Physical examination and cardiac auscultation are unreliable for differentiating supraventricular from ventricular premature beats. The least expensive yet reliable method to document these arrhythmias is a standard 12-lead ECG with a short rhythm strip. Unfortunately, with an ECG the cardiac rhythm is monitored only for a short period. Considering that the commonly accepted definition of “frequent” ventricular ectopy is more than 10 to 30 PVCs an hour, it becomes easy to see how even “frequent” PVCs can be overlooked by this method. On the other hand, if any PVCs are noted on a short rhythm strip, it is likely that the patient has both frequent and complex ventricular ectopy. Both would probably be detected during a longer period of monitoring, such as a Holter monitor study.
In the past, Holter recordings of only a few hours’ duration were used for arrhythmia detection. Although practical and economical, such brief recordings do not accurately reflect the severity of cardiac arrhythmias in many individuals. This point is best illustrated by reviewing what is known about the frequency of ventricular arrhythmias over the course of a 24-hour period. Simply stated, even with the same patient, a tremendous amount of spontaneous variability in PVC frequency exists between one Holter recording and another. Similarly, marked variability in PVC frequency also occurs in patients with chronic ventricular arrhythmias. PVC frequency varies greatly from one day to the next, between successive 8-hour monitoring periods, and even from hour to hour within a single day. Certain individuals exhibit PVCs primarily during the day; others manifest them principally at night. As might be expected, PVC frequency often varies with physical activity and emotional state. However, in many individuals, marked spontaneous variability in PVC frequency persists even when monitoring conditions are kept absolutely constant.
Because of such fluctuations in PVC frequency, a monitoring period of at least 24 hours has become the standard for adequate characterization of an arrhythmia, and thus Holter monitors are generally worn for 24 hours, though occasionally the time period is extended to 48 hours. For most individuals, 24-hour monitoring not only permits recognition of diurnal variations in arrhythmias, but it also allows detection of the maximal grade of ectopy.
The key caveat of 24-hour Holter monitoring is that no conclusions can be reached about whether a symptomatic arrhythmia exists unless symptoms occur during the 24 hours of monitoring. As noted previously, a patient may even have a malignant symptomatic ventricular arrhythmia that occurs only intermittently, sometimes as infrequently as once every few weeks. Event monitors, either in the form of a “postevent” device that necessitates patient activation or more commonly a continuously recording pre-event (“loop”) device, circumvent the short time limitation of the Holter monitor, as patients use these devices for several weeks at a time.
Although many variations of event monitoring exist, patients are generally issued a device that transmits the patient’s rhythm over the telephone. Usually the equipment remains with the patient for a few days or weeks. For cases of extremely infrequent arrhythmias, subcutaneously implanted units may be used for months. The principal weakness of the postevent monitor is that patients must be aware of arrhythmias when they occur, and they must maintain consciousness long enough to capture or transmit the rhythm. In the case of pre-event (“loop”) recorder, the patient can activate the device after regaining consciousness, and the preceding data will be saved. Some loop recorders can be programmed to detect asymptomatic arrhythmias and alert the patient to transmit data for evaluation. These automatic detection devices typically have greater data storage capability because they may not reliably discriminate arrhythmias from artifact, potentially creating a lot of false-positive events.
In the past, most clinicians began with full 24-hour Holter monitoring and then proceeded to event monitoring only for those cases when symptoms persisted despite negative Holter findings. However, because asymptomatic Holter results are often complicated and confusing and there is a low yield of positive findings on Holter monitoring when arrhythmias are infrequent, event monitoring is now more commonly ordered than Holter monitoring. Overall, event monitoring is at least as effective as Holter monitoring for detection of symptomatic arrhythmias; event monitoring also has the advantage of less frequently recording asymptomatic background arrhythmias (for which treatment is unnecessary). In the case of syncope and the evaluation of unexplained palpitations, the diagnostic yield of pre-event loop recorders over Holter monitors has been validated, and is the preferred initial AECG modality (Kinlay and colleagues, 1996).
When Holter or event monitoring results are equivocal, EP studies may be helpful. Although EP is an invasive study, the information obtained may be critical. Patients in whom a clinically relevant arrhythmia can be induced during EP testing usually have a worse prognosis, even if asymptomatic, than patients in whom an arrhythmia cannot be induced. However, EP testing does have a small but significant false-negative rate; results in patients with nonischemic cardiomyopathy are also difficult to interpret.
SAECG is a noninvasive test that has been advocated for risk stratification in potentially lethal ventricular arrhythmias. Although its main initial use was following MI, SAECG use has expanded to include patients with cardiomyopathies, Brugada syndrome, arrhythmogenic right ventricular dysplasia, mitral valve prolapse, ventricular aneurysms, and idiopathic VT. By computer-averaging signals for several hundred recorded beats, background “noise” can be filtered out to allow detection of low-amplitude, high-frequency late potentials after the QRS. These late potentials are suggestive of areas of slower conduction that may facilitate development of ventricular reentry. Unfortunately, the positive predictive accuracy of late potentials on SAECG following MI is less than optimal, around 15% to 20% for prediction of VT or ventricular fibrillation (VF). Therefore, negative findings on this test are more useful. SAECG is of established value in the evaluation of the syncope patient, but only in the setting of ischemic heart disease, and again its value is in its negative predictive accuracy.
Exercise ECG testing (EET; see Chapter 93, Exercise Electrocardiography [Stress] Testing) is a common method for evaluating PVCs (especially in older patients or those with coronary risk factors) and other arrhythmias (especially exercise-induced arrhythmias). It serves as a convenient, noninvasive test to screen for or to diagnose underlying CAD. EET may be indicated if ischemia is diagnosed with AECG. If CAD is diagnosed, EET can also evaluate its severity and assist with its management. EET also demonstrates what effect exercise has on arrhythmias. In general, PVCs that diminish with progressively increasing activity are less worrisome and tend to be associated with a better prognosis than those brought on by low levels of exercise. Recent evidence suggests that PVCs occurring during recovery from EET are associated with increased mortality, whereas PVCs during the EET are not (Dewey and colleagues, 2008). Although not nearly as accurate as Holter monitoring for quantitative or qualitative assessment of PVCs, complex ventricular arrhythmias (including VT) and symptoms are sometimes elicited only by vigorous exercise. Chronotropic incompetence (unable to obtain heart rate >120 beats per minute) on EET may suggest sick sinus syndrome, which is best diagnosed with a Holter monitor. Holter monitoring and EET may thus be complementary procedures that provide different information, and both tests should sometimes be considered for the complete evaluation of patients with ventricular arrhythmias.
It should be emphasized that detection of PVCs per se on EET is not indicative of an ischemic response. However, PVCs are cause for more concern when they occur in association with evidence of ischemia, such as ST segment depression or substernal chest pain in patients who are likely to have CAD. Thus, it is inadvisable to allow a middle-aged individual who has coronary risk factors to exercise in an unsupervised manner if EET produces frequent PVCs and ST segment depression or symptoms. Instead, further evaluation for CAD or ischemic or structural heart disease may be warranted.
On the other hand, many clinicians are much more comfortable allowing healthy young adults who have frequent PVCs to exercise vigorously if EET does not produce ST segment depression or if PVCs resolve with exercise. When these younger, asymptomatic, and otherwise healthy adults go out and exercise, their PVCs and symptoms will probably resolve with activity. Moreover, such individuals are much less likely to have underlying ischemic heart disease. Rare, life-threatening complex arrhythmias, seen only at peak exercise, will also be excluded with EET.
Mobile cardiac outpatient telemetry (MCOT) is an emerging technology that allows up to 2 weeks of continuous “real-time” ECG monitoring. Data collected are automatically transmitted via cell phone to a monitoring center. Benefits include less patient error because the device does not require patient activation, unlike postevent and loop recorders. A small industry-sponsored study suggested that MCOT devices may have a higher yield of arrhythmia detection or exclusion than loop recorders, although full validation is still in progress (Rothman and colleagues, 2007).
An all-too-often-ignored adjunct for monitoring is the patient’s history (perception) of symptoms compatible with an arrhythmia. Although many individuals are totally unaware of their arrhythmias, others are able to sense each and every ectopic beat. For individuals with non-life-threatening arrhythmias who have this awareness—and in whom AECG has confirmed a temporal relation between symptoms and the occurrence of their arrhythmias—the patient’s account of symptoms may serve as a fairly reliable and cost-effective adjunct for long-term monitoring (i.e., it may greatly reduce the need for [and expense of] repeated Holter recordings for judging the effect of treatment).
Consider the case of a young patient who is markedly symptomatic from extremely frequent ventricular ectopy. Baseline Holter monitoring reveals several thousand PVCs during the day of monitoring but no runs of VT and no evidence of ischemia. The echocardiogram is normal; there is no evidence of pericarditis, cardiomyopathy, or a metabolic cause for the PVCs, and the patient’s diary confirms a definite temporal relationship between symptoms and periods of greatest ectopy. If treatment with a beta-blocker (or a reduction in stimulants such as caffeine) leads to complete resolution of symptoms, does the Holter recording need to be repeated? The answer to this key question is often found by asking two additional questions: Would repeating the Holter recording alter treatment? Will the patient’s account of symptoms (i.e., the “poor person’s Holter”) be adequate for guiding management? In many instances, such as in this particular case, experts would consider monitoring the patient’s symptoms alone to be adequate.