Indications

EP testing can provide important diagnostic information in patients presenting with syncope. The results of EP testing can be useful in establishing a diagnosis of sick sinus syndrome, carotid sinus hypersensitivity, heart block, supraventricular tachycardia (SVT), and ventricular tachycardia (VT). The indications for EP testing in the evaluation of patients with syncope are outlined in detail in the European Society of Cardiology (ESC) Guidelines on Management of Syncope (Table 29-1).¹ It is generally accepted that EP testing should be performed in patients when the initial evaluation suggests an arrhythmic cause of syncope (class 1). This group of patients includes those with an abnormal electrocardiogram (ECG), structural heart disease, or both. Patients whose clinical history suggests an arrhythmic cause of syncope and those with a family history of sudden death are also included in this group. It is also generally accepted that EP testing should not be performed in patients with a normal ECG and no heart disease and in whom the clinical history does not suggest an arrhythmic cause of syncope (class 3). Class 2 indications for performing an EP study are shown in Table 31-1. These indications suggest that EP testing is appropriate when the results may affect treatment and in patients with “high-risk” occupations, in which case every effort should be expended to determine the probable cause of syncope.

Table 29-1 Indications for Electrophysiology Testing in the Evaluation of Patients with Syncope

Electrophysiology Testing Protocol

When EP testing is undertaken in a patient with syncope, a comprehensive EP evaluation should be performed. This should include an evaluation of sinus node function by measuring the sinus node recovery time (SNRT) and an evaluation of atrioventricular (AV) conduction by measurement of the H-V interval (His bundle to ventricle conduction time) at baseline, with atrial pacing, and following pharmacologic challenge with intravenous procainamide. In addition, programmed electrical stimulation using standard techniques should be performed to evaluate the inducibility of ventricular and supraventricular arrhythmias. The minimal suggested EP protocol recommended by the ESC is provided in Table 29-2. Although the minimal suggested EP protocol recommended by the ESC includes only double extrastimuli and two basic drive train cycle lengths, it is common practice in the United States to include triple extrastimuli and three basic drive train cycle lengths. It is also common practice to limit the shortest coupling interval to 200 ms. In select patients, when a ventricular arrhythmia is highly suspected, EP testing with atrial and ventricular programmed stimulation may be repeated after an infusion of isoproterenol. In my experience, this is of particular importance in the presence of suspicion of a supraventricular arrhythmia such as AV nodal re-entrant tachycardia or orthodromic AV reciprocating tachycardia as the cause of syncope.

Table 29-2 Minimal Suggested Protocol for Electrophysiology Testing for the Diagnosis of Syncope

Assessment of Sinus Node Function

Sinus node function is evaluated during EP testing primarily by determining the SNRT, which is determined by pacing the right atrium at cycle lengths between 600 and 350 ms for 30 to 60 seconds. The SNRT is defined as the interval between the last paced atrial depolarization and the first spontaneous atrial depolarization resulting from activation of the sinus node. The SNRT is corrected for the underlying sinus cycle length (SCL) and expressed as the corrected SNRT (CSNRT = SNRT – SCL). An SNRT longer than 1.6 seconds or a corrected SNRT greater than 525 ms is generally considered abnormal. A secondary pause is defined as an inappropriately long pause between the beats that follow the first sinus recovery beat after atrial overdrive pacing. Evaluation of secondary pauses increases the sensitivity of the SNRT in the detection of sinus node dysfunction. Identification of sinus node dysfunction as the cause of syncope is uncommon during EP tests (<5%). The sensitivity of an abnormal SNRT or CSNRT is approximately 50% to 80%. The specificity of an abnormal SNRT or CSNRT is greater than 95%.² The prognostic value of an abnormal CSNRT or SNRT has not been well defined. Gann and colleagues demonstrated a relationship between an abnormal SNRT and the effect of pacemaker placement on symptoms.³ Another study reported that patients with a markedly prolonged CSNRT (>800 ms) had a risk of syncope eight times higher than that with CSNRTs less than 800 ms.⁴ It is important to note that the absence of evidence of sinus node dysfunction during EP testing does not exclude a bradyarrhythmia as the cause of syncope.⁵

Assessment of Atrioventricular Conduction

During EP testing, AV conduction is assessed by measuring the A-H interval (AV node to His bundle conduction time) and the H-V interval by determining the response of AV conduction to incremental atrial pacing and atrial premature stimuli. If the results of an initial assessment of AV conduction in the baseline state are inconclusive, procainamide (10 mg/kg) may be administered intravenously and atrial pacing and programmed stimulation repeated. According to the 2004 ESC Guidelines on Management of Syncope, the findings at EP study that establish heart block as the probable cause of syncope are bi-fasicular block and a baseline HV interval longer than 100 ms or demonstration of second- or third-degree His-Purkinje block during incremental atrial pacing or when provoked by an infusion of procainamide (Table 29-3).¹ According to these guidelines, the finding of an H-V interval between 70 and 100 ms is of less certain diagnostic value. Among studies that have reported the results of EP testing in evaluating patients with syncope, AV block was identified as the probable cause of syncope in approximately 10% to 15% of patients. Donateo and colleagues reported the results of a systematic evaluation of patients with syncope in the setting of a bundle branch block on their baseline ECG.⁶ Of 347 patients referred for evaluation of syncope, 55 had a baseline bundle branch block pattern. Systematic evaluation of these patients, including EP testing, resulted in a diagnosis of cardiac syncope in 25 patients (45%): AV block in 20 (36%), sick sinus syndrome in 2 (3.6%), VT in 1 (1.8%), and aortic stenosis in 2 (3.6%). Neurally mediated syncope was diagnosed in 22 patients (40%) and syncope remained unexplained in 8 (15%).

Table 29-3 Diagnostic Findings of Electrophysiology Testing for Syncope

The role of EP testing in the assessment of AV conduction and as a predictor of AV block in patients with syncope has been derived from a large number of studies. Scheinman et al evaluated the prognostic value of the HV interval.⁷ The rate of progression to AV block at 4 years was 4%, 2%, and 12%, respectively, for patients with H-V intervals less than 55 ms, 55 to 69 ms, and greater than 70 ms, respectively. The risk of progression to AV block was 24% among those with an H-V interval greater than 100 ms. Other studies have investigated the prognostic value of development of intra-His block or infra-His block with incremental atrial pacing. These studies demonstrated that the presence of these blocks in response to incremental atrial pacing is a specific but insensitive parameter. Dini et al, for example, demonstrated that pacing-induced AV block was observed in 7% of 85 patients who were evaluated.⁸ Complete AV block developed within 2 years in 30% of these patients. The diagnostic value of acute intravenous pharmacologic stress testing has been performed with ajmaline, procainamide, and disopyramide. High-degree AV block is seen in approximately 15% of these studies.^8–10 During 24 to 63 months of follow-up, 43% to 100% of these patients develop spontaneous AV block. It has therefore been concluded that induction of AV block during pharmacologic stress testing of AV conduction is highly predictive of development of AV block. It is important to note, however, that a negative EP assessment of AV conduction does not eliminate AV block as the cause of syncope, nor does it exclude that AV block may develop over time. Link et al reported that at 30 months of follow-up, permanent AV block occurred in 18% of patients with syncope who had a negative EP test.¹¹ Similarly, Gaggioli reported that 19% of patients with syncope and a negative EP evaluation developed permanent AV block within 62 months of follow-up.¹²