560 CHAPTER 11 Invasive electrophysiology Complications of catheter ablation The general complications associated with ablation are d escribed here. The overall major complication rate for ablation of SVT is <1 % and for comp lex arrhythmia (AF, VT) 3 % . Speci \201 c issues in AF ablation are discussed later. Major complications \200 Death (<0.1 % ) \200 Bleeding : generally only venous access i s used, so major vascular damage requiring surgery is rare. This may be exacerbated by proc edural use of heparin or warfarin. Haematoma can be due to persistent arterial or venous bl eeding, arteriovenous \201 stula, or pseudoaneuysm. Large local or retroperitoneal haemat oma may require transfusion. Compression and reversal of anticoagulation with protamine, re combinant factor VIII (or fresh frozen plasma (FFP)) and vitamin K may be needed. Ultrasoun d and contrast CT (CT angio) are used to diagnose the cause and extent of bleeding Stroke (<0.2 % for supraventricular tachycardia (SVT)): the risk is higher for left-sided procedures or where cardioversion to SR from AF or \202 utter occur s. Minimize risk by: preoperative transoesophageal echocardiography (TOE), intraoperative h eparin guided by activated clotting time (ACT), postoperative anticoagulation (aspirin or w arfarin), irrigated catheters, continuous pressured heparinized saline administration throu gh left-sided sheaths, cryoablation Cardiac tamponade (<0.2 % for SVT): the risk is higher if trans- septal puncture is performed, but can occur even during diagnostic procedures. Blood pressu re (BP) is monitored throughout the procedure, and in any hypotensive episode tamponade is suspected. The EP lab should be equipped with a hand-held ECHO machine and emergency perica rdial aspiration sets. Doctors performing trans-septal punctures need to be experts in peri cardial aspiration AV nodal block (<1 % for SVT): high risk for septal AP or AVNRT (slow pathway) ablation. During RF, continuously image the catheter position and atrial and ventricular electrograms. If AV, VA block, or catheter movement occurs, STOP . Cryoablatio n may be preferred for high-risk cases Deep vein thrombosis (DVT) and pulmonary embolism (PE): due to placement of multiple catheters in small veins for prolonged periods. If patients have a te ndency to thrombosis, use heparin and continuous irrigation of sheaths Coronary artery spasm/MI : transient ST elevation and chest pain may occur without any long-term effect due to spasm Pneumothorax : only if a subclavian approach is used for catheters (coronary sinus) X-ray exposure : EP cases may be prolonged. Deterministic effects such as skin damage can b e avoided with care to \202 uoroscopy technique. Women of fertile age should be counseled and have pregnancy tests if necessary. Non- \202 uoroscopic catheter location (Carto, Nav X) is increasing COMPLICATIONS OF CATHETER ABLATION 561 Minor complications These are common. Liberal use of local anesthetic and conscious sedatio n (combined opiates and benzodiazepines administered IV) can prevent these. \200 Chest pa in : occurs transiently during energy delivery \200 Vasovagal episode : often occurs duri ng initial percutaneous sheath insertion; ensure the patient has an IV cannula before entering the lab Groin pain, bruising, or haematoma : common at puncture site, particularly if anticoagulation is used. 562 CHAPTER 11 Invasive electrophysiology Trans-septal puncture This permits a direct route to the LA via the intra-atrial septum and systemic venous system. Previously, the technique was used infrequently by cardiologists f or mitral valvuloplasty; however, due to the massive expansion in ablation of AF, it is now a routine skill of the modern cardiac electrophysiologist. A detailed description of the t echnique is available. 1 Electrophysiology (catheter ablation) indications \200 AF \200 Left atrial tachycardia \200 VT \200 Left-sided accessory pathways. Other indications \200 Percutaneous mitral valvuloplasty \200 Haemodynamic study of the left heart with prosthetic AV present. Technique (see Fig. 11.5) This is described using a Brockenbrough needle and Mullin \200 \231s sheath/dilator set. Other needles and sheaths are available. \200 Preparation: if T OE is performed, review the anatomy of the RA, LA, and intra-atrial septum. Optimal patient preparation \200\224 fasted but well hydrated, IV cannula, etc. Percutaneous access using Seldinger technique via right femoral vein for trans-septal sheat hs and access for other catheters. Trans-septal sheaths and dilator are delivered to the SV C over a long guide wire. The needle has a lumen to allow pressure monitoring. This is pass ed up the dilator but kept just within the tip of the sheath. An EP catheter is positioned on the His or in the coronary sinus, as an anatomical marker. Trans-septal puncture: the needle and sheath are held together, with the handle pointing to ward 4 o \200\231clock. The entire rig is pulled inferiorly while screening in LAO (left an terior oblique) projection, until the tip of the catheter and needle are seen to \200\230j ump \200\231 medially as it falls from the SVC to the RA, and then a more subtle jump as it falls into the fossa ovalis. The position is imaged in right anterior oblique (RAO) projec tion, to ensure it is posterior to the aortic root. The needle is then advanced through the septum to the LA. The pressure wave changes to LA trace. The dilator and sheath are advanc ed over the needle into the LA. Monitoring: the dilator and needle are removed to leave the sheath in the LA as access for EP catheters. Pressurized heparin saline \202 ush is attached to the sheath. Heparin is g iven in boluses to keep the ACT over 300 s, while the catheters are in the left heart. 1 Earley MJ (2009). How to perform a transseptal puncture. Heart 95 : 85 \200\22392. TRANS-SEPTAL PUNCTURE 563 Complications Occur in <1 % of cases: \200 pericardial effusion or tamponade \200 aorti c root needle puncture \200 right or left atrial wall needle puncture \200 pleuritic ch est pain \200 stroke/transient ischaemic attack (TIA) \200 transient ST elevation of in ferior leads \200 persistence of atrial septal defect (ASD). MV TV FO CS da2008 da2008 Fig. 11.5 A diagram showing the position of the trans-septal needle optimally positioned in the fossa ovalis (FO) ready for puncture through into the left atrium, on the left, LAO pr ojection; right, RAO projection. The most important structure to avoid is the aortic root, in which a pigtail catheter can be sited to visualize it. Alternatively, a catheter marking the os of the coronary sinus (CS) or the bundle of His (not shown) can be used. TV = tricu spid valve; MV = mitral valve. 564 CHAPTER 11 Invasive electrophysiology Atrial arrhythmias: mechanism There are only two main types of atrial arrhythmias: atrial t achycardia and atrial \201 brillation. Atrial tachycardia is characterized by repetitive single electrical wavefronts following the same course, causing regular atrial acti- vation . The source of these wavefronts can either be focal or a re-entry circuit. AF is character ized by multiple wavefronts following chaotic, con- stantly varying, courses. Focal atrial tachycardia Atrial cells with enhanced automaticity \201 re more quickly tha n the SAN. Any atrial cells can do this, but common foci are the crista terminalis, PV \200 \223LA junction, vena cavae \200\223RA junction, and triangle of Koch. It is pos- sible for re-entrant circuits to form within a very small group of cells, termed \200\230micro-re-e ntrant \200\231; however, distinguishing this from a focal mech- anism is very dif \201 cu lt even at EP study. Macro-re-entrant atrial tachycardia This is due to a re-entrant circuit bordered by areas o f \201 xed conduction block \200\224 either anatomical barriers (e.g. valve annulus) or areas of scar. The commonest form is typical atrial \202 utter , where the circuit is con tained within the RA, rotating anticlockwise around the tricuspid valve (see Fig. 11.6 ). T he opposite (clockwise) of this is reverse typical \202 utter. Any other macro-re- entran t atrial tachycardia in the right or left atrium can be termed atypical atrial \202 utter . Most atypical circuits are around areas of scar, most commonly due to catheter ablation o f AF, cardiac surgery, or congenital heart disease. These circuits need to be carefully map ped before ablation can be per- formed. The term \202 utter is an ECG diagnosis, i.e. P-w ave rate > 240/min. Atrial \201 brillation The mechanism underlying the chaotic electrical wavefronts that ch arac- terize AF is both focal and re-entry. Paroxysmal AF usually has a focal mechanism, an d persistent AF is due to multiple re-entry wavefronts. Focal: Wavefronts from a single source emerge from either cells of enhanced automaticity (l ike focal atrial tachycardia) or a single small re-entry circuit (micro-re-entrant). The pu lmonary veins are the source of these wavefronts in > 80 % of cases. The wavefronts are of such a high frequency that the rest of the atrial myocardium cannot conduct them uniformly. This causes them to break up to give multiple wavefronts (= \201 brillatory conduction, Fig. 11.6 ). This is usually the mechanism of paroxysmal AF and these foci are considered t riggers of AF. Multiple re-entry: 4 \200\2236 separate re-entry circuits of constantly varying course and velocity rotate around the atria, colliding with each other and anatomical structures such as veins and valves. They are self-perpetuating. The larger the atria, the more room these wavefronts have to rotate and the more likely it is that they will be sustained. Remodeling: This is a key concept in understanding the mechanism of AF. Episodes of AF, no matter how short, will alter the electrical properties of the myocytes due to downregulatio n of calcium channels and shortening ATRIAL ARRHYTHMIAS: MECHANISM 565 of action potential duration (electrical remodeling). This makes it easier for the myocardi um to support re-entry wavefronts. Thus, after multiple paroxysms, AF may become sustained, i.e. persistent. After months of AF, the atria will become dilated and \201 brosis will occur (structural remodeling), further promoting re-entry. Remodeling explains the untreate d natural history of AF to progress from paroxysmal to persistent to permanent. This is the pathophysiological explanation of the phrase \200\230AF begets AF \200\231. D A 2 0 1 0 Fig.11.6 Cartoon depicting AF being driven by the source of electrical wavefronts emerging from the left superior pulmonary vein (star). The arrows represent electrical wavefronts br eaking up to give multiple wavefronts \200\224 the hallmark of AF. Electrical isolation of this vein by ablation will prevent future episodes. 566 CHAPTER 11 Invasive electrophysiology Ablation of atrial tachycardias Focal atrial tachycardia (FAT) \200 Tachycardia must be i nduced and sustained to map the location in the atria of earliest activation (the focus) an d this may need an isoprenaline infusion. The hallmark of atrial tachycardia is dissociation of the atrial electrograms from ventricular during tachycardia. This may occur spontaneously (AV block), or it may be necessary to pace the ventricle faster than the atrium. The morphology of P waves on ECG may be used to identify the location of the source. ( + ve I and aVL, \210\222 ve V 1 = high lateral RA; \210\222 ve II, III and aVF = LA or RA posteroseptal; + ve I, aVL and V 1 = right PVs; \210\222 ve I a nd avL, + ve V 1 = left PVs,). Detailed algorithms are available. 1 \200 Catheters in the RA and CS will identify whether the LA or RA activates \201 rst. Beware: FAT from the right superior pulmonary vein (RSPV) may give th e appearance of having an RA origin. The RA is easily mapped with an ablation catheter via the inferior vena cava (IVC), but the LA requires a trans-septal puncture. A successful site usually has a local electrogram at least 30 ms ahead of of the P wave. Success rates are > 90 % . Typical atrial \202 utter \200 The re-entry circuit can be interrupted by creating a se ries of ablation lesions adjacent to one another so that a line of conduction block is crea ted between the IVC and tricuspid valve (see Fig. 11.7). This is therefore a purely anatomi cal procedure that can be performed in SR or tachycardia. Patients in atrial \202 utter will need perioperative anticoagulation with warfarin. Commonly, the tricuspid valve (TV) annulus is mapped with a 20-pole catheter, but this is not necessary. Success is proved by termination of tachycardia (if present) and demonstrating conduction block in both directions across the RA isthmus (bidirectional bloc k). Acute success occurs in 90 % of cases, with a 10 % relapse. \200 30 % of patients who und ergo atrial \202 utter ablation later develop AF. 1 Kistler PM, Roberts-Thomson KC, Haqqani HM, et al (2006). P-wave morphology in focal atri al tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Co ll Cardiol 48 : 1010 \200\22317. ABLATION OF ATRIAL TACHYCARDIAS 567 D A 2 0 1 0 Fig. 11.7 Ablation of typical atrial \202 utter. The arrows represent the re-entry ciruit activating around the RA with the critical isthmus of slowed conduction (zig-zag arrow) be tween the inferior vena cava (IVC) and tricuspid valve (TV) An ablation catheter is passed up from the IVC, and a series of ablation lesions delivered to join the TV to the IVC with a line of scar. In this way, no activation can pass through, and the re-entry circuit of ty pical atrial \202 utter is broken. 568 CHAPTER 11 Invasive electrophysiology Catheter ablation of atrial \201 brillation This is now the \200\230bread and butter \200\231 of modern interventional EP practice. For paroxysmal AF, the strategy is to electr ically isolate the PV, hence pre- venting triggering of these episodes. Ablation of persist ent AF starts with PV isolation and is followed by more extensive ablation in the left and right atrium aimed at modifying the atrial myocardial substrate so that it cannot support t he re-entry waves that sustain AF. High-volume EP units expect a success rate of > 90 % and > 80 % for paroxysmal and persistent AF, although multiple procedures may be required. Patient preparation The indication for ablation is symptomatic AF despite antiarrhythmic dr ugs. Patients need to be counseled of the 3 % risk of a major complication, long procedure time (up to 4 hours), and need for multiple procedures. A TOE is usually performed to ensur e the left atrium (LA) and left atrial appendage (LAA) are free of thrombus and to view the intra-atrial septum. A CT or MRI of the thorax may be performed to provide a LA reconstruc tion for image integration. A 3D mapping system is used (see b p. 556). Generally, the proc edure is performed under local anesthetic, with conscious sedation by a combination of opia tes and benzodiazepines. Percutaneous access is via the femoral veins. Heparin is administe red to maintain an ACT between 300 and 400s. Pulmonary vein isolation Trans-septal punctures are performed to deliver an irrigated RF ab lation and circular PV mapping catheter to the LA. There are two methods for isolating the PVs using RF energy. Segmental ostial isolation selectively ablates the individual electric al connections between the LA and each PV until the electrical signals disappear in the vei n. In wide area circumferential ablation , a continuous line of lesions is delivered well o utside the PV, to form a circle that encloses an ipsilateral pair of PVs (Fig. 11.8 ). Rega rdless of technique, the end-point is that the electrical signals in the PV disap- pear. It is also possible to isolate the SVC and coronary sinus if there are triggers of AF present here. New tools are available to deliver a \200\230one shot \200\231 ablation lesion that can is olate a PV. The most widely tested is the cryoballoon that delivers cryoablation via a ball oon in \202 ated in the LA and advanced into each PV over a guide wire. Clinical results a re similar to conventional techniques but a higher incidence of phrenic palsy has been obse rved. Substrate modi \201 cation Multiple strategies are adopted to achieve this. A catheter maz e is when the LA and RA are compartmentalized by creating long lines of abla- tion within t hem to interrupt the multiple re-entry circuits. Common lines are; LA roof (from the left ( LSPV) to the right superior pulmonary vein (RSPV)), mitral isthmus (left inferior pulmonary vein (LIPV) to the mitral valve (MV) annulus), CS roof (LA septum to LIPV along the poster ior MV annulus), intercaval (SVC to IVC along the lateral RA), RA isthmus (TV to IVC), with in the CS. In addition, complex and fractionated atrial electrograms (CFAEs) are ablated. T hese signals have high-frequency components and little isoelectric baseline. Several hypoth eses exist as CATHETER ABLATION OF ATRIAL FIBRILLATION 569 to their genesis: turning or collision points for wavefronts, spiral rotas that drive AF, o r autonomic nerve ganglia. Regardless of their cause, their ablation slows and terminates A F. AF may organize into a regular atrial tachycardia . This is usually a macro- re-entrant mec hanism and the circuit is de \201 ned by a combination of activation mapping with a 3D sys tem and entrainment. Ablation is delivered to interrupt this. A common circuit runs around the MV and this can be interrupted by a line of ablation between the MV and LIPV. If sinus rhythm is not restored by ablation alone, electrical cardioversion is performed. A \201 nal check is made of PV isolation, and the integrity of lines of block created. D A 2 0 1 0 Fig. 11.8 Cartoon depicting pulmonary vein isolation by wide area circumferential ablation. A catheter is delivered to the left atrium via a trans-septal puncture. Ablation lesions h ave been delivered point by point to create a continuous line around the left superior and inferior PV together. The catheter is seen delivering lesions around the right PVs. 570 CHAPTER 11 Invasive electrophysiology Complications of AF ablation The risk exceeds that of standard SVT, with immediate procedural major complications occurr ing in 3 % . \200 Bleeding : groin complications are higher risk due to procedural use of heparin and/or warfarin Stroke/TIA (1 % ): risk higher due to extensive ablation in LA \200 Cardiac tamponade (2 % ): the most frequent major problem due to a hole created during ablation. Small pericardi al effusions may need no treatment but tamponade requires pericardiocentesis and reversal o f anticoagulation. An ECHO is mandatory if there is any episode of hypotension in the posto perative period Pulmonary vein stenosis : this is now unusual as ablation is performed at the atrial aspect of the PV. To give symptoms, \211 1 PV needs to be severely narrowed ( > 75 % ) or occlu ded. It presents insidiously with progressive dyspnoea, fatigue, cough, haemoptysis, and re current chest infections. Investigate by contrast CT, MR and ventilation \200\223perfusion (V/Q) scan. Angioplasty can be performed Atrio-oesophageal \201 stula : a rare but usually fatal complication caused by ablation t hrough the posterior LA. Great caution should be taken when ablating in this area (low powe r, short RF times) Phrenic nerve palsy : the course of the right phrenic nerve makes it vulnerable to damage during ablation of the lateral RA or right PVs. Paralysis of the right hemidiaphragm can occur; however, there is almost always full recovery within a few months , with long-term problems being unusual Atrial tachycardia occurs in 10 \200\22340 % of patients within 3 months; persistent > paroxysmal. This may cause much worse symptoms than AF, as the ventricular rat e is faster and more dif \201 cult to control. Cardioversion, antiarrhythmic drugs, AV nod al blocking drugs can be used as a temporizing measure but further ablation is often needed . This page intentionally left blank 572 CHAPTER 11 Invasive electrophysiology Mechanism of AV re-entry tachycardias In young patients with paroxysmal regular narrow comp lex tachycardia, the diagnosis is either atrioventricular node re-entrant tachycardia (AVNR T) or atrioventricular re-entrant tachycardia (AVRT). The mech- anism of both is re-entry ( see b Fig. 11.10 , p. 575). 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. 11.2) and an EPS carrie d out (see b Table 11.2, p.551). Look for evidence of dual AVN physiology and presence of a n 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, BB block, and at the onset and te rmination of tachycardia. His synchronous ventricular premature beats (HSVPBs) are introduc ed 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 AVN jump immediately followed by tachycardia: AVNRT. \200 Loss of pre-excita tion followed by tachycardia: AVRT. Termination \200 Last tachycardia complex atrial (blo ck 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 The aim is to introduce a ventricular paced bea t exactly coincidental with the His potential during tachycardia, to see whether the ventri cle is an essential component of the re-entry circuit (Fig. 11.8). To do this the cycle len gth of the tachycardia is measured and a single sensed extrastimulus is delivered from the catheter in the RV at 20 ms less than the cycle length. This is repeated, reducing the coup ling interval by 10 ms each time, until it is clear the sensed extra is pre-His. Tachycardi a is then terminated and the electrograms analyzed. Analysis (Fig. 11.9): the HH and AA intervals are measured to ensure a stable tachycardia. The paced VPB must be synchronus with the His potential. The AA interval before and after t he 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 potential) and that the ventricle is part of the re-entry circuit hence AVRT. If the A is not advanced it suggests this is AVNRT. MECHANISM OF AV RE-ENTRY TACHYCARDIAS 573 1000 HRA 298 ms 260 ms 302 ms 350 ms HIS 9 \200\22310 HIS 7 \200\2238 HIS 5 \200\2236 HIS 3 \200\2234 H H H HIS 1 \200\2232 304 ms 306 ms CS 9 \200\22310 CS 7 \200\2238 CS 5 \200\2236 CS 3 \200\2234 CS 1 \200\2232 I aVf V1 V6 1000 Fig. 11.9 HSVPBs resetting tachycardia. From top to bottom; intracardiac electro- grams fro m high right atrium, His bundle catheter (proximal to distal), CS catheter (proximal to dis tal), and 4 surface ECG leads. The tachycardia cycle length is approximately 300 ms. During tachycardia the earliest atrial activation is at the distal coronary sinus (lateral left a trium) \200\224 see 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 by a left lateral pathway. 574 CHAPTER 11 Invasive electrophysiology Ablation of AV re-entry tachycardias AVRT Ablation must be performed during ventricular pac ing or AVRT to identify the location of the AP (unless it is manifest on the resting ECG i. e. WPW). The earliest atrial activation is looked for with an almost continuous V then A el ectrogram. Its general location is found by bracketing it with a diagnostic catheter on the valve annulus, i.e. the CS catheter on the left side or a multipolar catheter on the right side. The precise location is then found with the ablation catheter. A true annular site i s needed for success, so an equal-sized atrial and ventricular component on the mapping cat heter is looked for. Left-sided APs are approached either retrogradely (via the aortic valv e and LV) or anterogradely (trans-septal puncture). AVNRT The target is the slow AVN pathway (see b Fig. 10.9, p. 499). This is found inferior to the His bundle, close to the mouth of the CS. The pres- ence of a slow pathway signal (b ump and spike) with a small A and large V component should be seen. Energy is delivered, an d usually transient slow junctional escape beats are seen as the cells die. If the catheter moves or any AV or VA block occurs, ablation is stopped immediately. If the lesion is ther apeutic, a full EP study is then repeated to test and ensure no AVN damage. A successful pr ocedural outcome is the inability to induce tachy- cardia, and complete loss of dual AV nod al physiology. Conventionally, the presence of a jump and a single ECHO beat is permitted, providing tachycardia cannot be induced. If isoprenaline was needed to induce tach- ycardia , it must also be used during 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. ABLATION OF AV RE-ENTRY TACHYCARDIAS 575 D A 2 0 1 0 D A 2 0 1 0 Fig. 11.10 Cartoon exhibiting mechanisms of SVT. Wavefronts depicted by arrows. Orthodromic AVRT (top panel) via a left-sided accessory pathway (AP). Activation from A to V is down t he atrioventricular node (AVN), then across the ventricular myocardium and back from V to A up the AP, thus completing the circuit. The ventricle therefore is an essential part of th e circuit. Antidromic AVRT (not shown) would activate in the opposite direction. Typical AV NRT (bottom panel) activates from the atrium to the AVN via the slow pathway (zig-zag arrow ) and from the AVN to the atrium via the fast pathway (FP), thus completing the circuit. Th e ventricle is activated as a bystander via the bundle of His and is not an essential part of the circuit. 576 CHAPTER 11 Invasive electrophysiology Accessory pathways (Wolff \200\223Parkinson \200\223White syndrome) De \201 nitions and EC G 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 connection in normal hearts. Abnorma l accessory pathways can occur at any position along these annuli and are named accordingly (see Fig. 11.11 ). They may conduct in one or both directions. They 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 predicts the location of the accessory pathway. An AP that conducts only retrogradely is described as concealed. Wolff \200\223Parkinson \200\223White (WPW) syndrome strictly refers to APs that are both m anifest as pre-excitation on the resting ECG and cause tachycardia. Tachycardias An AP can be associated with tachycardia by several mechanisms: \200 orthodr omic AVRT (commonest, accounts for 95 % of AP mediated tachycardias) \200\224 narrow complex tachycardia \200 antidromic AVRT \200\224 broad c omplex tachycardia \200 bystander \200\224 SVT of another etiology that conducts down th e AP. Prognosis AF in the presence of an AP can be dangerous, as the ventricle is not protected b y the decremental behavior of the AV node. This can pre- cipitate VF and sudden death. If p atients are discovered incidentally, and are truly asymptomatic, then sudden death is extre mely rare (between 1 in 2000 and 1 in 20 000 per annum). Invasive EP can be used to risk st ratify patients. A worse prognosis is predicted by: invasive EP testing: 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 \200 multiple APs symptomatic tachycardia \200 Ebstein \200\231s anomaly. ACCESSORY PATHWAYS (WOLFF \200\223PARKINSON \200\223WHITE SYNDROME) 577 Anterior Left lateral His TV Septal MV CS Right lateral Posterior Fig. 11.11 Tricuspid (TV) and mitral valve (MV) annuli. Accessory pathways can be positione d anywhere on the annuli. They are named anatomically, i.e. anterior, left anterolateral, l eft lateral, left posterolateral, etc. Anteroseptal pathways are close to the His bundle an d AV node and are termed parahisian. 578 CHAPTER 11 Invasive electrophysiology Accessory pathways: localization See Fig. 11.12 . R/S \211 1 V2 Yes No \224 (+) \224 (+) III Yes No Yes No LL/ LAL \224 (+) \224 (+) \224 ( \200\223) V1 Yes Yes Yes No No No RAS/ RA LL/ LAL RPS MS V1 R/S \211 1 AVF \224 No Yes \200\223 + LP/ LPL RP/ RPL LPS RL RAL Fig. 11.12 Algorithm to locate the accessory pathway from the ECG with pre-excitation. G = delta wave; reprinted from Chiang et al (1995). Am J Cardiol 76 (1): 40 \200\2236, with per mission. ACCESSORY PATHWAYS: MANAGEMENT 579 Accessory pathways: management Ablation APs can be cured by catheter ablation, and this is \201 rst-line treatment for symptomatic patients. A catheter is moved around the MV or TV annulus until the AP is located by \201 nding the exact point of: \200 earliest ventri cular activation during SR or atrial pacing \200 earliest atrial activation during ventri cular pacing \200 earliest atrial activation during orthodromic AVRT. Acute success is > 90 % . The complication rate is very low (death 0 \200\2230.2 % , AV nodal block <1 % ). Fo r parahisian AP, the risk of AV nodal block is higher and cryoablation used if available. L eft-sided pathways can be approached via the femoral artery, aorta, and left ventricle, or from the RA by a trans-septal puncture. All symptomatic patients (with tachycardias) should be offered ablation. Asymptomatic young patients (<35 years) or those in a high-risk profession (pilots, divers, etc.) should be c onsidered for invasive EP testing and ablation. However, the risk of sudden death must be b alanced against the 2 % serious complication rate of ablating the pathway (particularly if left sided or parahisian). Pharmacological Flecainide and propafenone slow conduction in the AP without affecting the AV node, and are the preferred agents. Drugs that slow AV nodal conduction only (verapamil and digoxin) should not be used unless inva- sive EP has demonstrated that the AP does not conduct anterogradely (or conducts only very slowly). Unusual pathways Mahaim pathways: These are APs between the RA and RV (atrioventricular) or RA and right bundle branch (atriofasicular). Unlike ordinary APs, they exhibit AV nodal pr operties of decremental conduction and sensitivity to adenosine. They only conduct anterogr adely and mediate an AVRT with a broad complex left bundle branch block (LBBB) appearance. They are successfully treated by catheter ablation. 580 CHAPTER 11 Invasive electrophysiology Mechanism of ventricular tachycardia The improved survival from MI and widespread use of IC Ds has led to a much greater need for invasive management of VT, i.e. ablation. In structur al heart disease, VT almost always has a re-entry mechanism. Normal heart VT may be focal o r re-entry. Structural heart disease (see Fig. 11.13 ) Scarred ventricular myocardium (due to infarctio n, cardiomyopathy etc.) provides the substrate for re-entry as described previously (see b p. 524). Scar acts as a barrier to conduction ( \201 xed block); however, damaged but viab le myocardium will provide areas of slow conduction, which are critical to allow re-entry c ircuits to form. This acts as a source of wavefronts that repeatedly depolarize the rest of the ventricle \200\224 hence monomrphic VT. LV scarring is much more common than RV other than in ARVC. A stable re-entry circuit can break down into chaotic activa- tion, i.e. VF, hence the link between VT and sudden death. Bundle branch VT occurs in severely impaired v entricles, with damage to the conducting system and usually pre-existing bundle branch bloc k. It is due to a re-entry circuit involving the right and left bundles. Normal heart VT RV (and LV) out \202 ow tract VT has a focal mechanism with cells exhibiti ng enhanced automaticity. Fasicular VT is probably a re-entry circuit within either the pos terior (usually) or anterior (rare) hemifascicles of the left bundle. MECHANISM OF VENTRICULAR TACHYCARDIA 581 D A 2 0 1 0 Fig. 11.13 Mechanism of VT in structural heart disease, e.g. post-MI. An area of scar in th e LV myocardium (black) provides \201 xed conduction block. Electrical wavefronts (arrows ) rotate around and slowly through the scar to form a re-entry circuit. This acts as a sour ce of wavefronts to the rest of the ventricle. The area of slow conduc- tion (zig-zag arrow s) is termed the diastolic pathway as it activates during ventricular diastole. During VT, intracardiac electrograms recorded here time with the midpoint between successive QRS compl exes. This is the target for ablation of VT. 582 CHAPTER 11 Invasive electrophysiology Ablation of ventricular tachycardia Clinical indications \200 Recurrent symptomatic parox ysms of VT \200 To reduce the number of therapies delivered by an automated ICD (AICD) \200 Incessant VT Activation mapping VT (see Fig. 11.14) To successfully map the re-entry circuit, the patient must be in VT and therefore it needs to be haemodynamically well toler ated. Remote de \201 - brillation paddles are attached to the patient so that if VF or hyp otensive VT occurs, it can be immediately cardioverted. If feasible, the LV is accessed both retrogradely via the femoral artery and aortic valve a nd anterogradely via the femoral vein and a trans-septal puncture. Using a 3D mapping syste m, the ablation catheter is moved around the LV, recording ICegrams at different sites and timing them to a stable \201 xed reference. The aim is to identify the critical diastolic pathway at which the circuit is most susceptible to destruction. Entrainment of VT This can only be performed on tachycardias with a re-entry mechanism. The ablation catheter is moved around the ventricle to sites where the circuit is expected (i. e. adjacent to areas of scar). By pacing with this cath- eter 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-lead match to the clinical VT, then this i s concealed entrainment. This implies the pacing catheter is within the critical diastolic portion of the circuit. To con \201 rm this when pacing is stopped, the return cycle lengt h (the time from the \201 nal paced beat to the next activation at the catheter) should b e almost identical to the tachycardia cycle length. Ablation technique The standard steps of a VT ablation are: \200 induce VT (Wellen \200 \231s); ensure it is similar to clinical VT and well tolerated \200 map VT to identify th e critical diastolic pathway: very early local ICegram occurring mid-diastole (50 \200\223150 ms ahead of ECG) concealed entrainment during pacing \200 return cycle length (=post pacing interval) < ta chycardia cycle length + 30 ms. deliver RF energy via an irrigated catheter (for deeper lesion) at the site meeting the criteria above if VT is terminated, attempt to reinduce. Substrate ablation of VT If VT is not haemodynami cally tolerated or cannot be induced, then acti- vation and entrainment mapping cannot be p erformed. An alternative is to use a 3D mapping system to create a map of the LV during sin us rhythm. The map displays the voltages of the ICegrams, and hence areas of scar are ident i \201 ed. The re-entry circuit of the clinical VT can be estimated from the 12-lead ECG a nd by pacing at sites on the edge of scar, which, if they are the location of the re-entry circuit driving VT, will give a similar ABLATION OF VENTRICULAR TACHYCARDIA 583 12-lead ECG appearance to the clinical VT. Ablation is delivered between two areas of \201 xed conduction block (scar, mitral annulus) to interrupt theoretical re-entry circuits . Failed ablation If conventional ablation fails, alternative approaches are: \200 ablate t he epicardial surface of the heart by delivering the catheter via the pericardium (as for a pericardial aspiration) alcohol ablation via a small terminal coronary branch subtending the scarred area supporting re-entry. Hence, give the patient a controlled, small MI that destr oys the critical portion of the re-entry circuit cardiac surgical ablation. + 160 Arterial 0 HRA HBEp HBEd RVA I aVF Fig. 11.14 An induced VT at a cycle length of 320 ms (187/min). From top to bottom, a traci ng of arterial pressure, high right atrial ICegram, proximal then distal His bundle ICegram , RV ICegram, then two suface ECG leads. There is no V to A conduction at this rate and the atrium is dissociated form the ventricle. Despite the rapid rate, the systolic BP is maint ained at 100 mmHg, enabling the VT to be mapped if necessary. 584 CHAPTER 11 Invasive electrophysiology Automatic implantable cardioverter de \201 brillators Mirowski implanted the \201 rst au tomatic implantable cardioverter de \201 bril- lator (AICD) in 1980 to manage SCD. Since t hen there has been dramatic improvement in technology, and randomized controlled trial evid ence to support their use in primary and secondary prevention. Initial devices were large a nd placed surgically in abdominal pockets attached to epicar- dial leads. AICDs are now imp lanted in the same way as pacemakers and are often part of a biventricular pacing system. Components The bulk of an AICD box is the battery and capacitors that generate and store th e energy to deliver a de \201 brillation shock. The box is attached to a ventricular \200 \230shock \200\231 lead and often an atrial \200\230pace-sense \200\231 lead. The V lead c ontains one or two shocking coils and a bipolar set of pacing electrodes at its tip. This b oth senses electrograms and can deliver low-voltage pulses to pace the heart if it is too s low (bradycardia pacing), or overdrive if it is too fast, e.g. a ventricular tachycardia (a ntitachycardia pacing, ATP). Microprocessors contain the algorithms that interpret the sens ed elec- trograms to: (1) detect tachycardias; (2) discriminate VT/VF from non- life-threat ening arrhythmia (e.g. AF); (3) deliver therapy. These algorithms contain features that are both programmable and non-programmable.