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Original Article Contents Journal Watch 750 Preventive strategies against infective endocarditis: Are these worthless? 753 Jagdish C. Mohan, MD, DM; Vishwas Mohan, Resident News and Views Department of Cardiac Sciences, Fortis Hospital, Shalimar Bagh, Delhi, India Forthcoming Events 755 Instruction to Contributors Abstract 756 In the past, we have expended considerable effort and resources in devising strategies for antibiotic prophylaxis against infective endocarditis. There has been several sets of guidelines and strategies enunciated in this regard without any hard evidence, since 1955. Antibiotic prophylaxis given before invasive dental and non-dental interventional procedures have been the focus for infective endocarditis prevention for more than 50 years and remains the standard of care for patients at high risk in most parts of the world. Anesthetists, dentists, cosmetologists, urologists, and gynecologists are the ones who have to implement these guidelines primarily. In the past half a century, a tendency can be seen towards shorter duration and lower dose of antibiotics, and that fewer patients are considered to be at risk of infective endocarditis (IE). There has never been a randomised study into the use of antibiotic prophylaxis in this context. The American Heart Association published updated guidelines for IE prevention in 2007 that markedly restricted the use of antibiotic prophylaxis in certain at-risk patients undergoing dental and other invasive procedures. The French had begun this 2002 onward. National Institute of Health and Clinical Excellence (NICE) in United Kingdom took a drastic step in 2008 in recommending a policy of “no antibiotic prophylaxis”. There has been support and criticism for this policy. This minimalistic approach has found good support in Europe. However, newer research presented at end-2014 has shown that implementation of these guidelines may have resulted into 25% greater increased number of infective endocarditis in the United Kingdom. Safety of the 2008 NICE guidelines is under review. In this short write-up, the whole gamut of antibiotic prophylaxis of infective endocarditis is revisited with special regard to developing countries. Key Words • Trans fats/trans-fatty acids • Partially hydrogenated vegetable oils Introduction Infective endocarditis (IE) is an uncommon but deadly disease with an inhospital mortality of 20% and 1-year 1 mortality approaching 40%. The incidence is about 2 5/100,000 population. Incidence of IE in India is hard to guess in view of lack of population studies. Applying worldwide data to Indian population would yield an incidence of about 50,000 to 100,000 cases per year. About 5% of the entire population is abnormally Received: 30-11-14; Revised: 06-07-15; Accepted: 07-07-15 Disclosures: This article has not received any funding and has no vested commercial interest Acknowledgments: None Please send in your letters to the Editor at [email protected] J. Preventive Cardiology Vol. 4 No. 4 May 2015 725 Mohan JC, et al susceptible if bicuspid aortic valve, mitral valve prolapse, and degenerative valvular heart disease alone are included as criteria of susceptibility. It is apparent that one in 1000 susceptible subjects develops IE every year (with a risk multiple of 50). Bacteremia secondary to an interventional procedure in a susceptible subject (with a pre-existing cardiac lesion) is the underlying risk factor. In an attempt to prevent this disease, over the past 50 years, at-risk patients have been empirically given antibiotic prophylaxis before dental and certain nondental interventional procedures. The efficacy of this regimen in humans has never been properly investigated and clinical practice has been dictated by guidelines based on expert opinion. Antibiotics not only entail cost and the spectrum of developing resistance, but may lead to adverse events including anaphylaxis. Hence, definite evidence and cost-effectiveness needs to be demonstrated for this strategy. Can we rely only on good oral hygiene and cleanliness during medical (catheter insertion, dialysis, etc.) and non-medical procedures like tattooing, piercing, etc., for preventing IE? IE epidemiology 3 Epidemiology of IE has changed over last half a century. IE caused by Streptococcal viridans is decreasing and that caused by Staphylococcus aureus is increasing.4 Viridans group streptococci are part of the normal skin, oral, respiratory, and GI tract flora, and they earlier caused at least 50% of cases of community-acquired native valve IE not associated with intravenous drug use. However, streptococcal IE is decreasing in frequency even in the population-based studies.5 Staph infections are associated with longer hospital stay, more frequent embolic complications, greater need for surgery, increased cost, and higher in-hospital mortality. 6 Coagulase-negative staph is getting implicated more because of healthcare-associated infections. 4 Enterococcal infection is rising due to increasing age, immunosuppressive therapy, hemodialysis, etc. Enterococci are notorious for multidrug resistance. Reuse of disposable material in catheterisation laboratories in the developing world is fuelling IE caused by gram-negative bacilli. Healthcare associated IE now accounts for more than one-third of all IE and this has changed microbial profile of the disease. Although, intravenous drug abusers may not be a big problem in the developing countries, reuse of syringes by unqualified personnel in the remote areas, and unsafe deliveries in villages, certainly contribute to our share of right-sided IE. As of now, about 50% of staph infections are methicillin-sensitive and this number is declining. In India, culture-positive IE is only about 50% and, hence, 726 the exact microbiology remains under cloud.7–13 Portal of entry of infection is not clear in vast majority of patients and hence prophylaxis can never be very effective. Patients at risk Following categories are at special risk of developing IE: 1. Patients with congenital structural heart diseases (excluding atrial septal defects, closed ductus arteriosus, and devices for closures) 2. Patients with acquired valvular heart disease 3. Patients with prosthetic heart valves 4. Previous IE 5. Hypertrophic cardiomyopathy 6. Patients with implanted cardiac rhythm devices 7. Patients with percutaneous intravenously inserted long-term use catheters and ports Both the American and European guidelines initially suggested dividing patients into high risk and moderate risk.14,15 High risk 1. Previous IE 2. Prosthetic heart valves 3. Unoperated congenital cyanotic heart disease or complex congenital heart disease with residual lesions or with prosthetic material used during repair 4. Valvulopathy post cardiac transplantation Moderate risk for individuals who did not have a history of type I hypersensitivity reaction to penicillin, such as anaphylaxis, urticaria, or angioedema. The major changes in the updated recommendations included the following: 1. Only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100% effective. 2. Infective endocarditis prophylaxis for dental procedures is reasonable only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis (previous IE), unoperated cyanotic congenital heart disease, complex congenital heart disease with residual lesions or with prosthetic material having been used in repair, prosthetic heart valves, valvular heart disease in post-transplant patients. 3. For patients with these underlying cardiac conditions, prophylaxis is reasonable for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. 4. Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of infective endocarditis. 5. Administration of antibiotics solely to prevent endocarditis is not recommended for patients who undergo a genitourinary or gastrointestinal tract procedure. NICE guidelines 2008 1. Valvular heart disease 2. Hypertrophic cardiomyopathy 3. Previous rheumatic fever 4. Heart murmur 5. Uncomplicated ventricular septal defects, etc. Prophylaxis against IE The AHA made radical changes in their IE prevention guidelines in 200715 that recommended use of antibiotic prophylaxis for invasive dental procedures to only four groups of patients who would be at higher risk from complications and mortality if they developed endocarditis. A single dose of amoxicillin or ampicillin was considered safe and the preferred prophylactic agent J. Preventive Cardiology Vol. 4 Preventive strategies against infective endocarditis No. 4 May 2015 In March 2008, the National Institute for Health and Clinical Excellence (NICE) in the United Kingdom produced controversial new guidance recommending the cessation of antibiotic prophylaxis for all patients at risk of infective endocarditis undergoing dental and a 16 wide range of other invasive procedures. Summary of these guidelines is shown below: 1. Good oral hygiene for all including susceptible subjects 2. Discourage chlorhexidine mouthwash before dental procedures 3. Proper asepsis before body piercing and tattooing 6. Suspected IE should be vigorously investigated at the earliest Why “no antibiotic prophylaxis”? Active or potential infection treatment needs antibiotics. Premise of antibiotic prophylaxis is that invasive procedures on teeth, gums, respiratory tract, and genitourinary system lead to bacteremia. This bacteremia may be the underlying mechanism of IE in susceptible individuals. However, bacteremia occurs in many daily activities like tooth brushing or massaging the gums, etc. and also routine diagnostic procedures like endoscopy, bronchoscopy, transesophageal echocardiography, urinary catheterisation, vaginal 17 examination, etc. One can’t be prescribing antibiotics in every scenario which can cause transient bacteremia. There are no published prospective, randomized, placebo-controlled trials to evaluate either the risk of IE attributable to dental or non-dental procedures or the efficacy of antibiotic prophylaxis in these setting.18 Consequence of “no antibiotic policy” Given the lack of demonstrated efficacy of IE antibiotic prophylaxis, it is of paramount importance to identify any increase in viridans group streptococcal IE that would and could result from the restricted/no use of antibiotic prophylaxis. Twelve months before the NICE guidelines were introduced, dentists accounted for 91.9% of prescriptions for antibiotic prophylaxis, whereas 14 to 25 months after the introduction of the guidelines, the number of prescriptions written by dentists decreased significantly by 79.9%.19 For the first two years, there was no increase in incidence of IE. However, after that the incidence showed a rising trend and, overall, the incidence of infective endocarditis in England has increased significantly by 25% between 2008 and 2013.20 This increase in incidence has affected both high-risk and lower-risk individuals. Infective endocarditisassociated inhospital mortality also increased, although this increase was not significant, possibly because of the lower mortality associated with infective endocarditis caused by oral streptococci. Although, there is temporal relationship between cessation of antibiotic prophylaxis and increase in incidence of IE, it is difficult to establish a causative relationship. On the other hand, after a highly restrictive policy regarding antibiotic prophylaxis, there has been no 4. No routine antibiotic use J. Preventive Cardiology Vol. 4 5. Antibiotic prophylaxis only if instrumentation of an infected area No. 4 May 2015 727 Mohan JC, et al susceptible if bicuspid aortic valve, mitral valve prolapse, and degenerative valvular heart disease alone are included as criteria of susceptibility. It is apparent that one in 1000 susceptible subjects develops IE every year (with a risk multiple of 50). Bacteremia secondary to an interventional procedure in a susceptible subject (with a pre-existing cardiac lesion) is the underlying risk factor. In an attempt to prevent this disease, over the past 50 years, at-risk patients have been empirically given antibiotic prophylaxis before dental and certain nondental interventional procedures. The efficacy of this regimen in humans has never been properly investigated and clinical practice has been dictated by guidelines based on expert opinion. Antibiotics not only entail cost and the spectrum of developing resistance, but may lead to adverse events including anaphylaxis. Hence, definite evidence and cost-effectiveness needs to be demonstrated for this strategy. Can we rely only on good oral hygiene and cleanliness during medical (catheter insertion, dialysis, etc.) and non-medical procedures like tattooing, piercing, etc., for preventing IE? IE epidemiology 3 Epidemiology of IE has changed over last half a century. IE caused by Streptococcal viridans is decreasing and that caused by Staphylococcus aureus is increasing.4 Viridans group streptococci are part of the normal skin, oral, respiratory, and GI tract flora, and they earlier caused at least 50% of cases of community-acquired native valve IE not associated with intravenous drug use. However, streptococcal IE is decreasing in frequency even in the population-based studies.5 Staph infections are associated with longer hospital stay, more frequent embolic complications, greater need for surgery, increased cost, and higher in-hospital mortality. 6 Coagulase-negative staph is getting implicated more because of healthcare-associated infections. 4 Enterococcal infection is rising due to increasing age, immunosuppressive therapy, hemodialysis, etc. Enterococci are notorious for multidrug resistance. Reuse of disposable material in catheterisation laboratories in the developing world is fuelling IE caused by gram-negative bacilli. Healthcare associated IE now accounts for more than one-third of all IE and this has changed microbial profile of the disease. Although, intravenous drug abusers may not be a big problem in the developing countries, reuse of syringes by unqualified personnel in the remote areas, and unsafe deliveries in villages, certainly contribute to our share of right-sided IE. As of now, about 50% of staph infections are methicillin-sensitive and this number is declining. In India, culture-positive IE is only about 50% and, hence, 726 the exact microbiology remains under cloud.7–13 Portal of entry of infection is not clear in vast majority of patients and hence prophylaxis can never be very effective. Patients at risk Following categories are at special risk of developing IE: 1. Patients with congenital structural heart diseases (excluding atrial septal defects, closed ductus arteriosus, and devices for closures) 2. Patients with acquired valvular heart disease 3. Patients with prosthetic heart valves 4. Previous IE 5. Hypertrophic cardiomyopathy 6. Patients with implanted cardiac rhythm devices 7. Patients with percutaneous intravenously inserted long-term use catheters and ports Both the American and European guidelines initially suggested dividing patients into high risk and moderate risk.14,15 High risk 1. Previous IE 2. Prosthetic heart valves 3. Unoperated congenital cyanotic heart disease or complex congenital heart disease with residual lesions or with prosthetic material used during repair 4. Valvulopathy post cardiac transplantation Moderate risk for individuals who did not have a history of type I hypersensitivity reaction to penicillin, such as anaphylaxis, urticaria, or angioedema. The major changes in the updated recommendations included the following: 1. Only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100% effective. 2. Infective endocarditis prophylaxis for dental procedures is reasonable only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis (previous IE), unoperated cyanotic congenital heart disease, complex congenital heart disease with residual lesions or with prosthetic material having been used in repair, prosthetic heart valves, valvular heart disease in post-transplant patients. 3. For patients with these underlying cardiac conditions, prophylaxis is reasonable for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. 4. Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of infective endocarditis. 5. Administration of antibiotics solely to prevent endocarditis is not recommended for patients who undergo a genitourinary or gastrointestinal tract procedure. NICE guidelines 2008 1. Valvular heart disease 2. Hypertrophic cardiomyopathy 3. Previous rheumatic fever 4. Heart murmur 5. Uncomplicated ventricular septal defects, etc. Prophylaxis against IE The AHA made radical changes in their IE prevention guidelines in 200715 that recommended use of antibiotic prophylaxis for invasive dental procedures to only four groups of patients who would be at higher risk from complications and mortality if they developed endocarditis. A single dose of amoxicillin or ampicillin was considered safe and the preferred prophylactic agent J. Preventive Cardiology Vol. 4 Preventive strategies against infective endocarditis No. 4 May 2015 In March 2008, the National Institute for Health and Clinical Excellence (NICE) in the United Kingdom produced controversial new guidance recommending the cessation of antibiotic prophylaxis for all patients at risk of infective endocarditis undergoing dental and a 16 wide range of other invasive procedures. Summary of these guidelines is shown below: 1. Good oral hygiene for all including susceptible subjects 2. Discourage chlorhexidine mouthwash before dental procedures 3. Proper asepsis before body piercing and tattooing 6. Suspected IE should be vigorously investigated at the earliest Why “no antibiotic prophylaxis”? Active or potential infection treatment needs antibiotics. Premise of antibiotic prophylaxis is that invasive procedures on teeth, gums, respiratory tract, and genitourinary system lead to bacteremia. This bacteremia may be the underlying mechanism of IE in susceptible individuals. However, bacteremia occurs in many daily activities like tooth brushing or massaging the gums, etc. and also routine diagnostic procedures like endoscopy, bronchoscopy, transesophageal echocardiography, urinary catheterisation, vaginal 17 examination, etc. One can’t be prescribing antibiotics in every scenario which can cause transient bacteremia. There are no published prospective, randomized, placebo-controlled trials to evaluate either the risk of IE attributable to dental or non-dental procedures or the efficacy of antibiotic prophylaxis in these setting.18 Consequence of “no antibiotic policy” Given the lack of demonstrated efficacy of IE antibiotic prophylaxis, it is of paramount importance to identify any increase in viridans group streptococcal IE that would and could result from the restricted/no use of antibiotic prophylaxis. Twelve months before the NICE guidelines were introduced, dentists accounted for 91.9% of prescriptions for antibiotic prophylaxis, whereas 14 to 25 months after the introduction of the guidelines, the number of prescriptions written by dentists decreased significantly by 79.9%.19 For the first two years, there was no increase in incidence of IE. However, after that the incidence showed a rising trend and, overall, the incidence of infective endocarditis in England has increased significantly by 25% between 2008 and 2013.20 This increase in incidence has affected both high-risk and lower-risk individuals. Infective endocarditisassociated inhospital mortality also increased, although this increase was not significant, possibly because of the lower mortality associated with infective endocarditis caused by oral streptococci. Although, there is temporal relationship between cessation of antibiotic prophylaxis and increase in incidence of IE, it is difficult to establish a causative relationship. On the other hand, after a highly restrictive policy regarding antibiotic prophylaxis, there has been no 4. No routine antibiotic use J. Preventive Cardiology Vol. 4 5. Antibiotic prophylaxis only if instrumentation of an infected area No. 4 May 2015 727 Mohan JC, et al definite increase in IE in France21 and the United States.5 Duval and colleagues4 reported a follow-up study in three French regions (with a total adult population of about 11 million) where a guideline change in 2002 restricted antibiotic prophylaxis to patients at high risk of infective endocarditis (roughly 10% of the total cases). They identified no significant increase in the incidence of oral streptococcal infective endocarditis in 2008 compared with their findings from 1991 and 1999. However, there was an increase in staphylococcal infections (36% of all IE vs 12% streptococcal in 2008), mostly in those subjects with no pre-existing valvular heart disease. What to do in India? In India, we cannot ignore rheumatic valvular heart disease, with its peculiar structural and immunological characteristics, nor the poor oral health of the general Indian population, which has not improved significantly over the past decades. Therefore, it is not wise to ignore our epidemiological peculiarity of valvular heart disease and general level of hygiene. In India, it may be still reasonable to recommend antibiotic prophylaxis before starting dental interventional procedures that bear a high probability of significant bacteremia to patients who have either valvular or congenital heart diseases that represent a risk for IE, regardless of assumptions on differences of disease course. In addition, there is the need for prospective and controlled studies to support the probability of the effect of antibiotic prophylaxis. References 1. Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: Executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:e57–e185. 2. Tleyjeh IM, Abdel-Latif A, Rahbi H, Scott CG, Bailey KR, Steckelberg JM, et al. A systematic review of population based studies of infective endocarditis. Chest. 2007;132:1025–35. 3. Selton-Suty C, Célard M, Le Moing V, DocoLecompte T, Chirouze C, lung B, et al; on behalf of he AEPEI Study Group (2012) Preeminence of Staphylococcus aureus in Infective Endocarditis: A 1Year Population-Based Survey. Clin Infect Dis. 2012;54:1230–9. 728 4. Duval X, Delahaye F, Alla F, Tattevin P, Obadia JF, Le Moing V, et al. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. J Am Coll Cardiol. 2012;59:1968–76. 5. Desimone DC, Tleyjeh IM, Correa de Sa DD, Anavekar NS, Lahr BD, Sohail MR, et al. Incidence of infective endocarditis due to viridans group streptococci before and after publication of the 2007 American Heart Association’s endocarditis prevention Guidelines. Circulation. 2012;126(1): 60–4. 6. Benito N, Miró JM, de Lazzari E, Cabell CH, del Río A, Altclas J, et al; ICE-PCS (International Collaboration on Endocarditis–Prospective Cohort Study) Investigators. Health care–associated native valve endocarditis: importance of non-nosocomial acquisition. Ann Intern Med. 2009;150:586–94. 7. Datta BN, Khattri HN, Bidwai PS, Suri RK, Gujral JS, Agarwal KC, et al. Infective endocarditis at autopsy in northern India. A study of 120 cases. Jpn Heart J. 1982;23:329–37. 8. Choudhury R, Grover A, Varma J, Khattri HN, Anand IS, Bidwai PS, et al. Active infective endocarditis observed in an Indian hospital 1981-1991. Am J Cardiol. 1992;70:1453–8. 9. Garg N, Kandpal B, Garg N, Tewari S, Kapoor A, Goel P, et al. Characteristics of infective endocarditis in a developing country: Clinical profile and outcome in 192 Indian patients, 1992-2001. Int J Cardiol. 2005;98:253–60. 10. Senthilkumar S, Menon T, Subramanian G. Epidemiology of infective endocarditis in Chennai, South India. Indian J Med Sci. 2010;64:187–91. 11. Math RS, Sharma G, Kothari SS, Kalaivani M, Saxena A, Kumar AS, et al. Prospective study of infective endocarditis from a developing country. Am Heart J. 2011;162:633–8. 12. Jain SR, Prajapati J, Manjunath A. Clinical Spectrum of Infective Endocarditis in a Tertiary Care Centre in Western India: A Prospective Study. Int J Clin Med. 2014;5:177–187 13. Gupta A, Gupta A, Kaul U, Varma A. Infective endocarditis in an Indian setup: Are we entering the ‘modern’ era? Indian J Crit Care Med. 2013;17:140–7. 14. The task force on the prevention, diagnosis, and treatment of infective endocarditis of the European Society of Cardiology (ESC): Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009). Eur Heart J. 2009;30:2369–413. J. Preventive Cardiology Vol. 4 No. 4 May 2015 Preventive strategies against infective endocarditis 15. Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007;116:1736–54. 16. National Institute for Health and Clinical Excellence. Prophylaxis against infective endocarditis 2008 (NICE clinical guideline No. 64). 17. Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani-Mougeot FK. Bacteremia associated with toothbrushing and dental extraction. Circulation. 2008;117:3118–25. 18. Gould FK, Elliott TSJ, Foweraker J, Fulford M, Perry JD, Roberts GJ, et al. Guidelines for the prevention of J. Preventive Cardiology Vol. 4 No. 4 May 2015 endocarditis: report of the Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother. 2006;57:1035–42. 19. Thornhill MH, Dayer MJ, Forde JM, Corey GR, Hock G, Lockhart PB. Impact of the NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and after study. BMJ. 2011;342:d2392. 20. Dayer MJ, Jones S, Prendergast B, Baddour LM, Lockhart PB, Thornhill MH. Incidence of infective endocarditis in England, 2000–13: a secular trend, interrupted time-series analysis. The Lancet. 2014. doi: 10.1016/S0140-6736(14)62007-9 21. Chirouze C, Hoen B, Duval X. Infective endocarditis prophylaxis moving from dental prophylaxis to global prevention? Eur J Clin Microbiol Infect Dis. 2012;31:2089–95. Address for correspondence Dr. J. C. Mohan: Email: [email protected] 729 Mohan JC, et al definite increase in IE in France21 and the United States.5 Duval and colleagues4 reported a follow-up study in three French regions (with a total adult population of about 11 million) where a guideline change in 2002 restricted antibiotic prophylaxis to patients at high risk of infective endocarditis (roughly 10% of the total cases). They identified no significant increase in the incidence of oral streptococcal infective endocarditis in 2008 compared with their findings from 1991 and 1999. However, there was an increase in staphylococcal infections (36% of all IE vs 12% streptococcal in 2008), mostly in those subjects with no pre-existing valvular heart disease. What to do in India? In India, we cannot ignore rheumatic valvular heart disease, with its peculiar structural and immunological characteristics, nor the poor oral health of the general Indian population, which has not improved significantly over the past decades. Therefore, it is not wise to ignore our epidemiological peculiarity of valvular heart disease and general level of hygiene. In India, it may be still reasonable to recommend antibiotic prophylaxis before starting dental interventional procedures that bear a high probability of significant bacteremia to patients who have either valvular or congenital heart diseases that represent a risk for IE, regardless of assumptions on differences of disease course. In addition, there is the need for prospective and controlled studies to support the probability of the effect of antibiotic prophylaxis. References 1. Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: Executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:e57–e185. 2. Tleyjeh IM, Abdel-Latif A, Rahbi H, Scott CG, Bailey KR, Steckelberg JM, et al. A systematic review of population based studies of infective endocarditis. Chest. 2007;132:1025–35. 3. Selton-Suty C, Célard M, Le Moing V, DocoLecompte T, Chirouze C, lung B, et al; on behalf of he AEPEI Study Group (2012) Preeminence of Staphylococcus aureus in Infective Endocarditis: A 1Year Population-Based Survey. Clin Infect Dis. 2012;54:1230–9. 728 4. Duval X, Delahaye F, Alla F, Tattevin P, Obadia JF, Le Moing V, et al. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. J Am Coll Cardiol. 2012;59:1968–76. 5. Desimone DC, Tleyjeh IM, Correa de Sa DD, Anavekar NS, Lahr BD, Sohail MR, et al. Incidence of infective endocarditis due to viridans group streptococci before and after publication of the 2007 American Heart Association’s endocarditis prevention Guidelines. Circulation. 2012;126(1): 60–4. 6. Benito N, Miró JM, de Lazzari E, Cabell CH, del Río A, Altclas J, et al; ICE-PCS (International Collaboration on Endocarditis–Prospective Cohort Study) Investigators. Health care–associated native valve endocarditis: importance of non-nosocomial acquisition. Ann Intern Med. 2009;150:586–94. 7. Datta BN, Khattri HN, Bidwai PS, Suri RK, Gujral JS, Agarwal KC, et al. Infective endocarditis at autopsy in northern India. A study of 120 cases. Jpn Heart J. 1982;23:329–37. 8. Choudhury R, Grover A, Varma J, Khattri HN, Anand IS, Bidwai PS, et al. Active infective endocarditis observed in an Indian hospital 1981-1991. Am J Cardiol. 1992;70:1453–8. 9. Garg N, Kandpal B, Garg N, Tewari S, Kapoor A, Goel P, et al. Characteristics of infective endocarditis in a developing country: Clinical profile and outcome in 192 Indian patients, 1992-2001. Int J Cardiol. 2005;98:253–60. 10. Senthilkumar S, Menon T, Subramanian G. Epidemiology of infective endocarditis in Chennai, South India. Indian J Med Sci. 2010;64:187–91. 11. Math RS, Sharma G, Kothari SS, Kalaivani M, Saxena A, Kumar AS, et al. Prospective study of infective endocarditis from a developing country. Am Heart J. 2011;162:633–8. 12. Jain SR, Prajapati J, Manjunath A. Clinical Spectrum of Infective Endocarditis in a Tertiary Care Centre in Western India: A Prospective Study. Int J Clin Med. 2014;5:177–187 13. Gupta A, Gupta A, Kaul U, Varma A. Infective endocarditis in an Indian setup: Are we entering the ‘modern’ era? Indian J Crit Care Med. 2013;17:140–7. 14. The task force on the prevention, diagnosis, and treatment of infective endocarditis of the European Society of Cardiology (ESC): Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009). Eur Heart J. 2009;30:2369–413. J. Preventive Cardiology Vol. 4 No. 4 May 2015 Preventive strategies against infective endocarditis 15. Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007;116:1736–54. 16. National Institute for Health and Clinical Excellence. Prophylaxis against infective endocarditis 2008 (NICE clinical guideline No. 64). 17. Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani-Mougeot FK. Bacteremia associated with toothbrushing and dental extraction. Circulation. 2008;117:3118–25. 18. Gould FK, Elliott TSJ, Foweraker J, Fulford M, Perry JD, Roberts GJ, et al. Guidelines for the prevention of J. Preventive Cardiology Vol. 4 No. 4 May 2015 endocarditis: report of the Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother. 2006;57:1035–42. 19. Thornhill MH, Dayer MJ, Forde JM, Corey GR, Hock G, Lockhart PB. Impact of the NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and after study. BMJ. 2011;342:d2392. 20. Dayer MJ, Jones S, Prendergast B, Baddour LM, Lockhart PB, Thornhill MH. Incidence of infective endocarditis in England, 2000–13: a secular trend, interrupted time-series analysis. The Lancet. 2014. doi: 10.1016/S0140-6736(14)62007-9 21. Chirouze C, Hoen B, Duval X. Infective endocarditis prophylaxis moving from dental prophylaxis to global prevention? Eur J Clin Microbiol Infect Dis. 2012;31:2089–95. Address for correspondence Dr. J. C. Mohan: Email: [email protected] 729