Discussion
Infective endocarditis in hypertrophic cardiomyopathy is a serious
complication associated with high morbidity and mortality.[1]
Although it is not common, it has been reported in the literature, but
the data are limited to single cases or groups of cases.
The most cited study was that of Spirito and colleagues who followed the
evolution of 810 patients with HCM and the incidence was reported to be
1.4 cases/person/year and the main risk factors were outlet obstruction
and OG dilatation [2].
Another chinese study of Wang et al [7] showed that the proportion
of HCM patients with IE was 0.19%,with the estimated incidence of
0.15/1 000 person-years in HCM patients.
The mitral valve was the most affected in studies conducted by Spirito
et al in 1999 and Fernando et al in 2013 with a percentage of 70 and
71% respectively [2]
An obstructive HCM was present in all cases of infective endocarditis
[10] with a statistically significant association between
obstruction and infective endocarditis in the study of Spirito et al
[2] but the multicenter, prospective, cohort study of Dominguez et
al [3] and Sims et al [8] found a similar incidence of IE with
or without left ventricular outflow tract obstruction (LVOTO).
Nevertheless, the small sample size could be just a statistical outlier,
limiting its universality . In addition, the latter study found no
clinical difference between infective endocarditis in HCM patients with
and without obstruction..
Because HCM is a disorder of the myocardium and not the endocardium, it
has been considered to have low risk of IE. In fact the occurrence of
infective endocarditis in HCM patients can be explained by endocardial
lesions secondary to turbulent flow during ejection and contact between
the anterior leaflet of the mitral valve and the septum during systole
which is called « Venturi effect » , thus direct trauma resulting from
septal-anterior mitral leaflet contact may predispose to infection and
vegetation formation [2,4]
We note that the vegetation in our case was indeed located on the
anterior leaflet of mitral valve.
The most common germs found in the literature were staphylococcus aureus
and streptococcus , with this latest being more found among native-valve
HCM patients [2, 3].
The germ in our case was not identified with blood culture remaining
negtive.
Mitral valve replacement surgery and septal myomectomy are the two
accepted therapeutic methods for symptomatic obstructive HCM refractory
to medical treatment but the larger series on the surgical treatment of
HCM suggests that the two operations are rarely combined [5,6].
We recall that our patient had both operations at the same time.
The occurrence of a complication such as rupture of an intracerebral
mycotic aneurysm with hematoma, as was the case in our patient, is very
rare and limited to a few isolated cases reported in the literature
[7, 8], in a recent study of
Jason
R Sims et al [8], symptomatic embolic complications occurred in
33% of cases.