ATRIAL FLUTTER ABLATION
EP PROCEDURE NOTE
DATE:
ELECTROPHYSIOLOGIST:
ASSITANT CARDIOLOGIST:
PRE-PROCEDURE DIAGNOSIS:
1. Atrial Flutter
POST-PROCEDURE DIAGNOSIS:
1. Atrial Flutter - Cavotricuspid Isthmus Dependent, Typical Flutter
PROCEDURE PERFORMED
1. Atrial Flutter Ablation
2. Comprehensive EP Study with Induction
3. Left Atrial Pacing and Recording
4. 3D Mapping using the Carto 3 System
5. Intracardiac Echocardiography (ICE)
COMPLICATIONS: None
ESTIMATED BLOOD LOSS: 10 cc
CLINICAL PROFILE:
FLUORO TIME: 0.0 minutes (Fluoroless)
DAP: 0.0 Gycm2
AIR KERMA: 0.0 mGy
SHEATHS AND CATHETERS:
Access the femoral veins were obtained using the seldinger technique: The
right femoral vein was successfully cannulated with the needle. A guidewire
was then passed through the needle easily. A blade was used to make a nick
at the entry site to widen the entry site. The needle was then retracted.
A sheath was then placed over the guidewire and then flushed. This was
repeated in a similar fashion for the following access points:
Right Femoral Vein:
8Fr Sheath: The sheath was exchanged out for a Carto Vizigo steerable
medium curl sheath through which an Biosense Webster 3.5
mm tip smart touch DF curve mapping and ablation
catheter was placed through this sheath into the right
atrium and right ventricle.
7Fr Sheath: A deflectable decapolar catheter was placed through the
sheath and positioned into the coronary sinus.
Left Femoral Vein:
6Fr Sheath: A non-deflectable quadripolar catheter was positioned
into the Right Ventricle.
9Fr Sheath: Soundstar Intracardiac Echocardiographic (ICE) Catheter
placed into the RA and RV.
RESULTS:
I. Basic Intervals
After the ablation, the following measurements were obtained:
AA Sinus Cycle Length = msec
PR = msec
QRS = msec
QT = msec
AH = msec
HV = msec
II. Arrhythmias Observed or Induced
A. Atrial Flutter - Cavotricsupid isthmus dependent, typical atrial
flutter
DETAILS OF PROCEDURE:
I. DIAGNOSTIC PORTION OF PROCEDURE:
The patient was brought to the EP lab in a fasting and hemodynamically
stable condition. The patient was prepped and draped in a sterile fashion.
The Right and Left groin areas was anesthetized with lidocaine solution.
Sheaths and multipolar electrode catheters were placed and positioned as
described in the above section labeled, "Sheaths and Catheters." There
afterwards, catheters were placed through these sheaths into the heart.
***The patient was noted to be in atrial flutter at the start of the study.***
We placed the Soundstar Catheter into the RA and RV, and baseline survey
showed no significant pericardial effusion, no LAA thrombus, and normal LV
systolic function.
Next, we took our Octaray catheter and constructed a 3D geometric shell and then made an activation map of the RA. We then placed our coronary sinus catheter and then our RV catheter. We then took our ablation catheter and marked the His Bundle location, immediately adjacent to the non-coronary cusp of the aortic valve, which we were able to visualize on ICE.
The A-A tachycardia cycle length was ____ msec. The activation pattern on
the coronary sinus catheter was proximal to distal (concentric). We then
sought to entrain the tachycardia. Differential pacing from the proximal
coronary sinus and the distal coronary sinus while entraining (PPI - TCL) was
consistent with a right sided flutter. In comparing the two intervals (PPI-
TCL), the shorter PPI-TCL interval obtained from the proximal coronary sinus (as opposed to the left atrium or distal coronary sinus) suggested a right sided atrial flutter.
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Entrainment pacing within the CTI demonstrated a PPI - TCL < 30 msec, thus proving that the circuit wsa CTI dependent
Our propagation map demonstrated that the flutter rotated in a counter clockwise firection.
Thus, based on the following, we felt that this was a CTI dependent typical flutter:
(a) Typical Morphology on 12 Lead ECG
(b) Differential pacing from Coronary Sinus was consistent with a right
atrial flutter
(c) The entirety of the TCL was covered on mapping
(d) Propagation map demonstrating a counter clockwise electrical
wavefront rotation
(e) Entrainment pacing within the CTI demonstrated the circuit's
dependence upon the CTI
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****************SINUS - HAVE TO INDUCE*********************************
The patient was noted to be in sinus rhythm at the beginning of the study. Therefore, we sought to induce the clinical tachyarrhythmia. Pacing was performed from the coronary sinus, with burst pacing as fast as 220 msec.
While pacing at _____ we were able to induce a tachyarrhythmia
Despite this, we were unable to induce any tachyarrhythmias. Given the clinical presentation however, we felt that it was reasonble to proceed with modification of the CTI.
***********************SINUS********************************
II. Intervention Portion of Procedure
To enhance catheter stability, the 8Fr sheath was exchanged over a guidewire
for an Biosense Webster Vizigo steerable sheath. A soft J wire was advanced into the SVC. The 8Fr short sheath was then retracted, and then the Vizigo sheath was then positioned into the right atrium using ICE for guidance.
The ablation catheter was advanced into the cavotriscupid isthmus to a
position where there was a large ventricular signal, and a small atrial
signal (an approximate 1:4 to 1:5 ratio). The position of the catheter was
checked in the both the RAO and LAO projections. Radiofrequency energy was
applied at this location, with power controlled setting of 35 watts and we
did not observe any abrupt drops in wattage. We used a target ablation index of 500. A series of coalescing ablation
lesions were applied that connected the tricuspid annulus to the IVC, forming
a line of conduction block.
*******During the formation of the line, the AA TCL lenghtened followed by termination of atrial flutter, back to sinus rhythm.********
We reinterrogated our line, looking for areas of gaps and double potentials
and ablating them apropriately.
We then assessed whether we had reached the proper end point of the ablation.
END POINTS:
(1) Voltage Map
We remapped the CTI, and there were no gaps visible. Compared to pre and post
images, there was a clear line of voltage reduction along our CTI line with no
detectable gaps in voltage. This also correlated with our interrogation of our
CTI line, looking for atrial signal EGMs.
(2) Mapping
While pacing from the coronary sinus at a Pacing Cycle Length of 600 msec, we
took our Pentaray and mapped our line, and just lateral and septal to it, with
no break out locations identified on propagation map and activation mapping.
(3) Transithmus Conduction Time (TICT)
While pacing form the coronary sinus at a Pacing Cycle lenght of 600 msec, our
TICT from the proximal CS to the low lateral RA wall was ___ msec.
In addition, differential pacing was performed, wtih placing the catheter closer towards the CTI line, and at the same Pacing Cycle Length, the TICT was longer, consistent with block across the isthmus.
(4) Induction
We paced from the proximal coronary sinus, pacing all the way down to 220 msec without induction of any tachyarrhythmias.
Thus we felt that our end points had been achieved.
We then turned back to our ICE catheter to examine if there was any significant pericardial effusion, which there was not.
The procedure was then terminated. The catheters were removed, the sheaths
were pulled with figure of eight stitches applied. The patient was
then transported back to a monitored bed.
IMPRESSION:
1. Atrial Flutter - Cavotriscupid isthmus dependent, typical flutter
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2. Status post successful CTI ablation with termination of tachyarrhythmia
during RF application
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-In regards to anticoagulation, his CHADS2-VASc score is at least 2 (HTN
+ DM) and has been anticoagulated. Given the association of co-
existant atrial fibrillation with atrial flutter, as well as taking
into considering the fact that he has risk factors for the development
of AFib / substrate for AFib (obesity, suspicion for OSA, HTN, DM), it
is not unreasonable to continue anticoagulation following ablation.
-In fact, there is evidence in the literature that demonstrated
a 33% risk of developing new onset atrial fibrillation AFTER a
CTI ablation, and a 54.7% risk of deveoping AFib (new onset +
non-new onset) afterwards (Raposeiras-Roubin, S et al. "Is
safe to discontinue anticoagulation after successful ablation
of atrial flutter?" International Journal of Cardiology. Vol
201, P631-632 December 15, 2015)
-In regards to anticoagulation, per the 2023 ACC / AHA / HRS Guidelines
on AFib, "Patients with typical AFL who have undergone successful CTI
ablation and are deemed to be at high thromboembolic risk, without any
known previous history of AF, should receive close follow-up and
arrhythmia monitoring to detect silent AF if they are not receiving
ongoing anticoagulation in view of significant risk of AF"
-In regards to anticoagulation, per the 2023 ACC / AHA / HRS Guidelines
on AFib, "In patients with typical AFL who have undergone successful
CTI ablation without any known previous history of AF who are at high
risk for development of AF (eg, LA enlargement, inducible AF, chronic
obstructive pulmonary disease [COPD], HF), it may be reasonable to
prescribe long-term anticoagulation if thromboembolic risk assessment
suggests high risk (>2% annual risk) for stroke" (Joglar, Jose et al.
"2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of
Atrial Fibrillation" Circulation Vol 149 No 1; January 2, 2024
PLAN:
1. Bedrest x 2 hours.
2. Zio patch at discharge
3. Continue anticoagulation for now
4. No lifting anything heavier than 5 lbs for one week.
5. Return to clinic on ______