Abstract
Background
Alterations in atrial metabolism may play a role in the perpetuation of atrial fibrillation (AF). This study sought to compare 18F-fluorodeoxyglucose (FDG) uptake on PET, in patients with LV dysfunction versus those without AF.
Methods
Seventy-two patients who underwent myocardial viability assessment were evaluated. AF patients (36) had persistent or permanent AF based on history and ECG. Patients without AF (36) were matched to AF patients based on sex, diabetes, age, and LVEF. Maximum and mean FDG Standard Uptake Values (SUV) in the left atrial (LA) wall and right atrial (RA) wall were measured. Tissue-to-blood ratios (TBR) were calculated as atrial wall to blood-pool activity. Atrial volumes were measured by echocardiography.
Results
Maximum and mean FDG SUV and TBRs were significantly increased in the RA (but not the LA) of patients with AF compared to those without (P < 0.01). When accounting for changes in atrial volume, the presence of AF remained a significant predictor of higher RAMAX, but not RAMEAN FDG uptake.
Conclusion
In patients with LV dysfunction from ischemic cardiomyopathy, LA and RA glucose metabolism are differentially altered in those with persistent atrial fibrillation. Further investigations should elucidate the temporal relationship between AF and glucose metabolic changes, as a potential target for therapy.
Spanish abstract
Antecedentes
Las alteraciones en el metabolismo auricular pueden desempeñar un papel en la persistencia de lafibrilación auricular (FA). Este estudio buscó comparar la captación del PET con 18F fluorodesoxiglucosa(FDG), en pacientes con disfunción del VI con y sin FA.
Métodos
Se evaluaron setenta y dos pacientes que se sometieron a evaluación de viabilidad miocárdica. Los pacientes con fibrilación auricular (36) tenían fibrilación auricular persistente o permanente según su historia clínica y el ECG. Los pacientes sin FA (36) se compararon con los pacientes con FA en base a género, diabetes, edad y FEVI. Se midieron los valores de captación estándar (SUV) máximos y medios de FDG en la pared de la aurícula izquierda (LA) y la pared de la aurícula derecha (RA), y se calcularon las relaciones de tejido al pool sanguíneo (TBR) como pared-a-pool sanguíneo. Volúmenes auriculares fueron medidos por ecocardiografía
Resultados
Los SUV y TBR de FDG máximos y medios se encontraron significativamentemayores en la RA(pero no en la LA) de los pacientes con FA en comparación con los que no la tenían (p<0.01). Al tener en cuenta los cambios en el volumen auricular, la presencia de FA siguió siendo un predictor significativo de una mayor captación de FDG en RAMAX pero no de RAMEAN
Conclusión
En pacientes con disfunción del VI por miocardiopatía isquémica, el metabolismo glucolítico en laLA y en la RA se altera de manera diferencial en quienes tienen fibrilación auricular persistente.Futuras investigaciones deberían dilucidar la relación temporal entre la FA y los cambios metabólicos de la glucosa, como un objetivo potencial para la terapia.
Chinese abstract
背景
心房代谢的改变可能在心房颤动 (AF) 的持续中起作用。本研究旨在比较有无合并房颤 左心室 (LV) 功能障碍患者中, 18F-氟脱氧葡萄糖 (FDG) 在PET 中的摄取量有无差异。
研究方法
本研究纳入了72 名接受心肌活力评估的患者。根据病史和心电图, 房颤患者 (36 人) 诊 断为持续性或永久性房颤。根据性别、糖尿病、年龄和LVEF, 对应匹配无房颤患者36 人。 本研究测量了左心房 (LA) 壁和右心房 (RA) 壁的最大和平均FDG 标准摄取值 (SUV), 并计算了组织-血液比率 (TBR), 即心脏壁-血液池。心房容积由超声心动图测量。
结果
与无房颤患者相比, 房颤患者的RA (但不包括LA) 的最大和平均FDG 标准摄取值 (SUV) 和组织-血液比率 (TBRs) 都明显增加 (P<0.01)。当考虑到心房容积的变化时, 患者是 否合并房颤仍然是右房最大标准化摄取值 (RAMAX) 升高的重要预测因素, 但不是右房平 均标准化摄取值 (RAMEAN) FDG摄取的重要预测因素。
结论
在缺血性心肌病导致的左心室功能障碍的患者中, LA 和RA 的葡萄糖代谢在持续房颤的患 者中会有显著的改变。后续研究应进一步阐明房颤和葡萄糖代谢变化之间的时间关系, 并 作为治疗的潜在靶点。
French abstract
Mise en contexte
Les changements du métabolisme auriculaire peuvent jouer un rôle dans la perpétuation de la fibrillation auriculaire (FA). La présente étude avait pour but de comparer la captation du 18F-fluorodeoxyglucose (FDG) en TEP ( tomographie par émission de positrons) chez les patients avec une dysfonction du VG avec FA versus sans FA.
Méthodologie
Soixante-douze patients chez qui une étude de viabilité myocardique a été effectuée ont été évalués. Les patients avec FA (36) avaient une FA persistante ou permanente basée sur l’histoire clinique et l’ECG. Les patients sans FA (36) ont été assortis aux patients avec FA selon leur sexe, diabete, leur age et FEVG. Les ICN (indice de captation normalisée) du FDG maximal et moyen au niveau des parois de l’oreillette gauche (OG) et de l’oreillette droite (OD) ont été mesurées et les rapport tissus-sang (RTS) ont été calculés comme parois-pool sanguin. Les volumes auriculaires ont été mesurés par échocardiographie.
Résultats
Les ICN maximaux et moyens du FDG et les RTS étaient significativement augmentés dans OD (mais pas dans OG) chez les patients avec FA comparativement à ceux qui n’ont pas de FA (p < 0.01). Lorsque les changements du volume auriculaire sont pris en considération, la présence avec FA demeure un facteur prédicteur significatif d’une captation du FDG OD maximale plus élevée mais pas pour la captation OD moyenne.
Conclusion
Chez les patients avec dysfonction du VG reliée à une cardiomyopathie ischémique, le métabolisme du glucose dans OG et OD est altéré différemment chez les patients avec une FA persistante. D’autres études devront être effectuées afin d’élucider la relation temporelle entre la FA et les changements du métabolisme du glucose comme cible potentielle pour la thérapie.
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Change history
08 December 2022
Spanish, Chinese, and French translations of the Abstract and a note of thanks to the providers of the translated Abstracts added to the article.
Abbreviations
- AF:
-
Atrial fibrillation
- RA:
-
Right atrium
- LA:
-
Left atrium
- LV:
-
Left ventricle
- EF:
-
Ejection fraction
- PET:
-
Positron emission tomography
- FDG:
-
Fluorodeoxyglucose
- ROI:
-
Region of interest
- SUV:
-
Standard uptake value
- TBR:
-
Tissue-to-blood ratio
References
Feinberg WM, Blackshear JL, Laupacis A, Kronmal R, Hart RG. Prevalence, age distribution, and gender of patients with atrial fibrillation. Analysis and implications. Arch Intern Med 1995;155:469‐73.
Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV. Prevalence of diagnosed atrial fibrillation in adults: National implications for rhythm management and stroke prevention: The AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 2001;285:2370‐5.
Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 1998;98:946‐52.
Wijffels MC, Kirchhof CJ, Dorland R, Allessie MA. Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation 1995;92:1954‐68.
Issac TT, Dokainish H, Lakkis NM. Role of inflammation in initiation and perpetuation of atrial fibrillation: A systematic review of the published data. J Am Coll Cardiol 2007;50:2021‐8.
White CW, Kerber RE, Weiss HR, Marcus ML. The effects of atrial fibrillation on atrial pressure-volume and flow relationships. Circ Res 1982;51:205‐15.
Barth AS, Merk S, Arnoldi E, Zwermann L, Kloos P, Gebauer M, et al. Reprogramming of the human atrial transcriptome in permanent atrial fibrillation: Expression of a ventricular-like genomic signature. Circ Res 2005;96:1022‐9.
Ghezelbash S, Molina CE, Dobrev D. Altered atrial metabolism: An underappreciated contributor to the initiation and progression of atrial fibrillation. J Am Heart Assoc 2015;4:e001808.
Allessie MA, Boyden PA, Camm AJ, Kleber AG, Lab MJ, Legato MJ, et al. Pathophysiology and prevention of atrial fibrillation. Circulation 2001;103:769‐77.
Mayr M, Yusuf S, Weir G, Chung YL, Mayr U, Yin X, et al. Combined metabolomic and proteomic analysis of human atrial fibrillation. J Am Coll Cardiol 2008;51:585‐94.
Ono N, Hayashi H, Kawase A, Lin S-F, Li H, Weiss JN, et al. Spontaneous atrial fibrillation initiated by triggered activity near the pulmonary veins in aged rats subjected to glycolytic inhibition. Am J Physiol Heart Circ Physiol 2007;292:H639‐48.
Qiu J, Hu H, Zhou S, Liu Q. Alteration of myocardium glucose metabolism in atrial fibrillation: Cause or effect? Int J Cardiol 2016;203:722‐3.
Lenski M, Schleider G, Kohlhaas M, Adrian L, Adam O, Tian Q, et al. Arrhythmia causes lipid accumulation and reduced glucose uptake. Basic Res Cardiol 2015;110:40.
Oral H, Knight BP, Tada H, Özaydin M, Chugh A, Hassan S, et al. Pulmonary vein isolation for paroxysmal and persistent atrial fibrillation. Circulation 2002;105:1077‐81.
Hussein AA, Saliba WI, Barakat A, Bassiouny M, Chamsi-Pasha M, Al-Bawardy R, et al. Radiofrequency ablation of persistent atrial fibrillation: Diagnosis-to-ablation time, markers of pathways of atrial remodeling, and outcomes. Circ Arrhythm Electrophysiol 2016;9:e003669.
Peterson LR, Gropler RJ. Radionuclide imaging of myocardial metabolism. Circ Cardiovasc Imaging 2010;3:211‐22.
McArdle B, Dowsley TF, Cocker MS, Ohira H, deKemp RA, DaSilva J, et al. Cardiac PET: Metabolic and functional imaging of the myocardium. Semin Nucl Med 2013;43:434‐48.
Fujii H, Ide M, Yasuda S, Takahashi W, Shohtsu A, Kubo A. Increased FDG uptake in the wall of the right atrium in people who participated in a cancer screening program with whole-body PET. Ann Nucl Med 1999;13:55‐9.
Maurer AH, Burshteyn M, Adler LP, Steiner RM. How to differentiate benign versus malignant cardiac and paracardiac 18F FDG uptake at oncologic PET/CT. Radiographics 2011;31:1287‐305.
Dong A, Zhao T, Gong J, Zuo C. Diffuse FDG uptake of the bilateral atrial walls in a patient with atrial fibrillation. Clin Nucl Med 2014;39:167‐9.
Lange PS, Avramovic N, Frommeyer G, Wasmer K, Pott C, Eckardt L, et al. Routine (18)F-FDG PET/CT does not detect inflammation in the left atrium in patients with atrial fibrillation. Int J Cardiovasc Imaging 2017;33:1271‐6.
Beanlands RS, Nichol G, Huszti E, Humen D, Racine N, Freeman M, et al. F-18-fluorodeoxyglucose positron emission tomography imaging-assisted management of patients with severe left ventricular dysfunction and suspected coronary disease: A randomized, controlled trial (PARR-2). J Am Coll Cardiol 2007;50:2002‐12.
Vitale GD, deKemp RA, Ruddy TD, Williams K, Beanlands RS. Myocardial glucose utilization and optimization of (18)F-FDG PET imaging in patients with non-insulin-dependent diabetes mellitus, coronary artery disease, and left ventricular dysfunction. J Nucl Med 2001;42:1730‐6.
Dilsizian V, Bacharach SL, Beanlands RS, Bergmann SR, Delbeke D, Dorbala S, et al. ASNC imaging guidelines/SNMMI procedure standard for positron emission tomography (PET) nuclear cardiology procedures. J Nucl Cardiol 2016;23:1187‐226.
Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015;28:1‐39.
Nattel S. Molecular and cellular mechanisms of atrial fibrosis in atrial fibrillation. JACC Clin Electrophysiol 2017;3:425‐35.
Park JH, Lee JS, Ko Y-G, Lee SH, Lee BS, Kang S-M, et al. Histological and biochemical comparisons between right atrium and left atrium in patients with mitral valvular atrial fibrillation. Korean Circ J 2014;44:233‐42.
Zhang L, Huang B, Scherlag BJ, Ritchey JW, Embi AA, Hu J, et al. Structural changes in the progression of atrial fibrillation: Potential role of glycogen and fibrosis as perpetuating factors. Int J Clin Exp Pathol 2015;8:1712‐8.
Acknowledgments
BWJC is the UOHI Goldfarb Chair in Cardiac Imaging. RSB is a Tier 1 Research Chair supported by the University of Ottawa and was a career investigator supported by the Heart and Stroke Foundation of Ontario.
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BWJC receives research support from CV Diagnostix and educational support from TeraRecon Inc and has equity interest in GE. RdK has received research grant support and honoraria from Lantheus Medical Imaging, Jubilant DraxImage, and GE Healthcare. RdK receives royalty revenues from Rubidium-82 PET technologies licensed to Jubilant DraxImage and INVIA Medical Solutions. RSB has received research grant support and honoraria from Lantheus Medical Imaging, Jubilant DraxImage, and GE Healthcare.
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JNC thanks Erick Alexanderson, MD, and Isabel Carvajal-Juárez, MD, Instituto Nacional de Cardiología Ignacio Chávez, Mexico, for providing the Spanish abstract; Weihua Zhou, Ph.D., Michigan Technological University, Michigan, for providing the Chinese abstract; and Raymond Taillefer, MD, Hopital du Haut-Richelieu, Canada, for providing the French abstract.
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Santi, N.D., Wu, K.Y., Redpath, C.J. et al. Metabolic activity of the left and right atria are differentially altered in patients with atrial fibrillation and LV dysfunction. J. Nucl. Cardiol. 29, 2824–2836 (2022). https://doi.org/10.1007/s12350-021-02878-2
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DOI: https://doi.org/10.1007/s12350-021-02878-2