Infective endocarditis (IE) is an inflammatory disease of cardiac valves or septal defectscaused by bacteria or fungi. Incidence of IE is around 3 - 7 per 100 000 cases with in-hospital mortality ranging between 13% and 25%. Although transient bacteraemia is common, IE is not that common because intact endothelium is usually resistant to formation of microbial colonies. That is the reason why IE is mostly present on left-sided valves (mitral and aortic) which are exposed to increased stress caused by higher blood pressures in systemic circulation. Clinical features of IE are persistent fever, malaise, skin lesions, hemodynamic instability and dyspnea. Modified Duke criteria are the golden standard for diagnosis of IE. Two major (echocardiographic manifestation and positive blood cultures), 1 major and 3 minor or 5 minor (pre-existing cardiac conditions, fever, vascular phenomena, immunological phenomena and positive blood cultures) criteria need to be present to confirm the diagnosis of IE. IE can be caused by bacteria originating from oral cavity, mostly streptococci, but most often it is caused by staphylococci. Oral pathogens as causes of IE are usually present in the bloodstream after invasive dental procedures, but their release can also be triggered by routine dental activities such as using dental floss, especially in patients with poor levels of dental hygiene. Poor levels of dental hygiene have been linked with higher incidence of periodontal disease which can lead to higher affinity to development of atherosclerotic disease, as well as increased mortality and rate of complications after cardiac surgery. Aims: Aim of this prospective observational study is to assess whether oral pathogens as cause of IE in patients surgically treated for IE are linked to increase in in-hospital mortality rate compared to patients who had IE caused by pathogens which are not of oral origin. Length of stay in the intensive care unit (ICU), duration of mechanical ventilation, rate of ICU re-admissions and surgical revisions were assessed, as well as differences of cumulative fluid balance, need for renal replacement therapy and PaO2/FiO2 indices measured at ICU admission, 3, 6, 12 and 24 hours post admission were compared between groups. Quantitative values were also compared between survivors and non-survivors. Primary hypothesis of this research is that patients who were surgically treated for IE caused by oral pathogens will have higher in-hospital mortality rate compared to patients who had IE caused by other pathogens. Patients and methods: Following the approval of institutional ethics board, 65 patients surgically treated for native valve IE were included in this research. Patients who have had valvular surgery earlier in their lifetime, as well as patients with acute pneumonia or chronic lung disease were excluded. Demographical data, aerobic and anaerobic blood culture results, microbiology analysis of excised valve, laboratory data and clinical parameters needed to assess preoperative SOFA score and other measured variables were analysed from medical documentation. Dental plaque was sampled at ICU admission and microbiologically analysed where applicable. PaO2/FiO2 ratios at 0, 3, 6, 12 and 24h after ICU admission were calculated using blood gas analysis values sampled from radial or femoral artery. Dental procedure anamnestic data was collected from medical documentation and from patients or their families. All patient related data was coded to preserve patient anonymity. After data collection, statistical analysis using StatsDirect (StatsDirect Ltd, Altrincham, UK) v3.0.187 and jamovi v0.8.1.11. (www.jamovi.org) software was performed to compare measured data between groups. Results: 25 patients had IE caused by oral pathogens and 40 patients had IE caused by other pathogens. Primary hypothesis that in-hospital mortality will be higher in patients surgically treated for IE caused by oral pathogens was disproven. There was no statistically significant difference between groups. There was also no statistically significant difference between groups regarding valve involvement (aortic, mitral or tricuspid). However, patients who had IE caused by oral pathogens had significantly higher incidence of positive plaque swab cultures (64% vs 5%, p<0,001) and dental procedures 60 days preceding surgery (32% vs 10%, p=0,026). These patients also had lower SOFA scores (4 vs 7,5, p < 0,001) before surgery, as well as shorter length of ICU stay (44 h vs 67,5h, p=0,02) and shorter duration of mechanical ventilation(16h vs 18,5h, p=0,028). There was no statistically significant difference in rates of reintubation and ICU readmission between groups. There was also no difference in dynamics of changes in PaO2/FiO2 ratio at 0, 3, 6, 12 and 24 hours after ICU admission between groups. Survivors had statistically significant lower SOFA scores preoperatively, shorter duration of ICU stay, as well as higher PaO2/FiO2 ratio at 24h post ICU admission. Lower SOFA scores had predictive values for length of ICU stay and duration of mechanical ventilation. Conclusion: Although the primary hypothesis of this research was disproved, results such as incidence of IE which occurred in patients who had dental procedures performed 60 days before surgery show that IE prophylaxis for dental procedures is still not adequately enforced. Due to the fact that patients who were included in this research had native valve IE, and as such were not the population which is routinely prophylactically treated with antimicrobial drugs, further prospective multicentre trials are needed to determine the optimal prophylactic treatment for this preventable disease. Also, these results show that the course of disease is not as severe in patients who had IE caused by oral pathogens, and that lower preoperative SOFA scores are a good prognostic factor for length of ICU stay and duration of mechanical ventilation.