Bundlebranch Block

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Patients with bundle-branch block (BBB) are at increased risk of high-grade AV block and sudden cardiac death. Large epidemiologic studies have contributed substantially to our knowledge about the natural history of this disorder. For example, Rotman and Triebwasser reviewed the records of 237,000 presumably healthy personnel at the United States School of Aerospace Medicine (39). They found 394 people with right bundle-branch block (RBBB) and 125 with left bundle-branch block (LBBB), a combined incidence of 0.0002%. Over a 10-yr follow-up period, there were no sudden deaths, and only two people progressed to high-grade AV block. In contrast, in the Framingham study, 5209 people initially free of clinically manifest cardiovascular disease were followed for a period of 18 yr (40,41). The Framingham population was older and had a higher prevalence of cardiac risk factors. BBB developed in 125 people, and in this subgroup, there was a high incidence of sudden cardiac death and four progressions to high-grade block. Thus, it appears that although conduction system disease in these individuals is progressive, the progression is slow and does not warrant prophylactic permanent pacing. The prognosis appears closely related to the presence and severity of underlying cardiovascular disease.

In the 1970s, several large prospective studies were initiated that attempted to identify individuals with BBB who were likely to require permanent pacing (42-44). Since it

Left Bundle Branch Block Prognosis

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Fig. 3. An intracardiac electrogram recorded with four simultaneous surface leads in a patient with left bundle-branch block (LBBB) and PR prolongation. Type II second-degree atrioventricular (AV) block is shown with every other beat blocked distal to the His bundle depolarization. I, AVF, V1, V6 are standard surface leads, and HBE is the His bundle electrogram. A = atrial depolarization and H = His bundle depolarization.

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Fig. 3. An intracardiac electrogram recorded with four simultaneous surface leads in a patient with left bundle-branch block (LBBB) and PR prolongation. Type II second-degree atrioventricular (AV) block is shown with every other beat blocked distal to the His bundle depolarization. I, AVF, V1, V6 are standard surface leads, and HBE is the His bundle electrogram. A = atrial depolarization and H = His bundle depolarization.

was recognized that the standard 12-lead electrocardiogram (ECG) provides only limited information about the functional status of the specialized conduction system (it does not differentiate between block at the level of the AV node and block in the His-Purkinje system), intracardiac recordings were utilized (Fig. 3). These studies determined that prolongation of the infranodal conduction time (HV interval) is a significant risk factor for heart block, although the specificity of this finding is relatively low. Based upon this information, it has become common practice to implant permanent pacemakers in individuals with BBB who present with unexplained syncope and are found to have marked (>100 ms) HV prolongation. However, the validity of this approach remains open to question. Scheinman et al. examined the use of "prophylactic" (defined as the absence of electrocardiographic evidence of high-degree block) permanent pacing in a large, nonrandomized cohort of patients with BBB and HV prolongation, more than one-third of whom had presented with syncope (44). Interestingly, they found no difference in mortality, incidence of sudden cardiac death, or recurrence of syncope in the paced patients compared with a similar group of unpaced patients. A possible explanation of these findings was provided by Morady and colleagues, who performed programmed ventricular stimulation in 25 patients with BBB and unexplained syncope (45). They found inducible ventricular tachycardia (VT) in 14 (56%), suggesting that tachyarrhythmias may be a more common cause of syncope than high-grade AV block in patients with BBB and structural heart disease.

In an effort to improve the diagnostic approach to patients with BBB, especially those with syncope, various techniques have been suggested to "stress" the conduction system. The induction of infranodal block by means of atrial pacing has been reported to be a relatively specific, although insensitive, means of predicting subsequent high-degree block (46,47). Similar findings have been reported for the development of second-degree AV block during exercise stress testing (48). The infusion of various conduction-depressing pharmacologic agents, most notably procainamide, disopyra-mide, and ajmaline (an investigational drug not commercially available in the United States) has also been suggested as a means of "stressing" the conduction system (49-51). As with the other methods, the induction of high-grade block has been found to be a relatively specific, although insensitive, predictor of future events. The significance of drug-induced HV prolongation is considerably less clear.

The recommended clinical approach to the patient with BBB is summarized in Table 3. It should be noted that to warrant a class I indication for permanent pacing in chronic BBB, even in patients presenting with syncope, high-grade block (Type II second-degree AV block or higher degrees of block) must be documented electrocardiographically (1). AV block, induced by provocative maneuvers in asymptomatic individuals, receives a class IIa indication. Isolated fasicular block, with or without first-degree AV block, is a class III indication for permanent pacing.

NEUROCARDIOGENIC SYNCOPE, CAROTID SINUS HYPERSENSITIVITY, AND RELATED DISORDERS

The term "neurocardiogenic syncope" includes a relatively common group of disorders characterized by abnormalities in autonomic control of the cardiovascular system. Clinically, the spectrum ranges from the person who experiences an occasional vaso-vagal "faint," precipitated by an especially strong stimulus such as fright, severe pain, or emotional upset, to the individual with recurrent disabling syncope without a clear precipitating factor. Although the exact mechanism of neurocardiogenic syncope has not been completely elucidated, the initiating factor appears to involve an exaggerated response of the parasympathetic nervous system to noxious stimuli. The diagnosis of neurocardiogenic syncope usually involves head-up tilt testing, in which an individual is strapped to a specially designed table and tilted up at an angle of 60-80 degrees for a period of time, usually 30-60 min. There are three general types of positive responses: vasodepressor, where there is vasodilatation and symptomatic hypotension without a major change in heart rate; cardioinhibitory, in which the heart rate drops precipitously without accompanying vasodilatation; and mixed response, where there is both bradycardia and vasodilatation. In carotid sinus hypersensitivity and related disorders (such as deglutition syncope, micturition syncope, and post-tussive syncope), symptomatic bradycardia and/or hypotension is elicited by an appropriate stimulus such as pressure on the neck (e.g., wearing a tight collar or using an electric razor), swallowing, bladder emptying, or coughing.

The first line of therapy for neurocardiogenic syncope has traditionally been medication, usually beta-blockers. Other drugs that have been used with variable success included disopyramide, theophylline, steroids that induce salt retention (such as fludro-cortisone), serotonin-reuptake inhibitors, alpha agonists (e.g., midodrine), and anticho-linergic mediations such as scopolamine.

Initial experience with permanent pacing was relatively discouraging, even with dual-chamber rate-adaptive units. The development of the "rate-drop response" (whereby a

Table 3

Diagnostic and therapeutic approach to BBB

Table 3

Diagnostic and therapeutic approach to BBB

Clinical setting

Syncope

Workup

Therapy

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