Konstantinos Toutouzas1, John Skoumas2, Iosif Koutagiar2, Georgios Benetos2, Nikoletta Pianou3, Alexandros Georgakopoulos3, Spyros Galanakos2, Alexios Antonopoulos4, Maria Drakopoulou2, Evangelos K Oikonomou5, Pavlos Kafouris6, Emmanouil Athanasiadis7, Marinos Metaxas3, George Spyrou8, Zoi Pallantza2, Nikolaos Galiatsatos2, Constantina Aggeli2, Charalampos Antoniades5, Georgia Keramida9, Adrien M Peters9, Constantinos D Anagnostopoulos10, Dimitris Tousoulis2. 1. First Department of Cardiology, Hippokration Hospital, Athens, Greece. Electronic address: ktoutouz@gmail.com. 2. First Department of Cardiology, Hippokration Hospital, Athens, Greece. 3. Center for Experimental Surgery, Clinical and Translational Research, Biomedical Research Foundation, Academy of Athens, Athens, Greece. 4. First Department of Cardiology, Hippokration Hospital, Athens, Greece; Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK. 5. Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK. 6. Department of Informatics and Telecommunications, University of Athens, Athens, Greece; Center of Systems Biology, Biomedical Research Foundation of the Academy, Academy of Athens, Athens, Greece. 7. Center of Systems Biology, Biomedical Research Foundation of the Academy, Academy of Athens, Athens, Greece. 8. Bioinformatics ERA Chair, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. 9. Division of Clinical and Laboratory Investigation, Brighton and Sussex Medical School, Brighton, UK. 10. Center for Experimental Surgery, Clinical and Translational Research, Biomedical Research Foundation, Academy of Athens, Athens, Greece. Electronic address: cdanagnostopoulos@bioacademy.gr.
Abstract
BACKGROUND: Familial dyslipidemias of either heterozygous (heFH) or combined (FCH) type lead to accelerated atherogenesis and increased cardiovascular risk. OBJECTIVE: The aim of this study was to investigate in statin-naïve adult patients with familial dyslipidemias whether inflammatory activation and liver, spleen and bone marrow metabolic activity differ compared with normolipidemic subjects and between dyslipidemic groups. METHODS: Fourteen patients with FCH, 14 with heFH, and 14 normolipidemic individuals were enrolled. Serum lipids, high-sensitivity C-reactive protein, and fibrinogen levels were measured, followed by 18F-fluorodeoxyglucose positron-emission tomography/computed tomography imaging. Radiotracer uptake in the aortic wall, spleen, bone marrow, and liver was quantified as tissue-to-background ratio (TBR). RESULTS: Patients with heFH had significantly higher low-density lipoprotein levels compared with those with FCH and controls (P < .001). However, aortic TBRs were higher in FCH compared with heFH patients and controls (P = .02 and P < .001, respectively). FCH patients exhibited higher FDG uptake in the spleen compared with controls (P = .05). In addition, FCH exhibited higher bone marrow FDG uptake compared with heFH patients and controls (P = .03 and P = .02, respectively). FCH had higher liver uptake compared with heFH patients and controls (P < .001 for both). Significant correlations were observed between inflammatory biomarkers and imaging indices as well as between aortic TBR and FDG uptake of hematopoietic organs and liver. CONCLUSIONS: Systemic, as well as vascular inflammation and spleen, bone marrow, and hepatic metabolic activity are increased in patients with FCH despite lower levels of low-density lipoprotein.
BACKGROUND: Familial dyslipidemias of either heterozygous (heFH) or combined (FCH) type lead to accelerated atherogenesis and increased cardiovascular risk. OBJECTIVE: The aim of this study was to investigate in statin-naïve adult patients with familial dyslipidemias whether inflammatory activation and liver, spleen and bone marrow metabolic activity differ compared with normolipidemic subjects and between dyslipidemic groups. METHODS: Fourteen patients with FCH, 14 with heFH, and 14 normolipidemic individuals were enrolled. Serum lipids, high-sensitivity C-reactive protein, and fibrinogen levels were measured, followed by 18F-fluorodeoxyglucose positron-emission tomography/computed tomography imaging. Radiotracer uptake in the aortic wall, spleen, bone marrow, and liver was quantified as tissue-to-background ratio (TBR). RESULTS: Patients with heFH had significantly higher low-density lipoprotein levels compared with those with FCH and controls (P < .001). However, aortic TBRs were higher in FCH compared with heFH patients and controls (P = .02 and P < .001, respectively). FCH patients exhibited higher FDG uptake in the spleen compared with controls (P = .05). In addition, FCH exhibited higher bone marrow FDG uptake compared with heFH patients and controls (P = .03 and P = .02, respectively). FCH had higher liver uptake compared with heFH patients and controls (P < .001 for both). Significant correlations were observed between inflammatory biomarkers and imaging indices as well as between aortic TBR and FDG uptake of hematopoietic organs and liver. CONCLUSIONS: Systemic, as well as vascular inflammation and spleen, bone marrow, and hepatic metabolic activity are increased in patients with FCH despite lower levels of low-density lipoprotein.
Authors: Georgia Keramida; Alexander Dunford; Guven Kaya; Constantinos D Anagnostopoulos; Adrien Michael Peters Journal: Am J Nucl Med Mol Imaging Date: 2018-06-05
Authors: Charalambos V Vlachopoulos; Iosif P Koutagiar; Alexandros T Georgakopoulos; Anastasia G Pouli; Anastasia Κ Sioni; Stavroula Ε Giannouli; Spiros D Chondropoulos; Ioanna Ε Stergiou; Eirini G Solomou; Dimitrios G Terentes-Printzios; Ioannis G Karakitsios; Pavlos P Kafouris; Anastasios Gaitanis; Nikoletta K Pianou; Aikaterini Petrocheilou; Constantina I Aggeli; Euaggelia Stroumpouli; Theodoros P Marinakis; Michael Voulgarelis; Dimitrios M Tousoulis; Constantinos D Anagnostopoulos Journal: JACC CardioOncol Date: 2020-12-15