Ventricular Premature Complexes Workup
- Author: Jatin Dave, MD, MPH; Chief Editor: Jeffrey N Rottman, MD more...
Obtain laboratory studies to evaluate or correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI. Obtain serum electrolyte and magnesium levels.
Imaging studies may help to identify any underlying structural heart abnormalities that can predispose to VPCs. Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging. Echocardiography may be the preferred imaging modalitybecause it also provides structural information about the heart.
Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.
In patients suspected of having coronary artery disease, a noninvasive evaluation to rule out this possibility or even a cardiac catheterization may be helpful diagnostically. This is based on not just the presence of VPCs, but on all risk factors and symptoms. Onset in an elderly patient should be a red flag to consider the possibility of progressive structural heart disease.
The diagnosis of VPCs is typically established by electrocardiography. The presence of a VPC on a 12-lead ECG provides essential information about the origin of that extrasystole, as well as providing important information about the ventricular site-of-origin of the VPC. Accordingly, an ECG should be performed to look for pathophysiologic cardiac abnormalities as well as documenting the presence of VPCs and potentially providing information about their specific mechanism and frequency.
Diagnostic criteria include the following:
Wide (duration exceeding the dominant QRS complexes) and bizarre QRS complexes are present.
No preceding premature P waves occur, and, rarely, a sinus P wave is conducted.
The T wave usually is in the opposite direction from the R wave.
Full compensatory pause is common.
VPCs originating from the left ventricle typically produce a right bundle-branch block (BBB) pattern on QRS.
VPCs originating from right ventricle typically produce left BBB-like pattern on QRS.
Idiopathic VPCs often originate from the right ventricular outflow tract and have a left bundle inferior axis morphology. See the image below.
Noninvasive mapping of cardiac arrhythmias is also possible with a 252-lead ECG and computed-tomography scan–based three-dimensional electroimaging.
In high-risk patients, ie, those with reduced ejection fraction (EF) and VPCs, a 24-hour Holter monitor may help establish the degree of electrical instability.
The severity of LV dysfunction, along with the complexity and frequency of the VPC, determines the aggressiveness of management.
Suppression of VPCs by beta-blocker or calcium blocker, together with a typical VPC morphology (inferior axis, LBBB morphology) can be helpful in establishing typical right ventricular outflow tract ectopy.
Suppressing the VPCs themselves is not the focus of treatment unless patients are significantly symptomatic.
Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.
Electrophysiologic study (EPS) may be indicated for 2 types of patients with VPCs, (1) those with a structurally normal heart with symptomatic VPCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with VPCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
According to the American College of Cardiology/American Heart Association guidelines,[15, 16] class I indications for EPS are patients with CAD, low EF (< 0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of VPC, couplets, and nonsustained VT.
Classification of Ventricular Premature Contractions
VPCs can be classified in different ways. The Lown classification was introduced to gauge effects of antiarrhythmic drugs and widely assumed to encapsulate prognostic significance—it is not clear that it fulfills either of these goals, but this classification is still employed.
Table 1. Lown Classification (Open Table in a new window)
|1||Unifocal; < 30/h|
|2||Unifocal; ≥ 30/h|
|4B||≥ 3 consecutive|
The Lown classification does not necessarily imply a continuum of increasing risk.
Clinical classification is as follows:
Classification according to frequency is as follows:
Frequent - 10 or more VPCs per hour (by Holter monitoring) or 6 or more per minute
Occasional - Fewer than 10 VPCs per hour or fewer than 6 per minute
Classification according to relationship to normal beats is as follows:
Bigeminy - Paired complexes, VPC alternating with a normal beat
Trigeminy - VPC occurring every third beat (2 sinus beats followed by VPC)
Quadrigeminy - VPC occurring every fourth beat (VPC following 3 normal beats)
Couplet - 2 consecutive VPCs
Nonsustained VT - 3 or more consecutive VPCs (< 30 s)
Classification according to origin is as follows:
Number of foci: Unifocal/unimorphic (beats originate from 1 focus; ie, all VPCs have the same morphology) or multifocal/multimorphic (VPCs have more than one morphology and may originate from more than one site)
Site of origin: Left or right ventricular
Associated heart disease: None (idiopathic) or structural heart disease is present
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