IJCS | Volume 33, Nº1, January / February 2019

20 Lott Bezerra et al. Insulin use and infective endocarditis Int J Cardiovasc Sci. 2020;33(1):14-21 Original Article in our sample. The initial search for medical records through the International Classification of Diseases codes may have underestimated the total number of IE cases that occurred in these hospitals during the assessed period, considering the records may not have been performed in the presence of other diagnoses. Conclusion According to our results, diabetic patients did not show higher mortality rates in comparison to the others, even those who used insulin. In turn, we observed a statistically significant difference regarding the higher prevalence of IE by S. aureus and the greater involvement of the tricuspid valve among insulin users. Only two studies separately analyzed diabetics with IE who used or did not use insulin, and some of our results are in agreement and others in disagreement with these studies, which makes it difficult to generalize the results. Nevertheless, it is reasonable to infer that these microbiological and valvular characteristics found in the insulin users of our sample may signal a particular IE profile in these patients. New observational studies considering the insulin use variable are necessary to understand whether these characteristics are identified in observational studies with significant samples and in different locations. Thus, by establishing and controlling the previous insulin use variable, it may be possible to obtain a better understanding of the factors involved in the association between DM and IE, aiming to clarify the current controversy. Despite the limitations of observational and retrospective studies to confirm causal inferences, the analogy between themicrobiological and valvular profile of the insulin user and the intravenous drug user is notable. The analogy is a piece of evidence of contestable strength; however, when associated with the fact that both are injectable substances and could share the same pathophysiological mechanism, it raises a hypothesis to be confirmed or rejected in future studies. Acknowledgments We thank Isabel Cristina Gomes for statistical support; Luiz Wellington Pinto, Maria do Carmo Pereira Nunes, Teresa Cristina de Abreu Ferrari, Milton Henriques Guimarães Junior and Beatriz Pinto Coelho Lott for technical-scientific support; Gilmar Alves Costa, Flávia Martins Alves Godinho, Jéssica Paula Gonçalves, Elcy de Oliveira Silva and Mirian Gonçalves Soares from Santa Casa BH; David da Silva from Hospital Universitario Ciências Médicas; Vivian Ribeiro Miranda, Alessandra Barbosa de Oliveira Andrade and Kenia Coeli Patrício Viana from Hospital Márcio Cunha. Author contributions Conception and design of the research: Bezerra R. Acquisition of data: Bezerra RL, Carvalho TF, Batista RS, Silva YM, Fiuza-Campos B, Castro JHM, Filho RMB, Monteiro PIP. Analysis and interpretation of the data: Bezerra RL, Carvalho TF, Batista RS, Silva YM, Fiuza- Campos B, Castro JHM, Filho RMB, Monteiro PIP. Statistical analysis: Bezerra RL, Alves MC. Obtaining financing: Bezerra RL, Batista RS, Monteiro PIP, Machado ELG. Writing of the manuscript: Bezerra RL. Critical revision of the manuscript for intellectual content: Bezerra RL, Machado ELG, Batista RS, Silva YM, Carvalho TF, Alves MC, Castro JHM. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding This study was funded by CNPq and FAPEMIG. Study Association This study is not associated with any thesis or dissertation work. Ethics Approval and Consent to Participate This study was approved by the Ethics Committee of the Pesquisa da Ciências Médicas – MG (CEPCM-MG) under the protocol number 1.856.064. All the procedures in this study were in accordance with the 1975 Helsinki Declaration, updated in 2013.