THE ELECTROPHYSIOLOGY STUDY (EPS) 517 wraps around the left posterior atrioventricular groove. From this position Egrams are reco rded from the left atrium and ventricle. The CS catheter is often inserted via the left or right subclavian veins. The intracardiac electrocardiograms conventionally ordered are HRA, His, CS, and RV (not di splayed here), with an ECG lead at the bottom. On each catheter, bipolar electrode pairs ar e then ordered proximal to distal. In SR the activation starts at the HRA, passes across th e His, and then along the CS catheter proximally to distally. Earliest ventricular activati on is at the RVA (where the Purkinje \201 bers insert). Normal intervals are PA 25 \200\22355 ms; atrium \200\223His (AH) = 50 \200\223120 ms; His \200\223 ventricular (HV) = 35 \200\22355 ms; QRS <120 ms; and corrected QT <440 ms men, <4 60 ms women. HRA His9 \200\22310 His1 \200\2232 CS 9 \200\22310 CS 1 \200\2232 I aVF V1 V6 Figure 13.2 Standard positions of catheters in the EPS and intracardiac electrograms at tho se sites. CHAPTER 13 Invasive electrophysiology 518 Uses of the EPS Sinus node function The corrected sinus node recovery time (CSNRT) and sinoatrial conductio n time (SACT) are both measures of SAN function. Unfortunately, they are unreliable tests, as SAN function is greatly in \202 uenced by autonomic tone, drugs, and observer error. SA N dysfunction is best assessed with ambula- tory monitoring and exercise testing. EPS can be considered for patients who have symptoms consistent with bradyarrhythmia (synco pe) and for whom noninvasive evaluations have been unrevealing. EPS for SAN function has hi gher speci \201 city than sensi- tivity. Therefore, a positive test is much more informati ve than a negative one. AV conduction (see Table 13.2) Heart block The degree of heart block is assessed via the EC G, which can also suggest the level (i.e., AV node or His Purkinje system). The true level of block is easily ascertained via EPS. The AH time is prolonged in nodal block and the HV interval, in infranodal block. The AH (but not the HV) time may be shortened by exercise, i soproterenol, or atropine and prolonged by vagal maneuvers. AV nodal function This is assessed in both the anterograde (A to V) and retrograde (V to A) directions, using both incremental pacing and extrastimuli. By incremental pacing in the H RA, conduction is observed in the His and RVA until block occurs. The longest pacing interv al at which block occurs in the AVN is the anterograde Wenckebach cycle length (WCL). Normal values are <500 ms; however, this increases with age and auto- nomic in \202 uences . The retrograde WCL is also measured, although absent VA conduction can be normal. Extrastimulus pacing is also performed from the HRA. As the coupling interval between S1 an d S2 is reduced, AV conduction is observed. The longest S1S2 interval at which AV block occ urs is the anterograde AVN effective refractory period (ERP). This is usually measured at d rive trains of 600 and 400 ms. If VA conduction is present, the retrograde AVN ERP is measu red. Decremental conduction This is the key physiological property of the AV node. As the interv al between successive impulses passing through the AV node decreases, the conduction veloci ty within the AV node also decreases. In AV conduction this is manifest as a prolongation o f the AH (and AV) interval as the atrial pacing interval decreases. This phenomenon can be observed during incremental and extrastimu- lus pacing. During extra stimulus pacing if the AH interval is plotted against the S1S2 (= A1A2), an anterograde con duction curve can be plotted. USES OF THE EPS 519 Table 13.2 A standard basic electrophysiology study Pacing protocol Measure Comments Is there AV conduction block? 1. Sinus rhythm Basic sinus intervals (PA, AH, HV, QRS, corrected QT) 2. Incremental ventricular pacing (IVP) RWCL Is VA conduction present? If so, is atrial activation normal and decremental? 3. Incremental atrial pacing (IAP) AWCL Is AV conduction decremental? Is pre-excitation manifest during pacing? 4. Extrastimulus pacing from atrium at 600 and 400 ms Anterograde AVNERP at 600 and 400 ms Is AV conduction decremental? Is pre-excitation manifest during pacing? Is there dual AV-no dal physiology? 5. Extrastimulus pacing from ventricle at 600 and 400 ms Retrograde AVNERP at 600 and 400 ms Is VA conduction present? If so, is atrial activation normal and decremental? 6. Arrhythmia induction from atrium. Use 2 \200\2234 extrastimuli, sensed extrastimuli, and burst pacing. . Note pacing protocol that induces arrhythmia. Is it reproducible? Compare arrhythmia induce d to clinical arrhythmia 7. If VT suspected, perform PES with up to 3 extrastimuli VERP at 600 and 400 ms Observe induced arrhythmia 8. Repeat steps 2 \200\2237 during isoproterenol infusion. Essential for tachycardias associated with enhanced automaticity AVNERP, atrioventricular nodal effective refractory period; AWCL, anterograde Wenckebach cy cle length; PES, programmed extra stimuli; RWCL, retrograde Wenckebach cycle length; VERP, ventricular effective refractory period. Dual AV nodal physiology It is possible in many patients (but not all) to identify two elec trical con- nections between the atrial myocardium surrounding the compact AV node and the node itself, which have different conduction properties. The slow pathway has slower conduc tion velocity but a shorter ERP than the fast pathway, with faster conduction and a longer ERP. This is observed by plotting an anterograde conduction curve. For longer A1A2 intervals AV conduction is preferentially via the fast pathway; however, on ce the fast pathway ERP is reached, conduction is via the slow pathway and consequently the AH time suddenly prolongs. This is called an AH interval jump and is de \201 ned as a len gthening of the AH by >50 ms, following reduction in the A1A2 interval by 10 ms (see Fig. 1 3.3). Dual AV-nodal pathways are the substrate for AVNRT. CHAPTER 13 Invasive electrophysiology 520 Identifying abnormal AV connections \200\224accessory pathways In normal hearts there is on ly one connection between the atrium and ventricle, the AV node. Activation of the atrium ( during V pacing) or ventricle (during A pacing or SR) should therefore start at the AV node . Accessory pathways (AP) do not decrement. Their presence can be iden- ti \201 ed by both abnormal activation patterns and conduction physiology using incremental and extrastimulus pacing. Atrial pacing As the AV node decrements, a greater proportion of ventricular activa- tion w ill occur via an AP if present. Thus, nondecremental AV conduction times and broadening of the QRS complex will be observed as the pacing interval shortens. If the ERP of the AP is l onger than the ERP of the AV node, then the QRS will suddenly narrow and the AV time sudden ly pro- long when the AP blocks. Ventricular pacing The normal order of atrial activation is His, then CS (proximal to dista l), and \201 nally the HRA, termed concentric activation. If the atrium is activat- ing v ia an AP, an eccentric activation pattern is usually observed. The site of the earliest atr ial activation will localize the AP. Nondecremental VA conduction is also seen. Induction of arrhythmia The presence of an AP, dual AV-nodal physiology, or ventricular sca r provides the substrate for a tachycardia but does not necessarily indi- cate that it will occur. A diagnosis can only be con \201 rmed by inducing the tachycardia. In addition to the pacing techniques described here, burst pacing, extra- stimulus pacing w ith multiple extrastimuli, and sensed extras are used. If this fails, pacing maneuvers can be repeated during an isoproterenol infusion (1 \200\2234 g/min) or boluses (1 \200\2232 g). This is particularly important for tachycardias due to enhanced automaticity. \200 \234Aggressive \200\235 induction protocols increase the likelihood of inducing an unwanted , nonspeci \201 c arrhythmia such as AF or VF. Once a tachycardia is initiated, it is useful to compare it with a 12 lead ECG of the tachy cardia recorded during symptoms to ensure that this is the clinical arrhythmia. How individ ual tachycardias are diagnosed and treated is considered in subsequent sections. U S E S O F Figure 13.3 Example of AH interval jump during extrastimulation. T H E E P S 5 2 1 CHAPTER 13 Invasive electrophysiology 522 Programmed ventricular stimulation An EP study focusing on induction of ventricular arrhyth mias (the VT stimulation study) has been used to risk stratify for sudden cardiac death (SC D), to decide on the effectiveness of antiarrhythmic drugs and deter- mine the need for ICD therapy. Evidence has now accumulated, however, that its predictive value is limited and t hat, in general, decisions regard- ing ICD therapy should be based on other risk factors, p articularly LV function. The EP study can be useful in the diagnosis and assessment of VT/VF and prior to ICD implant for other reasons: \200 \200 \200 \200 Does a patient with borderline LVEF (35% \200\22340%) have inducible VT? To assess suitabil ity for VT ablation (e.g., bundle branch VT) Are other arrhythmias present and easily induc ed? To aid programming of device: \200 \200 \200 Is VT well tolerated hemodynamically? Is it easily terminated with overdrive pacing? Is the re VA conduction? During V pacing or VT? Programmed ventricular stimulation is performed using the protocol devised by Wellens or a modi \201 cation thereof (see Box 13.1). Clinical indications \200 Documented symptomatic tachycardia (as \201 rst stage of diagnostic and ablation procedur e) Risk strati \201 cation for sudden cardiac death Suspected but not documented symptomat ic tachycardia (diagnostic only) Wolff \200\223Parkinson \200\223White syndrome Unexplained syncope (suspicious of arrhythmic cause) Symptomatic SAN or AVN heart block suspected but not documented \200 \200 \200 Thus the pacing protocol becomes gradually more aggressive. The more aggressive the inducti on protocol, the more nonspeci \201 c the result may be. The most useful result is inducti on of a sustained monmorphic VT with one or two extrastimuli. This indicates a potential su bstrate for ventricular arrhythmias. Nonsustained VT, polymorphic VT, and VF induced by an aggressive protocol are all nonspeci \201 c results and of little predictive value. PROGRAMMED VENTRICULAR STIMULATION 523 Box 13.1 Protocol for programmed ventricular stimulation End points for the EPS \200 \200 >10 beats of inducible and reproducible ventricular tachycardia Completion of protocol with out induction of ventricular tachycardia Pacing sequences from RV apex \200 Step 1: ventricular refractoriness at 3 drive cycle lengths (600, 500, 400) Step 2: ventric ular refractoriness at 3 drive cycle lengths Step 3: ventricular refractoriness at 3 drive cycle lengths Step 4: intervals to ventricular refractoriness single extrastimulus at decreasing coupling intervals to double extrastimuli at decreasing coupling intervals to triple extrastimuli at decreasing coupling intervals to 8 \200\22312 incrementally paced beats at decreasing coupling If no ventricular arrhythmia is induced, repeat from RV out \202 ow tract. If no ventricular arrhythmia is induced, isoproterenol can be infused and pacing repeated. CHAPTER 13 Invasive electrophysiology 524 New technologies EP procedures have become increasingly complex (e.g., for AF or congeni- t al heart disease) and require greater radiation exposure. Both of these problems have been overcome by non \202 uoroscopic, 3-D mapping systems. A computer-generated image of the ca rdiac chamber of interest is formed and onto this the electrical activation in the heart an d the EP catheter location are superimposed (see Fig. 13.4). In some cases it is now possible to perform a complete EP study and ablation without the us e of X-ray. Also, 3-D CT or MR images of the patient can be imported and integrated with th e electrical map to create a 3-D electroanatomical map of the chamber of interest. Figure 13.4 An Ensite NavX image of the left atrium. The torso demonstrates that this is an LAO projection. The catheter positions are located without the use of X-ray. CATHETER ABLATION 525 Catheter ablation In medical terms, ablation is the removal of tissue. As many tachycardias depend on discreet foci or pathways to be sustained, they are amenable to cure by destruct ion of these areas. Energy sources for ablation Radiofrequency (RF) energy Cells are destroyed by heating >50 C. The RF generator delivers an alter- nating current of 500 \200\223750 KHz between the ac tive catheter electrode and a large indifferent electrode placed on the patient \200\231s s kin. The ions within cells immediately adjacent to the catheter are agitated and generate h eat (resistive heating). The heating power generated in this way dramatically decreases as the distance form the catheter increases. The remaining heat is conducted away to the surro unding tissue. A lesion of 5 mm depth is formed after 30 \200\22360 seconds, which is suf \201 cient to destroy the full thickness of atrial myocardium. Catheters are 7 Fr with tip electrodes of 4 mm as standard or 8 to 10 mm where larger lesions are desired. If the temperature approaches 100 C, boiling of cell water occurs, gen- erating steam that escapes either by exploding through the endocardium, causing a large lesion (cavitation, \200\234steam-pop \200\235), or the pericardium (per- foration tamponade). Temperature is monitored at the tip of the catheter and power delivery automatically limite d to prevent such overheating. The generator allows the power, temperature, and duration of each RF delivery to be adjusted. Cooled RF The tip of the catheter is cooled during RF by the \202 ow of blood, so the hot test part of an RF lesion is 1 mm beneath the surface. Stasis of \202 ow occurs as the le sion is formed, hence the temperature rises, limiting the amount of power delivered and thu s the size of the lesion. Normal saline passed through a lumen (closed or open) in the tip of the catheter at a rate of 10 \200\22330 mL/hr continuously cools the catheter, allows higher powers and bigger les ions to be formed. This is needed where the myocardium is thick, e.g., left ventricle (VT) or Eustachian ridge (typical atrial \202 utter). Low- \202 ow (2 mL/hr) external irrigation with RF ablation may be useful for keeping the tip of the catheter free of thrombus, thus reducing stroke risk during RF in the LA or LV. Cryoablation Completely contained within the specialized ablation catheter, liquid nitrous oxide is released into the tip, rapidly vaporizes, and removes heat from the tissue in cont act with the catheter. The gas is rapidly recycled back to the catheter console. The tissue temperature (monitored at the tip of the catheter) falls to \210\22230 C, at w hich stage there is reversible loss of cell function. If an appro- priate response is seen (e.g., loss of pre-excitation during AP ablation), CHAPTER 13 Invasive electrophysiology 526 then the tissue is further cooled to \210\22260 C for 4 minutes to cause perma- nent dest ruction. The formation of ice adheres the catheter to the tissue, making it very stable. If , however, an adverse change is seen (e.g., AVN block) at \210\22230 C, the tissue can be rewarmed. Other Other energy sources under investigation are microwave, ultrasound, and laser. CATHETER ABLATION: COMPLICATIONS 527 Catheter ablation: complications SVTs (other than AF) are cured in >90% of cases with ablat ion. For AVNRT, the rate is >97%. Registry data demonstrate that signi \201 cant com- plic ations occur in <2% \200\2233% of cases; however, this varies with speci \201 c procedures . Major complications \200 \200 Death Stroke risk by: using preoperative TEE, intraoperative heparin guided by activated cl otting time, postoperative anticoagulation (aspirin or warfarin), irrigated catheters, cont inuous pressured heparinized saline administration through left-sided sheaths, and cryoabla tion. Cardiac tamponade puncture, but can occur even during the diagnostic procedure. BP is monitored throughout the procedure and in any hypotensive episode tamponade is suspected. The EP lab should have a readily available ECHO machine and emergency pericardial aspiratio n sets. AV nodal block (1%). High risk for septal accessory pathway (AP) or AVNRT (slow-pat hway) ablation. During RF continuously image the catheter position and atrial and ventricul ar electrograms. If AV, VA block, or catheter movement occurs, STOP. Cryoablation may be pr eferred for high-risk cases. Coronary artery spasm/MI: occur without any long-term effect d ue to spasm. Pneumothorax catheter placement. X-ray exposure . EP cases may be prolonged. D eterministic effects such as skin damage can be avoided with attention to \202 uoroscopy technique. Women of fertile age should be counseled and have pregnancy tests. Non \202 uor oscopic catheter location (Carto, LocaLisa, Ensite NavX) is increasingly used. (0.1% \200\2230.3%) (0.2%). Risk is higher for left-sided procedures. Minimize (0.5% \200\2231%). Risk is higher with trans-septal Transient ST elevation and chest pain may occurs only if the subclavian approach is used for Minor complications \200 Bruising/hematoma is used. Chest pain benzodiazepines may be nec essary. Vasovagal episode insertion or at sheath removal. Ensure that patient has IV access prior to entering the lab. is common at the puncture site if anticoagulation occurs transiently during energy delivery; IV opiates or often occurs during initial percutaneous sheath CHAPTER 13 Invasive electrophysiology 528 Atrial tachyarrhythmias: mechanism All regular atrial tachyarrhythmias should be named mech anistically, i.e., either focal atrial tachycardia or macro-reentrant atrial tachycardia (w hich includes atrial \202 utter). Focal atrial tachycardia The mechanism may be due to enhanced automaticity or micro-reentry . Common foci are the crista terminalis, PV \200\223LA junction, vena cava \200\223RA junct ion, and triangle of Koch. Macro-reentrant atrial tachycardia The most common form is typical atrial \202 utter. Thi s is an ECG diagnosis, i.e., P wave rate >240/min. There is a reentry circuit contained wit hin the RA, rotating counterclockwise around the tricuspid valve and dependent on conductio n through the tricuspid isthmus (see Fig. 13.5). The opposite of this is reverse typical \202 utter. Reentry circuits are also found in the left atrium, following cardiac sur- gery or ablation of atrial \201 brillation, or in congenital heart disease. These have varying circuits t hat need to be carefully mapped before ablation can be performed. Atrial \201 brillation The chaotic electrical wavefronts are seen because the atria do no t acti- vate uniformly. Two potential mechanisms account for this. Focal A single source of wavefronts emerges from cells with either enhanced automaticity (s uch as an atrial tachycardia located in a PV) or a single small reentry circuit (micro-reen try). These depolarize so rapidly that the rest of the atria cannot conduct them uniformly and the wavefronts break up to give multiple wavefronts (= \201 brillatory conduction). T his is usually the mechanism of paroxysmal AF, and these foci are considered triggers of AF . Multiple reentry This underlies permanent AF. Four to six separate reentry circuits or roto rs of constantly varying course and velocity rotate around the atria, colliding with each o ther and anatomical structures such as veins and valves. They are self-perpetuating. The la rger the atrium, the more room these wave- fronts have to rotate and the more likely they w ill be sustained. As any episode of AF persists, atrial dilation due to mechanical stunning increases (remode ling), which explains the natural progression of AF from paroxysmal to persistent to perman ent: AF begets AF. ATRIAL TACHYARRHYTHMIAS: MECHANISM 529 SVC CT FO CSO IVC TV Figure 13.5 Mechanism of typical atrial \202 utter. A diagram of the right atrium with an terior surface cut open and swung out to the left. The arrow represents the wavefront passi ng up the septum, over the roof of the RA, anterior to the crista terminalis (CT), and then passing through the isthmus between the inferior vena cava (IVC) and tricuspid valve (TV). Conduction is slowed as it passes transisthmally. CSO, coronary sinus os; FO, fossa ovalis ; SVC, superior vena cava. CHAPTER 13 Invasive electrophysiology 530 Ablation of atrial tachycardias Focal atrial tachycardia (FAT) Tachycardia must be induced and sustained to map location in the atria of earliest activation (the focus) and this may require an isoproterenol infu- sion. The hallmark of AT is dissociation of the atrial and v entricular elec- trograms during tachycardia. This may occur spontaneously (AV block) or it may be necessary to pace the ventricle faster than the atrium to demonstrate this phenomen on. ECG may indicate the origin (positive I and aVL, negative V1 = high lat- eral RA; negative II, III, and aVF = posteroseptal LA or RA; positive I, aVL, and V1 = right PVs; negative I and aVL, positive V1 = left PVs). Catheters in the RA and CS will identify whether the LA or RA activates \201 rst. Beware: AT from the right superior pulmonary vein (RSPV) may give the appearance of having an RA o rigin. The RA is easily mapped with an ablation catheter via the IVC, but the LA requires a transeptal puncture. A successful site usually has a local electrogram at least 30 ms ahead of the onset of the P wave. Success rates are >90%. Typical atrial \202 utter The reentry circuit can be interrupted by creating a series of ablation lesions creating a line of conduction block between the IVC and tricuspid valve th at disrupts conduction through the RA isthmus (see Figs. 13.5 and 13.6). This is therefore a purely anatomical procedure that can be per- formed in SR or during tachycardia. The TV annulus is usually mapped with a 20-pole catheter. Alternately, non \202 uoroscopic catheter location systems can be used to map the RA and isthmus and guide the catheter dur ing ablation. Success is proven by demonstrating that there is conduction block in both directions across the RA isthmus (bidirectional block). Acute success occurs in 90% of cases with a 10% rela pse. Thirty percent of patients who undergo atrial \202 utter ablation later develop AF. ABLATION OF ATRIAL TACHYCARDIAS 531 IVC TV Figure 13.6 Ablation of typical atrial \202 utter. An ablation catheter is passed up from the IVC, and a series of burns is made in the RA isthmus to join the TV to the IVC with a line of scar. In this way, no activation can pass through and the reentry circuit of typica l atrial \202 utter is broken. (See Fig. 13.5 for landmarks on the diagram.) CHAPTER 13 Invasive electrophysiology 532 Catheter ablation of atrial \201 brillation There are two main catheter strategies to pre vent recurrences of AF \200\224abolishing the focal triggers, and changing the atrial subst rate such that multiple reentry circuits cannot be sustained. Single focal trigger An example is focal AT from the PV. This is selectively ablated in the same way as described above. This is rarely a cure of AF, as there are often multiple trig gers. In addition, ablation within the PVs increases the risk of developing pulmonary vein stenosis and is not generally a \201 rst-line approach. Abolish potential triggers from affecting the atrial myocardium All four PVs are isolated. This is done in two ways: 1. Create a line of conduction block outside the ostia of the vei ns (anatomical isolation, see Fig 13.7b), isolating not just the vein but also the LA tissue a djacent to the veins. The risk of PV stenosis is virtually eliminated. PVI is currently the preferred method for RFA of AF 2. Selectively ablate all the electrical connections betwee n the LA and each PV (electrical isolation, see Fig. 13.7a). An important risk if ablating in the PV is PV stenosis (3%), which causes progressive dyspnea and is very dif \201 cult to manage . In some centers it is common to also ablate electrical signals in the supe- rior vena cava and coronary sinus. For paroxysmal AF, clinical success rates using this technique are 60% \200\22370% in published series. Newer approaches also include mapping the LA for complex fraction- ated electrograms (CFEs) and then ablating the CFEs that may serve as triggers or drivers of atrial \201 brillati on. Linear ablation The LA and RA can be compartmentalized by creating long lines of ablation w ithin them. These interrupt the multiple reentry circuits and hence AF cannot be sustained. This treatment was pioneered by the car- diac surgeons performing the surgical Maze with g reat success; however, improvements in catheter technology and non \202 uoroscopic localiz ation systems (e.g., Carto or Ensite NavX) have made it feasible to do this percutaneously. This treatment is suitable for symptomatic patients with persistent or permanent AF. In add ition to isolating the PVs, lines are drawn across the roof of the LA, between the LIPV and MV, the RA isthmus, and between the SVC and IVC. Success rates are lower than for paroxysm al AF. Procedures are long (4 hours) and carry a higher risk of stroke than with standard a blation. CATHETER ABLATION OF ATRIAL FIBRILLATION 533 (a) Lasso catheter Ablation catheter (b) Figure 13.7 (a) Electrical isolation of the left superior pulmonary vein. A lasso catheter is placed well up inside the vein to record pulmonary vein potentials. The ablation cathete r is back at the mouth of the vein. Where potentials are found linking the pulmonary vein t o the surrounding LA, energy is applied. The procedure continues until no potentials are re corded in the vein or potentials are dissociated. (b) Anatomical isolation of the right sup erior pulmonary vein. This is a Carto image of the LA from the front with the four pulmonar y veins posterior. Lesions can be seen well outside the vein, therefore not risking pulmona ry vein stenosis. CHAPTER 13 Invasive electrophysiology 534 Mechanism of AV reentry tachycardias In young patients with paroxysmal regular narrow compl ex tachycardia, the diagnosis is either AVNRT or AVRT. The mechanism of both is reen- try ( see Fig. 9.7). The substrate for AVNRT is dual AVN pathways and for AVRT the presence of an AP. Occasionally, an atrial tachycardia may give an identical ECG appearance. Diagnostic testing Four standard catheters are positioned (see Fig. 13.2) and an EPS is car ried out (see Table 13.2). Look for evidence of dual AVN physiology and pres- ence of an AP . If tachycardia is induced, atrial activation is observed to see whether it is via the AVN (AVNRT) or an AP (AVRT). Look closely for AVN block and BB block, especially at the onset and termination of tachyca rdia. HSVPBs (His synchronous premature beats) are introduced to identify whether an AP is mediating the tachycardia (AVRT). AV block If AVN block occurs, but tachycardia persists, it is almost always an atrial tachy cardia. Onset \200 \200 AVN jump immediately followed by tachycardia indicates AVNRT. Loss of pre-excitation follow ed by tachycardia indicates AVRT. Termination \200 Last tachycardia complex atrial (block in AVN): AVNRT or AVRT (almost certainly not atrial tachycardia) Last tachycardia complex ventricular: atrial tachycardia (AVNRT or AVRT still possible) His synchronous ventricular premature beats (HSVPBs) The aim is to introduce a ventricular paced beat exactly coincidental with the His potential during tachycardia, to see whether t he ventricle is an essential component of the reentry circuit (Fig. 13.8). To do this, the cycle length of the tachycardia is measured and a single sensed extrastimul us is delivered from the catheter in the RV at 20 ms less than the cycle length. This is re peated, reducing the coupling interval by 10 ms each time, until it is clear that the sense d extra is pre-His. Tachycardia is then terminated and the electrograms are analyzed. Analysis (Fig. 13.8) The HH and AA intervals are measured to ensure a stable tachycardia. T he paced VPB must be synchronous with the His potential. The AA intervals before and after the HSVPB are measured. If the subsequent A is premature, this implies that the atrium must have been activated via an AP (as we know the His bundle is refractory due the presence of the anterograde potential) and that the ventricle is part of the reentry circuit, hence AV RT. If the A is not advanced, it suggests that this is AVNRT, but does not preclude AVRT. MECHANISM OF AV REENTRY TACHYCARDIAS 535 1000 298 ms 260 ms 302 ms 350 ms 304 ms 306 ms 1000 Figure 13.8 His synchronous ventricular premature beats (HSVPBs) resetting tachycardia. Fro m top to bottom: intracardiac electrograms from high right atrium, His bundle catheter (pro ximal to distal), CS catheter (proximal to distal), and four surface ECG leads. The tachyca rdia cycle length is approximately 300 ms. During tachycardia, the earliest atrial activati on is at the distal coronary sinus (lateral left atrium) \200\224see arrows. A sensed extra (the HSVPB) is introduced just ahead of the His potential (H). The next atrial complex is advanced (see cycle lengths measured at the HRA). This strongly suggests an AVRT mediated b y a left lateral pathway. CHAPTER 13 Invasive electrophysiology 536 AV reentry tachycardias: ablation AVRT Ablation must be performed during ventricular pacing or AVRT to iden- tify the locatio n of the AP (unless it is manifest on the resting ECG i.e., WPW). The earliest atrial activ ation is identi \201 ed with an almost continu- ous V-then-A electrogram. Its general loca tion is found by bracketing it with a diagnostic catheter on the valve annulus, i.e., the C S catheter on the left side or a multipolar catheter on the right side (see Fig. 10.9). The precise location is then found with the ablation catheter. A true annular site is needed for success, so an equal-sized atrial and ventricular compone nt on the mapping catheter is looked for. Left-sided APs are approached either retrogradely (via the aortic valve and LV) or anterogradely (trans-septal puncture). Following ablation, full EP testing is repeated. VA conduction should be absent or via the AVN (concentric). If VA conduction persists, adenosine boluses are given to demonstrate bot h VA and AV block. AVNRT The target is the slow AVN pathway (see Fig. 13.9b). This is found inferior to the Hi s bundle, close to the mouth of the CS in the inferior aspect of the triangle of Koch. Anat omically guided slow pathway ablation is con- ducted in the area along the inferior part of Koch \200\231s triangle extending from the TV annulus to the anterior edge of the CS os. With continuous ECG monitoring, RF energy is delivered, and usually transient slow junction al escape beats are seen as the cells die. If the cath- eter moves or any AV or VA block oc curs, ablation is stopped immedi- ately. If the lesion is therapeutic, a full EP study is t hen repeated to test and ensure that there is no AVNRT. A successful procedural outcome is the inability to induce tachycardia and complete loss of dual AV-nodal physiology. Conventionally, the pres- ence of a jump and a single echo beat is permitted, providing tachycardia cannot be induced. If isoproterenol was needed to induc e tachycardia before the ablation, it should also be used during post-ablation testing. Following ablation, full EP testing is repeated. VA conduction should be absent or via the AVN (concentric). If VA conduction persists, adenosine boluses are given to demonstrate bot h VA and AV block. AV REENTRY TACHYCARDIAS: ABLATION 537 (a) AVN Left sided AP (b) FP SP Figure 13.9 (a) Orthodromic AVRT via a left-sided accessory pathway (AP). Activation from A to V is down the atrioventricular node (AVN), then across the ventricular myocardium and b ack from V to A up the AP, thus completing the circuit. The ventricle therefore is an essen tial part of the circuit. Antidromic AVRT (not shown) would activate in the opposite direct ion. A left-sided AP as shown here would be accessed by a trans-septal puncture or retrogra dely (via aortic valve and LV). (b) Typical AVNRT activates from the atrium to the AVN via the slow pathway (SP) and from the AVN to the atrium via the fast pathway (FP), thus comple ting the circuit. The ventricle is activated as a bystander via the bundle of His and is no t an essential part of the circuit. Atypical AVNRT (not shown) activates in the opposite di rection. Ablation targets the slow pathway. CHAPTER 13 Invasive electrophysiology 538 Ablation of ventricular tachycardia Clinical indications Only a small percentage of patients with VT and structural heart disea se are suitable for ablation. The VT needs to be relatively well tolerated (see Fig. 13.10) and ideally is monomorphic. In this group, success rates of 70% are expected. Ablation sho uld be offered to patients whose VT is well tolerated and have one of the following feature s: \200 \200 \200 \200 Recurrent symptomatic paroxysms The number of therapies delivered by an ICD needs to be red uced Incessant VT VT in normal hearts: ablation offers a cure for these patients (>90% cure ). RVOT and fascicular tachycardia are mapped during VT, looking for the earliest ventricul ar activation. Mechanism of VT In structural heart disease VT almost always has a reentry mechanism. Scarr ed ventricular myocardium (due to ischemia, cardiomyopathy, etc.) provides the substrate fo r reentry as described previously. A stable reentry circuit can break down into chaotic act ivation of \201 brillation (VF), hence the link between VT and sudden death. Mapping reentry VT To successfully map the reentry circuit, the patient must be in VT (acti va- tion mapping). Thus the VT needs to be hemodynamically well tolerated. Remote de \201 brillation paddles are attached to the patient so that if VF or hypotensive VT occurs, it c an be immediately cardioverted. The aim is to identify the critical pathway at which the circuit is most susceptible to des truction. This is achieved by entrainment mapping. Alternately, 3-D noncontact scar mapping can be performed in SR and \200\234escape pathways \200\235 can be eliminated by ablation . Entrainment of VT This can only be performed on tachycardias with a reentry mechanism. The ablation catheter is moved around the ventricle to sites where the cir- cuit is expected (i .e., adjacent to areas of scar). By pacing with this catheter at a rate just faster than th e tachycardia cycle length, a VT is entrained if it is following the same circuit but at a faster rate. If the ECG during pacing is a 12/12 surface lead match to the clinical VT, then this is con cealed entrainment. This implies that the pacing catheter is within the critical portion of the circuit. To con \201 rm this when pacing is stopped, the return cycle length or post- pacing interval (the time from the \201 nal paced beat to the next activation at the cath eter) should be almost identical to the tachycardia cycle length. Ablation technique The standard steps of a VT ablation are as follows: \200 \200 Induce VT. Ensure similar to clinical VT and well tolerated. Map VT to identify critical di astolic pathway: \200 Very early local electrogram occurring mid-diastole (50 \200\223150 ms ahead of ECG) ABLATION OF VENTRICULAR TACHYCARDIA 539 +160 Arterial 0 HRA HBEp HBEd RVA I aVF Figure 13.10 An induced VT at a cycle length of 320 ms (187/min). From top to bottom a trac ing of arterial pressure, high right atrial Egram, proximal then distal His bundle Egram, R V Egram, then 2 surface ECG leads. There is no V-to-A conduction at this rate and the atriu m is dissociated form the ventricle. Despite the rapid rate, the systolic BP is maintained at 100 mmHg, enabling the VT to be mapped if necessary. \200 Concealed entrainment during pacing Return cycle length (= post-pacing interval) < tachycar dia cycle length + 30 ms \200 Deliver energy at site, meeting criteria above. If VT is terminated, attempt to reinduce ag ain. Failed ablation If conventional ablation fails, alternative approaches are as follows: \200 \200 Arrhythmia cardiac surgery. Ablate the epicardial surface of the heart by delivering the ca theter via the pericardium (as for a pericardial aspiration). Alcohol ablation via a small terminal coronary branch subtending the scarred area supporting reentry. This gives the pat ient a controlled, small MI that destroys the critical portion of the reentry circuit. CHAPTER 13 Invasive electrophysiology 540 Accessory pathways (Wolff \200\223Parkinson \200\223 White syndrome) De \201 nitions and ECG The atria and ventricles are separated by the \201 brous annuli of the TV on the right and MV on the left. The AV node is the only electrical connec- tion in normal hearts. Abnormal accessory pathways can occur at any position along these annuli and are named accordingly (see Fig. 13.11). They may conduct in one or both directions. The y are the substrate for AVRT to occur. If an AP conducts anterogradely (A to V) it will be manifest on the ECG as pre-excitation ( short PR interval and delta wave). The morphology of the delta wave helps to predict the lo cation of the AP. An AP that con- ducts only retrogradely is described as concealed. Wolff \200\223Parkinson \200\223White syndrome refers strictly to APs that are both manifest as pre-excitation on the resting ECG and cause tachycardia. Tachycardias An AP can be associated with tachycardia by several mechanisms: \200 Orthodromic AVRT (most common, accounts for 95% of AP-mediated tachycardias) \200\224narrow complex tachycardia with anterograde conduction over the AVN and retrograde conduction via the AP wide complex tachycardia with anterograde Antidromic AVRT \200\224 conduction via t he AP and retrograde conduction via the AVN Bystander \200\224SVT of another etiology that conducts down the AP Prognosis AF in the presence of an AP with anterograde conduction can be danger- ous, as th e ventricle is not protected by the decremental behavior of the AV node. This can precipita te VF and sudden death. If patients are discov- ered incidentally to have an AP and are tru ly asymptomatic, then sudden death is extremely rare (2 deaths in 600 patients followed for 3 \200\22320 years). Invasive EP can be used to risk stratify patients. A worse prognosis is predicted by the following: Invasive EP testing \200 Anterograde ERP of the AP <250 ms (the longest interval that will not conduct down the AP d uring atrial extrastimulus pacing or AF) Inducible AVRT Multiple APs \200 Symptomatic tachycardia Ebstein \200\231s anomaly \200 ACCESSORY PATHWAYS (WOLFF \200\223PARKINSON \200\223WHITE SYNDROME) 541 Anterior Left lateral His Septal MV TV CS Right lateral Posterior Figure 13.11 Tricuspid (TV) and mitral valve (MV) annuli. Accessory pathways can be positio ned anywhere on the annuli. They are named anatomically, i.e., anterior, left anterolateral , left lateral, left posterolateral, etc. Anteroseptal pathways are close to the His bundle and AV node and are termed parahisian. CHAPTER 13 Invasive electrophysiology 542 Accessory pathways: localization R/S(cid:1)1 V2 Yes No \210\206 (+) \210\206 (+) III Yes Yes No No LL/ LAL \210\206 ( \200\223) \210\206 (+) \210\206 (+) V1 Yes Yes Yes No No No RAS/ RA LL/ LAL RPS MS AVF \210\206 V1 R/S(cid:1)1 No Yes \200\223 