Summary Syncope is defined as a transient loss of consciousness due to transient cerebral hypoperfusion. It is a frequent reason for consultation in the emergency department and cardiac arrhythmias play an important role in the differential diagnosis. This review article describes the different arrhythmic causes of syncope and their management, as well as the warning signs that should lead one to suspect an arrhythmia. |
Syncope is defined as a complete loss of consciousness characterized by sudden onset, short duration , and spontaneous complete recovery. It is a common condition, representing ~1% of all care in the emergency unit. Syncope occurs due to transient cerebral hypoperfusion, which can be triggered by many different causes. Heart disease represents the second most common cause, accounting for 5-21% of all syncope, with a significant contribution from arrhythmias.
Cardiac syncope occurs due to transient low cardiac output. Loss of consciousness may be facilitated by other concomitant factors that contribute to decreased cerebral perfusion, such as valvular heart disease or left ventricular dysfunction. Atherosclerosis of the cerebral arteries could increase the phenomenon, making arrhythmogenic syncope a frequent event in elderly patients.
A thorough history is a crucial point in the evaluation of patients presenting with syncope. Some findings in the first evaluation of patients presenting with syncope should prompt the clinician to include arrhythmogenic syncope in the diagnostic workup, such as the onset of syncope while sitting or lying down, or syncope preceded by palpitations. Similarly, in patients with structural heart disease (especially in the case of a severely depressed left ventricular ejection fraction) or a pathological resting electrocardiogram (ECG), an arrhythmic cause should always be considered. A list of 12-lead ECG red flags that should prompt the search for an arrhythmic cause is presented in Table 1 .
Syncope related to bradycardia
In this group, syncope is related to a marked decrease in heart rate, which can be transient or persistent over time. Decreased heart rate can be caused by two conditions: sinus node dysfunction or AV conduction disturbances . Many external factors can facilitate bradycardia, such as drugs, electrolyte disorders, or acute myocardial ischemia. These reversible causes should be looked for and corrected before considering other therapies.
Bradycardia-related syncope should be suspected in the presence of sinus bradycardia or conduction abnormalities on the resting ECG. However, these findings do not automatically imply that bradycardia is the cause of syncope. This point needs careful evaluation. In case of an established relationship between syncope and bradycardia and in the absence of reversible factors, cardiac stimulation is the treatment of choice.
Advanced AV conduction disturbances, such as documented third-degree AV block, Mobitz II type second-degree AV block, or alternate bundle branch block, represent clear indications for pacing. Bifascicular block, with or without associated first-degree AV block, and sinus node disease are more complicated conditions.
Donateo et al. conducted a study in patients with syncope and bundle branch block. All patients underwent a standardized conventional evaluation of their syncope, which included echocardiography, Holter monitoring, and stress testing if syncope occurred during exercise. They found that less than half of these patients had a final diagnosis of syncope due to paroxysmal AV block and, therefore, an indication for a pacemaker.
Proceeding to pacemaker implantation without having documented the causality of arrhythmias for syncope ( empirical pacemakers ) may end up with implanted patients presenting with recurrences of syncope. In fact, implantation of patients with undocumented suspected AV block due to bifascicular block can lead to syncope recurrences in 11-14% of patients over one to two years. These figures are even higher for sinus node dysfunction, with recurrences of syncope in up to 25% of patients after two years. This is due to the fact that sinus node disease is frequently associated with a vasodepressor reflex mechanism, which also contributes to syncope, but is not balanced by cardiac stimulation. Finally, empirical stimulation has not been shown to improve survival.
The diagnostic study in case of syncope in combination with sinus bradycardia should include at least 24 hours of ECG monitoring. In patients with documented asymptomatic sinus pauses > 6 seconds, stimulation may be indicated, but only after other concurrent diagnostic options have been ruled out. Implantable loop recorders are a good option in unclear cases to match symptoms and arrhythmia. In case of bifascicular block without documented AV block , the recommended strategy is to perform an electrophysiological study (EPS) to measure the HV interval and implant an event recorder if the EPS findings are inconclusive.
Echocardiography should be performed in all patients before implanting a device to choose the best pacing option. In general, ventricular pacing should be avoided whenever possible as it may cause reduced left ventricular systolic function, especially if it is already impaired or borderline. If a high rate of ventricular pacing is anticipated, patients with a reduced left ventricular ejection fraction <40% should have a resynchronization device implanted . It is worth noting that in patients with left ventricular dysfunction and/or structural heart disease, ventricular arrhythmias should be included in the differential diagnosis even if bradycardia is the most prominent finding on initial evaluation.
Finally, atrial arrhythmias with alternating fast ventricular rates and bradycardic sinus rhythms ( bradycardia-tachycardia syndrome ), can be treated with catheter ablation, avoiding pacemaker implantation. Indeed, in a retrospective analysis, Chen et al. found that 95% of patients with tachycardia-bradycardia syndrome who underwent catheter ablation no longer had an indication for a pacemaker 20.1+/-9.6 months after the procedure. In these patients, including those with symptomatic sinus pauses after cardioversion of spontaneous atrial fibrillation, it is appropriate to consider ablation as first-line treatment.
Syncope related to tachycardia
Tachycardia-related syncope can be divided into supraventricular and ventricular tachyarrhythmias . Differentiating them is crucial, as it has important therapeutic and prognostic implications. Therefore, efforts should always be made to obtain 12-lead documentation of tachycardia. Although supraventricular tachycardias are much less frequently syncopal than ventricular tachycardias, hemodynamic tolerance should not be considered a reliable diagnostic clue . Treatment options for these tachyarrhythmias are much broader than for bradyarrhythmias, including antiarrhythmic medications, catheter ablation, and implantable cardiac defibrillators (ICDs).
Benign supraventricular tachycardia may be a cause of arrhythmogenic syncope, especially in elderly patients with concomitant significant valvular heart disease and atherosclerosis of the supra-aortic vessels. Differential diagnoses include AV nodal reentry tachycardia, atrial flutter, or atrial fibrillation, and more rarely, orthodromic atrioventricular reentry tachycardia and focal atrial tachycardia. Catheter ablation often represents the first-line treatment for these arrhythmias, considering the serious clinical repercussions.
A pattern of ventricular pre-excitation on the ECG should raise suspicion of pre-excited atrial fibrillation as a possible cause of syncope. Catheter ablation would then be the first-line therapy, as this condition could lead to ventricular fibrillation.
Syncope in atrial fibrillation and atrial flutter may be related to rapid ventricular rates, but is more commonly related to concomitant sinus node dysfunction. As mentioned above, treatment of tachyarrhythmia can prevent the need for pacemaker implantation.
Antiarrhythmic drugs can be weighed, taking into account the patient’s concomitant conditions and preferences, but must be carefully selected and monitored, as all antiarrhythmic drugs can also be proarrhythmic and a possible cause of recurrent syncope, whether due to bradycardia or tachyarrhythmia.
Regarding ventricular arrhythmias , if they are documented in a patient with structural heart disease, the ICD is indicated for secondary prevention. Whenever cardiac syncope is suspected based on history and/or resting ECG, ventricular arrhythmia should always be considered in patients with structural heart disease . Therefore, echocardiography has a central role in the initial evaluation. Often, other cardiac imaging modalities will be required, such as cardiac MRI , supplemented or not by other modalities depending on the clinical context, such as 18-FDG positron emission tomography.
Implantable cardiac defibrillators (ICDs) should always be considered in case of syncope, when the left ventricular ejection fraction is ≤35%.
Patients with monomorphic ventricular tachycardia and a structurally normal heart less frequently present with syncope. In these patients, the indication for an ICD is weaker, since a comprehensive study that usually includes cardiac MRI has ruled out structural heart disease. Implantable cardiac defibrillator (ICD) will certainly be considered if the arrhythmia cannot be cured with catheter ablation or if antiarrhythmic medications fail to prevent recurrences of the arrhythmia. Arrhythmogenic right ventricular dysplasia should be considered in the differential diagnosis in case of premature ventricular extrasystoles of the left bundle branch block type.
It is important to note that an implantable cardiac defibrillator (ICD), when indicated, will treat the arrhythmia once it is present, but will not be able to prevent it . Therefore, in case of documented ventricular arrhythmias, catheter ablation and/or antiarrhythmic medications should also be used in these patients for arrhythmia prevention.
Finally, arrhythmogenic syncope may be due to polymorphic ventricular tachycardia or torsade de pointes in the context of congenital or acquired channelopathies. A positive family history or a pathological 12-lead ECG may indicate hereditary arrhythmogenic heart disease. If suspected, patients should be referred for a comprehensive workup, including exercise testing for catecholaminergic polymorphic ventricular tachycardia (CPVT) or ajmaline testing for Brugada syndrome . Genetic testing based on clinical data may also be considered to complete the examination.
Congenital long QT syndrome can be very difficult to diagnose and may require the use of provocative maneuvers to unmask it (such as an exercise test or dynamic measurement of the QT interval during acceleration of the heart in response to standing). The management of catecholaminergic polymorphic ventricular tachycardia (CPVT) and congenital long QT syndrome includes beta blockers, with nadolol and propranolol having the best evidence. Patients should be instructed to avoid some medications and situations, depending on the condition. ICD implantation may be indicated, but should be carefully considered, especially in young patients and according to the suspected diagnosis.
The most prevalent condition is the acquired form of long QT syndrome, which can cause torsade de pointes . A severely prolonged QT interval > 500 ms confers a two- to threefold risk of developing torsade de pointes . A prolonged QT interval (corrected QT interval of ≥450 ms in men or ≥460 ms in women) is common and often overlooked.
In a study published by Pasquier et al in 2012, 22.3% of patients admitted to internal medicine had a prolonged QT interval, especially in the case of liver diseases or polypharmacy. Furthermore, in this study, 50.8% of these patients received QT prolonging drugs during their hospitalization. The QT interval should always be assessed on a 12-lead ECG before initiating medications that may prolong the QT interval. You can find a complete list of these medications online at www.crediblemeds.org. In patients with a prolonged QT interval, reversible factors , such as drugs and electrolyte disorders, should be sought and corrected. Bradycardia-induced QT prolongation can also cause torsade de pointes that can be treated with pacemakers.
Key points
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