important numbers of a pathogen which is generally
a bacteria but could sometimes be a fungus that hap-
pened to be circulating in the blood stream. Therefore
a vegetation is formed and can hitherto damage the
neighboring endocardial tissue or valves 8 .
As we all know, valves are what maintains
blood‘s one-way flow through the heart and circulato-
ry system. Once the function of these valves is jeopar-
dized by a large vegetation for example, important he-
modynamic consequences may occur: from pulmonary
oedema and hypertension to cardiac failure and shock.
Extension of germ colonization to endocardial tissue
could also cause mechanical complication such as
perivalvular abscess, or cordage rupture. Nodal tissue
involvement can occur and conduction blocks could
also result 8,9 .
The vegetation could be source of septic em-
boli which is the migration of its detached parts and
thereof the occlusion of any artery in the pulmonary
or systemic circulation. This could cause a widespread
of manifestation from pulmonary embolism and pneu-
mopathy to stroke or paralysis, consequences of a
brain injury 8 .
Anatomically speaking, a vegetation located in the
right-heart’s valves would embolize to the lungs, while
a left-heart vegetation would mostly embolize to the
systemic arteries (brain, legs, spleen, kidneys…) 8 .
The most common form of infective endocar-
ditis in drug users involves the tricuspid valve (This is
explained by the fact that injecting drugs is done in
veins which blood is drained to the right heart) and
is due to S. aureus 6 (No surprise there!). It manifests
clinically by a fever, pleuritic chest pain and cough 7 .
The classic heart murmur can be absent. Although the
mortality of this form is quite low (5%), a large vegeta-
tion size > 2cm or a fungal etiology might make things
worse (25% and 65% mortality rates respectively) 10 .
In all cases, isolating the responsible germ (staph or
other) in blood-cultures and visualizing the vegeta-
tion through imaging methods (mainly transthoracic
echocardiography and sometimes trans-esophageal
one) are the two major criteria in diagnosing an in-
fective endocarditis. They belong to an ensemble of
criteria known as Duke’s 9 .
Last but not least, let us speak of blood-borne
viruses, mainly HIV and HCV. The use of non-sterile sy-
ringes is the main source of contamination. Addition-
ally, the existence of blood on drug sniffing straws is
thought to vehicle HCV between users who share this
paraphernalia 11 .
Remember when we said that tricuspid valve
endocarditis has a low death tow of 5%? That rate be-
comes higher in HIV-infected users with a low CD4
count 7 . In fact, the highes