Vicente F Corrales-Medina1, Robert A deKemp2, Julio A Chirinos3, Wanzhen Zeng4, Jerry Wang2, Grant Waterer5, Rob S B Beanlands2, Girish Dwivedi6. 1. Ottawa Hospital Research Institute, Ottawa, ON, Canada; Department of Medicine, University of Ottawa, ON, Canada. 2. National Cardiac PET Centre, University of Ottawa Heart Institute, Ottawa, ON, Canada; Division of Cardiology, Department of Medicine, University of Ottawa, ON, Canada. 3. University of Pennsylvania, Philadelphia, PA. 4. Department of Medicine, University of Ottawa, ON, Canada. 5. Royal Perth Hospital, Perth, WA, Australia; School of Medicine, University of Western Australia, Perth, WA, Australia. 6. National Cardiac PET Centre, University of Ottawa Heart Institute, Ottawa, ON, Canada; Division of Cardiology, Department of Medicine, University of Ottawa, ON, Canada; School of Medicine, University of Western Australia, Perth, WA, Australia; Department of Advanced Clinical and Translational Cardiovascular Imaging, Harry Perkins Institute of Medical Research, Murdoch, WA, Australia; Department of Cardiology, Fiona Stanley Hospital, Murdoch, WA, Australia. Electronic address: girish.dwivedi@perkins.uwa.edu.au.
Abstract
BACKGROUND: Survivors of community-acquired pneumonia (CAP) are at increased risk of cardiovascular disease, cognitive and functional decline, and death, but the mechanisms remain unknown. RESEARCH QUESTION: Do CAP survivors have evidence of increased inflammatory activity in their lung parenchyma on 2-deoxy-2-[18F]fluoro-d-glucose (18FDG)-PET/CT imaging after clinical resolution of infection? STUDY DESIGN AND METHODS: We obtained 18FDG-PET/CT scans from 22 CAP survivors during their hospitalization with pneumonia (acute CAP) and 30 to 45 days after hospital discharge (post-CAP). In each set of scans, we assessed the lungs for foci of increased 18FDG uptake by visual interpretation and by total pulmonary glycolytic activity (tPGA), a background-corrected measure of total metabolic activity (as measured by 18FDG uptake). We also measured, post-CAP, the glycolytic activity of CAP survivor lung areas with volumes similar to the areas in 28 matched historical control subjects without pneumonia. RESULTS: Overall, 68% of CAP survivors (95% CI, 45%-85%) had distinct residual areas of increased 18FDG uptake in their post-CAP studies. tPGA decreased from 821.5 (SD, 1,140.2) in the acute CAP period to 80.0 (SD, 81.4) in the post-CAP period (P = .006). The tPGA post-CAP was significantly higher than that in lung areas of similar volume in control subjects (80.0 [SD, 81.4] vs -19.4 [SD, 5.9]; P < .001). INTERPRETATION: An important proportion of CAP survivors have persistent pulmonary foci of increased inflammatory activity beyond resolution of their infection. As inflammation contributes to cardiovascular disease, cognitive decline, functional waning, and mortality risk in the general population, this finding provides a plausible mechanism for the increased morbidity and mortality that have been observed post-CAP.
BACKGROUND: Survivors of community-acquired pneumonia (CAP) are at increased risk of cardiovascular disease, cognitive and functional decline, and death, but the mechanisms remain unknown. RESEARCH QUESTION: Do CAP survivors have evidence of increased inflammatory activity in their lung parenchyma on 2-deoxy-2-[18F]fluoro-d-glucose (18FDG)-PET/CT imaging after clinical resolution of infection? STUDY DESIGN AND METHODS: We obtained 18FDG-PET/CT scans from 22 CAP survivors during their hospitalization with pneumonia (acute CAP) and 30 to 45 days after hospital discharge (post-CAP). In each set of scans, we assessed the lungs for foci of increased 18FDG uptake by visual interpretation and by total pulmonary glycolytic activity (tPGA), a background-corrected measure of total metabolic activity (as measured by 18FDG uptake). We also measured, post-CAP, the glycolytic activity of CAP survivor lung areas with volumes similar to the areas in 28 matched historical control subjects without pneumonia. RESULTS: Overall, 68% of CAP survivors (95% CI, 45%-85%) had distinct residual areas of increased 18FDG uptake in their post-CAP studies. tPGA decreased from 821.5 (SD, 1,140.2) in the acute CAP period to 80.0 (SD, 81.4) in the post-CAP period (P = .006). The tPGA post-CAP was significantly higher than that in lung areas of similar volume in control subjects (80.0 [SD, 81.4] vs -19.4 [SD, 5.9]; P < .001). INTERPRETATION: An important proportion of CAP survivors have persistent pulmonary foci of increased inflammatory activity beyond resolution of their infection. As inflammation contributes to cardiovascular disease, cognitive decline, functional waning, and mortality risk in the general population, this finding provides a plausible mechanism for the increased morbidity and mortality that have been observed post-CAP.
Authors: Anke H W Bruns; Jan Jelrik Oosterheert; Mathias Prokop; Jan-Willem J Lammers; Eelko Hak; Andy I M Hoepelman Journal: Clin Infect Dis Date: 2007-09-12 Impact factor: 9.079
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Authors: Vicente F Corrales-Medina; Karina N Alvarez; Lisa A Weissfeld; Derek C Angus; Julio A Chirinos; Chung-Chou H Chang; Anne Newman; Laura Loehr; Aaron R Folsom; Mitchell S Elkind; Mary F Lyles; Richard A Kronmal; Sachin Yende Journal: JAMA Date: 2015-01-20 Impact factor: 56.272
Authors: Joshua P Metlay; Grant W Waterer; Ann C Long; Antonio Anzueto; Jan Brozek; Kristina Crothers; Laura A Cooley; Nathan C Dean; Michael J Fine; Scott A Flanders; Marie R Griffin; Mark L Metersky; Daniel M Musher; Marcos I Restrepo; Cynthia G Whitney Journal: Am J Respir Crit Care Med Date: 2019-10-01 Impact factor: 21.405
Authors: Benjamin Bartlett; Herbert P Ludewick; Shipra Verma; Vicente F Corrales-Medina; Grant Waterer; Silvia Lee; Girish Dwivedi Journal: Sci Rep Date: 2022-07-01 Impact factor: 4.996