Alterations of platelet aggregation while treating cardiac arrhythmias with radiofrequency ablation

Abstract

To find out if radiofrequency ablation as method of treatment of cardiac arrhythmia influences platelet aggregation and if intensity of this process depends on the number of radiofrequency ablation episodes for one patient.
We analyzed platelet aggregation before, right after and in 24 hours after radiofrequency ablation in whole blood and platelet rich plasma in 39 cases with cardiac arrhythmias. Adenosine diphosphate and adrenaline were used for aggregation induction. Three groups of patients were formed based on the number of radiofrequency ablation episodes: A-- <10, B--10-20, C-- >20 for one patient.
We detected a decrease in spontaneous, adenosine diphosphate and adrenaline induced platelet aggregation in plasma right after radiofrequency ablation, and also the same tendency was noted in adenosine diphosphate induced aggregation in whole blood. In 24 hours after radiofrequency ablation platelet aggregation tended to return to pre-radiofrequency ablation levels. Based on the number of radiofrequency ablation episodes we detected significant changes in spontaneous and adrenaline-induced aggregation in plasma. In group A adrenaline induced aggregation after radiofrequency ablation increased by 0.4%, in group B it decreased by 15.7% and in group C it decreased by 19.4% from pre-radiofrequency ablation level (p<0.05, between groups A and C). Spontaneous platelet aggregation after radiofrequency ablation decreased in group A 41.9%, in group B--20.8% and in group C--18.4% from pre-radiofrequency ablation level (p<0.05 between groups A and C). The greater decrease in adenosine diphosphate induced aggregation in plasma and in whole blood was detected in the group with larger number of radiofrequency ablation episodes.
This study found that platelet aggregation decreased in plasma and in whole blood after radiofrequency ablation. And this alteration was significant in groups B and C, when the number of radiofrequency ablation episodes were >10. In 24 hours platelet aggregation increased again to pre- radiofrequency ablation level.

Full text

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Alterations of platelet aggregation while treating cardiac arrhythmias
with radiofrequency ablation
Vilma Kozlovaitė, Pranas Grybauskas, Jūratė Cimbolaitytė, Aušra Mongirdienė,
Aras Puodžiukynas
1
, Vytautas Šileikis
1
,
Tomas Kazakevičius
1
, Vytautas Zabiela
1
Insitute of Cardiology, Kaunas University of Medicine
1
Clinic of Cardiology, Kaunas University of Medicine Hospital, Lithuania
Key words: platelet aggregation, radiofrequency catheter ablation.
Summary. Objective. To find out if radiofrequency ablation as method of treatment of
cardiac arrhythmia influences platelet aggregation and if intensity of this process depends
on the number of radiofrequency ablation episodes for one patient.
Material and methods. We analyzed platelet aggregation before, right after and in 24
hours after radiofrequency ablation in whole blood and platelet rich plasma in 39 cases
with cardiac arrhythmias. Adenosine diphosphate and adrenaline were used for aggrega-
tion induction. Three groups of patients were formed based on the number of radiofrequency
ablation episodes: A – <10, B – 10–20, C – >20 for one patient.
Results. We detected a decrease in spontaneous, adenosine diphosphate and adrenaline
induced platelet aggregation in plasma right after radiofrequency ablation, and also the
same tendency was noted in adenosine diphosphate induced aggregation in whole blood.
In 24 hours after radiofrequency ablation platelet aggregation tended to return to pre-
radiofrequency ablation levels. Based on the number of radiofrequency ablation episodes
we detected significant changes in spontaneous and adrenaline-induced aggregation in
plasma. In group A adrenaline induced aggregation after radiofrequency ablation increased
by 0.4%, in group B it decreased by 15.7% and in group C it decreased by 19.4% from pre-
radiofrequency ablation level (p<0.05, between groups A and C). Spontaneous platelet
aggregation after radiofrequency ablation decreased in group A 41.9%, in group B – 20.8%
and in group C – 18.4% from pre-radiofrequency ablation level (p<0.05 between groups A
and C). The greater decrease in adenosine diphosphate induced aggregation in plasma
and in whole blood was detected in the group with larger number of radiofrequency abla-
tion episodes.
Conclusions. This study found that platelet aggregation decreased in plasma and in
whole blood after radiofrequency ablation. And this alteration was significant in groups B
and C, when the number of radiofrequency ablation episodes were >10. In 24 hours plate-
let aggregation increased again to pre- radiofrequency ablation level.
Medicina (Kaunas) 2004; 40(9) - http://medicina.kmu.lt
Correspondence to V. Kozlovaitė, Institute of Cardiology, Kaunas University of Medicine, Sukilėlių 17,
50157 Kaunas, Lithuania. E-mail: vkozlovaite@yahoo.com
Introduction
Cardiac arrhythmias (atrial fibrillation etc.) caused
by thrombus in cardiac chambers are one of the main
thromboembolic complications and the cause of the
stroke. Prevention of embolization with antithrombotic
medications in these cases is essential.
Using modern electrophysiologic test for
assessment of causes of arrhythmia and detection
of topography of active focus the radiofrequency
ablation (RFA) became an effective and safe method
of radical treatment for various arrhythmias.
However, since RFA has a mechanical and thermal
effect on a relatively wide area of the tissue
(endocardium, endothelium, etc.) that may lead to a
clot formation, and it is being discussed if embolization
prevention with coagulation system modulating
(usually suppressing) medications (antiplatelet drugs
and/or anticoagulants) is beneficial. Evaluating
relations between thromboembolism and RFA it was
established that it is important to distinguish effects
on coagulation system and clot formation caused by
electrophysiologic procedure and RFA itself (1).

851
There are early and late post-RFA thromboembolic
complications. The early complications are caused by
local haemostatic disruption in the catheter zone and
the late ones by endothelial damage (2). Up to 1-2%
of post-RFA complications of both types have been
reported (3-7), even after one month of antiplatelet
drug therapy (8). The complications are more common
after the left heart procedures (2).
The process of clot formation involves plasma
coagulation factors and is completed by platelets.
Although plasma's and platelets coagulation systems
are different, the end result is mutual - thrombus/clot
(9, 10). The purpose of this study is to find out if RFA
affects the platelet function (i. e. aggregation) and
whether the intensity of this process depends on the
number of RFA episodes irrespective of medications
used and the disease substrate.
Material and methods
In this study we examined 39 cases of cardiac
arrhythmias (atrial flutter, supraventricular tachycardias
and extrasystoles), in Clinic of Cardiology of Kaunas
University of Medicine Hospital. The main diagnosis
of a case was based on clinical and electrophysiologic
test data. Patients had no meal and antiarrhythmic
medications and did not smoke 12-16 hours before the
RFA.
The RFA procedure was performed using a
standard Seldinger method. Through the puncture of
the right femoral vein or artery, multicontact electrodes
were inserted into the heart and directed to the certain
cardiac areas with the accuracy of 1-2 mm. Their
electric activity and the spread of the impulse were
registered in the intracardiac ECG by computer system
(PRUCKA). Arrhythmogenic substrate was destroyed
using radio-frequency 500 kHz 30-60 W energy which
produces 50-70° temperature irreversibly coagulating
2-4 mm
3
area of tissue at the side where a special
destructive electrode-catheter contacts the
endocardium (11).
The blood for platelet aggregation testing was
drawn from the antebrachial vein into 5 ml vacuum
test-tube with 3.8% sodium citrate before, right after,
and 24 hours after RFA. The platelet rich plasma was
separated from red blood cells by blood centrifuging
1000/min (100 g) 15 min at the room temperature.
Platelet-free plasma was obtained by further
centrifuging the rest of the blood 3000/min (1000 g),
30 min.
We tested platelet aggregation in the whole blood
and platelet rich plasma. Platelet aggregation in the
whole blood was analyzed using a special whole blood
aggregometer (WBA, Chrono-Log, USA) that
measures platelet aggregation by the principle of
electric resistance variation in units of resistance
(ohms). Adenosine diphosphate (ADP, 10 mcmol/l)
was used for induction of platelet aggregation. Platelet
aggregation was analyzed using aggregometer
(Chrono-Log, USA) by classic Born method (12) based
on platelet plasma optical density variation in the
process of aggregation, expressed in relative percents.
ADP in 2 concentrations (ADP
1
- 3.8 mcmol/l and
ADP
2
- 0.45 mcmol/l) and adrenaline (ADR 4.5
mcmol/l) were used for aggregation induction.
Spontaneous aggregation (SP) was recorded without
any inductor, only under the mechanical effect of
centrifuge.
Statistic calculations were made using "Excel" and
"Statistica" statistic packages.
Results
In order to evaluate RFA effect on platelet
aggregation 3 groups of the examined patients were
formed: group A - the number of RFA episodes given
to the patient £9; group B - 10-20 RFA episodes; group
C >20 RFA episodes (Table 1).
The results of platelet aggregation obtained before,
right after, and in 24 hours after RFA are shown in
Fig. 1.
The results revealed a significant decrease in
spontaneous, ADP
1
and ADR induced platelet
aggregation in plasma. The same tendency was noted
for aggregation induced by lower ADP concentration
(ADP
2
) and in the whole blood (WBA). Platelet
aggregation in 24 hours after RFA tended to return to
the pre-RFA levels.
Table 2 contains data of platelet aggregation based
on the number of RFA episodes. These results
demonstrate a significant change in spontaneous and
adrenaline-induced platelet aggregation in plasma
based on the number of RFA episodes.
In group A (number of RFA episodes 1-9) there
practically was no change (increase by 0.4%) in
adrenaline - induced post - RFA platelet aggregation,
in group B (number of RFA episodes 10-19) there was
a decrease by 15.7% in platelet aggregation, in group
C (number of RFA episodes ³20) there was a decrease
by 19.4% from a pre-RFA level (p<0.05, between group
A and C). The opposite tendency was noted in a
decrease in spontaneous platelet aggregation after RFA
based on the number of episodes: in group A there
was the most noticeable (evident) decrease - 41.9%
in group B - 20.8%, and in group C - 18.4% from the
pre-RFA level (p<0.05, between groups A and C).
Alterations of platelet aggregation while treating cardiac arrhythmias
Medicina (Kaunas) 2004; 40(9) - http://medicina.kmu.lt

852
Fig. The effect of RFA on platelet aggregation
* p<0.05, ** p<0.001, comparing with intensity of pre-RFA platelet aggregation (t-test for dependent values).
Table 1. Clinical characteristic of the examined patients
Patients Number of Mean Mean number of Total RFA Total duration of RFA
groups patients age (years) RFA episodes energy (J) coagulation (min)
A 14 49±11 4.4±2.7 2365±2248 1.6±0.7
B 12 55±9.5 14±2.6 11295±6064 5.7±2.07
C 13 44±11 37±11 26898±15236 14±4.0
Table 2. The dependence of the intensity of platelet aggregation on the number of RFA episodes
60
62
64
66
68
70
72
74
76
78
Before
RFA
After
RFA
24 h
after
RFA
Platelet aggregation
ADP1
ADR
**
**
2
3
4
5
6
7
8
9
Before
RFA
After
RFA
24 h
after
RFA
Platelet aggregation
ADP2
SP
WBA
*
Aggregation Number of RFA Platelet aggregation (X±SD)
inductor episodes
WBA <10 4.3±2.2 3.5±3.0 4.1±2.7
ADP (ohms) 10–20 4.3±3.3 3.6±3.3 4.3±2.7
>20 4.8±3.5 3.6±2.8 5.2±2.9
Spontaneous (%) <10 6.2±4.4 3.6±2.5 ** 7.7±9.4
10–20 5.3±4.0 4.2±2.8 6.2±4.1
>20 7.6±6.4 6.2±3.4 5.2±3.0
ADP
2
(%) <10 8.0±6.5 7.2±8.5 6.9±6.6
10–20 11.9±21.1 7.0±8.4 12.1±18.9
>20 7.0±5.7 4.9±3.3 * 6.5±5.8
ADP
1
(%) <10 77.9±10.5 75.5±11.0 69.8±15.2
10–20 77.6±8.1 70.2±8.4 ** 79.6±13.6
>20 73.5±14.8 67.8±15.4 * 68.7±17.8
ADR (%) <10 72.0±17.4 72.3±15.4 66.7±18.8
10–20 81.3±6.3 68.5±16.2 * 74.3±20.4
>20 67.1±17.9 54.1±24.5 *** 64.5±23.9
* p<0.005; ** p<0.001; *** p<0.0001 comparing with pre-RFA platelet aggregation (t-test for dependent
values). WBA - whole blood aggregation, ADP - adenosine diphosphate, ADP
1
ADP
2
- adenosine diphosphate
of different concentration for rich platelet plasma, ADR - adrenaline.
Before RFA After RFA 24 h after RFA
Vilma Kozlovaitė, Pranas Grybauskas, Jūratė Cimbolaitytė et al.
Medicina (Kaunas) 2004; 40(9) - http://medicina.kmu.lt

853
ADP-induced platelet aggregation in plasma and in
whole blood also tended to demonstrate a greater
decrease with a higher number of RFA episodes.
Although these 2 parameters demonstrated similar
changes, correlation between whole blood and plasma
platelet aggregation in the examined patients is very
low (r=0.004-0.28) and not reliable.
Discussion
All 39 patients had an uneventful RFA procedure.
Testing platelet activity it was not taken account of a
disease substrate as well as patients taking antiplatelet
drugs and anticoagulants. In this study we tried to detect
if RFA influences platelet aggregation and whether
the number of RFA episodes may affect the intensity
of aggregation.
Discussing these problems, we should address to
multiple effects of RFA: hemocoagulation changes
inserting the catheters, direct thermal effect on
surrounding tissues, and endothelial damage in all stages
of the procedure. Authors who studied these problems
emphasize the activation of platelet and coagulation
system in the early and late post - RFA stages. The
increase in blood thrombogenicity was confirmed by
definite markers. The increase in concentrations of
prothrombin fragments F
1+2
D - dimmers and thrombin
- antithrombin complex was noted (13-16). Anfinsen
A.G. (17) who detected an increase of concentration
of intracellular platelet component beta-
thromboglobulin in plasma, related it to platelet
degranulation and increase in their activation.
Our study demonstrated a post-RFA decrease in
platelet aggregation in blood and plasma and this change
was statistically significant in group B and C, where
the number of RFA episodes >10. In 24 hours platelet
aggregation returned to pre-RFA level.
The mechanism of post-RFA thromboembolism
remains unclear. Increase (18) in both platelet
aggregation and thromboxane B2 concentration is
noted 10 min after RFA. These parameters returned
to the previous levels 30 min after RFA. Mean values
(17) of beta-thromboglobulin were somewhat higher
at the end of RFA procedure and returned to normal
in 24 hours. There was no change in beta-
thromboglobulin concentration 10 min after RFA. Also,
there was no correlation between beta-thromboglobulin
concentration and the duration and number of RFA
episodes.
Using RFA procedure, fibrinolytic activity measured
by D-dimers concentration was higher after RFA (19)
in patients who did not take antiplatelet drugs. In 24
hours D-dimers' quantity went down but their
concentration was increased up to 48 hours and it did
not correlate with the duration and number of RFA
episodes.
Michelucci A. and others (3) surveyed spontaneous
platelet aggregation in the blood, increase in coagulation
activation markers (prothrombin 1+2 fragments,
thrombin - antithrombin complex) and activation of
fibrinolytic system (inhibitor of plasminogen activator
and D-dimers). A significant post-RFA increase in
spontaneous platelet aggregation in blood returned to
the previous level in 24 hours. A marked
hypercoagulation (prothrombin 1+2 fragments) was
detected in patients in whom RFA duration exceeded
23.5 s.
There was no correlation noted between clot
formation and total RFA energy in experiments with
dogs (20) when in 20% of cases post-RFA thrombosis
at the ablation sites was documented macro- and
microscopically.
In the normal state of organism or in the presence
of minor tissue injury declining hemostatic physiologic
function does not manifest clinically and dynamic
balance is preserved between activating and
suppressing hemostatic mechanisms. Platelet adhesion
to the intact blood vessel wall is inhibited by
antithrombogenic factors of the endothelium
(endothelium - derived factors, increased blood flow,
etc.)
More serious damage of the endothelium results
in 2 different types of platelet reaction: a) morphologic
structure changes stimulating clot formation, and b)
biochemical changes leading to antithrombotic
substance expression in the endothelium. Numerous
factors that stimulate or inhibit platelet function appear
at the site of endothelial damage: strong agonist -
collagen (exposed in endothelial damage), thrombin
(produced under influence of thromboplastin and tissue
factor), weak agonist - ADP (present in each cell),
adrenaline (in the endothelial damage) and others,
antagonists - prostacyclin PGI
2
, NO (endothelial
relaxation factor). Activated platelets release active
substances (serotonin, adrenaline, platelet factors 3 and
4, beta - thromboglobulin, etc.) (9, 10).
Under the influence of weak stimulus platelet
activation terminates at the stage of their shape
changes. In the case of a strong stimulus the process
proceeds to adhesion, aggregation, and final secretion
stages. However, fibrinolysis activation is a parallel
process to hemostasis activation.
The experiments with pigs revealed that endocardial
endothelium has a stronger antiplatelet action than the
endothelium of coronary arteries. Endocardial cells inhibit
Alterations of platelet aggregation while treating cardiac arrhythmias
Medicina (Kaunas) 2004; 40(9) - http://medicina.kmu.lt

854
platelet aggregation though PG I
2
more than it does
through the endothelial relaxation factor (EDRF) (21).
During the procedure of RFA transesophageal
echocardioscopy documented a spontaneous post-RFA
echogenicity (22-24) however failure to detect thrombi
at the site of ablation may be due to minor RFA
damages and massive blood flow at this site (21).
Perhaps therefore platelets do not remain in activated
form for a prolonged period of time as the largest
platelet aggregation and clot formation is observed 10
min after the injury.
Results provided in the literature about RFA effects
on hemostatic markers are ambiguous. Data we
obtained demonstrated a decrease in platelet
aggregation right after RFA procedure. In the presence
of marked tissue damage this change could be
explained by intensive mobilization of anticoagulation
system factors or a certain remaining effect of used
antiplatelet drugs and anticoagulants. Further tests are
needed to disclose the mechanism of post-RFA
thromboembolism and to assess the necessity for its
prophylaxis with antiplatelet drugs and anticoagulants.
Although the number of post-RFA thromboembolism
cases is not high it does not prevent some patients
from suffering from it and therefore the question about
preventive measures should not be neglected.
Conclusions
Decrease in spontaneous and in natural platelet
aggregation (induced by two aggregates (adenosine
diphosphate and adrenaline)) was detected in vitro in
the whole blood and platelet rich plasma right after
the procedure in patients in whom arrhythmias were
treated with radiofrequency ablation. These
parameters almost returned to pre-RFA levels in 24
hours. The intensity of platelet aggregation right after
RFA was decreasing depending on the number of
episodes used for treatment.
Trombocitų agregacijos pokyčiai gydant širdies aritmijas radiodažnine abliacija
Vilma Kozlovaitė, Pranas Grybauskas, Jūratė Cimbolaitytė, Aušra Mongirdienė,
Aras Puodžiukynas
1
,Vytautas Šileikis
1
,
Tomas Kazakevičius
1
, Vytautas Zabiela
1
Kauno medicinos universiteto Kardiologijos institutas
1
Kauno medicinos universiteto klinikų Kardiologijos klinika
Raktažodžiai: trombocitų agregacija, radiodažninė abliacija.
Santrauka. Darbo tikslas. Ištirti, ar aritmijų gydymui taikoma radiodažninė abliacija turi įtakos trombocitų
agregacijai, ar šio proceso intensyvumas priklauso nuo radiodažninės abliacijos epizodų skaičiaus.
Medžiaga ir metodai. Ištyrėme 39 ligonių, sergančių širdies ritmo sutrikimais, trombocitų agregaciją prieš
radiodažninę abliaciją ir praėjus 24 val. po jos kraujyje ir plazmoje, indukuotą adenozino difosfatu ir adrenalinu.
Ligonius suskirstėme į tris grupes pagal radiodažninės abliacijos epizodų skaičių: A – <10, B – 10–20, C – >20
epizodų ligoniui.
Rezultatai. Iškart po radiodažninės abliacijos pastebėta sumažėjusi spontaninė, indukuota adenozino difosfato
ir adrenalino sužadinta trombocitų agregacija plazmoje. Tokią pačią tendenciją nustatėme sužadinę agregaciją
kraujyje adenozino difosfatu. Kitą parą po radiodažninės abliacijos trombocitų agregacija turėjo normalizuotis
iki reikšmių, buvusių iki radiodažninės abliacijos. Priklausomai nuo radiodažninės abliacijos epizodų skaičiaus,
reikšmingai pakito spontaninė ir adrenalino indukuota trombocitų agregacija plazmoje. A grupėje adrenalino
indukuota agregacija po radiodažninės abliacijos padidėjo 0,4 proc.; B grupėje sumažėjo 15,7 proc.; C grupėje
sumažėjo 19,4 proc. nuo pradinės agregacijos reikšmės iki radiodažninės abliacijos (p<0,05 tarp grupių A ir C).
Spontaninė trombocitų agregacija sumažėjo A grupėje 41,9 proc., B grupėje – 20,8 proc. ir C grupėje – 18,4
proc. nuo pradinės reikšmės iki radiodažninės abliacijos (p<0,05 tarp grupių A ir C). Adenozino difosfato indukuota
trombocitų agregacija plazmoje ir kraujyje po radiodažninės abliacijos taip pat mažėjo daugiau, kai radiodažninės
abliacijos epizodų skaičius didesnis.
Išvada. Tyrimas parodė, kad trombocitų agregacija kraujyje ir plazmoje po radiodažninės abliacijos sumažėjo
ir kad šis pokytis buvo statistiškai reikšmingas tiriant B ir C grupių ligonius, kai radiodažninės abliacijos epizodų
skaičius daugiau nei 10. Po 24 val. trombocitų agregacija vėl padidėjo iki pradinių reikšmių.
Adresas susirašinėjimui: V. Kozlovaitė, KMU Kardiologijos institutas, Sukilėlių 17, 50157 Kaunas
El. paštas: vkozlovaite@yahoo.com
Vilma Kozlovaitė, Pranas Grybauskas, Jūratė Cimbolaitytė et al.
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855
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Received 19 May 2004, accepted 28 June 2004
Alterations of platelet aggregation while treating cardiac arrhythmias
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