CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 4, July/August 2014
AFRICA
167
development of DVT in patients with PFO, other studies found
no difference between PFO patients and controls.
15-18
Accordingly, the majority of strokes associated with PFO
cannot be explained by paradoxycal embolism. We hypothesised
that increased platelet activity may be a factor in the pathogenesis
of cryptogenic stroke in patients with PFO, and found that PFO
patients with and without stroke had similar MPV, which was
decreased after percutaneous closure.
Increased platelet activity in patients with right-to-left shunt
may be a precipitating factor in thrombus formation in the
conduit of PFO, which is one of the proposed pathogenic links
between PFO and stroke. The absence of recurrent neurological
events during the mean follow-up period of 26.5
±
1.3 months in
the intervention group may also suggest that decreased MPV and
platelet activity may have a possible protective role for recurrent
ischaemic events after the closure procedure. However, why
patients with right-to-left shunt have increased platelet activity
is a dilemma.
Forty-four per cent of patients in the intervention group
were receiving aspirin before the procedure, after which dual
antiplatelet therapy was prescribed to all patients for three
months. Finally, aspirin monotherapy was recommended
lifelong. Although there are limited data regarding the effect
of antiplatelet agents on MPV, aspirin does not seem to
significantly affect platelet volume.
19,20
Likewise, large platelets
exhibit increased reactivity even after dual antiplatelet therapy in
patients with stable coronary artery disease.
21
These data support
the hypothesis that post-procedural decline in MPV cannot be
solely attributed to a higher rate of usage of antiplatelet therapy
after the intervention.
This study is limited by its small sample size. The lack of
significant difference in MPV between patients with and without
stroke may be a type 2 error due to insufficient sample size. Mean
platelet volume may be greater in patients with cryptogenic
stroke and PFO compared with asymptomatic patients with
PFO. This should be clarified in further randomised studies with
larger patient populations.
Additionally, the observed post-procedural decline in MPV
may be related to factors such as different rates of pre- and
post-procedural antiplatelet and anticoagulant therapy usage
as well as the PFO closure device itself. Therefore, performing
other laboratory tests in addition to platelet count and MPV to
estimate platelet activity would have strenghtened our results.
On the other hand, this is the first study to our knowledge
that demonstrates a decrease in platelet activity in patients with
PFO undergoing percutaneous closure. Our findings warrant
further studies to investigate the platelet activity in PFO patients
as a risk factor for cryptogenic stroke and its possible association
with percutaneous closure.
Conclusion
Our findings suggest interatrial communication through a PFO
may be related to increased MPV and increased platelet activity.
The authors gratefully thank M Erdinc Arikan for his assistance in language
editing.
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