Lithuanian University of Health Sciences

Lithuanian University of Health Sciences

Final Master Thesis

Medical Faculty

Kaunas Clinics

Department of Cardiology

Changes of intracardiac ECG in patients with Typical Atrial

Flutter after Radiofrequency Ablation of the Cavo-Tricuspid

Isthmus; implication of age and prevalence of post ablative

Atrial Fibrillation

Supervisor Aras Puodžiukynas, Consultant Cardiologist

Table of Contents

6.0 PERMISSION ISSUED BY THE ETHICS COMMITTEE……….…....6

7.0 ABBREVIATIONS……….…….7

8.0 TERMS……….…7

9.0 INTRODUCTION………....8

10.0 AIMS AND OBJECTIVES ………...9

10.1 Aims 10.2 Objectives 11.0 LITERATURE………....9

11.1 Normal conducting system and conduction within the heart 11.2 Electrophysiologic mechanism of typical Atrial flutter (AFL) 11.3 Types of AFL 11.4 Management of Type 1 AFL 11.5 Radiofrequency ablation 11.6 Equipments used 11.7 Possible complications during and after procedure 11.8 Structural changes of cardiac tissue with age 12.0 METHODOLOGY………...16

12.1 Patient selection 12.2 Data obtained

12.3 Method in obtaining the result 12.4 Data interpretation

13.0 RESULTS………...18 14.0 DISCUSSION OF RESULTS………...20 15.0 CONCLUSION………...22 16.0 PRACTICAL RECOMMENDATION………..…..22 17.0 REFERENCE………...……...24

3.0 Summary

3.1 Summary in English

Author Anish Thomas

Title of the research: Changes of intracardiac ECG in patients with Typical Atrial Flutter after Radiofrequency Ablation of the Cavo-Tricuspid Isthmus (CTI); implication of age and prevalence of post ablative Atrial Fibrillation

In this research I will explore the changes in intracardiac ECG in AFL patients in various age groups before and after RF ablation of the CTI. I will also assess the correlation between post ablative Stimulus-A wave time and the prevalence of new onset AF. A brief review of the conducting tissues of the cardia will be done as well as the different types of AFL. The method of ablation will also be explained along with the changes seen in the intracardiac ECG.

A random sample of n=109 patients were selected from a population size of 150 patients who all have Type 1 AFL. Prior to the ablation a Sti-A time is generated, this pre ablation time will be analyzed alongside the post ablation Sti A time. The ablation is carried out using catheters in the right atrium which uses radiofrequency waves to cause permanent damage to the myocytes, inturn disrupting the electrical pathway causing the AFL. A 6 month follow up was also carried out on the subjects to evaluate the development of AF as a complication of the ablation.

It is widely accepted that there is an increase in atrial size with the older population due to histological changes that occur with age. The results indicated that a 40 year old will have a post ablation Sti-A of 144ms, while an 80 year old will have a post ablation time of 205ms. These results support the prediction. Out of 109 subjects, 13 patients developed AF since after the procedure (prevalence rate of 11.93%).

It was seen that the age group with the highest prevalence of AF was 71-90y/o with 17.65% whilst the youngest age group 31-50y/o had the lowest prevalence of AF, 4.17%. In 13 subjects that suffered AF post ablative Sti-A was an average of 185.75ms while the 96 subjects without this particular complication had an average time of 145.32ms. From this it was concluded that a lower Sti-A time (usually associated with younger age) results in a lower

chance of AF occurrence and on the other hand a higher Sti-A time (usually associated with older age) resulted in a higher chance of AF occurrence.

3.2 Summary in Lithuanian

109 pacientams su prieširdžių plazdėjimu buvo atlikta kavotrikuspidalinės sąsmaukos radiodažninė abliacija. Buvo analizuotas santykis tarp ir poabliacinio laiko. Taip pat buvo tiriama poabliacinio prieširdžių virpėjimo pasireiškimo dažnis.

4.0 Acknowledgement

I would like to express my sincere appreciation to Dr Aras Puodziukynas, who enabled me to complete this thesis.

5.0 Conflict of interests

I would like to declare that there was no conflict of interest encountered whilst conducting this research.

6.0 Permission of the Ethics Committee

7.0 Abbreviations

TAFL - Typical Atrial Flutter y/o - Years old (age)

AFL - Atrial Flutter

CTI - Cavo Tricuspid Isthmus RFA – Radiofrequency Ablation Hz - Hertz

AF - Atrial Fibrillation

Sti-A - Time from Stimulus to A wave (pacing from coronary sinus) SA node - Sinoatrial node

SVC - Superior Vena Cava RA - Right Atrium

AV node - Atrioventricular node IVC - Inferior Vena Cava

CS - Coronary sinus BPM - Beats per Minute

COPD - Chronic Obstructive Pulmonary Disease DC - Direct Current

CCB - Calcium Channel Blocker PPI - Post Pacing Interval

TA - Tricuspid annulus

8.0 Terms

Radiofrequency ablation - high frequency ((500–750 Hz) _​electrical current produced by a generator which is used to heat up and consequently necrotize part (or all) of a particular area CavoTricuspid Isthmus – an area between the inferior vena cava and tricuspid valve, which the site ablated during RFA

9.0 Introduction

Typical Atrial flutter (TAFL), also known as anti-clockwise Cavotricuspid Isthmus (CTI) dependent AFL, is caused by a macro reentrant atrial tachycardia, between the tricuspid valve annulus and coronary sinus. Usually rates of atrial activation are above 220 bpm till 350 bpm. Anatomically the CTI is bordered anteriorly by the tricuspid annulus and posteriorly by the crista terminalis/eustachian ridge and the endocardial cavity. The term anticlockwise refers to the direction of the electrical activity inside the right atrium, when the view is in an anteroposterior plane. These flutter waves manifest as negative saw toothed deflections in the II, III and avF leads but as positive deflections on the V1 lead of surface ECGs. TAFL can be confirmed using intracardiac catheters to map the activation patterns in the right atrium. Local activation patterns are seen as the low to high activation of the septum and the high to low activation of the lateral wall of the right atrium [1].

Within this thesis, I shall assess how the time elapsed between Stimulus A which is paced locally from proximal coronary sinus (CS) and the local A wave (recorded on ablation electrode placed on cavotricuspid isthmus (CTI)) seen on the intracardiac ECG changes when comparing pre and post radiofrequency ablation (RF) in relation to the age of the samples used. Thus drawing a comparison and relation, if any, between the age of the subject and the alterations that will be seen.

Atrial fibrillation (AF) is an another rhythm disturbance that may appear as a complication in patients who have undergone AFL ablation. Dilation of atria increases the distance between pacing site and CTI as a result of proliferating fibrotic tissue. Therefore, slowing down the velocity of electrical activation could serve as substrate promoting development of atrial fibrillation. In this research I will examine the prevalence of AF in selected patients and further examine the results to see if there is any significant correlation between post ablation Sti-A time and the occurrence of AF. I believe that, if a correlation is identified, this can be later used as an indicator for predicting whether a person may or may not have episodes of AF post ablative treatment of AFL.

10.0 Aims and Objectives

10.1 Aims

1. Determine the changes in intracardiac ECG after RF ablation of typical AFL and understand the implications of age

2. Describe the relationship between Stimulus A (post ablation) and new onsets of Atrial Fibrillation

10.2 Objectives

● Evaluate the procedures used in radiofrequency ablations of AFL and how intra cardiac ECGs are used to obtain values such as Sti A time

● Collect the age of patients who have undergone therapeutic RF ablation for AFL and to note the differences in Sti-A time in intracardiac ECG before and after ablation for these patients

● Using graphs and other statistical tools access the relation between age and postablative Sti A

● Identify the patients who have had AF as a complication after the ablation procedure and draw correlations between post ablative Sti A values and the occurrence of AF using analytic tools

● Evaluate the relevance of this research in terms of using patients information and data obtained during ablation to predict possible occurrences of AF

11.0 Literature review

11.1 Normal conducting system and conduction within the heart

The conducting system of the heart consists of various components including the SA node, AV node, Bundle of His, bundle branches and Terminal Purkinje fibers. Electrical activity originates from the densely innervated SA node, located laterally in the right atrial terminal sulcus and the anteromedial part of the SVC. Electrical impulses propagates through the right atria in one of three routes; anterior, middle and posterior internodal tracts. As these tracts are

not histologically different to adjacent cells, these tracts are better known as longitudinally oriented fibers of atrial myocardium.

Fig.1 Schematic illustration of the cardiac conduction system [2]

The AV node is also located in the RA, situated at the apex of the triangle formed by the tendon of Todaro and the tricuspid annulus. The AV node is responsible in conducting the electrical impulses from the SA node to the ventricles via bundle of His and it’s branches and then via the Purkinje Fibers [3]. The maximum rate at which the AV node conducts in adult patients is usually about 140 - 160 beats/minute.

11.2 What happens during a typical Atrial flutter

Typical AFL is caused by a macro reentrant circuit that propagates through the RA (most often in a counterclockwise manner), within this circuit lies an area of slower conduction which is the area of ablation, known as CTI [4]. Certain anatomical features of the RA provides a functional or anatomical block to the pathway of electrical current and thus determines the route of this reentry circuit. The boundaries including the tricuspid annulus, crista terminalis, IVC

orifice, eustachian ridge and CS opening provide, as mentioned earlier, a line of conduction block. Included in these boundaries is the CTI. This area of slow conduction is located more laterally in younger patients and medially in older. The reason behind the slower conduction at the CTI is uncertain but some sources suggest that it is due to the anisotropic orientation of the fibers in that region. Age is also said to play a key role in the orientation of these fibers. As the atria dilates with increasing age, the density of the cells in CTI also changes thus, changing its electrical properties [5]. Essentially these structures result in an arrhythmia producing 220-300 bpm causing an AV nodal block. Atrial flutters manifest symptomatically as palpitations, fatigue, mild dyspnea and presyncope [6,7].

The etiology of AFL is multifactorial but generally originates from a structural or functional abnormality affecting conduction. Incisional scars or ablation sites from previous surgeries or from congenital defects, idiopathic fibrosis, thyrotoxicosis, chronic alcoholism and pericarditis all maybe contributing etiological factors of AFL. Risk factors include increasing age, valvular dysfunction, atrial septal defect, atrial dilation, heart failure, asthma, pneumonia and COPD, to name a few [7,8].

11.3 Types of AFL

There are various types of AFL based on anatomical location and direction of electrical activity. These may vary according to rates and how they are seen on ECGs. Typical AFL, also known as Type 1 AFL, is characterized with atrial rates ranging from 220-300 bpm. Two variant of type 1 AFL are present: counter-clockwise re-entry and clockwise re-entry. The direction mentioned is in regards to the path taken by the electrical activity around the tricuspid annulus. The former, counter-clockwise re-entry is more common in comparison to clockwise, producing inverted flutter waves in leads II, III and avF, while producing positive flutter waves in V1. In contrast, the clockwise re-entry flutters manifests as positive waves in lead II, III and avF while in V1 they appear as broad and inverted [8].

Type 1 AFLs can be further diagnosed with the use of intracardiac catheters to obtain visual depiction of electrical activity within the RA. Three catheters are typically used named, TA (Halo), ABL and CS. These are placed in a manner that records the circuitry of the RA explained further in Fig.2 below. Atypical AFL or type 2, usually represents less that 8% of AFL

cases [11]. These AFL produce a higher rate of atrial activity and are far more unstable than type 1 resulting in deterioration to AF. This type of AFL is also less susceptible to RF ablation treatment [9]. Therefore in this research I will only be examining the RFA of patients with TAFL.

As seen in Fig. 3 a 20 pole catheter is placed around the right atrium with the distal end near the posterior free wall and the proximal side closer to the anterior septum. In the top illustration the catheter is activated in counterclockwise manner resulting in the activation being registered on the proximal end first and propagates to the distal end. In contrast the illustration on the bottom shows the opposite. The clockwise activation results in the distal part of the catheter to be activated first and then continues to the proximal end.

Fig 2.Surface 12-lead ECGs during counterclockwise (left) and clockwise (right) typical atrial flutter (AFL) in a patient on flecainide therapy [9]

Fig 3. Endocardial electrical activity measured during Counterclockwise AFL and Clockwise AFL (red arrow) using a Halo catheter placed around the TA, another placed at the ablation site and a final catheter at the CS[5] 11.4 Management of Type 1 AFL

Acute management of type 1 AFL include 3 options: antiarrhythmic drug, DC cardioversion and atrial pacing to terminate atrial flutter. Clinical presentation and availability of

equipment,resources and ease of using these techniques determine which option is used and is the best. Rate control of atrial flutter is achieved by IV administration of calcium channel blockers (verapamil, diltiazem) or beta blockers (esmolol, propranolol) as well as Digoxin and Amiodarone. DC cardioversion is done using usually 150 - 200 joules of energy. are antiarrhythmic drugs which have proven to convert atrial flutter to sinus rhythm effectively [5,11]. Rhythm control is achieved with the use of class _​I_​A (_{​Procainamide)​, ​}I_​C (_{​Flecainide,} Propafenone_{​) and ​}III (_​Sotalol, Amiodarone, Ibutilide, Dofetilide) _​drugs. Stroke prophylaxis also plays a major role in the management of typical AFL. Coumadin, Dabigatran, Rivaroxaban and Apixaban are used to prevent the occurrence of further complications.

The use of Beta blockers and CCB in conjunction with class 1C drugs have also proven to be effective in managing typical AFL [12]. Catheter ablation is performed for patients who meet certain criteria such as; patients who are symptomatic post pharmaceutical treatment, patients with CTI dependent flutter after failure of at least one antiarrhythmic agent, CTI dependent AFL that occurs after the use of flecainide, propafenone or amiodarone to treat AF and as a first choice treatment in patients preferring elective ablation [13,14]. The rate of positive results post ablation is 92% after the first procedure and 97% after multiple ablations. These values are further lowered if structural abnormalities are present in the heart making the ablation more difficult [15].

11.5 Radiofrequency ablation

Three weeks prior to the ablation procedure, patients are asked to take Vitamin K antagonists (VKA) or a non VKA oral anticoagulants for patients on ongoing persistent AFL. An INR of 2.5-3 or more and APTT of 30s or more is preferred [16]. Patients are requested to stop eating for 6-8 hours leading up to the operation[17]. Transesophageal echocardiography can be done in patients prior to the ablative procedure to visualize the anatomy of the right atrium and exclude the presence of the thrombus in a left atrial appendage. I.V. access is placed in the arm to give anesthesia. The patients’ right groin is shaved and cleaned with iodine, local anesthetics are also used to achieve numbness of the disinfected area [18]. Surface ECG leads are placed to monitor the heart throughout the procedure. Catheters are inserted into the femoral vein and then progressed up through the IVC into the RA, using X ray guidance. The use of coronary

sinus catheter and multi electrode catheter is used in the RA, in some cases an electroanatomic mapping system and mapping catheter is used [19].

WIth the electrode catheters in place, AFL is now induced using programmed electrical stimulation from various locations. Usually pacing from proximal coronary sinus induces a counterclockwise flutter. Isoproterenol (a beta adrenergic agonist) may be used to enable the induction of tachycardia. A maneuver known as entrainment is used to confirm the diagnosis and also determines whether the AFL is CTI dependent or independent. RFA is only carried out if the AFL is found to be CTI dependent, this achieved by atrial pacing at a shorter cycle length than the total cycle length to entrain. Using post pacing interval we can determine whether the pacing site is inside the circuit or not. If the PPI is within 20ms of the TCL, it is considered to be within the circuit. The same method is used to determine if the CTI is in the circuit by pacing slightly shorter in relation to TCL from an electrode placed in CTI. As before a PPI of less than 20ms is considered to be within the circuit and thus the AFL is confirmed to be CTI dependent [28]. The CTI is then ablated using RF waves delivered by the catheter along the CTI. After ablation of the CTI the end point is considered to be when a bidirectional block is achieved.

11.6 Equipments used

There are different types of catheters that can be used in this ablation procedure. The use of multi electrode catheter or simply repositioning a bipolar catheter is used to assess the activation patterns. The CTI is located and bi-directional block is then formed using RF energy which causes necrosis of the tissue in the area, resulting in the disruption of the re-entrant circuit [19,20]. Thus, after the effective ablation, stimulation (stimulus A) of the right atrium at the free lateral wall using the ablation electrode will cause an A wave to be measured at the coronary sinus catheter much later than earlier. The time elapsed increases as a result of the extended (caudocranial route along the free lateral wall) path the circuit has to take due to the ablation of the prior pathway. Furthermore, evidence of counterclockwise isthmus block shows that, when paced from the lateral aspect of the atrium, adjacent to the ablation site,the anterior septum is activated (evident by the His-bundle potential seen in the ablation catheter) before the coronary sinus [22]. This research will take this notion further by examining how the time elapsed between

stimulus A wave and changes in the A wave in accordance to age. From this we can examine the idea that as age increases the atrial size increases and causes changes to cycle lengths.

11.7 Complications related with procedure

The complications related to the ablation of CTI can include injury to normal conducting system (particularly AV node) in turn causing conduction issue, cardiac tamponade, peripheral vascular complications or embolic phenomenon and AF. The occurrence of complications is relatively low in ablative surgeries [23,24].

A single centered research conducted in _{​Łódź​, Poland to explore the occurrence of AF} after radiofrequency ablation of typical AFL. _{​Warchoł I and his team found that out of the 110} patients (average age _{​67±10 years​) who underwent radiofrequency ablation of CTI, 45%} developed AF as complication. However, only 40 patients out of the 110 were included in the follow up that was carried out in the time frame of _{​46±23 months after their ablation procedure} [4].

In another study it was found that the group of patients who previously presented with AF had a higher chance of developing AF post RFA for AFL. 54% of patients who had previous episodes of AF suffered AF post ablation as opposed to 13.9% who only developed AF after the ablation and had no previous AF. In this research it was noted that patients who have had structural or valvular heart disease were more prone to suffer from AF after AFL ablation [27].

11.8 Structural changes of cardiac tissue with age

Heart wall thickness increases with age and this is caused by myocytes size increasing or histological changes such as collagen deposition in the walls. It is also known that the atrial size of the heart also increases with age and this is thought to cause AF as a clinical manifestation [29]. More changes in structure can be seen at the CTI as a result of age, studies show that the slow conducting are of the CTI is located more medially in older patients as opposed to more laterally in younger patients [30].

12.0 Methodology

The subjects that were selected from a population of typical atrial flutter patients who were ablated within the time frame of 2016/01-2018/04 at the department of Cardiology of LSMU University Hospital. This time frame was selected as the population sample was registered on the online system. The use of the online system have reduced errors while obtaining data in comparison to retrieving data from a paper backed system.

109 subjects who underwent RFA for AFL were selected however information about any cardiac structural abnormalities were not obtained from the online database. Therefore, I have, for the purpose of this research kept this as a practical limitation. As this research mainly focuses on new onset of AF post ablation procedure, I have omitted patients with previous AF diagnosis from the population used to ensure that the chances seen in the intracardiac ECG are direct representations of the radiofrequency ablation therapy for Atrial Flutter patients and not influenced by any other pathological arrhythmical abnormalities.

The required information about the patients was obtained from their medical histories. Later, the information listed below were reviewed and analyzed to assess how the changes found before and after the ablations can be interpreted.

12.2 Data obtained

● Age of patient

● Time elapsed from stimulus to A wave before the ablative procedure ● Time elapsed from stimulus to A wave after the ablative procedure

● Whether new onset of AF occurs within the timeframe till 2019/04 after ablative procedure

12.3 Method in obtaining the result

There are four data points that are required to conduct this thesis; the age of the selected patients, the time elapsed from stimulus to A wave before and after the ablative procedure and the presence of new AF since the ablation procedure.

The time elapsed from stimulus till the A wave is measured intraoperatively using intracardiac ECG, pre and post ablation of the CTI. The two catheters (CS, ABL) are placed on two sides of the patient’s right atrium which will provide us with the following result. The stimulus will be induced by the CS catheter close to the septum while the other measuring catheter (ABL)

is lateral to the ablation site. This value will illustrate the path that the electrical impulses took during both times.

The patients’ online medical history log was used to see if episodes of AF followed post ablation. I acknowledge that there may be errors in patient history when logged onto the system. Additionally these patients may have been treated in other hospitals for the AF that may follow and those results won‘t be available to me. These may affect the accuracy of the results of this research.

12.4 Data interpretation

To interpret the results I will be using two softwares, firstly I will use Microsoft Excel to collect all the numerical data including age, pre and post ablation Sti-A times. The patients who had AF episodes after the ablative procedures were also noted. Secondly, I used a software called Minitab 8 to generate the tables and graphs, and also to draw statistical conclusion between sets of data.

13.0 Results

Within this research, I have gathered the case history of 109 typical AFL patients (within the age range of 31-90) with no known previous occurrence of AF, the presence of structural abnormalities were not explored. All of the 109 patients have undergone radiofrequency ablation for AFL after which some have developed AF in a time frame extending till 2019/04. Firstly, I examined how the Sti-A time changed in relation to age before and after ablation. I then divided the patients into three age groups of 31-50, 51-70 and 71-90 and evaluated the post and pre ablation Sti-A time of each group. Within each group the percentage prevalence of AF was also calculated. Furthermore, I have examined the correlation, if any, between the prevalence of AF and the post ablation Sti-A time within each group.

Fig 4. The graph above shows the relationship between age and Pre ablation Sti A time(ms), in AFL patients (n=109) who have undergone RF ablation

Table 1: The table shows the average pre and post Ablation Sti-A time seen in each Age Groups

Age group Average pre Ablation Sti-A (ms) _{Average post Ablation Sti-A}

(ms)

31-50 95.88 _141.96

51-70 127.92 _181.43

71-90 140.29 _196.35

Table 2: The table displays the number of people per age group and how many people in each group had AF since the procedure. The percentage prevalence of AF per age group is also included

Age Range Groups

Number of candidates age group AF Prevalence (%) per group 31-50 24 1 4.17% 51-70 51 6 11.76% 71-90 34 6 17.65%

Table 3: The table below shows the average Sti-A value in both patients with and without AF after ablation

Post ablation patients: n Average Sti-A (ms)

Without AF 96 145.32

With AF 13 185.75

Table 4: The table below shows the average Sti-A (ms) times for people with and without AF, after the RFA procedure. The data is also further divided into 3 age groups

Age Range Groups

Post ablation patients: 31-50 51-70 71-90

With AF 151.75 185.76 205.18

14.0 Discussion

The result shown in Fig 4, displays the relationship between age and Pre ablation Sti A time(ms), in AFL patients (n=109) who have undergone RF ablation it clearly indicates an upward trend in the pre ablation Sti-A as age increases. Using the trendline we can estimate that a 40 year old will have a pre ablation Sti-A of 96ms, while an 80 year old will have a time of 143ms, approximately. These results indicate that the pathway taken by the stimulus wave prior to ablation is longer in older patients as opposed to the pathway taken in a younger patient. This is evident from the difference in the elapsed time.

Fig 5 supports this trend and a steady increase in the post ablation Sti-A time as age increases is also observed. The trendline suggests that a 40 year old will have a post ablation Sti-A time for 144ms, while an 80 year old patient will have a post ablation time of 205ms. As before the Sti-A time indicates the time taken between the Stimulus and the A wave. Thus, a longer Sti-A time coincides with a longer pathway taken by the Stimulus wave. Therefore, using the results it is easy to understand that in older patients the Stimulus wave propagates via a larger pathway as the Sti-A times are comparatively larger.

These were expected trends as the histological composition of the cardiac tissue changes with age to include more elastin, collagen tissue and reticular fibers [25]. However, other researches in the field have used diastolic filling rates to determine the difference in heart size implicated by age. Their results suggests that the changes in heart size is only seen after the 7th decade of life [26].

Table 1, shows the average pre and post Ablation Sti-A time seen in each age group. The table is divided into 3 age groups 31-50, 51-70 and 71-90. Two patterns are obvious from the data. Firstly, as indicated by the graphs the pre and post ablation Sti-A time in each age group increases with the age of the group. The highest pre and post ablative Sti-A times are seen in the oldest age group 71-90, while the lowest is seen in the youngest age group 31-50. Secondly, for the age group of 31-50, an increase of 46.08ms was seen between the two Sti-A times. While in age groups 51-70 and 71-90 has Sti-A times increase by 53.51ms and 56.06ms respectively. These provide additional numerical support to the data observed in the graphs.

Table 2 shows the number of people per age group and how many people in each group had AF since the procedure and the percentage prevalence of AF is also indicated. A total of 13 patient of the 109 (11.93%) patients had at least one episode of AF since the radiofrequency ablation procedure. Table 2 indicates how these cases were distributed within the various age groups. Due to the unbalanced number of patients in each group a percentage of prevalence was calculated for each group. It shows that the age groups 31-50, 51-70 and 71-90 had percentage prevalences of 4.17%, 11.76% and 17.65% respectively. It is easily observable that with age the prevalence of AF increases. This data therefore agrees with the findings of _​Warchoł I et al. [4].

Table 3 displays the average Sti-A value in both patients with and without AF after ablation. It shows that the average Sti-A time for patients (n=13) who had AF is 185.75ms and the average Sti-A time for patients (n-96) who didn‘t have AF since their ablation procedure to be 145.32. Thus, these data coincides with the findings of _{​Warchoł I et al. [4].}

Table 4 shows the average Sti-A (ms) times for the 3 age groups with and without AF, after the RFA procedure. The average post ablative Sti- A times in each age group is higher for patients who had AF as opposed to patients without AF. This further solidifies the information obtained in Table 3. It is also evident that the average post ablative Sti-A time for both patients with and without AF increases with each older age group. However, the only anomaly that is seen in this trend is seen in the age group of 71-90 who didn‘t suffer from AF, where the average Sti-A time is lower in comparison to the younger age group of 51-70.

15.0 Conclusions

1. Changes in pre and post RF ablation Sti-A times in comparison with age which indicated a longer Sti-A wave was seen in older populations. As the time elapsed between the stimulus wave and A wave represents the pathway of the electrical impulse, we can assume that the larger time difference was due to the longer pathway the stimulus electrical impulse had to travel.

2. Patients with a smaller post ablative Sti-A time were less likely to have AF as a complication, when compared to patients with larger Sti-A times. Younger patients had

lower post ablative Sti-A times and interestingly these patients had the lowest prevalence of having AF within the follow up period after undergoing the ablative procedure.

16.0 Practical Recommendation

The subjects for this study had no other known disorders of arrhythmia however, these patients may have had other forms of cardiac pathologies or structural pathologies. This could have affected the data collected for this research and caused changes in the outcome of the results. If I were to repeat this research once more, I would use a patient database spanning over a longer period of time, so that I would be able to select patients with only AF and no other cardiac comorbidities including structural variations. The use of cardiac echograms can be used to find structural variations. Gender also plays a crucial role in the size of the heart tissue, however this was omitted from this research to obtain a large sample size.

There were slight discrepancies with the pre and post ablation Sti-A time values. These values are obtained during surgery and are noted into the patient’s medical records after the operation. Lapses and limits in memory may cause errors when recording these values which does impact the findings. As a result, it is recommended to document the results as soon as they are obtained during the surgery.

The prevalence of AF was taken from the patient's medical records using KK numbers, however, this would hinder results if the patients were taken to another hospital and the record of the visit wasn’t recorded in the patient's medical history kept in Kaunas Clinics. Therefore, a thorough follow through would also be required and this would help in achieving better results.

17.0 Reference

1. Katherine C_{​. Atrial flutter - Symptoms, diagnosis and treatment | BMJ Best Practice} [Internet]. Bestpractice.bmj.com. 2018 [cited 4 March 2019]. Available from:

https://bestpractice.bmj.com/topics/en-gb/183

2. Gambino B. High Incidence of Atrial Fibrillation After Atrial Flutter Ablation - The Cardiology Advisor [Internet]. The Cardiology Advisor. 2016 [cited 4 March 2019].

Available from:

https://www.thecardiologyadvisor.com/arrhythmia/atrial-fibrillation-after-atrial-flutter-ablati on/article/499143

3. Park DS, Fishman GI. The cardiac conduction system. Circulation. 2011 Mar 1;123(8):904-15.

4. Warchoł I, Bińkowski BJ, Kucejko T, Sobiczewska J, Lubiński A. A Retrospective Study of Atrial Fibrillation Following Cavotricuspid Isthmus Ablation for Atrial Flutter. Med Sci Monit. 2019 May 5;25:3316-20.

5. Clinical G. Typical Atrial Flutter [Internet]. Clinical Gate. 2015 [cited 4 March 2019]. Available from: _​https://clinicalgate.com/typical-atrial-flutter/#cebib0010

6. Mayo Clinic. Atrial fibrillation - Symptoms and causes [Internet]. Mayo Clinic. 2018 [cited

4 March 2019]. Available from:

https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20 350624

7. Katherine C. Atrial flutter Risk Factors - Epocrates Online [Internet]. Online.epocrates.com. 2018 [cited 4 March 2019]. Available from:

https://online.epocrates.com/diseases/18332/Atrial-flutter/Risk-Factors

8. Unknown. Atrial Flutter Topic Review | LearntheHeart.com [Internet]. Healio.com. 2017

https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/atrial-fl utter

9. Burns D. Atrial Flutter • LITFL Medical Blog • ECG Library Diagnosis [Internet]. Life in the Fast Lane • LITFL • Medical Blog. 2019 [cited 4 March 2019]. Available from:

https://lifeinthefastlane.com/ecg-library/atrial-flutter/

10.Garan H. Atypical atrial flutter [Internet]. heartrhythmjournal.com. 2008 [cited 7 March

2019]. Available from:

https://www.heartrhythmjournal.com/article/S1547-5271(07)01086-7/pdf

11.Waldo A. ELECTROPHYSIOLOGY: Treatment of atrial flutter [Internet]. 2000 [cited 4 March 2019]. Available from: _​https://heart.bmj.com/content/84/2/227

12.Katherine C. Atrial flutter Treatment Approach - Epocrates Online [Internet]. Online.epocrates.com. 2018 [cited 4 March 2019]. Available from:

https://online.epocrates.com/diseases/18341/Atrial-flutter/Treatment-Approach

13.Page RL, Joglar JA. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology 2016;67(13):e27-e115.

14.Spector P, Reynolds MRI. Meta-analysis of ablation of atrial flutter and supraventricular tachycardia. The American journal of cardiology 2009;104(5):671-7.

15.Pérez FJ, Schubert CM. Long-term outcomes after catheter ablation of cavo-tricuspid isthmus dependent atrial flutter: a meta-analysis. Circulation. Arrhythmia and electrophysiology 2009;2(4):393-401.

16.Passman R. Uptodate.com. 2017 [cited 4 March 2019]. Available from:

https://www.uptodate.com/contents/catheter-ablation-to-prevent-recurrent-atrial-fibrillation -anticoagulation#subscribeMessage

17.De Ruvo E, Sagone A, Rovaris G, Marchese P, Santamaria M, Solimene F, et al. A comparison of 8-mm and open-irrigated gold-tip catheters for typical atrial flutter ablation: Data from a prospective multicenter registry. J Arrhythm. 2018 Aug;34(4):402-9.

18.Kim JO, Shim J, Lee SH, Yu HT, Kim TH, Uhm JS, et al. Clinical characteristics and rhythm outcome of catheter ablation of hemodynamically corrected valvular atrial fibrillation. J Cardiol. 2019 Jun;73(6):488-96.

19.Glover B. Catheter ablation for atrial flutter: a survey by the European Heart Rhythm Association and Canadian Heart Rhythm Society [Internet]. https://academic.oup.com. 2016 [cited 7 March 2019]. Available from:

https://academic.oup.com/europace/article/18/12/1880/2960772

20.Iwasawa J, Iesaka Y. Cavotricuspid isthmus ablation using a catheter equipped with mini electrodes on the 8 mm tip: a prospective comparison with an 8 mm dumbbell-shaped tip catheter and 8 mm tip cryothermal catheter [Internet]. https://academic.oup.com. 2016

[cited 7 March 2019]. Available from:

https://academic.oup.com/europace/article/18/6/868/2467089

21.Sullivan D. Cardiac Ablation Procedures: Uses, Preparation, and Risks [Internet]. Healthline. 2017 [cited 7 March 2019]. Available from:

https://www.healthline.com/health/cardiac-ablation-procedures#procedure

22.Melo S. Ablation of typical atrial flutter: a prospective randomized study of cooled-tip versus 8-mm-tip catheters [Internet]. http://www.scielo.br. 2007 [cited 7 March 2019].

Available from:

http://www.scielo.br/scielo.php?pid=s0066-782x2007000300004&script=sci_arttext&tlng= en

23.Al-Jazairi MIH, Rienstra M, Klinkenberg TJ, Mariani MA, Van Gelder IC, Blaauw Y. Hybrid atrial fibrillation ablation in patients with persistent atrial fibrillation or failed catheter ablation. Neth Heart J. 2019 Mar;27(3):142-51.

24.Baman TS, Jongnarangsin K. Prevalence and predictors of complications of radiofrequency catheter ablation for atrial fibrillation. Journal of cardiovascular electrophysiology 2011;22(6):626-31.

25.Nikitin N. Effect of Age and Sex on Left Atrial Morphology and Function. European Journal of Echocardiography. 2003;4(1):36-42.

26.Fleg JL, Strait J. Age-associated changes in cardiovascular structure and function: a fertile milieu for future disease. Heart failure reviews 2012;17(4-5):545-54.

27.Maskoun W, Pino M, Ayoub K, Llanos O, Almomani A, Nairooz R et al. Incidence of Atrial Fibrillation After Atrial Flutter Ablation. JACC: Clinical Electrophysiology. 2016;2(6):682-690.

28.Bonakdar H. Atrial Flutter: Diagnosis and Management strategies. Cardiac Arrhythmias. 2018;.

29.Fleg JL, Strait J. Age-associated changes in cardiovascular structure and function: a fertile milieu for future disease. Heart Fail Rev. 2012 Sep;17(4-5):545-54.

30.Waldo AL, Atienza OF. Atrial flutter: Mechanisms, features, and management. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology: From Cell to Bedside. 5th ed. Philadelphia: Saunders; 2009. pp. 567-576