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Alterations of platelet aggregation while treating cardiac arrhythmias with radiofrequency ablation

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  • Lietuvos sveikatos mokslų universitetas Biochemijos katedra

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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.
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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 (SD)
inductor episodes
WBA <10 4.3±2.2 3.5±3.0 4.1±2.7
ADP (ohms) 1020 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
1020 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
1020 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
1020 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
1020 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.
Medicina (Kaunas) 2004; 40(9) - http://medicina.kmu.lt
855
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Received 19 May 2004, accepted 28 June 2004
Alterations of platelet aggregation while treating cardiac arrhythmias
Medicina (Kaunas) 2004; 40(9) - http://medicina.kmu.lt
... In our previous study (9), we found that platelet aggregation (PA) right after RFA significantly decreased while in 24 h after RFA it increased again. ...
... The arrhythmogenic substrate was destroyed by using radiofrequency energy (500 kHz, 30-60 W), which produces temperature of 50-70°C and hence irreversibly coagulates a tissue area of 2 to 4 mm 3 at the site of contact between the special destructive electrode-catheter and endocardium. Commonly treating supraventricular Medicina (Kaunas) 2009; 45 (9) lation analyzer STA COMPACT with a STA-Liatest D-Di reagent (Diagnostica Stago, France). ...
... Medicina (Kaunas) 2009; 45 (9) ...
Article
Full-text available
To determine an influence of radiofrequency ablation on changes in coagulation system. We investigated 30 patients with cardiac arrhythmias. Platelet aggregation, fibrinogen and D-dimer level were analyzed before, right after, 24 and 72 h after radiofrequency ablation. Platelet aggregation was explored in whole blood and platelet-rich plasma using adenosine diphosphate (ADP), epinephrine, and collagen for induction. Platelet aggregation induced by ADP and collagen in whole blood plasma increased significantly (P<0.01) (by 45% and 43%, respectively) in 24 h after radiofrequency ablation and remained increased in 72 h after radiofrequency ablation (by 11% and 35%, respectively) (P<0.01) as compared with baseline results. Spontaneous aggregation of platelet-rich plasma as well as ADP- and collagen-induced platelet aggregation tended to decrease right after radiofrequency ablation. Epinephrine-induced platelet aggregation significantly decreased by 17.5% after radiofrequency ablation (P<0.01) and started to increase in 24 h after radiofrequency ablation. In 72 h after radiofrequency ablation, platelet aggregation induced by different agonists increased by 7-45% significantly (P<0.05), and values were higher than baseline ones. Fibrinogen level after radiofrequency ablation did not differ from that of the baseline (3.08+/-0.7 g/L), but D-dimer level increased significantly (from 0.39+/-0.3 to 1.29+/-2.4 mg/L, P<0.01). In 24 h after radiofrequency ablation, an increase in fibrinogen level and a decrease in D-dimer level were found. Fibrinogen level increased to 3.32+/-0.6 g/L significantly in 72 h after radiofrequency ablation (P<0.05). Meanwhile, D-dimer concentration decreased to 0.78+/-0.8 mg/L, but it was still significantly higher (P<0.05) than the baseline value. Despite diminished platelet aggregation and increased D-dimer level right after radiofrequency ablation, a risk of thrombosis increased in the next few days after radiofrequency ablation.
... Interesting findings also emerged from a recent study which explored platelet biology in vitro after exposure to electromagnetic radiation 19 . In brief, exposure of a suspension of platelets for 30 min to electromagnetic radiation emitted by car electronics 20 . Although a significant reduction of platelet aggregation using both agonists was observed immediately after RF ablation, the decrease of platelet aggregation was more than double using epinephrine than using ADP (i.e., 19% vs 8%). ...
Article
Full-text available
Background. Significant concerns are now regularly raised about the safety of excessive mobile phone use. This study was aimed to assess the acute effects of radiofrequency waves emitted by a commercial smartphone on platelet function. Materials and methods. Two sequential citrated blood samples were collected from 16 healthy volunteers recruited from laboratory staff. The first sample was placed in a plastic rack, 1 cm distant from a commercial smartphone receiving a 30-min call and emitting 900 MHz radiofrequency waves. The second sample was placed in another plastic rack, isolated from radiofrequency wave sources, for the same period. The platelet count and the mean platelet volume were then assessed in all blood samples, whereas platelet function was evaluated using the platelet function analyser-100 (PFA-100). Results. A 30-min exposure of citrated blood to smartphone radiofrequency waves induced significant prolongation of collagen-epinephrine aggregation (median increase, 10%) and a considerable increase of mean platelet volume (median increase, 5%), whereas collagen-adenosine diphosphate aggregation and platelet count remained unchanged. Discussion. This study demonstrates that smartphone radiofrequency waves induce significant perturbation of platelet structure and function, thus providing further support to concerns regarding excessive use of mobile phones. Caution should also be taken with regards to blood products containing platelets, which should be kept far away from mobile phones and smartphones throughout the production pipeline and storage period.
Article
Ablation and Coagulation Activation. Introduction: Although thromboembolism is an uncommon complication of radiofrequency (RF) ablation, some preliminary reports have suggested that RF ablation results in activation of the coagulation system, possibly increasing this risk. We hypothesized that the insertion of intravenous catheters and their prolonged intravenous placement rather than RF ablation activates the coagulation cascade. Methods and Results: Thirty-seven patients, group 1 (n = 21) during RF ablation, and group 2 (n = 16) during routine electrophysiologic studies (EPS), were studied prospectively. Blood was drawn for coagulation and fibrinolytic studies following insertion of venous sheaths (TO), following catheter placement (T1), and 1 hour after completion of RF ablation or EPS {T2). Conversion of prothrombin to thrombin was measured using thrombin-antithrombin complex (TAT) and prothrombin activation peptide (F1+2). and fibrinolytic activity was assessed using D-dlmer concentration. Levels of D-dimer increased in group 1 from 823.52 ± 323.52 ng/mL at TO to 1,314.28 ± 297.63 ng/mL at T2 (P= 0.005), and in group 2 from 658.15 ± 161.70 ng/mL at T0 to 1625 641.45 ng/mL at T2 (P=±0.064). TAT levels increased from to 27.74 ± 5.6 μg/L at T0 to 52.99 ± 5.93 μg/L at T2 in group 1 (P= 0.09), and from 19.79 ± 5.14 μg/L at T0 to 73.5 ± 24.15 μg/L at T2 in group 2 (P= 0.05). F1+2 concentration increased from 1.52 ± 0.30 nmol/L at T0 to 3.06 ± 0.41 nmol/L at T2 in group 1 (P= 0.004), and from 1.32 ± 0.30 nmol/L at T0 to 3.11 ± 0.46 nmol/L at T2 in group 2 (P= 0.087). There was no significant difference in the concentration of the three coagulation variables between group 1 and group 2 at any given time point. No correlation was demonstrable between concentration of D-dimers, TAT, or F1+2 and variables of RF delivery such as cumulative energy, number of RF energy applications, or number of impedance rises. However, a significant positive correlation (r = 0.65, P < 0.01) was noted between the duration of the RF ablation procedure and the concentration of D-dimers. Conclusion: We conclude that activation of the coagulation cascade in RF ablation procedures is not related to the delivery of RF energy, but is related to the placement of intravascular catheters and to the duration of the ablation procedure.
Article
Catheter ablation of accessory pathways (APs) provides a definitive therapy for patients with Wolff-Parkinson-White Syndrome. The reported incidence of thrombus formation on ablation-induced injuries with direct current shock varies from 0%-20% in animal studies. The purpose of this study was to determine the prevalence of mural thrombus following catheter ablation with radiofrequency current of accessory pathways in humans. Radiofrequency current (30-35 watts) was applied through a catheter electrode placed against the mitral or tricuspid annulus guided by catheter recordings of AP potentials. Transthoracic (TTE) and transesophageal echocardiography (TEE) were performed in 95 of 111 patients, at 18 +/- 6 hours following catheter ablation. After ablation, no thrombus was identified at or near the ablation site in any patient. Two out of 95 patients had a mural thrombus at a remote site that was detected by TEE but not by TTE. No new wall motion abnormality was detected in any patient. No significant regurgitant valvular lesion was found in any patient. Intracardiac thrombus was not identified at the site of catheter ablation, possibly owing to the small lesions produced by radiofrequency energy and high blood flow normally present in those areas. However, patients may be at small risk for mural thrombus at a remote site from prolonged placement of catheters.
Article
64 ablation catheter-induced injuries were studied macroscopically and microscopically to determine the incidence of endocardial thrombus formation. Ablation was performed in 16 mongrel dogs, 7 days before necropsy, 16 endocardial necroses were located in the right atrioventricular (AV) junction, 16 in the non-coronary cusp of the aortic valve or the subaortic valve area, 16 in the right and 16 in the left ventricle. Cathodal discharge at the distal electrode was employed against an external anodal plate for ventricular ablation. Necroses in the right AV junction and in the aortic area where the result of transseptal His bundle ablation. Energies ranged from 100–360 J. Pathologic examination was performed 1 week after ablation. 13 thrombi were observed attached to the endocardial necrosis area, of sizes ranging from 1–25 mm diameter (mean 6.9 mm). Six thrombi were found in the septal valve of the tricuspid valve, two in the aortic valve, two in the subaortic region, and three related to ventricular necroses. We conclude that the incidence of thrombosis is 20% in ablation injuries, the majority, 77%, having a diameter ≤ 10 mm. No correlation was found between thrombus formation and delivered energy or catheter polarity.
Article
We report the incidence of cardiovascular complications in patients receiving RF catheter ablation for supraventricular tachyarrhythmias. To reduce the incidence of complications, a rigid guideline or policy for the personnel and facilities should be followed. A prospective, multicenter registry program may be needed to further define the complications associated with this procedure.
Article
Radiofrequency (RF) catheter ablation has developed into a new non-pharmacological therapy for the definitive treatment of patients with cardiac arrhythmias. Although an increasing number of recent reports have indicated the widespread use of the procedure, no data are available to estimate the number of procedures performed in Europe. Furthermore, currently no data on a large series of patients are available that provide information on the risk of procedure-related complications. This report presents the results of the Multicentre European Radiofrequency Survey (MERFS) that was conducted by the Working Group on Arrhythmias of the European Society of Cardiology. The objectives of this voluntary retrospective survey were to assess the number of radiofrequency catheter ablation procedures performed in 86 European institutions from January 1987 until March 1992 and the incidence of procedure-related complications with respect to the different types of ablative procedures. A total of 4398 patients were reported on from 68 out of 86 institutions (79%) from 15 European countries that agreed to participate in MERFS. From 1987 to 1991, the number of patients who underwent RF ablation per year increased from 45 to 2000. In the first 3 months of 1992, a total of 1640 patients were reported on. The number of patients reported on in relation to the different types of ablative procedures were: ablation of atrial tachycardialatrial flutter: n = 141 (3.2%); ablation of the atrioventricular junction: n = 900 (20.5%); modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: n = 815 (18.5%); ablation of accessory pathway: n = 2222 (50.5%); ablation of ventricular tachycardia: n = 320 (7.3%). Procedure-related complications occurred in 223 patients (5.1%). The incidence of complications in relation to the ablative procedure was: ablation of atrial tachycardia/atrial flutter: 5.0%; ablation of the atrioventricular junction: 3.2%; modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: 8.0%; ablation of accessory pathway: 4.4%; ablation of ventricular tachycardia: 7.5%. Complications occurred significantly more often in patients who underwent modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia, when compared to ablation of the atrioventricular junction (P < 0.001) or ablation of accessory pathway (P < 0.001), and in patients who underwent ablation of ventricular tachycardia, when compared to ablation of the atrioventricular junction (P < 0.002) or ablation of accessory pathway (P < 0.02). The highest incidence of complications was reported after modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
Article
Predictors and comparisons of complications in patients with electrophysiologic study or radiofrequency ablation have not been assessed in previous published reports. The purpose of this study was to prospectively evaluate the procedure-specific complications and investigate the possible causes and predictors of complications in electrophysiologic study and radiofrequency ablation. Data of diagnostic electrophysiologic studies and radiofrequency ablation were prospective, and represented a consecutive series of 2,593 patients with 3,966 procedures. The present study showed that a significantly higher complication rate occurred in radiofrequency ablation than in electrophysiologic study (3.1% vs. 1.1%, respectively, p = 0.00002) and a significantly higher complication rate occurred in elderly than in young patients with electrophysiologic study (2.2% vs 0.5%, p = 0.0002) or radiofrequency ablation (6.1% vs 2.0%, p = 0.00015). Multiple logistic analysis found that older age (p < 0.01) and systemic disease in elderly patients (p < 0.01) were the independent predictors of complications in both procedures. Furthermore, there was no temporal trend in the incidence of complication. We conclude that the incidence of complication was higher in radiofrequency ablation, and elderly patients had a higher incidence of complications in both electrophysiologic study and radiofrequency ablation; these procedures, when performed by experienced personnel in an appropriately staffed and equipped laboratory, can be undertaken with an acceptable risk.
Article
Forty-two consecutive patients were checked for profiles of platelet aggregability before, during, and 10 and 30 minutes after catheter ablation. They were randomized into Group A (n = 20) who accepted intravenous aspirin (in 0.015 g/kg body weight) and Group P (n = 22) who accepted only placebo treatment. Blood samples were drawn from ascending aorta (Ao) and main pulmonary artery (MPA) simultaneously at each time period. In Group P, the EC50 of substrate induced platelet aggregability decreases significantly during (for ADP, from 1.72 to 0.78 mumol/L for samples from Ao, P < 0.0001; and from 1.68 to 0.69 mumol/L for MPA, P < 0.0001; for collagen, from 2.26 to 1.34 micrograms/mL for Ao, P < 0.005, and from 2.40 to 1.64 micrograms/mL, P < 0.0001) and 10 minutes after successful ablation (for ADP, to 0.70 mumol/L for Ao, P < 0.000, and to 0.61 mumol/L for MPA, P < 0.0001; for collagen, to 1.54 micrograms/mL for Ao, P < 0.01, and to 1.63 micrograms/mL, P < 0.0001), and then returned to baseline levels 30 minutes later (all P = NS) compared with comparative baseline levels. The levels of thromboxane B2 (TXB2) had the similar evolution. The evolution of platelet aggregability profiles was not associated with total energy dose, duration of energy application, duration of procedure, impedance, and ablation site. However, there were moderate positive correlations between the TXB2 levels and tip temperatures (r = 0.56, P < 0.05 for Ao and r = 0.65, P < 0.01 for MPA). These results suggest that increased platelet aggregability can occur during and 10 minutes after radiofrequency current ablation and antiplatelet therapy can maintain "flat" response of platelet aggregability to radiofrequency energy, which may provide possible benefits in preventing the occurrence of the complication.
Article
Both early and late thromboembolic events are known complications of radiofrequency catheter ablation. This review of 758 patients undergoing 830 radiofrequency ablation procedures finds that embolic complications after radiofrequency ablation in patients without other risk factors for thromboembolism are rare (<0.2%).
Article
By measuring plasma levels of D-dimer, a product of fibrin degradation, we sought to investigate whether the application of radiofrequency (RF) energy might activate endogenous thrombotic mechanisms. Quantitative determination of D-dimer, a bio-chemical marker of thrombus formation and reactive fibrinolysis, helps to diagnose activation of the coagulation system. It remains controversial whether endocardial lesions produced during RF catheter ablation of arrhythmogenic foci have a thrombogenic effect, and the issue of the need for antithrombotic therapy after RF ablation is still unresolved. We made serial determinations of plasma D-dimer levels by enzyme immunoassay before insertion of catheters, after completion of electrophysiologic study (EPS) but before RF ablation, immediately after RF ablation and before discharge (at 48 h) from the hospital in 37 patients undergoing RF ablation (22 men, 15 women; mean [+/-SD] age 37 +/- 18 years, range 12 to 74; 16 +/- 16 lesions produced) of accessory (n = 17) or slow (n = 12) pathways, atrial (n = 4) or ventricular foci (n = 3) or the atrioventricular node (n = 1). D-dimer levels were also measured in 26 age-matched control subjects undergoing EPS only. In the RF ablation group, the mean D-dimer levels increased from a baseline value of 29 +/- 28 to 62 +/- 56 micrograms/liter after EPS (p < 0.0001). However, after RF ablation, D-dimer levels increased to much higher levels (188 +/- 138 micrograms/liter, p < 0.0001). There was no correlation of D-dimer levels with the number of RF lesions produced or the duration of the procedure. At 48 h after the procedure, D-dimer levels decreased (75 +/- 67 micrograms/liter) but still remained significantly elevated compared with baseline values (p = 0.0001). Three were no significant differences in baseline (25 +/- 21 micrograms/liter) and post-EPS (51 +/- 50 micrograms/liter) measurements between control subjects and patients. During RF ablation, intravenous heparin was given to nine patients who still demonstrated high plasma D-dimer levels after RF ablation. As reflected by elevated plasma D-dimer levels, RF ablation has a thrombogenic effect that persists through 48 h after the procedure. This effect needs to be taken into account when considering antithrombotic therapy in patients undergoing RF ablation.