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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.
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Address for correspondence
Dr. J. C. Mohan: Email: [email protected]
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