Electrophysiology testing is usually performed using a femoral vein and/or artery. For recording of atrial activity and atrial pacing, a catheter is placed in the coronary sinus or the right atrial appendage. A multi-electrode catheter is placed at the His position near the anterior aspect of the tricuspid valve. A catheter is also placed in the right ventricular apex for recording and pacing. The following data are acquired from the surface electrocardiogram (ECG): heart rate, PR, QRS, and QT intervals. Pacing threshold, defined as the minimum output required to consistently capture the myocardium, is then determined for each pacing site.

The following basic intervals are measured by analysis of the intracardiac electrograms (Fig. 8-1): the atrial-His (AH) interval (the conduction time from the septal aspect of the right atrium through the atrioventricular [AV] node, and to the bundle of His), and His-ventricular (HV) interval (the conduction time from the His bundle to the earliest ventricular activation on the ECG). Atrial pacing and ventricular pacing are performed to determine the AV (Fig. 8-2) and ventriculo-atrial (VA) block cycle lengths. Thereafter, various refractory periods are determined during extrastimulus testing: an “S2” is delivered progressively shorter cycle lengths after
a series of consecutive “S1” complexes. The effective refractory period is defined as the longest coupling interval that fails to capture the myocardium (the atrial or ventricular effective refractory period) or fails to conduct to the AV node (the AV nodal effective refractory period). Further maneuvers and investigations depend upon the precise indication for the EP study.

A common indication for an EP study is a history of recurrent PSVT. Patients with PSVT typically report symptoms of rapid palpitations, dyspnea, chest discomfort, lightheadedness, and rarely syncope. Patients may also report that they are able to terminate the arrhythmia with vagal maneuvers. The ECG usually shows a regular, narrow-complex tachycardia without obvious P waves (Fig. 8-3). Patients seeking medical attention in the emergency room are usually hemodynamically stable. Intravenous adenosine terminates the tachycardia in most cases.

Patients with an initial episode of SVT without serious symptoms such as angina or syncope may be reassured and are instructed to avoid possible triggers, and to employ abortive maneuvers in case of recurrent symptoms. Electrophysiology study and catheter ablation is a class I indication for patients with recurrent SVT. During the EP study, determination of baseline electrophysiologic data as described above may help elucidate the mechanism of the tachycardia. AV nodal reentrant tachycardia (AVNRT), orthodromic reciprocating tachycardia (ORT) utilizing an accessory pathway as the retrograde limb of the reentry circuit, and atrial tachycardia (AT) account for >95% of cases of paroxysmal SVT.

The ECG during tachycardia may offer clues that help to narrow the differential diagnosis. During AVNRT, atrial and ventricular activation occur nearly simultaneously, resulting in a retrograde P wave at the end of the QRS complex. Electrocardiographically, this results in a pseudo R’ in lead V₁ or a pseudo S wave in the inferior leads (see Fig. 8-3).

In patients with AVNRT, one is usually able to demonstrate the presence of dual (“slow” and “fast”) AV-nodal pathways in the EP laboratory. The fast pathway
typically is associated with a longer effective refractory period and therefore blocks at a longer coupling interval during extrastimulus testing. After anterograde block in the fast pathway, conduction may proceed down the slow pathway resulting in a long AH (and PR) interval. Given adequate time for recovery, the fast pathway then may be engaged retrogradely, resulting in an AV-nodal echo beat. If this sequence of events repeats itself, the result is a sustained tachycardia or AVNRT (Figs. 8-4 and 8-5). The endpoint of the procedure is to render AVNRT noninducible by eliminating or significantly altering conduction over the slow pathway. Catheter ablation of the slow pathway is performed by delivering radiofrequency energy outside the ostium of the coronary sinus, that is, inferior and posterior to the bundle of His (Fig. 8-6).

Patients with a history of SVT and evidence of preexcitation on the ECG (i.e., WPW syndrome) should undergo electrophysiologic evaluation and catheter ablation to eliminate symptoms and the small risk of sudden death. The presence of a delta wave on the ECG during sinus rhythm (Fig. 8-7) suggests that the mechanism of the tachycardia is ORT. During ORT, anterograde conduction proceeds down the AV node and retrograde conduction occurs over the accessory pathway. The result is a narrow QRS-complex tachycardia with retrograde P waves that may be seen within the ST segment. In some patients, the reentry circuit may consist of anterograde conduction over the accessory pathway and retrograde conduction over the AV node, resulting in a wide QRS-complex tachycardia referred to as antidromic reciprocating tachycardia. Some patients with ORT may not demonstrate preexcitation on the 12-lead ECG owing to absent or very slow anterograde conduction over the accessory pathway. The end point of the procedure is elimination of pathway conduction during radiofrequency energy delivery at the atrial or ventricular insertion of the accessory connection (Fig. 8-8).

Atrial tachycardias may arise from the right or left atrium or from the musculature of the coronary sinus. Common sites of origin of focal atrial tachycardias include the crista terminalis, pulmonary veins, tricuspid or mitral annuli, and the inter-atrial

septum. The site of origin is determined by mapping the earliest activation with respect to the P wave on the ECG.

The success rate for ablation of PSVT is >95% and the recurrence rate is very low. The risk of a serious complication such as perforation or thromboembolism is
<1%. The risk of AV block requiring a pacemaker is approximately 0.5% in patients with AVNRT.

In the recent past, an EP evaluation was routinely used to risk stratify patients with coronary artery disease and left ventricular (LV) dysfunction. It was also performed to determine an effective anti-arrhythmic regimen for patients with sustained VT in the setting of structural heart disease. After publication of MADIT II, and SCD-HeFT, EP evaluation in patients with advanced heart disease has become less common. The MADIT (Multicenter Automatic Defibrillator Implantation Trial) II study randomized patients with a prior myocardial infarction and an LV ejection fraction ≤30% to conventional medical therapy or an implantable cardioverter-defibrillator (ICD). The all-cause mortality rate was significantly lower in the ICD group, and as a result ICD implantation in such patients has become standard clinical practice. Due to the clear benefit of device therapy in patients with coronary disease and severe LV dysfunction, electrophysiologic risk stratification is not needed.

Results from the SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) study have been helpful in the management of patients with whose LV performance was less severely impaired (ejection fraction ≤35%). In this study, patients with ischemic or nonischemic disease, and a history of New York Heart Association class II or III symptoms were randomized to optimal medical therapy or optimal therapy and an ICD. Device therapy was associated with a higher survival rate than optimal medical therapy (or optimal medical therapy plus amiodarone). As in the MADIT II study, an electrophysiologic testing was not required as an entry criterion.

Since MADIT II and SCD-HeFT have streamlined the management of patients with ischemic and nonischemic cardiomyopathy, one may question whether there is any role for invasive EP testing in ascertaining the risk of sudden death in this population. In patients who do not qualify for an ICD by way of these landmark studies, EP testing may still be helpful in risk assessment. For example, a patient with a history of myocardial infarction, nonsustained VT, and an ejection fraction of 35% but no history of heart failure would not meet criteria for an ICD according to the aforementioned studies. The results of the MADIT I and MUSTT (Multicenter Unsustained Tachycardia Trial) may be invoked in the management of such patients. In these randomized studies, patients with a history of ischemic cardiomyopathy and nonsustained VT underwent a diagnostic EP study to evaluate for the possibility of inducible, monomorphic ventricular tachycardia. Patients who had inducible sustained, monomorphic VT were randomized to therapy with antiarrhythmic medications or an ICD. In both of these studies, there was a clear benefit of device therapy. Therefore, EP testing may be useful in patients with structural heart disease who otherwise would not qualify for a prophylactic ICD.

Survivors of a cardiac arrest and patients with sustained VT in the setting of structural heart disease should undergo implantation of an ICD for secondary prevention given the demonstrated superiority of device therapy.

Although EP testing has a role in risk stratification in patients with coronary disease and moderate LV dysfunction, its negative predictive value is less than ideal.
For example, in the MUSTT trial, the 5-year rate of cardiac arrest or arrhythmic death was still 24% in patients who were noninducible for VT. Although the event rates were lower than those in patients with inducible VT who were assigned to no therapy, lack of VT inducibility is not necessarily indicative of a low risk of mortality. Also, patients in MUSTT who were inducible for VT were randomized to EP-guided therapy (consisting of antiarrhythmic therapy or possible ICD after drug failure) or no therapy. The results showed that there was no difference in mortality between patients in the EP-guided group who were treated with antiarrhythmic medications and those randomized to no treatment. In fact, a survival benefit was only seen among patients in the EP-guided group who received an ICD. Thus, medical treatment of patients with inducible VT guided by EP testing has little role as stand-alone therapy in patients with structural heart disease.