Pre-excitation/Wolf \200\223Parkinson \200\223White (WPW) Resting ST depression >1 mm (i.e. , LVH, digoxin effect) Prior revascularization Vasodilator stress perfusion imaging with adenosine or dipyridamole is recommended in patie nts with LBBB or ventricular pacemakers, as exer- cise SPECT often leads to false-positive septal defects. Patients who are unable to exercise should also undergo pharmacological (ei ther adenos- ine/dipyridamole or dobutamine) stress perfusion imaging (Table 12.8). Although exercise or vasodilator stress perfusion imaging is an AHA/ ACC Class IIB indicati on as the initial test in patients with a normal resting Table 12.7 Summed stress score Score Interpretation 0 \200\2233 Normal 4 \200\2238 Mild 9 \200\22313 Moderate >13 Severe Table 12.8 Indications for pharmacological stress agents Indication Preferred agent Inability to exercise Adenosine/dipyridamole Asthma/COPD Dobutamine High-grade AV block Dobutamine Caffeine/theophylline use Dobutamine LBBB Adenosine/dipyridamole Post-MI Adenosine/dipyridamole Speci \201 c A 2a receptor agonists are now available with fewer side effects. CHAPTER 12 Stress testing and cardiac imaging 496 ECG, this is an appropriate use according to the 2005 ACCF/ASNC Appropriateness Criteria. Other useful applications of SPECT perfusion imaging in patients with coronary disease include the following: \200 \200 \200 \200 Determine lesion severity prior to planned revascularization Assess the response to medical therapy Risk strati \201 cation post-MI Risk strati \201 cation prior to noncardiac surg ery Results of SPECT perfusion imaging provide important prognostic infor- mation in patients w ith coronary disease, in addition to other clinical vari- ables. The risk of future cardiac events is related to the extent and severity of perfusion defects. Viability testing \200 Thallium rest: 24-hour redistribution imaging. Normalization of perfusion on delayed imagin g following reinjection implies viability. Technetium-99m. Tracer uptake >50% of normal imp lies viability. Normal regional function on gated SPECT imaging also suggests viable myocar dium. \200 Acute chest pain \200 Normal rest myocardial perfusion during active chest pain excludes ischemia/infarction with a negative predictive value of 99%. Stress myocardial SPECT perfusion imaging is a valuabl e diagnostic modality in the evaluation of low- to intermediate-risk patients with chest pa in, a nondiagnostic ECG, and normal biomarkers in emergency department chest pain centers ( ACC/AHA Class I indication). High-risk \201 ndings on SPECT Findings with 3% \200\2235% risk of cardiac death or MI pe r year include the following: \200 Transient ischemic dilatation due to global subendocardial ischemia during stress. There is increased risk even if there are no perfusion defects. Large reversible anterior wall defe ct LV systolic dysfunction post-stress Defects in multiple coronary territories Ischemic EC G changes during vasodilator stress Increased lung tracer uptake (>0.5 for thallium-201) du e to increased pulmonary capillary wedge pressure \200 \200 \200 \200 Balanced ischemia Because SPECT imaging measures relative perfusion, a patient with multi- vessel coronary disease where perfusion is globaly reduced with stress may have a relativel y normal, though false-positive study. Ancillary data from the stress protocol (especially abnormal exercise ECG or hemodynamics) and gated SPECT images (i.e., global or regional LV dysfunction) should be carefully review ed for \201 ndings consistent with signi \201 cant coronary disease. PET SCANNING 497 PET scanning Positron emission tomography (PET) is a nuclear imaging technique that uses sh ort half-life radionuclides incorporated into radiopharmaceuticals allowing quantitative as sessment of various aspects of cardiac function in different regions of the heart: \200 \200 \200 Global and regional left ventricular function Myocardial blood \202 ow Myocardial metabol ism: glucose and fatty acid metabolism; myocardial oxygen consumption Pharmacology: innerva tion; myocardial ACE and angiotensin II receptors B-adrenergic and muscarinic receptors; sympathetic Clinical applications In current clinical practice, cardiac PET is used primarily for the a ssessment of myocardial viability and measuring myocardial perfusion in patients with equiv ocal SPECT imaging (i.e., obese patients) (see Fig. 12.14). Myocardial perfusion The radionuclides most commonly used in practice are Rb-82 and N-13 am monia. The advantage of these PET tracers over SPECT tracers is the higher energy of the re sulting photons (511 keV), which dramatically improves image resolution and test speci \201 city by decreasing soft tissue attenuation and scatter. The short half-life of these tracers, however, requires on-sight produc- tion and limits th e application with exercise stress. Interpretation of tomo- graphic PET imaging is similar to that described earlier for SPECT imaging. Identi \201 cation of myocardial viability A valuable clinical application of PET scanning is the determination of myo- cardial viability in patients with ischemic cardiomyopathy wh o may bene \201 t from surgical or percutaneous coronary revascularization. Studies have d emonstrated that PET imaging has high sensitivity for predicting recov- ery of contractile function after revascularization and have also provided major insights into the mechanisms underlying left ventricular dysfunction in patients with coronary artery disease. Perfusion is measured using either Rb-82 or N-13 as described above. Metabolism is assessed using 18- \202 uorine-labeled glucose (FDG), which is taken up by viable myocardial tissu e. A perfusion \200\223metabolism mismatch implies viable hibernating myocardium and predic ts functional recovery following revascularization. Research applications The large variety of compounds available for study using PET permits interro- gation of many facets of cardiac function, providing important in vivo mecha- nist ic information (see Box 12.9). These measurements also allow analysis of the mechanisms und erlying the bene \201 t of established and novel therapies. Examples include the following: Myocardial blood \202 ow and microvascular function: isch emic heart disease, hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic stenosis, s yndrome X. CHAPTER 12 Stress testing and cardiac imaging 498 Myocardial metabolism and cardiac energetics: ischemic cardiomyopathy, dilated cardiomyopat hy. Cardiac autonomic function: hypertrophic cardiomyopathy, dilated cardiomyopathy, arryht hmogenic right ventricular dysplasia, autonomic neuropathy, long QT syndrome. Figure 12.14 Example of an uninterpretable SPECT perfusion study in an obese patient due to signi \201 cant attenuation, scattering, and poor spatial resolution (top). A Rb-82 PET s tudy on the same patient clearly demonstrates normal myocardial perfusion (bottom). PET SCANNING 499 Figure 12.14 (Cont \200\231d.). CHAPTER 12 Stress testing and cardiac imaging 500 Box 12.9 Comparison of PET with conventional SPECT imaging Advantages \200 Short half-life of radionuclides allows ef \201 cient same-day rest/stress protocols \200 \200 \200 Better spatial resolution Accurate attenuation correction, allowing absolut e quanti \201 cation of radiopharmaceutical concentration Can assess perfusion and metabol ism 1/2 is 75 seconds 1/2 is 10 minutes Rb-82 T N-13 T O-15 water T 1/2 is 2 minutes \200 Disadvantages \200 Expensive \200 Limited availability \200 Most tracers require cycl otron for production. Rb-82 is generator produced Dif \201 cult to perform with exercise s tress because of short half-life of tracers EQUILIBRIUM RADIONUCLIDE ANGIOGRAPHY (ERNA) 501 Equilibrium radionuclide angiography (ERNA) ERNA, or multiple-gated (MUGA) blood pool imagi ng, is an accurate and reproducible noninvasive method for evaluating ventricular function using nuclear imaging techniques. Technetium-99m is the most commonly used radioisotope for this purpose. A patient \200\231s red blood cells (RBCs) are labeled, either in vivo or in vitro, with re duced 99mTc and allowed to equilibrate in the blood pool. A gamma camera then obtains image s (counts) gated to the ECG with each car- diac cycle divided into 16 \200\22332 frames whe re the counts are stored. Usually more than 2 million counts are acquired over hundreds of cardiac cycles for adequate image resolution. As with gated SPECT, a regular rhythm is required for optimal perform- ance. The standard views (see Fig. 12.15) are as follows: \200 \200 \200 Anterior Left anterior oblique (LAO) Left lateral A region of interest is drawn over the LV cavity, and LV ejection fraction is determined as End diastolic counts \200\223 End systolic counts End diastolic counts \200\223 Backgroun d counts x 100 The most widely used application of this technique is measurement of LV systolic function. This modality is particularly valuable in serial assessment of LVEF in patients receiving c ardiotoxic chemotherapy (i.e., doxorubicin). Other applications include the following: \200 \200 \200 \200 \200 Ventricular volumes Regional wall motion RV function Diastolic function (peak \201 lling rate, time to peak \201 lling) Stress testing An alternative to ERNA is \201 rst-pass radionuclide ventriculography. Instead of using r adiolabeled RBCs, a bolus of 99mTc-labeled radiopharmaceuti- cal is injected and tracer act ivity is measured in the superior vena cava, through the right heart and pulmonary circulat ion, and into the left heart and systemic circulation. This technique can be used to evalua te LV and RV function, as well as to detect right \200\223left shunts. CHAPTER 12 Stress testing and cardiac imaging 502 Basal Anterolateral Mid Anterior Basal Mid Inferoseptal Apical Septal Lateral LAO Inferolateral Inferoseptal Inferoapical Basal Anterior Mid RAO Inferior Mid Apex Figure 12.15 Standard ERNA views. LAO, left anterior oblique; RAO, right anterior oblique. CARDIAC CT 503 Cardiac CT Cardiac CT has recently become a powerful tool to study cardiac anat- omy. CT sc anning involves measuring the attenuation of a fan-shaped X-ray beam projected around a pat ient, using multiple detectors. The 3-D projection data set is then reformatted to display images in any plane. The most commonly used devices in practice today are multidetector or multislice CT scanner s (MDCT). MDCT scanners use rotating gantries with a temporal resolution high enough to all ow imaging of the beating heart as long as the cardiac rhythm is regular and fairly slow (i .e., <70 bpm). B-Blockers are often given to achieve this. Newer single-source MDCT scanners acquire 256 or 312 slices per gantry rotation. Dual-sourc e scanners have improved temporal resolution that does not necessitate slow heart rates. Electron beam CT (EBCT) has been used extensively for calcium scor- ing. One of the advanta ges of CT over conventional noninvasive testing (i.e., SPECT imaging) is the rapidity of im age acquisition. A comprehensive cardiac CT scan can be acquired in a matter of seconds. Common applications of cardiac CT include the following: Pericardial disease: presence of c alci \201 cation Coronary artery calcium (CAC) scoring CT coronary angiography measurement of pericardial thickness and determine \200 A concern with cardiac CT is incidental noncardiac \201 ndings. These images should be re viewed by or interpreted with a trained radiologist. Another concern, particularly with newer multislice scanners, is the radiation exposure to the patient, which needs to be considered when ordering these tests. ECG-triggered tube cur rent modulation and pro- spective gating can reduce the radiation dose administered. Coronary calcium scoring Because calcium highly attenuates X-rays, CT scanning can detect c alci \201 ed atheromas with great sensitivity. The amount of calcium can be quanti \201 e d using the Agatson score, which is proportional to the total burden of cor- onary atherosc lerosis (Table 12.9). Although the presence of coronary calcium does not necessarily imply obstructive coronary s tenosis, a normal calcium score can exclude signi \201 - cant coronary disease with very h igh accuracy. Likewise, in symptomatic patients with chest pain, the presence of coronary c alcium predicts sig- ni \201 cant coronary stenosis (>50%) with high sensitivity, albeit m oderate speci \201 city. In asymptomatic patients, an abnormal coronary calcium score is a risk factor for future ca rdiac events and may aid in primary prevention strate- gies, especially in patients at inte rmediate risk based on traditional scores (i.e., Framingham). Age- and gender-speci \201 c thresholds should be applied when interpret- ing a calcium score. CHAPTER 12 Stress testing and cardiac imaging 504 Table 12.9 CT coronary artery calcium scoring Score Plaque burden 0 None 1 \200\22399 Mild 100 \200\223399 Moderate (cid:116)400 Severe ACC/AHA 2007 Consensus \200 Routine screening with CAC scoring is not recommended in asymptomatic patients with low or high risk for coronary disease based on Framingham risk score. In patients at intermediate risk, a CAC is reasonable if the results will reclassify the patient as low or high risk an d alter management. Coronary CT angiography This technique evaluates coronary anatomy, unlike stress perfusion imag- ing with assesses the functional signi \201 cance of a coronary stenosis. Current sc anners can provide exquisitely detailed images of coronary anatomy, including bypass grafts . Like invasive angiography, coronary CT requires the administration of iodinated contrast dy e to enhance the vascular lumen and is thus con- traindicated in patients with severe dye a llergy or those at high risk for contrast nephropathy. Signi \201 cant coronary artery calci \201 cation and coronary stents can lead to reconst ruction artifacts, which may limit the ability to accurately interpret the images. Vessel s egments <1.5 mm in diameter may also be dif \201 cult to visualize. Per-patient sensitivity and speci \201 city for signi \201 cant (>50%) stenosis are 98% a nd 88%, respectively. Hybrid CT/SPECT scanners are being stud- ied with the advantage of al lowing the physiological as well as anatomical extent of coronary disease to be measured. Appropriate indications for CT coronary angiography are as follows: Congenital coronary ano malies Evaluate coronary bypass grafts not seen during cardiac catheterization in symptomat ic patients As an alternative to cardiac catheterization in patients with typical symptoms or abnormal stress testing who either refuse an invasive procedure or are at high risk of c omplications Evaluate coronary anatomy in symptomatic intermediate-risk patients with nondi agnostic or equivocal stress test results \200 Coronary CT is not recommended for patients with a low or high pre-test likelihood of signi \201 cant coronary disease. CARDIAC MAGNETIC RESONANCE IMAGING (CMR) 505 Cardiac magnetic resonance imaging (CMR) In the past decade, cardiac magnetic resonance ima ging (CMR) has emerged as an important investigative and clinical tool in the diagnosis and management of a variety of cardiovascular diseases (see Box 12.10). Technique \200 + ions, abundant in vivo due It uses signals produced from protons (H to the large proportion of body being water). When a magnetic \201 eld is applied, the protons align both parallel (majority) and antiparal lel to the \201 eld with a net vector between. Net vector can be altered by applying diff ering types of short radiofrequency pulses. On cessation of this secondary pulse, the vecto r returns or relaxes to its original position and releases energy in the form of radiowaves . There are two forms of net vector relaxation: longitudinal (T1) and transverse (T2). Type s of CMR \200 Spin-echo contrast, and \202 owing blood appears dark. Gradient-echo and LV function. Flo wing blood (i.e., \202 owing protons) across magnetic gradient has magnetic vectors with phase shift proportional to \202 ow velocity, thus allowing assessment of these dynamic l esions. It has lower soft-tissue contrast with blood \202 ow shown by high signal intensi ty. is used to assess morphology. There is higher soft-tissue is used to assess shunts, valvular lesions, great vessels Box 12.10 Cardiac magnetic resonance imaging Advantages \200 \200 Rapid scanning sequences Gives anatomical, hemodynamic and functional information from same scan Noninvasive High spatial resolution No ionizing radiation \200 \200 Disadvantages \200 \200 \200 \200 Claustrophobia \200\224tight, enclosed space within scanner Lack of adequate patient monito ring Expensive Metallic prosthetic implants \200\224becoming less of a problem CHAPTER 12 Stress testing and cardiac imaging 506 Uses of CMR Congenital heart disease \200 Anatomical and hemodynamic assessment of complex abnormalities of the heart and great vesse ls. Ventricular function \200 \200 Assessment of RV/LV function, volume, and mass Assessing response to novel therapies (e.g., stem cell therapy) Aortic disease \200 \200 \200 Aortic dissection \200\224origin, extent, and organ involvement Aneurysms \200\224serial sc ans to assess progression Intramural hematoma, aortic atheroma, penetrating ulcers Valvular heart disease \200 \200 Echocardiography remains the mainstay of assessment. CMR use may be more common as speci \201 city and sensitivity improve. Cardiomyopathies \200 Arrhythmogenic RV dysplasia (ARVD) \200\224RV enlargement/aneurysms, RV dysfunction, fatty replacement of RV myocardium DCM, myocarditis, HOCM, sarcoidosis \200\224mid-myocardial or subepicardial \201 brosis and perfusion abnormalities Cardiac tumors and pericardial disease \200 \200 Anatomical localization and extracardiac involvement Assess vascularity of tumor with gradi ent-echocardiogram Coronary artery disease \200 \200 \200 Coronary anatomy (inferior to CT) Pharmacological stress perfusion with \201 rst-pass gad olinium uptake Assessment of infarct size and viability by delayed myocardial enhancement w ith gadolinium (see Fig. 12.16) CARDIAC MAGNETIC RESONANCE IMAGING (CMR) 507 Figure 12.16 Comparison of in vivo delayed-enhancement CMR images (upper panel) to histopat hology (middle panel) in a canine with subendocardial inferior wall infarction. Correspondi ng SPECT-sestamibi images are also shown for comparison (bottom panel). Adapted with permis sion from Wagner A, Mahrholdt H, Holly TA, et al. (2003). Lancet 361(9355):374 \200\223379. CHAPTER 12 Stress testing and cardiac imaging 508 Metallic prostheses and CMR Ferromagnetism refers to metallic compounds attracted by a magn etic \201 eld; it initially referred to ferrous compounds and their properties in a mag- netic \201 eld (i.e., attraction). Four other metals are also strongly magnetic: cobalt, dysprosium, gadolinium, and nickel. Alloys of these compounds will also exhibit magnetism t o some degree. Most human prosthetic implants are not strongly magnetic as they have impurities added to t he iron to give them added strength and antioxidant properties. Potential for causing injury with CMR and metallic objects There are three main mechanisms for this (see also Table 12.10): \200 Projectile injury refers to external adjunctive equipment, e.g., O2 cylinders, forceps, sci ssors, etc., that is in the MR room. A strong magnetic \201 eld could launch these items across the room with obvious consequences. Ferrous compounds such as these must therefore b e barred from the room or special \200\234MR-safe \200\235 equipment used. Injury can resu lt from internal movement of Implanted prostheses these prostheses. Potential for movement will depend on magnetic properties of the device and on the restraining tissue surrounding it. Thus hip prosthesis has less potential to cause damage than an intracranial arterial cl ip. Electrical currents CMR can induce electrical currents in devices with conductance prop erties, which can cause heating and thermal injury. Examples include pacing wires, guide wi res, and PA catheters. METALLIC PROSTHESES AND CMR 509 Table 12.10 Risk associated with CMR use in patients with metallic devices Device Risk* Coronary stents Currently available stents are safe and can be tested <3T any time after implantation Other vascular stents Similar to coronary stents Guide wires May cause thermal injury (newer CMR-safe ones developed for CMR intervention) Prosthetic valves/rings All valves appear safe. Pacemakers and ICDs Potential for movement, thermal injury, and electrical inhibition. CMR use is associated wi th excess mortality, thus it is NOT currently recommended Intracardiac catheters Polyurethane and PVC ones are safe. Those with metallic component (e.g., PA catheters) will cause thermal injury and are NOT safe IABP/LVAD NOT safe due to thermal injury, movement, and mechanical malfunction ECG leads Standard metallic leads have been associated with burns. Newer carbon-based CMR-compatible leads are available Sternal wires/ epicardial pacing wires Safe, although may cause artifacts NB Always check with the MRI department if concerned. This page intentionally left blank 511 Chapter 13 Invasive electrophysiology Mechanism of tachycardias 512 Mechanism of arrhythmias 514 The electrophysiology study (EPS ) 516 Uses of the EPS 518 Programmed ventricular stimulation 522 New technologies 524 Cathe ter ablation 525 Catheter ablation: complications 527 Atrial tachyarrhythmias: mechanism 52 8 Ablation of atrial tachycardias 530 Catheter ablation of atrial \201 brillation 532 Mec hanism of AV reentry tachycardias 534 AV reentry tachycardias: ablation 536 Ablation of ven tricular tachycardia 538 Accessory pathways (Wolff \200\223Parkinson \200\223White syndrome ) 540 Accessory pathways: localization 542 Accessory pathways: management 543 Implantable c ardioverter de \201 brillators (ICDs) 544 Indications for ICD implantation 545 ICD therapi es 546 ICD: trouble shooting and follow-up 547 CHAPTER 13 Invasive electrophysiology 512 Mechanism of tachycardias Knowledge of how arrhythmia are initiated and perpetuated is fund amen- tal to understanding the techniques described in this chapter. The electrical wavefront The excitable impulse is generated at the cell membrane by the act ion potential (see Chapter 9). As one cell depolarizes, it causes a reduction in negativity of the resting potential in the adjacent cells, causing the adjacent cells to reach thresh old potential and depolarize. The shape, orientation, and presence of gap junctions between myocar- dial cells allow the rapid spread of depolarization, which can be described as an electrical wavefront. After a cell has depolarized, it cannot depolarize again until it repolarizes over a \201 xed per iod of time, the refractory period. Cells that are able to depolarize are excitable, and th ose that cannot are refractory. In sinus rhythm (SR) the source of these wavefronts is the sinoatrial (SA) node, and they a re conducted from the atria to ventricles via the atrioventricular node (AVN). SA nodal imp ulses are initiated at inter- vals largely regulated by the autonomic nervous system and ci rculating catecholamines. This control is lost in tachyarrhythmia and heart rates are inapp ropriate. Conduction block A wavefront will propagate as long as there are excitable cells in its pat h. Anatomical barriers such as the mitral valve annulus, vena cava, and aorta do not contai n myocardial cells; therefore, the progression of wavefronts is halted there. This is descr ibed as \201 xed conduction block, as block is always present. Dead cells are another imp ortant source of \201 xed conduction block, e.g., the left ventricular scar of a myocardi al infarction (MI). Functional conduction block describes block that is only present under certain conditions. An example is myocardial ischemia, which may alter the electrical properties of myocytes su ch that they do not conduct. It is also a functional block that prevents a wavefront from turning back on itself, as the cells behind the leading edge are temporarily refractory and force the wavefront to contin ue in one direction. Other causes of functional block are cyanosis, myocardial stretch, and the rate and direc- tion of the wavefront. Arrhythmia mechanisms Three distinct mechanisms are described: 1. Enhanced automaticity 2. Reentry 3. Triggered activity The \201 rst two mechanisms account for nearly all clinical tachycardias and their charac teristics are compared in Table 13.1. MECHANISM OF TACHYCARDIAS 513 Table 13.1 Characteristics of automatic and reentry tachycardias* Automatic Reentry Autonomic sensitivity? (e.g., to exercise, emotion) Often Unusual* Reproducible induction and termination by programmed stimulation No Yes Entrainment of the tachycardia by pacing? No Yes Induced by atropine/ isoproterenol infusion? Yes May augment induction by pacing Related to metabolic causes Often Unusual Onset/offset May be gradual (warm up and down) Sudden Speci \201 c tachycardias caused Inappropriate sinus tachycardia, focal atrial tachycardia, focal AF, junctional tachycardia SNRT, macro- reentrant atrial tachycardia, AF, AVNRT, AVRT, VT The conduction properties of, e.g., the AV node, are in \202 uenced by autonomic tone. Spo ntaneous or drug-induced changes in this may then in \202 uence the development of reentry tachycardias such as AV-nodal reentry tachycardia (AVNRT). AF, atrial \201 brillation; A VRT, atrioventricular reentrant tachycardia; SNRT, sinus node reentrant tachycardia; VT, ve ntricular tachycardia. CHAPTER 13 Invasive electrophysiology 514 Mechanism of arrhythmias Enhanced automaticity If a nidus of myocardial cells depolarizes faster (rapid phase 4 of t he action potential) than the SA node, it will act as the source of wavefronts that conduct through the heart. It may be atrial or ventricular, but if it occurs in the atria it will override the SA node. As it occurs from a single site it is often termed focal. Common sites are where myocardial cells suddenly change shape or size or are under abnormal pressures, such as the junction of veins and atrium (SVC, PVs), crista terminalis, coronar y sinus (CS), AV node area, mitral/tricuspid ring, and ventricular out \202 ow tracts. Reentry Reentry accounts for >75% of clinical arrhythmias. It is caused by a per- petually propagating wavefront that it is constantly meeting excitable myocardium. For reentry to occur, at least two distinct pathways must exist around an area of conductio n block. This is best described using the example of VT due to reentry around a LV myocardi al scar (see Fig. 13.1). 1. A myocardial scar acts as an area of block, around which a nor- mal sinus wavefront passes via normal myocardium (A) and slowly through it via diseased myo cardium (B) \200\224hence two distinct pathways. 2. The sinus beat is followed closely by a ventricular ectopic, which is conducted around A normally but is blocked in B, which is still refrac- tory following the last sinus beat. 3. The distal end of B, however, is now excitable and the wavefront passes backward up B, which has had time to fully recover by the time it reaches the proxim al end. Conduction is suf \201 ciently slow up B that now A is excitable again and the wav efront can pass down A. Thus a reentrant wavefront has been formed that is constantly meeting excitable myocardium. Triggered activity This has features of both of the above mechanisms. It is caused by spon- taneous (hence automatic) after-depolarizations (ADs) occurring late in phase 3 (early ADs ) or in phase 4 (delayed ADs) of the action potential. These ADs, however, are often trigge red by premature beats and thus are inducible (like reentry). If these ADs reach the thresh old level, then a single or burst of action potentials is set off. The ADs can be induced experimentally by ischemia, QT-prolonging drugs, cell injury, or low potassium. This mechanism underlies torsades de pointes and arrhythmias due to digoxin tox icity. MECHANISM OF ARRHYTHMIAS 515 1 A B A 2 A B A 3 A B A Figure 13.1 Reentry as a mechanism of tachycardia. 1 Normal sinus beat passing around and t hrough scar. 2 Ectopic beat passing around but blocked through scar. 3 Reentry circuit of t achycardia. Dark gray represents scar; light gray, normal myocardium; and white arrows repr esent electrical wavefronts. CHAPTER 13 Invasive electrophysiology 516 The electrophysiology study (EPS) The electrophysiology study (EPS) is most useful for the diagnosis of tach- ycardia. When tachycardia has been documented or is strongly suspected, it is generally the \201 rst part of a combined procedure with catheter ablation designed to cure the arrhythmia. In EP it is usual to discuss cycle lengths (in ms) rather than heart rates, e.g., 60/min = 1000 ms; 100/min = 600 ms; 150/min = 400 ms. Mapping electrical activity in the heart The EPS is wrongly considered to be complex. Funda mentally, it is just recording of the heart \200\231s electrical signals during sinus rhyth m, arrhythmia, or in response to pacing at speci \201 c sites. The ECG provides a great de al of this information and so a full 12 lead ECG is recorded throughout the procedure. The intracardiac electrogram (Egram) The ECG summarizes the entire cardiac activation. By p lacing 2-mm elec- trodes directly on the heart \200\231s endocardial surface, the electrica l activity at precise locations is known. The Egram is therefore much narrower than the ECG and is best appreciated at 100 mms \200\2231 sweep speed, four times faster than a standar d ECG recording. Either the potential difference between two closely spaced electrodes (a bipolar electrogra m) or that between one electrode and in \201 nity (a uni- polar electrogram) can be record ed. The unipolar electrogram is more accurate regarding direction and location of electrica l activity; however, it is subject to much greater interference. A pacing current can be passed through any of these electrodes. Standard catheter location is shown in Figure 13.2. Pacing protocols Pacing in the EPS is done in a prede \201 ned manner, termed programmed s timulation. This has three forms: 1. Incremental pacing: the pacing interval is started jus t shorter than the sinus interval and lowered in 10-ms steps until block occurs or a predetermined lower l imit (often 300 ms) is reached. 2. Extrastimulus pacing: following a train of eight paced beats at a \201 xed cycle lengt h, a further paced beat (the extrastimulus) is introduced at a shorter coupling interval (t he time between the last stimulus of the drive and the \201 rst extrastimulus). The stimu li of the drive train are conventionally termed S1, the \201 rst extrastimulus S2, the se cond extrastimulus S3, and so on. Extrastimuli can also be introduced after sensed heart be ats (singles in sinus or sensed extras). 3. Burst pacing is pacing at a \201 xed cycle length for a predetermined time. Catheters have been passed into the right heart from sheaths in the fem- oral and subclavia n veins under \202 uoroscopic guidance. These images from the right anterior oblique (abo ve) and left anterior oblique (below) dem- onstrate the standard positions at the high righ t atrium (HRA) close to the SA node, on the His bundle (HIS), and at the RV apex (RVA), as well as a catheter passed through the os of the coronary sinus (CS), which 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.