ABC | Volume 114, Nº4, April 2020

Original Article Albuquerque et al. Ser49Gly Polymorphism in heart failure Arq Bras Cardiol. 2020; 114(4):613-615 1. Brasil. Ministerio da Saude. [Internet]. DATASUS. Informaçes de saude, epidemiologicas emortalidade [acesso13mar. 2019 ]. Disponivel em: http:// datasus.saude.gov.br . 2. Luo N, Fonarow GC, Lippmann SJ, Mi X, Heidenreich PA, Yancy CW, et al. Early adoption of sacubitril/valsartan for patients with heart failure with reducedejection fraction: insights fromgetwiththeGuidelines-HeartFailure (GWTG-HF). JACC Heart Fail. 2017;5(4):305-9. 3. Small KM, Wagoner LE, Levin AM, Kardia S, Liggett SB. Synergistic polymorphisms of beta1- and alpha2C-adrenergic receptors and the risk of congestive heart failure. N Engl J Med. 2002;347(15):1135-42. 4. Abuzaanona A, Lanfear D. Pharmacogenomics of the natriuretic peptide system in heart failure. Curr Hear Fail Rep. 2017;14(6):536-42. 5. Albuquerque FN, Brandão AA, Silva DA, Mourilhe-Rocha R, Duque GS, Gondar AF, et al. Angiotensin-converting enzyme genetic polymorphism: its impact on cardiac remodeling. Arq Bras Cardiol. 2014;102(1):70-9. 6. Luzum JA, English JD, Ahmad US, Sun JW, Canan BD, Sadee W, et al. Association of genetic polymorphisms in the beta-1 adrenergic receptor with recovery of left ventricular ejection fraction in patients with heart failure. J Cardiovasc Transl Res. 2019;12(4):280-9. 7. BorjessonM,MagnussonY,HjalmarsonA,AnderssonB.Anovelpolymorphism inthegenecodingforthebeta(1)-adrenergicreceptorassociatedwithsurvival in patients with heart failure. Eur Heart J. 2000;21(22):1853-8. 8. Levin MC, Marullo S, Muntaner O, Andersson B, Magnusson Y. The myocardium-protective Gly-49 variant of the β 1-adrenergic receptor exhibits constitutive activity and increased desensitization and down- regulation. J Biol Chem. 2002;277(34):30429-35. 9. Liu WN, Fu KL, Gao HY, Shang YY, Wang ZH, Jiang GH, et al. β 1 adrenergic receptor polymorphisms and heart failure: a meta-analysis on susceptibility, response to β -blocker therapy and prognosis. Plos One. 2012;7(7):e37659. 10. Biolo A, Clausell N, Santos KG, Salvaro R, Ashton-Prolla P, Borges A, et al. Impact of β 1-adrenergic receptor polymorphisms on susceptibility to heart failure, arrhythmogenesis, prognosis, and response to beta-blocker therapy. Am J Cardiol. 2008;102(6):726-32. 11. Mialet-PerezJ,RathzDA,PetrashevskayaNN,HahnHS,WagonerLE,Schwartz A,etal.Beta1-adrenergicreceptorpolymorphismsconferdifferentialfunction and predisposition to heart failure. Nat Med. 2003;9(10):1300-5. 12. Lanfear DE, Peterson EL, Zeld N, Wells K, Sabbah HN, Williams K. Beta blocker survival benefit in heart failure is associated with ADRB1 Ser49Gly genotype. J Card Fail. 2015;21(8):S50. References The relatively small number of patients (178) is a limitation in this study and may have influenced the results, especially due to the low number of patients with the Gly-Gly genotype. However, the genotypic distribution pattern observed was the same in most studies and this is the study with the longest follow-up time with GP-R β 1 in the context of HF. It is also worth noting that, despite this reduced number, it was possible to find results with statistical significance. Another limitation refers to the collection of data from medical records. However, since all individuals are followed at a HF clinic, standardization of care routines and information records, as well as the care provided by the doctors involved with the treatment and follow-up of this syndrome, ensured higher quality of the information obtained. Nevertheless, if hospitalization occurred in another institution, there was no access to information and even the number of hospitalizations may be underestimated. This may have determined the absence of statistical differences between the genotypes and limited the evaluation of this clinical outcome. Conclusions In patients with HF with reduced ejection fraction, the presence of Gly-Gly GP-R β 1 was associated with better clinical outcome assessed by NYHA functional class and was a predictor of lower risk of mortality, regardless of other factors in 6.7 years of follow-up. Author contributions Conception and design of the research: Albuquerque FN, Brandão AA, Mourilhe-Rocha R; Acquisition of data: Albuquerque FN, Silva DA, Bittencourt MI; Analysis and interpretation of the data: Albuquerque FN, Brandão AA; Statistical analysis: Albuquerque FN, Pozzan R; Obtaining financing: Albuquerque FN; Writing of the manuscript Albuquerque FN, Brandão AA, Bittencourt MI; Critical revision of the manuscript for intellectual content: Albuquerque FN, Brandão AA, Bittencourt MI, Sales ALF, Spineti PPM, Duque GS, Albuquerque D. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding This study was funded by FAPERJ (Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro). Study Association This article is part of the thesis of Doctoral submitted by Felipe neves de Albuquerque, from Programa de Pós-Graduação em Ciências Médicas da Faculdade de Ciências Médicas da Universidade do Estado do Rio de Janeiro (FCM-UERJ) Ethics approval and consent to participate This study was approved by the Ethics Committee of the Hospital Pedro Ernesto under the protocol number CAAE: 0176.0.228-000-09. All the procedures in this study were in accordance with the 1975 Helsinki Declaration, updated in 2013. Informed consent was obtained from all participants included in the study. 622