Conduction Disturbances in Acute Myocardial Infarction

Anatomy

The sinus node, sinoatrial conduction system, atrioventricular (AV) node, bundle of His, right bundle, left bundle dividing into anterior and posterior fascicles and myocardial Purkinje fibers form the cardiac conduction system ( Fig. 17.1 ). The bundle of His divides into the right and left bundle branches after leaving the AV node. The right bundle traverses the right side of the interventricular septum without giving off branches for most of its course. Ultimately, it branches near the base of the right anterior papillary muscle with fascicles supplying the septal and free wall of the right ventricle. The left bundle divides into several discrete branches after penetrating the membranous septum under the aortic valve. The anterior fascicle crosses the left ventricular outflow tract and terminates in the Purkinje system of the anterolateral wall of the left ventricle. The posterior fascicle courses inferiorly and posteriorly. The septum is activated earliest in all hearts by either a discrete septal fascicle or branches of the posterior fascicle.

The sinoatrial node is supplied by the atrial branch of the proximal right coronary artery (RCA) in 55% of cases and by the proximal left circumflex coronary artery (LCX) in 45% of cases. The RCA perfuses the AV node and the proximal portion of the His bundle in 90% of patients with perfusion originating from the LCX in the remaining 10%. The septal branches of the left anterior descending coronary artery (LAD) supply the distal part of the His bundle, the right bundle branch, and the anterior fascicle of the left bundle branch. The proximal portion of posterior fascicle of the left bundle is supplied by the AV nodal artery or by septal branches of the LAD. The distal portion is supplied by septal branches from the LAD coronary artery and RCA.

Incidence

The overall incidence of new conduction disturbances, including bundle branch and fascicular block, during acute MI is difficult to accurately determine because these abnormalities may often be chronic and unrelated to the acute presentation. The National Registry of Myocardial Infarction 2 (NRMI-2) evaluated the incidence of bundle branch block in 297,832 patients admitted to a hospital in the United States with an acute MI between 1994 and 1997: 6.7% of patients had a left bundle branch block (LBBB) and 6.2% had a right bundle branch block (RBBB) on the initial electrocardiogram (ECG). A similar rate of LBBB (9%) was noted in a prospective analysis of over 88,000 acute MI patients in Sweden. Since both series only assessed the presence of a bundle branch block (BBB) on the initial ECG, these data provide no information on the incidence of new conduction disease in acute MI. The development of BBB complicating acute MI after initial presentation appears to be rare, with only 0.73% and 0.15% of patients developing RBBB and LBBB, respectively, in the first 60 minutes after presentation. However, this is likely an underestimate, as many patients probably develop an acute BBB prior to presenting to the hospital.

The largest experience with high-degree AV block in the fibrinolytic era comes from a review of almost 76,000 patients with ST-elevation MI (STEMI) enrolled in four large randomized trials. The overall incidence of high-degree AV block was 6.9%: 9.8% associated with an inferior MI and 3.2% with an anterior MI.

In the thrombolytic era, the incidence of complete block has been reported in 3.2% of patients, 5.9% of patients with RCA occlusion, and 1.5% of patients with other infarct-related arteries. These generally develop within the first 2 days. The incidence of complete heart block (CHB) in acute MI was about 4% to 5%, with CHB or second-degree AV block occurring in 7% to 10% of patients. Since the widespread use of primary PCI, the incidence of AV block appears to have declined. Among 2073 STEMI patients treated with primary PCI in the Danish National Patient Registry, only 3.2% presented with second- or third-degree AV block or developed it during hospitalization.

Among 6662 STEMI patients enrolled in a French prospective registry between 2006 and 2013, of whom 74% of patients underwent primary PCI and 90% had PCI at some point in the index hospitalization, 3.5% of patients developed Mobitz II or third-degree AV block—2.2% on admission and 1.3% later in the hospitalization. AV block was more common among those with RCA occlusion (5.9%) than those with other infarct-related arteries (1.5%). Rates of AV block developing during hospitalization were lower in patients who received primary PCI (1.2%) or thrombolysis (0.5%) than those with no reperfusion treatment (2.6%).

The Global Registry of Acute Coronary Events (GRACE) enrolled 59,229 patients with acute coronary syndromes (37% with STEMI, 33% with non-ST elevation MI [NSTEMI]) at 126 hospitals in 14 countries. Second-degree Mobitz II or third-degree AV block occurred in 2.9% of patients (5% of STEMI patients, 1.9% of NSTEMI patients). AV block was noted on presentation in about half the patients and developed following admission in the other half. The RCA was the culprit vessel in 65% of patients with AV block and 31% of patients without AV block. A total of 35% of patients with AV block underwent temporary pacemaker placement and 5.9% required a permanent pacemaker.

Most reports that have assessed the incidence and prognostic significance of high-degree AV block after MI have not distinguished between STEMI and NSTEMI. In the Second Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) of 610 patients with a first NSTEMI, second- or third-degree AV block developed in 7% of patients. In the GRACE registry, 5% of STEMI patients developed Mobitz II second- or third-degree AV block compared to 1.9% of NSTEMI patients.

Specific Conduction Abnormalities