Europace

Europace 2005 7(1):14-18; doi:10.1016/j.eupc.2004.11.001

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© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.

Proposed electrocardiographic classification of spontaneous syncope documented by an implantable loop recorder

Michele Brignole^a,*, Angel Moya^b, Carlo Menozzi^c, Roberto Garcia-Civera^d and Richard Sutton^e

^aDepartment of Cardiology, Ospedali del Tigullio 16032 Lavagna, Italy; ^bDepartment of Cardiology, Hospital Vall d'Hebron Barcelona, Spain; ^cDepartment of Cardiology, Ospedale S Maria Nuova Reggio Emilia, Italy; ^dDepartment of Cardiology, Hospital Clinico Universitario Valencia, Spain; ^eDepartment of Cardiology, Royal Brompton Hospital London, UK

Manuscript submitted 28 September 2004. Accepted after revision 17 November 2004.

^*Corresponding author. Tel.: +39 185 329 569; fax: +39 185 306 506. E-mail address: mbrignole{at}asl4.liguria.it (M. Brignole).

	Abstract

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Uniform data from the literature show that the mechanism of syncope recorded by implantable loop recorder is extremely heterogeneous and a wide variety of rhythm disturbances is recorded at the time of syncope. Therefore, the proposed classification aims to group the observations into homogeneous patterns in order to define an acceptable standard useful for future studies and clinical practice.

Key Words: syncope, electrocardiographic monitoring, implantable loop recorder

	Introduction

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Knowledge of what occurs during a spontaneous syncopal episode is ideally the gold standard for syncope evaluation. For this reason it is likely that implantable loop recorders (ILR) will become increasingly important in the assessment of the syncope patient, and their use will be definitive instead of the use of many conventional investigations. Uniform data from the literature show that the mechanism of syncope recorded by an ILR is extremely heterogeneous and a wide variety of rhythm disturbances is recorded at the time of syncope. Therefore, the proposed classification aims to group the observations into homogeneous patterns in order to define an acceptable standard useful for future studies and clinical practice.

	Methods

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All the electrocardiographic recordings of the first syncopal episodes observed after ILR implantation in the International Study on Syncope of Uncertain Etiology (ISSUE) study [1–4] were reviewed and classified. The classification has been validated using the consecutive series of the population of the hospitals of Lavagna and Reggio Emilia [5].

	Classification

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In the ISSUE study [1–4], 57 of 198 enroled patients affected by unexplained syncope had a syncopal recurrence recorded by ILR. Their tracings were classified as reported in the Table 1. Type 1 (asystole) was the most frequent finding which was observed in 63% of patients (Fig. 1–Fig. 3); type 2 (bradycardia) was observed in 5% of patients (Fig. 4); type 3 (no or slight rhythm variations was observed in 18% of patients (Fig. 5); and type 4 (tachycardia) was observed in 14% of patients (Figs. 6 and 7).

View larger version (28K): [in this window] [in a new window]   Figure 1 Type 1A, sinus arrest. Panel A. Heart rate trend during 42 minutes of loop recording. Initially, the heart rate is stable at approximately 70 bpm; at the beginning of the episode the heart rate increases to 100 bpm, then decreases rapidly to a very low rate. Panel B. The expanded electrocardiogram at the time of syncope shows prolonged multiple pauses due to sinus arrest. The noise recorded during the pauses of 8 s and 19 s of asystole probably reflects jerking movements of the patient. The finding of initial sinus tachycardia progressive sinus bradycardia frequently followed by sinus arrest has been regarded as highly suggestive of a neurally mediated mechanism.

 

View larger version (19K): [in this window] [in a new window]   Figure 2 Type 1B, Sinus bradycardia plus AV block. Progressive sinus bradycardia to <30 bpm followed by AV block (and long ventricular pauses) with concomitant severe bradycardia. The association between AV block and sinus arrest suggests a neurally mediated mechanism.

 

View larger version (25K): [in this window] [in a new window]   Figure 3 Type 1C, AV block. Panel A. Heart rate trend during the whole 21 min loop recording. Initially, the heart rate is stable at approximately 80 bpm and suddenly falls at the time of the syncope. Panel B. The expanded ECG shows blocked P waves with 2 main pauses of 5 and 6 sec duration. The sinus rate increases during AV block. The noise recorded during the second pause probably reflects jerking movements of the patient. The sudden onset AV block (and ventricular pause) with concomitant increase in sinus rate is opposite to the finding in Figs. 1 and 2 and suggests a different mechanism, namely intrinsic disease of the His-Purkinje system as observed in Stokes-Adam attacks.

 

View larger version (18K): [in this window] [in a new window]   Figure 4 Type 2, Bradycardia. The initial sinus tachycardia 90 bpm is followed by progressive sinus bradycardia to <30 bpm for >10 seconds.

 

View larger version (10K): [in this window] [in a new window]   Figure 5 Type 3 A. No variation or <10% variation in heart rate. Heart rate trend during 21 minutes of loop recording. Heart rate is approximately 60 bpm and remains stable throughout the recording period. The triangle () indicates the time when the patient activated the recording after resuming consciousness. The pattern of almost no variation in heart rate excludes the participation of a cardiac reflex in the genesis of the loss of consciousness; this means that reflex syncope is also unlikely, though it cannot be definitely ruled out.

 

View larger version (16K): [in this window] [in a new window]   Figure 6 Type 3 B. Heart rate trend during 7 minutes of loop recording. Initially, the heart rate is approximately 90 bpm; it progressively increases to 120 bpm in a few minutes, then progressively decreases to 100 bpm. That value is reached roughly 1 minute before multiple device activations by the patient () and thus is likely to coincide with the loss of consciousness. The pattern of a progressive increase and then decrease in heart rate is similar to the pattern observed during tilt testing in the patients who have a typical mixed vasovagal response.

 

View larger version (18K): [in this window] [in a new window]   Figure 7 Type 4 A. Progressive sinus tachycardia. Heart rate trend during 7 minutes of loop recording. Initially, the heart rate is approximately 100 bpm; it then progressively increases to 130 bpm, a value reached approximately 1 minute before device activation by the patient () and thus likely to coincide with the loss of consciousness. The pattern of progressive heart rate increase is similar to a pattern observed in some patients during tilt testing; this pattern is characterized by progressive tachycardia and hypotension and variously defined as ‘Excessive heart rate rise’ or ‘Orthostatic intolerance’. This behaviour suggests that heart rate increases as part of an inadequate compensatory attempt and indicates sympathetic arousal.

 

View this table: [in this window] [in a new window]   Table 1 The ISSUE classification of ECG-documented spontaneous syncope

 
In the validation cohort, 52 of 103 patients had a syncopal recurrence recorded by ILR. Type 1, 2, 3 and 4 were observed in 48%, 8%, 27% and 17% respectively of patients (P=0.6 vs ISSUE data, not significant).

	Discussion

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With ILR we have only electrocardiographic recordings but no information concerning arterial blood pressure and other factors that are involved in causing syncope. Despite this limitation, the ISSUE classification has some pathophysiological implications which are helpful to distinguish different types of arrhythmic syncope and have potentially different diagnostic, therapeutic and prognostic implications.

In types 1A, 1B, and 2 the findings of progressive sinus bradycardia, most often followed by ventricular asystole due to sinus arrest, or progressive tachycardia followed by progressive bradycardia and, eventually, ventricular asystole due to sinus arrest suggest that the syncope is probably neurally-mediated [1].

In type 1C, the finding of prolonged asystolic pauses due to sudden-onset paroxysmal AV block with concomitant increase in sinus rate suggests another mechanism, namely intrinsic disease of the His-Purkinje system as observed in Stokes-Adam attacks [2].

In type 3A, the finding of no variation in heart rate excludes participation of a cardiac reflex in the genesis of the loss of consciousness; this means that reflex syncope is also unlikely, though it cannot be definitely ruled out. Alternatively, this type of response could be observed in patients with chronic orthostatic intolerance. However, the cause of syncope remains largely unknown because of the lack of contemporary recording of blood pressure values with the available ILR technology [4]. In type 3B, mild rhythm variations reflect participation of a cardiac reflex in the genesis of the loss of consciousness, the exact nature of which remains uncertain because of the lack of contemporary recording of blood pressure values with the available ILR technology [4].

In type 4A, the finding of progressive heart rate increase at the time of syncope suggests a (primary or secondary) activation of the cardiovascular system. It is very similar to a pattern observed in some patients during tilt testing and variously defined as ‘Excessive heart rate rise’, ‘Orthostatic intolerance’ or ‘Progressive Orthostatic hypotension’ [4]. The patients with this feature are unable to achieve a steady-state adaptation to the upright position and, therefore, show a progressive fall in blood pressure until syncope occurs.

Finally, in types 4B, 4C and 4D a primary cardiac arrhythmia is typically responsible for syncope.

	References

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[1] Moya A, Brignole M, Menozzi C, et al. Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope. Circulation 2001; 104: 1261–1267.[Abstract/Free Full Text]

[2] Brignole M, Menozzi C, Moya A, et al. The mechanism of syncope in patients with bundle branch block and negative electrophysiologic test. Circulation 2001; 104: 2045–2050.[Abstract/Free Full Text]

[3] Menozzi C, Brignole M, Garcia-Civera R, et al. Mechanism of syncope in patients with heart disease and negative electrophysiologic test. Circulation 2002; 105: 2741–2745.[Abstract/Free Full Text]

[4] Brignole M, Menozzi C, Moya A, et al. Non-arrhythmic syncope documented by an implantable loop recorder (An ISSUE substudy). Am J Cardiol 2004; 90: 654–657.

[5] Solano A, Menozzi C, Maggi R. Incidence, diagnostic yield and safety of the implantable loop-recorder to detect the mechanism of syncope in patients with and without structural heart disease. Eur Heart J 2004; 25: 1116–1119.[Abstract/Free Full Text]

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