CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 4, July/August 2014
166
AFRICA
Percutaneous PFO closure was performed under fluoroscopic
and TEE guidance and under general anaesthesia. Procedural
success was defined as successful implantation of the occluder
at the closure site with no procedural complications. Dual
antiplatelet therapy including 75 mg clopidogrel for three months
and 100 mg aspirin lifelong was recommended after the closure
procedure. Patients in the intervention group were followed up
at one, three, six and 12 months after the procedure and closure
rates and residual shunt were evaluated at the six-month follow
up by contrast transthroracic echocardiography.
Statistical analysis
Continuous variables are presented as mean
±
standard deviation
and categorical variables are presented as percentages. Group
differences for continuous variables were examined by the Mann–
Whitney
U
-test. For categorical variables, comparisons between
groups were made with the
χ
2
or Fisher exact test, as appropriate.
Pre- and post-procedural MPV levels in the intervention group
were compared with the Wilcoxon signed-rank test.
Results
A total of 31 patients were enrolled in the study. Baseline
demographic and clinical characteristics of all patients are
presented in Table 1. The patients in the intervention group
were significantly older than those without a history of stroke
(48.25
±
12.1 vs 37.4
±
15.32 years;
p
=
0.028). The other baseline
characteristics were similar between the two groups. The mean
age of the patients in the intervention group at the time of their
first ischaemic attack was 45.38
±
12.01 years.
Procedural success rate was 100% in the intervention group.
Cardio Fix, BioSTAR, Amplatzer and Cardioseal/Starflex
devices were implanted in eight, six, one and one patients,
respectively. Residual shunt was detected in three (19%) patients
at the six-month follow up. None of the patients suffered a
recurrent ischaemic attack after the intervention during a mean
follow-up period of 26.5
±
1.3 months.
Forty-four per cent of the patients undergoing PFO closure
were receiving aspirin (100 mg/day), and the remainder (56%)
were taking oral anticoagulant therapy before the procedure.
After PFO closure, all patients were prescribed dual antiplatelet
therapy with asetylsalicilic asid (100 mg/day) and clopidogrel (75
mg/day).
The patients with PFO and cryptogenic stroke had similar
mean platelet volumes to the patients with PFO but without
stroke (9.34
±
1.64 fl vs. 9.1
±
1.34 fl;
p
=
0.526). On the
other hand, we observed a significant decline in MPV after
transcatheter PFO closure in patients with stroke compared
with their pre-procedural levels (9.34
±
1.64 fl vs 8.3
±
1.12 fl;
p
=
0.001). Pre- and post-procedural changes in MPV in patients
undergoing percutaneous closure is represented in Fig. 1.
There was no difference in platelet count in patients with and
without stroke. There were also no significant differences in pre-
and post-closure platelet count levels in the intervention group
(Table 1).
Discussion
We presumed that platelet activity may be increased in PFO
patients with stroke compared to those without stroke, but we
did not find a difference between these two groups. Interestingly,
we observed that MPV levels decreased after percutaneous PFO
closure in patients with previous stroke compared with their
pre-procedural levels.
Mean platelet volume is a measure of platelet size, and is a
determinant of platelet activity. Larger platelets are metabolically
and enzymatically more active than smaller platelets, containing
more prothrombotic material such as thromboxane A
2
and
serotonin, and expressing greater numbers of adhesion molecules
such as Glp IIb/IIIa receptor and P-selectin.
11-14
They also show
greater aggregation in response to ADP.
10
Previous studies have
shown that MPV was increased in myocardial infarction and
ischaemic stroke, both of which are atherothrombotic events
where platelets play a pivotal role.
The association of PFO with cryptogenic stroke has been
established previously,
1,4
but the pathogenic link between PFO
and stroke is still unclear in most cases. One of the postulated
mechanisms underlying the stroke in the presence of PFO is
paradoxycal embolism with an occult DVT. Although some
studies have shown increased frequency of prothrombotic
mutations, which may be a predisposing factor for the
Table 1. Demographic and clinical characteristics
of the patients
PFO patients
with stroke
PFO patients
without stroke
p
-value
Number
16
15
Male (%)
44
13
0.113
Age (years)
48.2
±
12.1
37.4
±
15.3 0.028
Current smoker (%)
44
47
0.870
Hypertension (%)
19
7
0.600
Diabetes mellitus (%)
25
0
0.101
Hyperlipidaemia (%)
6
0
1.00
Coronary artery disease (%)
0
0
1.00
Antiplatelet use at
baseline (%)
44
0
Oral anticoagulan therapy
at baseline (%)
56
0
MPV at baseline (fl)
9.34
±
1.64
9.10
±
1.34 0.526
Platelet count at baseline 288562
±
80180 267400
±
56368 0.527
16
14
12
10
8
6
4
2
0
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
Pre-procedural MPV Post-procedural MPV
MPV (fl)
Fig. 1.
Pre- and post-procedural mean platelet volume (MPV)
in PFO patients undergoing percuteneous closure.
