(126). The prevalence is likely higher when IMI is complicated by right ventricular infarction (13,127,128). CHB in IMI is frequently transient; the median duration in the TAMI cohort was 2.5 h (126). In the TIMI II study, there was a trend toward more second- and third-degree heart block in IMI patients who received iv beta-blockade (129). Although patients with CHB had a higher in-hospital mortality, there was no difference in long-term follow-up in patients who survived until discharge. The incidence of CHB in anterior MI is approx 3.9%, although the in-hospital mortality is much higher than when CHB complicates IMI (130). The long-term prognosis of hospital survivors remains unaffected. For both inferior and anterior MIs, it remains unclear whether CHB is an independent cause of poor in-hospital outcome or simply a marker for a large infarction. In IMI, in-hospital mortality is considerably higher in the setting of concomitant CHB and right ventricular infarction (131).
The GUSTO experience with AV block was recently reported. The frequency of second- and third-degree AV block was 11.6% and 3.8% in patients with IMI and AMI, respectively. Patients with AV block had more AF, ventricular arrhythmias, and a substantially higher in-hospital mortality than patients without heart block. Only 2.1% of patients with second- or third-degree AV block received permanent pacemakers, confirming that AV block complicating AMI is usually transient (132).
The pathophysiology and management of CHB differs in inferior and anterior MI (see Table 3). In IMI, block is typically intranodal; patients characteristically progress from first-degree to Mobitz I second-degree AV block before developing CHB (see Fig. 20). The escape rhythm is usually narrow, suggesting a focus in the proximal portion of the specialized conducting system. During the first 24 h of infarction, this is likely a manifestation of the Bezold-Jarisch reflex and therefore responds to atropine. CHB later in the course of an IMI usually may be caused by AV nodal ischemia, which
typically does not respond to atropine. Recent experimental evidence suggests that this late block may be mediated by adenosine at the cellular level; iv aminophylline, an adenosine antagonist, may improve such conduction disturbances (133,134). Several series have been published in which iv aminophylline at doses of 5-7 mg/kg infused over 15-20 min has improved AV block late in the course of IMI (133,134).
In anterior MI, block is usually within or below the bundle of His rather than within the AV node. The escape complex is generally wide, undependable, and poorly responsive to atropine. CHB usually develops in anterior MI patients who have previously displayed BBB rather than lower-grade AV block, as in IMI (see Fig. 21). In anterior MI, CHB usually results from proximal LAD occlusion, which causes ischemia/ infarction in the infranodal conducting system. Thus, CHB is a marker of extensive infarction in the setting of anterior MI. Beta-blocker therapy should be discontinued in patients with high-grade AV block. If a pacemaker (temporary or permanent) is placed, however, beta-blocker therapy may be resumed, as the benefits of beta-blockade extend beyond the negative chronotropic effects and continuation of these protective effects is desirable.
Like AV block, intraventricular conduction disturbances (IVCDs) occur frequently during AMI (135). More common in anterior than inferior MI, these defects reflect large infarctions, typically caused by proximal occlusions of the LAD coronary artery, and are associated with high in-hospital mortality (136-138). The incidence of the various IVCDs and approximate rates of progression to CHB are noted in Table 4. Prethrombolytic-era studies suggest that left anterior fascicular block (LAFB) and left posterior fascicular block (LPFB) occur in 3-5% and 1-2% of AMI patients, respec tively, and if isolated do not progress at high rates to CHB (139). Right bundle-branch block (RBBB) occurs in approx 2-5% of cases of AMI (136); approx 14-23% develop high-grade AV block (136,140). In anterior but not inferior MI patients, RBBB is associated with CHF, CHB, and a high in-hospital mortality, although this excess mortality is present only in patients with RBBB who also manifest CHF (141,142). There is also a high incidence of late VF in these patients (18). More common than RBBB during AMI, left bundle-branch block (LBBB) progresses less frequently to CHB, but also connotes a high in-hospital mortality (136). Patients with BBB and first-degree AV block are at higher risk (140), and patients with alternating BBB (see Fig. 22) extremely high risk of progressing to CHB (136). Finally, up to 50% of BBBs may actually be chronic and precede the index MI (136). In this case, there is a greater chance of developing CHB in anterior but not inferior MI (137).
Bifascicular block (RBBB with LAFB or LPFB, see Fig. 23) progresses at very high rates (27-34%) to CHB in the setting of anterior MI (136,140) and is associated with a very high in-hospital mortality. Bifascicular block with a prolonged PR interval is called "trifascicular block," because the prolonged PR interval may reflect delayed conduction in the "healthy" fascicle rather than in the AV node (see Fig. 24). Trifascicular block progresses in CHB in approx 38% of patients (140). Beta-blocker therapy should be suspended in patients with bifascicular or trifascicular block pending temporary pacemaker placement.
More recent data from the National Registry of Myocardial Infarction 2 suggests that newer therapies of AMI may have modified these findings. The prevalence of RBBB and LBBB with AMI were 6.2% and 6.7%, respectively. Patients with BBB were older and were more likely to develop CHF than patients without BBB. In-hospital mortality was almost double in patients with BBB compared without BBB, but the rate of progression to second- or third-degree AV block was relatively low—6.1% and 4.4%—with RBBB and LBBB, respectively (143).
Fewer data are available in patients treated with thrombolytic therapy. In GUSTO-I, the prevalence of RBBB and LBBB were 1.1% and 0.7%, respectively (144). Patients with BBB had a higher incidence of VT/VF, AV block, and cardiogenic shock than patients without BBB; mortality was also substantially higher in these patients (132). This probably reflects the fact that BBB occurs primarily in patients with large anterior MIs. In this trial, mortality was substantially higher with isolated RBBB or RBBB/ LAFB than with LBBB. Permanent BBB was associated with a higher mortality than transient BBB.
Indications for temporary pacemaker placement during AMI depend on the particular rhythm disturbance, hemodynamic consequence, and site of infarction (see Tables 3, 4). The availability of reliable temporary transcutaneous pacing has obviated the need for prophylactic transvenous pacing in some patients; in low-risk patients, a prophylactic transcutaneous system may be appropriate. Once a patient demonstrates a pacemaker dependence, however, a transvenous system should be placed. The risk of right ventricular perforation, infection, vascular complications, and bleeding must be carefully considered, especially in patients who have received thrombolytic and/or antithrombotic therapy.
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