In this chapter, we summarize the ECG patterns of risk of important arrhythmias and sudden death that have not been fully discussed in previous Chapters 14 to 17 (arrhythmias), 20 (ischemic heart disease), and 21 (inherited heart diseases). When pacemaker activity of the sinus node, or stimulus conduction from the sinus node to the atria, is diminished, passive arrhythmias occur, such as sinus bradycardia due to a decrease of automaticity and/or a sinoatrial block (see Chapter 17). In many situations—such as myxedema, drugs (beta blockers, some other antiarrhythmic agents), and ionic and metabolic disturbances—severe but often asymptomatic; sinus bradycardia may be present. Some asymptomatic cases of inherited severe bradycardia (related to HCN4 ion channel mutation) have been reported (Nof et al. 2007). These cases are usually associated with a good prognosis, and do not require pacemaker implantation in the long term. If there is a significant sinus bradycardia and symptoms are present (dizziness, syncope), a diagnosis of sick sinus syndrome is suspected (Figure 24.1). The most important cause of symptomatic sick sinus syndrome (SSS) is idiopathic fibrosis of the sinus node, which appears more frequently in elderly individuals. SSS is also related to many heart diseases, especially ischemic heart disease. The effects of some drugs must be ruled out at all times (see above, consider beta blockers, calcium blockers, digoxin, timolol eye‐drops, etc.). Bradyarrhythmias due to sinus node disease (significant sinus automaticity depression and/or sinoatrial block) are not associated with severe symptoms if a normal junctional escape rhythm exists. Most of the symptoms are caused by co‐existent associated alterations: junctional automaticity depression (resulting in a slower escape rhythm) and/or atrioventricular (AV) block. If a normal escape rhythm exists, the patient could be virtually asymptomatic or have only mild symptoms (tiredness, mild dizziness). Figure 24.1 Holter recording from a patient with sick sinus syndrome (SSS). (A) Note that the escape rhythm is quite slow with some sinus captures. In the first and fourth T‐waves, a sinus P is probably concealed (see Figure 6.8). The last QRS escape complex is retrogradely conducted to the atria. (B) A pause > 3.5 seconds between the first and second QRS escape complexes. The last QRS complex is also conducted to the atria. (C) Junctional slow escape rhythm, with slow atrial retrograde conduction. Sick sinus syndrome is frequently associated with supraventricular arrhythmias, which alternate with significant bradyarrhythmias (bradycardia–tachycardia syndrome) (Figures 24.2 and 24.3). Indeed, patients with SSS often experience intermittent supraventricular arrhythmias, especially atrial fibrillation (AF), and marked or very marked pauses are frequently found at the end of these crises (Figure 24.2). If this occurs, concerning symptoms may be present (presyncope or syncope, low cardiac output, paroxysmal dyspnea, etc.). In these cases, the immediate implantation of a pacemaker is recommended. The pacemaker has a dual effect: first, it prevents bradyarrhythmia, and second, if tachyarrhythmia episodes persist, an appropriate antiarrhythmic treatment may be safely administered to prevent future episodes by having appropriate back‐up provided by the pacemaker. Figure 24.2 A 65‐year‐old man with a normal baseline ECG (above) and a history of fainting falls. The ECG Holter recording showed a typical bradycardia–tachycardia syndrome (three bottom strips). Figure 24.3 A characteristic ECG pattern of advanced interatrial block in a 60‐year‐old patient with Ebstein’s disease. Note that the P ± is very wide in II, and in III and aVF. The patient also suffers from frequent episodes of supraventricular tachyarrhythmia (Bayés syndrome). The implanted pacemaker should provide: (i) normal ventricular activation whenever possible (avoid unnecessary ventricular pacing), (ii) physiologic AV synchrony, and (iii) physiologic chronotropic competence (heart rate increase). This may be achieved with an atrial single‐chamber pacemaker (AAI) when no AV block is present. However, as mentioned in Chapter 17, often a DDDR (universal dual chamber rate responsive) pacemaker should be implanted. This occurs especially when there is uncertainty about the appearance of an AV block in the future. About 2% of patients with SSS will develop AV block at 1–2 years (Andersen et al. 1998) (see Chapter 17, Choosing the best pacemaker). This type of advanced interatrial block produces a ± P‐wave in leads II, III, and aVF, with a duration ≥ 0.12 sec (Bayés de Luna et al. 1985) (see Figure 9.18). This infrequent morphology (≈1/1000 ECG taken in the University Hospital Sant Pau, Barcelona) is explained because right atrial activation has a craniocaudal sense, but the left atrium is activated retrogradely from the mid‐lower part of the septum. This retrograde activation of the left atrium occurs because the Bachman region, which is normally the way to cross the stimulus from the right to the left atrium, is blocked (see Figure 9.21). If the first part of the P‐wave has a very low voltage, due to atrial fibrosis the atrial wave seems negative in II, III, aVF, mimicking a junctional rhythm (Bayés de Luna et al. 2019). In the presence of this type of atrial block, the incidence of supraventricular tachyarrhythmias, especially AF, is very common (see Figures 24.4, and 24.5)(Bayés de Luna and Baranchuk 2017). Therefore, it has been considered that the combination of advanced interatrial block with left atrial retrograde conduction (P wave ± in II, III, and aVF) and supraventricular arrhythmias constitutes a new arrhythmogenic syndrome (Daubert 1996; Bayés de Luna et al. 1999) now called Bayes’ syndrome (Conde and Baranchuk 2014). Interatrial conduction block is generally present in patients with advanced heart disease who usually do not tolerate well fast atrial arrhythmias. Recently, has been demonstrated the association with stroke and dementia (Martínez‐Sellés et al. 2020a, 2020b; Herrera et al. 2020) of elderly patients with A‐IAB and structural heart disease. Therefore, in patients with this type of P‐wave (P‐wave ± in II, III, and aVF), may be advisable strict cardiac monitoring and antiarrhythmic or invasive approaches to control for rapid AF (Bayés de Luna et al. 1989; Baranchuk et al. 2014). Finally, a randomized trial (NOA vs placebo) is necessary to prove the potential benefit of anticoagulation in these patients. Figure 24.4 In this patient with advanced interatrial block, both types of atrial tachyarrhythmias (atrial fibrillation) and atrial flutter are observed. Figure 24.5 Patients with advanced interatrial block and left atrial retrograde activation show many more supraventricular paroxysmal arrhythmias during follow‐up when compared with patients from the control group with the same ECG and clinical characteristics (Bayés de Luna et al. 1988). A bundle branch block is a marker of bad prognosis in patients with heart disease, especially left bundle branch block (LBBB). The presence of LBBB, or even right bundle branch block (RBBB), in post‐infarction patients with ventricular dysfunction/heart failure (HF) is a marker of higher risk of sudden death, and, in the case of LBBB, it is also a marker for all‐cause mortality (Bogale et al. 2007). Patients with HF and LBBB who present with AF have the worst prognosis (Baldasseroni et al. 2002; Vázquez et al. 2009) (see Chapter 15, Atrial fibrillation). The “de novo” appearance of an advanced RBBB in the course of a serious acute episode with precordial pain and/or dyspnea constitutes a marker of bad prognosis. This situation obliges us to consider a diagnosis of acute coronary syndrome or pulmonary embolism. Naturally, in the course of an acute coronary syndrome with ST‐segment elevation in precordial leads (STEMI), a RBBB pattern is observed when the left anterior descending coronary artery proximal to the first septal branch is occluded. This is the artery branch perfusing the right bundle (see Figure 13.53) (Wellens et al. 2003; Fiol‐Sala et al. 2020). Additionally, the diagnosis of pulmonary embolism when a new RBBB pattern occurs in patients with an acute episode of dyspnea should be entertained (Digby et al. 2015). In this case, the ECG may also show an ST‐segment elevation in different leads, as well as sinus tachycardia, apart from the advanced RBBB pattern. The presence of a new RBBB is indicative of a massive pulmonary embolism, and thus is associated with a very poor prognosis. The cause of death is not usually a primary arrhythmia, but rather a hemodynamic failure with progressive impairment of automaticity leading to cardiac arrest (Qaddoura et al. 2017) (see Figure 10.16). Special attention to rule out RBBB aberrancy in relation to sinus tachycardia (tachycardia‐dependent block) should be given. In this case, the prognosis would not depend on the appearance of RBBB. Therefore, to determine the prognosis, it is important to know whether the patient had previously had an intermittent RBBB related to an increased heart rate (sometimes very difficult to prove). The possibility of progression to advanced AV block in the case of bifascicular block (i.e. RBBB plus superoanterior or inferoposterior hemiblock (SAH or IPH)) remains controversial (see Figures 11.50 and 11.54). Pacemaker implantation seems to reduce recurrence of syncope in comparison to monitoring with implantable loop recorders (Krahn et al. 2012). However, in asymptomatic individuals, pacemakers may not be indicated in cases of bifascicular block. However, close follow‐up is recommended. It is a special type of bifascicular block with a particular bad prognosis. The diagnosis of masquerading bifascicular block is confirmed when in the presence of a tall and wide R‐wave in lead V1 (the ECG is suggestive of advanced RBBB), no S‐wave is recorded in leads I and aVL. The presence of extreme left axial deviation is explained by an associated superoanterior hemiblock (see Figure 11.51) (Bayés de Luna et al. 1989). At first glance, in an ECG of this type, it seems that LBBB is present in the frontal plane (FP), whereas in the horizontal plane (HP), RBBB is observed. The fact that an R‐wave is recorded in lead V1 but no S‐wave is seen in leads I and aVL is due to a significant left ventricular enlargement and/or associated conduction block in the left ventricular free wall. The final activation forces (see Figure 11.53) are not directed forward and rightward, as in the classic bifascicular block (Vector 1), but forward and leftward (Vector 2). The masquerading bifascicular block rarely occurs intermittently (García‐Moll et al. 1994) (see Figure 11.52). In these cases, prognosis is poor regardless of whether a pacemaker is implanted or not (Bayés de Luna et al. 1989) because this type of block is usually detected in patients with advanced heart disease. Hence, the diagnosis in itself is a marker for poor prognosis (Elizari et al. 2013). Masked RBBB in a patient with an LBBB ECG pattern may be diagnosed if there is a QR pattern in lead aVR and high R‐wave in lead V1. In the presence of HF, this morphology may be explained by delayed activation of the basal part of the right ventricle (RV) (Van Bommel et al. 2011). In the absence of HF, this is probably explained by associated truncal partial RBBB pattern (Kukla et al. 2014). In 1968, Rosenbaum et al. described a type of intraventricular block that could lead to sudden death and that required urgent pacemaker implantation. Several consecutive ECGs showed RBBB and anterosuperior block, alternating with RBBB with posteroinferior hemiblock (Rosenbaum et al. 1968) (see Figure 11.56). This diagnosis, which usually has evident clinical characteristics (dizziness, near‐syncope, etc.), is named Rosenbaum–Elizari syndrome (Bayés de Luna and Baranchuk 2017). Pacemaker implantation is indicated and improves patient’s outcome. In the absence of advanced underlying heart disease, the prognosis can be excellent. In this case, the ECG alternatively shows LBBB and RBBB pattern, with or without associated hemiblocks, in the same patient (see Figure 11.49). In most cases, the patient presents with symptoms (dizziness, syncope), and it is necessary to implant a pacemaker as soon as possible because of the potential risk of complete AV block and sudden death. After pacemaker implantation, patients may have a good prognosis in the long‐term follow‐up when the block is due mainly to the involvement of the specific conduction system and there is no structural heart disease. Obviously, the presence of an acquired AV block requires pacemaker implantation in most cases. There may be exceptions, such as cases of AV block due to a reversible cause (ischemia, toxic substances, drugs, sarcoidosis, Lyme carditis, etc.) (Yeung and Baranchuk 2019). The implantation of a pacemaker for congenital AV blocks is a questionable procedure. This condition is already present at birth, often related to a systemic disease of the mother during pregnancy (presence of Ro/SS‐A and La/SS‐B antinuclear antibodies in the mother’s blood), which results in fetal myocarditis involving the specific conduction system. Using fetal kinetocardiography, it has been demonstrated (Rein et al. 2009) that 10% of fetuses whose mothers carried these antibodies experienced first‐degree AV block at 20–30 weeks’ gestation. When dexamethasone was prescribed, AV conduction was normalized and the infant showed no AV block or evidence of heart disease at birth. This type of AV block has sometimes been found in different members of the same family, although its genetic origin has not been demonstrated to date. Immune‐mediated cardiomyopathy has been recognized in infants born of mothers with antinuclear antibodies. The natural history of patients with isolated congenital AV block that requires pacing depends on their antibody status. If it is positive, it has been demonstrated that it is a predictor of HF and death. The cases with negative antibody status in a long follow‐up have a survival free of new HF after pacemaker implant (Sagar et al. 2010). Patients with advanced congenital AV block have a certain risk of sudden death. Although it is difficult to decide the best moment to implant a pacemaker, the tendency is to recommend pacemaker implantation even in the absence of symptoms if the escape rhythm is very slow (Friedman 1995). Pacemaker implantation is usually not indicated during childhood: (i) if the baseline rate is ≥ 50 bpm with a narrow escape rhythm, (ii) if the nighttime rate (Holter recording) is never < 30–35 bpm with a mean 24‐hour ventricular rate > 45–50 bpm, (iii) if the heart rate during an exercise test is > 100 bpm, (iv) if there is no lengthening of the QT interval, and (v) if there are no important ventricular arrhythmias (see Figure 17.15). If the previously mentioned parameters worsen during follow‐up, or if the patient becomes symptomatic, pacemaker implantation is recommended (Figure 24.6). The presence of premature ventricular complexes (PVCs) in the surface ECG in patients with chronic heart disease, especially ischemic heart disease, indicates that probably they are occurring frequently. In this case, Holter recordings (or event monitors) and exercise testing to establish their characteristics is recommended. In fact, the presence of any PVC in a routine 10 sec ECG in patients with moderate HF is a powerful predictor of cardiovascular mortality (Van Lee et al. 2010). Figure 24.6 A 12‐year‐old child with congenital complete atrioventricular (AV) block and no heart disease in whom the following findings were observed. (A) At rest, the heart rate, which was always greater than 60 bpm, now decreased to 45 bpm; (C) during the exercise stress testing, it did not exceed 80 bpm; and (B) at night (Holter), it frequently decreased to < 35 bpm. These findings, along with the occurrence of exercise dyspnea, suggest pacemaker implantation.
Chapter 24
Other ECG Patterns of Risk
Introduction
Severe sinus bradycardia
Advanced interatrial block with left atrial retrograde conduction (Figures 24.3–24.5)
Intraventricular conduction disturbances
High‐risk bundle branch block
High‐risk combined intraventricular blocks
Classic masquerading bifascicular block (see Chapter 11)
Masquerading RBBB pattern in the presence of advanced LBBB pattern
RBBB with alternating block in the two sub‐divisions of the left bundle
Alternating bundle branch block
Advanced atrioventricular block
The presence of ventricular arrhythmias in chronic heart disease patients
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