CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 7, August 2013
AFRICA
253
bioprosthetic heart valve implantation, haemolysis, platelet
activation and thromboembolic events resulting from clot
formation are commonly encountered in mechanical heart
valves.
8
Biomedical engineering studies revealed that these
complications might be related to non-physiological blood flow
patterns in the vicinity of the heart valves. In fact, the potential
of abnormal flow patterns to promote blood cell damage has
long been recognised. Abnormal flow patterns cause thrombus
formation by imposing forces on cell elements in high shear-
stress regions (so leading to haemolysis and platelet activation),
and changing the frequency of contact (particularly activating
platelets for thrombus formation). In addition, these abnormal
flow patterns might induce leaflet calcification, and tearing in
tissue and polymeric valves by high shear-force regions near the
leaflet surfaces.
8,9
For clinical interpretation, it has been reported in the literature
that mechanical valve dehiscence and pannus formation were
encountered with both bioprosthetic and mechanical valves.
Acute prosthetic valve thrombosis was commonly seen with
mechanical valves only.
10
In line with the literature, our results demonstrated that
thrombus and pannus formation were the leading indications
for re-operation, whereas left atrial thrombus and valvular
calcification were diagnosed in nearly one-quarter of the sample
group. We believe that a high risk of thrombus formation in
patients with left atrial thrombus and valvular calcification
in the initial surgery might indicate a tendency to thrombosis
and ongoing inflammatory processes. Correlated with this
process, MPV may indicate increased risk of thrombosis and the
inflammatory process.
No or inadequate oral anticoagulation (INR
<
2.5) or extreme
fluctuations of INR values were also reported as strong risk factors
in the aetiology of mechanical prosthetic valve thrombosis.
11
In
our study, no direct correlation was determined between valvular
thrombus formation and anticoagulant use. Similarly, we did
not observe any statistically significant relationship between
warfarin use/INR levels and thrombosis (
p
>
0.05).
The distance of the patient from a cardiac surgery centre
was another major factor in the management of the condition.
The postoperative life expectancy of patients undergoing
prosthetic valve replacement was closely related to reversibility
of myocardial or other organ damage. Therefore, the timing of
the operation was critical.
6
Bioprosthetic valves may be more
useful for patients who live in rural areas.
Although there was a statistically significant relationship
between the presence of calcification in the native valve and
valvular thrombus during the primary surgery (
p
>
0.05), it was
not significantly related to perivalvular leak (
p
> 0.5). However,
the incidence of perivalvular leak was expected to be increased
in patients with annular calcification. This may have been caused
by the small sample size of the study.
The aortic annulus is not only a circular structure that
supports the leaflets of the heart valve, it also allows opening
of the leaflets during the ventricular systole. The anatomical
structure and shape of the aorta as well as the ventricular outflow
tract are of utmost importance for maintaining blood flow.
Considering these anatomical and physiological characteristics,
non-conformity of the prosthetic valve and annulus may lead to
perivalvular leak.
In a study by Beghi
et al
., it was shown that perivalvular
leak led to aortic valve replacement.
12
The factors leading to
perivalvular leak include prosthetic valve endocarditis, Marfan
syndrome, bicuspid aorta and a highly calcific aortic annulus.
The major site for perivalvular leak is the mid-zone of the
non-coronary sinus and the right coronary sinus.
13
In the present
study, we suggest that the anatomical structure of the zone
resulted in perivalvular leak. In addition, Thubrikar
et al
.
demonstrated that non-conformity of the prosthetic valve and
aortic annulus led to perivalvular leak in these zones.
14
In another study investigating reasons for prosthetic mitral
valve regurgitation, it was shown that 46% of the patients
underwent re-operation due to structural degeneration of the
valve.
15
Structural degeneration was defined as valve stenosis
or regurgitation secondary to calcification or ruptured leaflets,
whereas non-structural degeneration was defined as valve
stenosis or regurgitation secondary to trauma, pannus formation
or surgery. In these patients, perivalvular leak was the leading
cause of re-operation in 20%, non-structural degeneration in
10%, progression of primary valve disease in 8%, and infective
endocarditis in 6%.
Mitral valve re-operation did not increase the length of
hospital stay, compared to the primary surgery. In addition,
re-operation was shown not to be a risk factor for peri-operative
mortality. Despite a higher incidence of perivalvular leak with
mechanical valves, structural degeneration was more often seen
with bioprosthetic valves. There was no difference in postoperative
complications and mortality rate between the groups.
The incidence of infective endocarditis was similar between the
groups. A total of 30.2% of the patients had infective endocarditis
Fig. 1. Distribution of pathologies on the prosthetic
valves.
18
16
14
12
10
8
6
4
2
0
Mitral
Aorta
Tricuspid
Valves
Thrombus (+)
Thrombus (–)
Leakage (+)
Leakage (–)
Pannus (+)
Pannus (–)
Fig. 2. ROC curve.
1.0
0.8
0.6
0.4
0.2
0.0
0.0
0.2
0.4
0.6
0.8
1.0
1 – Specificity
Sensitivity
