Concept and mechanisms

Premature ventricular complexes (PVCs) are premature impulses (complexes) that originate in the ventricles. Therefore, they have a different morphology from that of the baseline rhythm.

PVCs may be caused by extrasystolic or parasystolic mechanisms (Figures 16.1 and 16.2):

• Extrasystoles are much more frequent than parasystoles and are induced by a mechanism related to the preceding QRS complex. For this reason, they feature a fixed or nearly fixed coupling interval (Figure 16.1). This is generally a reentrant mechanism (usually micro‐reentry), but also branch to branch, or around a necrotic or fibrotic area (see Figure 14.10). They may also be induced by post‐potentials (triggered activity) (see Figure 14.16) or other mechanisms (see Bayés de Luna and Baranchuk 2017; Enriquez et al. 2017).
  
• Parasystoles are much less frequent (Figure 16.2). They are impulses that are independent of the baseline rhythm. The electrophysiologic mechanism is an ectopic focus protected from depolarization by the impulses of the baseline rhythm. In general, this is due to the presence of a unidirectional entrance block in the parasystolic focus (see Figure 14.18).

ECG findings

ECG forms of presentation

In the ECG, the PVCs are represented as premature wide QRS complexes with a different morphology from that of the basal QRS.

PVCs usually show a complete compensatory pause (the distance between the QRS complex preceding the PVC and the following QRS complex double the sinus cadence) (Figure 16.3A). This happens because the PVC usually fails to discharge the sinus node. In consequence, the distance BC doubles the distance AB, appearing as two sinus cycles.

If the PVC discharges the sinus node, a non‐complete compensatory pause may be observed (BC < 2AB) (Figure 16.3B).

When the sinus heart rate is slow, a PVC, although it may enter the atrioventricular (AV) junction, leaving it in a refractory period (RP), will not prevent the following sinus stimulus from being conducted toward the ventricles, usually with a longer PR interval. This is because of the concealed PVC conduction over the AV junction, leaving it in the relative refractory period (RRP) that slows, but does not prevent, the conduction of the following P wave. Thus, the PVC occurs between two sinus conducted P waves and does not feature a compensatory pause (Figure 16.3C). This type of PVC is known as an interpolated PVC (Figures 14.29 and 16.3C).

An isolated PVC may occur sporadically or with a specific cadence. In this case, they may produce a bigeminy (a sinus QRS complex and an extrasystolic QRS complex) (Figure 16.1B) or a trigeminy (two normally conducted QRS complexes and one extrasystolic QRS) (Figure 16.1A). As we have already said, they may also occur in a repetitive form (Figures 16.1B and 16.4D). Short and isolated runs of classical monomorphic ventricular tachycardia with a rather slow rate (Figure 16.4) are considered repetitive forms of PVCs and will be dealt separately within this section.

Grade 0	No PVC
Grade 1	<30/h
Grade 2	≥30/h
Grade 3	Polymorphic PVCs
Grade 4a	On pairs
Grade 4b	Runs of monomorphic ventricular tachycardia
Grade 5	R/T Phenomenon (PVC falls on the preceding T wave)

Modified from Lown and Wolf (1971).

Lown has classified the PVCs into different types, according to the characteristics shown in Table 16.1 and Figure 16.4 (Lown and Wolf 1971). Ventricular tachycardia (VT) runs correspond to class 4b in Lown’s classification (Figure 16.4). If the runs of VT are frequent and repetitive, they are named non‐sustained VT (see later). This classification is hierarchical and has prognostic implications (see later).

Characteristics of QRS complexes

Width of the QRS complex

Most PVCs originate in the Purkinje network or in the ventricular muscle. They usually display a QRS complex ≥0.12 sec. Occasionally, if they start in one of the two main branches of the bundle of His or in one of the two divisions of the left bundle branch (LBB), the QRS is <0.12 sec (narrow fascicular PVC), and the morphology, although variable, resembles an intraventricular conduction block with a QRS < 0.12 sec. Some of these are parasystolic impulses.

Morphology

QRS morphology varies according to its site of origin (Figure 16.5). If the QRS complex starts in the right ventricle, it may be similar (in lead V1) to that of a left bundle branch block (LBBB) (Figure 16.5B). Those originating in the left ventricle show a variable morphology: when QRS complexes arise mainly from the lateral or inferobasal walls of the heart, they appear positive in all precordial leads (Figure 16.5A); when QRS complexes originate next to the inferoposterior or superoanterior division of the left bundle, they resemble a prominent R wave, sometimes with notches in the descending limb of the R wave, but usually without the rsR morphology that is typical of right bundle branch block (RBBB) in lead V1. The ÂQRS may be extremely deviated to the right or to the left, depending on their origin in the inferoposterior or superoanterior division, etc. The presence of QR morphology suggests associated necrosis (see Monomorphic ventricular tachycardia). Recently, Enriquez et al. described an anatomical attitudinal approach to determination of the site of origin (SOO), indicating that some previously considered “right‐sided structures” are at the left of the middle line and vice versa. The importance of this preliminary ECG screening of the SOO relies on the ability of guiding the interventionist EP to the proper approach for an ablation (Enriquez et al. 2019a).

In general, all QRS of ventricular tachycardias show similar morphologic characteristics to the initial PVC. This is because they usually have the same origin and are caused by the same mechanism. In addition, the intraventricular conduction of the stimulus is usually the same. However, the morphology of QRS complexes may change during an episode of ventricular tachycardia (pleomorphism) (see Polymorphic ventricular tachycardia), or a PVC with a given morphology may produce a polymorphic rather than monomorphic ventricular tachycardia, as is often the case in Brugada’s syndrome (see Chapter 21).

In individuals with no evidence of heart disease, PVCs usually show high voltage and non‐notched QRS complexes. It is possible for them to have a QS morphology but rarely a notched QR morphology (Enriquez et al. 2019a). Repolarization shows an ST segment depression when the QRS is positive, and vice versa, whereas the T wave has asymmetrical branches (Figure 16.6A). This type of PVC may also be observed in patients with heart disease.

However, the PVCs of patients with significant myocardial impairment show symmetrical T waves more often than healthy subjects, because of the presence of an additional primary disturbance of repolarization. Also, the QRS complexes show notches and slurrings, often with a low‐voltage pattern and qR morphology (Moulton et al. 1990) (Figure 16.6B).

Extrasystole compared with parasystole (Figures 16.1 and 16.2): The extrasystolic PVC presents a fixed coupling interval. When they are very late (PVCs in the PR interval), they may present fusion complexes (Figure 16.21B). The parasystolic PVCs present usually marked variable coupling interval (>80 ms) and the interectopic intervals are multiples of each other. Lastly, the third key diagnostic point of parasystolic PVCs is the presence of fusion complexes that occur when the impulse from baseline and parasystolic foci both activate the ventricle at the same time. The presence of fusion complexes is not necessary for diagnosis of parasystole because they often only appear sporadically and when the diagnosis is already made (Figure 16.2) (consult Bayés de Luna and Baranchuk (2017) for more information, McIntyre and Baranchuk (2011)).

Differential diagnosis

Table 15.1 shows the most relevant data indicative of aberrancy or ectopy in cases of premature complexes with wide QRS. It is very important to determine whether a P wave preceding a wide premature QRS complex is present, because this is crucial for the diagnosis of aberrancy (Figure 16.7). It is also essential to thoroughly observe the PVC morphology, as the presence of patterns consistent with the typical bundle branch block is very much in favor of aberrancy, although we have already stated that fascicular PVC may mimic the pattern of an intraventricular conduction disorder with QRS complexes <0.12 sec.

Clinical implications

If the PVCs are repetitive, they form pairs (two consecutive PVCs) or ventricular tachycardia runs (≥3) (Figures 16.1B and 16.4). Conventionally, a ventricular tachycardia is considered to be sustained when it lasts for more than 30 sec.

PVCs both of extrasystolic and parasystolic origin may be observed in healthy subjects and in heart disease patients. PVCs are more troublesome while resting, particularly when the patient is lying in bed. When frequent, they can cause significant psychologic disturbances. The incidence increases with age, and is more frequent in asymptomatic men after the age of 50 (Hinkle et al. 1969). At times, healthy people present with PVCs as a result of consuming foods that cause flatulence, in addition to wine, coffee, ginseng, and some “energy drinks.” Emotion, stress, and exercise can also cause PVCs.

The characteristic auscultation finding is interruption of the normal rhythm by a premature beat or beats followed by a pause. If they are very frequent, and especially if they appear in runs, they may end up affecting the left ventricular function, even in patients without previous heart disease (tachycardiomyopathy). Nevertheless, in healthy subjects the prognosis is generally excellent.

The long‐term prognosis of healthy subjects with ventricular premature systoles is generally good (Kennedy et al. 1985; Kennedy 2002). Nevertheless, the following considerations should be taken into account: (i) if PVCs clearly increase with exercise, this indicates an increasing long‐term risk for cardiovascular problems (Jouven et al. 2000); (ii) it has been reported that during a stress test, the ST segment depression in the PVC may be a better marker for ischemia than the ST segment depression in the baseline rhythm (Rassouli and Ellestad 2001) (see Figure 20.33); (iii) very frequent PVCs (>10 000–20 000/day) (Niwano et al. 2009) or a PVC burden of >24% (Baman et al. 2010) may lead to ventricular function impairment, in which case ablation of the ectopic focus may be advisable (Bogun et al. 2008). In the catheter ablation era, the indications to approach the treatment of PVCs from an invasive perspective have significantly evolved. Today, ablation of PVCs is a common procedure; however, the following rules should be considered before sending a patient for ablation: 1. The PVC “density” should be high (i.e. more than 20 000/day), 2. PVCs should be impacting left ventricular performance (i.e. LVEF < 50%), and 3. symptoms should be debilitating (i.e. patient not able to perform daily activity). If 2/3 of the criteria are present, one should consider treating the PVC (either pharmacologically or by ablation) (Lamba et al. 2014; Enriquez et al. 2019b).

In addition, it should be noted that Lown’s classification is hierarchical (Table 16.1). However, the R/T phenomenon is currently considered to be dangerous, especially in the presence of acute ischemia.

It has been demonstrated (Moss 1983; Bigger et al. 1984) that in patients with chronic ischemic heart disease (IHD), especially post‐infarction, risk increases after one PVC per hour, especially when complex PVC morphologies and/or heart failure are present. Recently, it has been demonstrated (Haqqani et al. 2009) that the characteristics of myocardial infarction scar are more important than the number of PVCs in the triggering of sustained ventricular tachycardia.

In hypertrophic cardiomyopathy, the presence of frequent PVCs, especially the presence of ventricular tachycardia runs, during a Holter ECG recording is an indicator of risk for sudden death (McKenna and Behr 2002).

The severity of PVCs increases in patients with depressed ventricular function and especially in the presence of evident heart failure.

Treatment of PVCs largely depends on the clinical condition of the patient (Bayés de Luna and Baranchuk 2017).

Monomorphic ventricular tachycardia

When monomorphic ventricular tachycardias (VTs) originate in the upper septum/bundle of His branches, they may have a narrow QRS (<0.12 sec). However, if they originate in the Purkinje network, or in any area of the ventricular myocardium, they have wide QRS complexes (≥ 0.12 sec) (classical VT).

Classical ventricular tachycardia (QRS ≥ 0.12 sec)

Concept

By definition, sustained VTs are those lasting longer than 30 sec. However, from a clinical point of view, most sustained VTs are long enough to develop specific symptoms that may require hospitalization. Most VTs are triggered by extrasystolic PVC. Thus, the initial complex if there are several episodes has the same coupling interval. Parasystolic VTs are very rare and frequently occur at a slow rate. They are generally non‐sustained VTs, appearing in runs, and arise from a protected automatic focus, which explains the variable coupling interval (see Figure 16.24).

Classical VT generally originates in the subendocardial area. In a small number of cases in the subepicardium and the majority of these cases in presence of heart disease, especially ischemic and non‐ischemic CM. The basal superior region of the LV is the most frequent site of origin of VT of epicardial origin in cases of non‐ischemic CM (Valles et al. 2010). Localization of the SOO using the ECG has been deeply explored correlating the QRS morphology and sequence of activation with extensive endocardial mapping (Enriquez et al. 2019a).

Electrophysiologic mechanism

In subjects with heart disease

In acute myocardial infarction patients without previous scars, sustained VTs are relatively rare, and sudden death generally occurs due to ventricular fibrillation triggered by one isolated or repetitive PVC (Figures 16.31 and 16.32).

Post‐infarction VTs in the presence of ischemic CM are usually triggered by alterations in the autonomic nervous system (“modulating factors”) assessed by different parameters in the presence of frequent PVCs (Moss 1983; Bigger et al. 1984). It has been demonstrated (Haqqani et al. 2009) that the characteristics of the scar are more relevant to trigger VTs in chronic IHD patients without residual ischemia than the presence of PVCs (see before). The VT may be perpetuated in post‐infarction patients by a reentry mechanism in the area surrounding the infarction scar.

This reentry may be explained by the classical concept of anatomic obstacle or by the functional reentry (rotors).

VTs are also present in patients with non‐ischemic CM and in other heart diseases (valvular, congenital) especially in the presence of heart failure.

In some cases, particularly in patients with dilated or ischemic cardiomyopathy, VTs are produced by a reentry where both branches of the specific conduction system (SCS) are involved (Touboul et al. 1983).

Channelopathies present VT due to heterogeneous dispersion of repolarization (phase 2 reentry) (Figure 14.15) (Yan and Antzelevitch 1998; Opthof et al. 2007) that may induce SD. Also, other inherited heart diseases such as HC and ARVD/C may present VT and SD (see Chapter 21).

In subjects with no evidence of heart disease

The most frequent electrophysiologic mechanisms are as follows (Enriquez et al. 2017):

• A micro‐reentry, usually in the region of the inferoposterior fascicle of the left bundle branch.
  
• Triggered electrical activity: These VTs are sensitive to adenosine.
  
• Increased automatism: These VTs are sensitive to propanolol.

Table 16.3 shows the differences between these three types of idiopathic VTs.

ECG findings

ECG recording in sinus rhythm

If previous ECGs are available, it is useful to compare their morphologies with that of a wide QRS complex tachycardia. For instance, in the case of a tachycardia with a wide QRS complex ≥0.12 sec, the presence of an even wider QRS complex in sinus rhythm due to an advanced LBBB strongly supports the diagnosis of VT. Meanwhile, the presence of an AV block during sinus rhythm favors a wide QRS complex being a VT.

Idiopathic VT with LBBB morphology (generally with “r” in V1). May originate in both ventricles (although usually originates in the RV) b
Inferior (right) ÂQRS Superior (left) ÂQRS	VT originates in RVOT endocardium. Features a relatively late R transition (V3–V4); R/S in V3 < I) and an isolated unnotched R in V6 (see Figure 16.11). 50% of VT of ARVC show similar morphologies (RVOT) VT originates near the aortic valve. Features an early R transition (R/S V3 > I) and an isolated notched R in V6. With regard to origin (see Figure 16.9): (i) if QRS morphology in I is rS or QS, the zone close to the left coronary leaflet is involved; (ii) if a notched “r” is observed in V1, the VT originates near the non‐coronary valve; and (iii) if qrS pattern is present in V1–V3, the VT originates between the right and left coronary valves If the VT originates in the area surrounding the mitral ring, a morphology rsr′ or RS is observed in V1 VT originates in the RV free wall and/or near the tricuspid ring. R in I and QS or rS in V1–V2 and late R transition in precordials. ARVC should be ruled out (see Figure 21.7B)
Idiopathic VT with RBBB morphology (generally, R in V1 and “s” in V6; from Rs to rS). Always originates in the LV
Superior (left) ÂQRS Inferior (right) ÂQRS	Inferior–posterior fascicular VT: activation similar to RBBB + SAH (Figure 16.10) Anterior–superior fascicular VT VT originated in LVOT endocardium near anterior–superior fascicle } Activation similar to the RBBB + IPH

^a Idiopathic VTs with duration < 120 ms (narrow QRS) present partial RBBB or LBBB morphologies.

^b Ouyang et al. (2002); O’Donnell et al. (2003); Yamada (2008).

IPH: inferoposterior hemiblock; LBBB: left bundle branch block; LV: left ventricle; LVOT: left ventricular outflow tract; RBBB: Right bundle branch block; RV: right ventricle; RVOT: right ventricular outflow tract; SAH: superoanterior hemiblock; VT: ventricular tachycardia.

Onset and end

Sustained VT usually starts with a PVC with a morphology similar to the other QRS of the tachycardia, with a relatively short and fixed coupling interval but frequently without R/T phenomena, especially in sustained VT not related to acute ischemia. Sometimes, prior to the establishment of a sustained VT, the number of PVCs and runs increases significantly.

Sustained VT may trigger ventricular fibrillation (Figure 16.34A). This is often the final event in ambulatory patients dying suddenly while wearing a Holter device (Bayés de Luna et al. 1989). Tachycardization of sinus rhythm characteristically occurs prior to the sustained ventricular tachycardia, which leads to ventricular fibrillation and sudden death.

Ventricular tachycardia may end by reverting to sinus rhythm or triggering ventricular fibrillation, and, rarely, reverting to asystole (Figure 16.8).

Heart rate

Heart rate usually ranges from 130 to 200 bpm. RR intervals occasionally show some irregularities, especially at tachycardia onset and termination. The rate typically increases before ventricular tachycardia turns into ventricular fibrillation (Figure 16.34A).

QRS morphology

By definition, QRS complexes are monomorphic. The QRS complex patterns depend on the site of origin, the ventricular tachycardia pathways, and the presence of heart disease.

In subjects with no evidence of heart disease: (i) Usually, the QRS morphology does not have many notches, and the T wave is clearly asymmetric. The morphology is similar to that of a LBBB or RBBB. However, the bundle branch block pattern is usually atypical. (ii) Table 16.3 describes the different types of idiopathic VT according to ECG morphology: RBBB‐type with evidence of left or right ÂQRS deviation, or LBBB‐type with left or right ÂQRS deviation. (iii) Figure 16.9A,B shows the ECG characteristics of idiopathic VT, depending on their site of origin (Figures 16.10 and 16.11). (iv) Despite having different mechanisms, VTs often originate in areas very close to each other, and therefore have similar morphologies. (v) VTs originating in the left papillary muscles are similar to fascicular VTs; however, they show a wider QRS complex, and there is no Q wave in the frontal plane.