Cihan Cevik MDa
Correspondence to Cihan Cevik MD. Email: ccevik@sleh.com
SWRCCC 2014;2(6):1-2
doi: 10.12746/swrccc2014.0206.065
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“The infective endocarditis increases the physician’s interest in the development of an infectious process”.
- William Bart Osler, 1893Medical historians report that Mozart suffered
frequent attacks of tonsillitis, migratory polyarthritis,
and glomerulonephritis and almost certainly had
acute rheumatic fever. He underwent a dental extraction
before penicillin was discovered. Subsequently,
he developed fever and septic emboli and died at age
35 in 1791. The extent of infection in his heart still
remains a mystery since this happened before the
invention of ECGs, chest radiographs, and even the
stethoscope. An autopsy was never done.
Approximately one hundred years later, William
Osler was the first to describe infective endocarditis
by reviewing the records of 200 patients with socalled
ulcerative, malignant endocarditis in London.1
He included patients with fever and new murmurs,
and he described his experience with a woman who
developed erythematous, painful, swollen small spots
occurring on the fingertips and feet resembling “beehives”that became known as Osler’s nodes. In 1908, William Osler wrote that “with carefully made blood cultures one should now be able to determine the
presence of the septicemia; this was easily done in
three of my recent cases.2
Infective endocarditis was almost 100% fatal until 1950s. Cure rates with sulfonamides (5%) improved
up to 60-70% with the administration of penicillin.
The concept of removing the infected tissue
surgically from a patient with heart failure and fever
seemed imprudent until Andrew Wallace excised and
replaced the aortic valve with a Starr-Edwards prosthesis in a 45- year-old patient with Klebsiella endocarditis who was unresponsive to antibiotics 3 In the 21st century, the risk of infective endocarditis remains a major concern, especially in patients with device implants, indwelling catheters, and IV drug abuse.
These risk factors cause the tricuspid valve and the
right heart to be involved before the left heart. Interestingly,
the literature available on patients with rightsided
infective endocarditis is much less than the literature
available on mitral/aortic infective endocarditis
cases, even though there is an increasing number of
device implants and of IV drug users and decreasing
prevalence of rheumatic heart valve disease.
Dr. Sutamtewagul and coworkers report the
results of their chart review of the patients diagnosed
with right-sided infective endocarditis between 2000
and 2011 in the current issue of the Journal. The authors
speculated that embolic events associated with
vegetations would increase pulmonary artery pressures,
which, in turn, would predict hospital outcomes.
The authors found out that most of these patients had
mild pulmonary hypertension. Although they could not
demonstrate an association between the mean pulmonary
artery pressure and hospital outcomes, they
observed that patients with right-sided infective endocarditis
and abnormal chest radiographs stayed in
the hospital three times longer than the patients with
normal chest x-rays (7.5 vs. 21.4 days; p=0.008). Despite
having the drawbacks of a retrospective, observational
study using indirectly calculated pulmonary
artery pressure data, their findings still underscore
the utility of a simple chest x-ray for the triage, management,
and perhaps outcome prediction in these
patients. The lack of association between pulmonary
artery pressure and length of stay seems to be a Type
2 error in this small study.
We are very fortunate for the advances in
diagnosis and management of infective endocarditis in 21st century so that more than ninety percent of
patients have favorable outcomes. While utilizing the
best medical and surgical therapy, we should also
keep in mind that simple diagnostic tools, such as a
chest radiograph, may still help guide the management.
Finally, we must not forget that an abnormality
on the chest radiograph could also indicate other
diseases, such as pneumonia, lung abscess, or empyema,
conditions which caused Sir William Osler’s
death in 1916.
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Published electronically: 4/15/2014
Conflict of Interest Disclosures: None