The strength of a 12-lead ECG, the gold standard for arrhythmia detection, is the ability to assess rhythm from multiple lead vectors. This allows the diagnosis of cardiac structural, electrophysiologic, and metabolic abnormalities, but it is limited by the brief duration of rhythm detection.¹ Therefore, over the prior decades there has been a steady evolution in available options for extended cardiac rhythm monitoring (Figure 14.1).

The Holter monitor, first introduced in the 1960s, typically provides 24 or 48 hours of ambulatory rhythm recording.² This modality has the advantages of relative

simplicity of the device and capability to quantify the arrhythmia burden² but is limited by time-consuming data processing by health care professionals, negative patient acceptance, inability to detect arrhythmias for patients with relatively infrequent symptoms,³,⁴ and a reliance on the patient’s compliance with documenting symptoms.⁵ However, in spite of these limitations, Holter monitoring has been frequently used for the diagnosis, management, and evaluation for recurrence during the treatment of multiple arrhythmic conditions, including atrial fibrillation (AF), the most common arrhythmia encountered in clinical practice.

Because of the need for longer duration of monitoring, particularly among patients with infrequent symptoms suspected to be arrhythmogenic in origin, there has been a need to develop monitors capable of longer duration monitoring. Newer generation event recorders, designed with this need in mind, have been developed. These devices may be divided into two broad categories—loop recorders and postevent recorders. Loop recorders continuously analyze and retain pertinent rhythm information, which may be automatically detected by preset algorithms. Loop recorders may be either internal or external. In contrast, a postevent recorder relies on patient activation during symptoms. Event recorders are considered to be less sophisticated than loop recorders and rely on the patient being able to apply the device directly to the chest area once a symptom occurs.

Generally speaking, data are collected by external loop recorders over a 14- to 30-day interval and are usually transmitted transtelephonically to a monitoring station for analysis.⁵ A well-described limitation with loop and event recorders is the need for proper device activation and transmission of information by the patient. A second limitation with external loop devices is the patient’s reaction to the adhesive chemicals. These limitations have been partially overcome with the advent of the patch recorder. The purpose of this design is to provide a noninvasive extensive rhythm monitoring system utilizing a biosensor patch, which may be combined with cloud-based technology. These devices have become popular owing to their ease of use, leadless design, and minimal intrusion with daily activity.

Another new development in ambulatory rhythm monitoring is the introduction of real-time continuous cardiac monitoring systems that take advantage of the rapid advancement in wireless communication.⁶ The modern technology provided by these systems enables extended continuous cardiac rhythm monitoring, with the added advantage of automatically transmitting collected data to a portable monitor, which may be accomplished via smartphone technology. Software is provided to analyze data for arrhythmia detection. Any suspected arrhythmic event or patient activation is transmitted for prompt analysis. This advancement in design helps overcome the lag time between data collection and analysis, which is particularly useful in situations where potentially life-threatening arrhythmia or high-grade conduction block is identified.

Ventricular arrhythmia may present as sustained or nonsustained ventricular tachycardia (VT), or as premature ventricular complexes (PVCs). These occurrences may be asymptomatic or herald the onset of sudden cardiac arrest. When ventricular arrhythmia (in any form) is suspected, ambulatory rhythm monitoring may play a crucial role in diagnosis and in monitoring response to treatment.

A common referral to cardiology is for the evaluation of palpitations, which, of course, can be caused by a number of factors. Among these, PVCs are a common etiology. Although there is no clear evidence that PVC suppression with β-blockers or antiarrhythmic drugs improves overall survival among patients, the diagnosis can
provide patient satisfaction, offer an opportunity to relieve symptoms, and identify patients who would benefit from screening for structural heart disease. This is particularly relevant when a high PVC burden coexists with left ventricular (LV) dysfunction. Among such patients, LV dysfunction should be considered reversible if there is a high burden of ventricular ectopy, and PVCs should be treated aggressively via medical or catheter ablation therapy.⁷ In a study authored by Deyell et al, a greater than 80% reduction in PVC burden was achieved in 37 of 44 (84%) patients with baseline LV dysfunction undergoing radiofrequency ablation, and LV function normalized within 6 months in 24 of the 37 patients with a depressed baseline ventricular function.⁸ In addition, in a study authored by Singh et al, the hypothesis that amiodarone can reduce mortality among patients with congestive heart failure and asymptomatic ventricular arrhythmias was tested. Although this study demonstrated no significant difference in overall mortality between the two treatment groups, it did demonstrate a greater improvement in mean ejection fraction among patients in the amiodarone group (35.4 ± 11.5 vs 29.8 ± 12.2 at 24 months), presumably through suppression of ventricular arrhythmia.⁹ Based in part on the data from these trials, the Heart Rhythm Society issued a Class I indication for catheter ablation for instances in which declining ventricular function is suspected to be caused by frequent PVCs, and a IIa recommendation for consideration of pharmacologic options.¹⁰