate the prognostic impact of sarcopenia on coronary artery disease (CAD). A total of 475 patients with CAD who underwent successful percutaneous coronary intervention (PCI) and computed tomography (CT) were enrolled. The cross-sectional area of skeletal muscle at the first lumbar (L1) vertebral level was measured, and sex-specific cut-off values of L1 skeletal muscle index (L1 SMI; male <31.00 cm²/m², female <25.00 cm²/m²) were obtained. The primary outcome was 3-year all-cause mortality and the secondary outcome was 3-year major adverse cardiovascular events (MACEs). Low L1 SMI was present in 141 (29.7%) of 475 patients. The incidence of all-cause mortality (23.7% vs. 5.9%, p < 0.001) and MACEs (39.6% vs. 11.8%, p < 0.001) was significantly higher in patients with low L1 SMI than in those with high L1 SMI. In multivariate analysis, low L1 SMI was an independent predictor of higher risk of all-cause mortality (hazard ratio (HR): 4.07; 95% confidence interval (CI): 1.95–8.45; p < 0.001) and MACEs (HR: 3.76; 95% CI: 2.27–6.23; p < 0.001). These findings remained consistent after propensity score-matched analysis with 91 patient pairs (C-statistic = 0.848). CT-diagnosed low skeletal muscle mass is a powerful predictor of adverse outcomes in patients with CAD undergoing PCI.

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. 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. 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.

Background: Raoultella planticola was originally considered to be a member of environmental Klebsiella. The clinical significance of R. planticola is still not well known. Case presentation: We describe the first case of necrotizing fasciitis involving the chest and abdominal wall caused by R. planticola. The identity of the organism was confirmed using 16S rRNA sequencing. The patient was successfully treated with the appropriate antibiotics combined with operative drainage and debridement. Conclusions: R. planticola had been described as environmental species, but should be suspected in extensive necrotizing fasciitis after minor trauma in mild to moderate immunocompromised patients.