Case Report and Brief Review

Percutaneous Coronary Intervention for Persistent Complete Heart Block Complicating Inferior Myocardial Infarction

S. Ramamurthy, MD, DM, S. Anandaraja, MD, DM, Navin Matthew, MD, DM From the Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India. The authors report no conflicts of interest regarding the content herein. Manuscript submitted May 24, 2007, provisional acceptance given July 18, 2007, manuscript accepted August 3, 2007. Address for correspondence: S. Anandaraja, MD, DM, Assistant Professor, Ste. 25, Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India 110029. E-mail: saraja79@yahoo.com
S. Ramamurthy, MD, DM, S. Anandaraja, MD, DM, Navin Matthew, MD, DM From the Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India. The authors report no conflicts of interest regarding the content herein. Manuscript submitted May 24, 2007, provisional acceptance given July 18, 2007, manuscript accepted August 3, 2007. Address for correspondence: S. Anandaraja, MD, DM, Assistant Professor, Ste. 25, Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India 110029. E-mail: saraja79@yahoo.com
ABSTRACT: Current guidelines recommend implantation of permanent pacemakers for advanced atrioventricular block complicating acute myocardial infarction (MI) when the block is present beyond the usual hospital course. In patients with inferior MI, such blocks are usually transient, but they can also be persistent. However, they are not considered as primary indications for early reperfusion by percutaneous coronary intervention (PCI) in the absence of ongoing ischemia. We describe a patient with inferior MI in whom a successful PCI was effective in reversing persistent complete heart block, thus avoiding implantation of a permanent pacemaker. In selected patients with inferior MI and advanced atrioventricular block, PCI should be considered as a treatment option before recommending permanent pacemaker implantation. J INVASIVE CARDIOL 2007;19:E372–E374
Acute inferior wall myocardial infarction (MI) is often complicated by atrioventricular (AV) block, the incidence of which is reported to be 6–13%.1–3 High incidence of inhospital complications, an increased short-term mortality rate and an association with larger infarct size have been documented in these patients. Thrombolytic therapy has decreased the incidence of high-grade AV block in acute MI. However, even in the thrombolytic era, complete AV block continues to be a strong independent predictor of inhospital mortality.4 The current guidelines for pacing in acute MI recommend permanent pacemakers for patients with high-degree AV block associated with any MI.5 The decision to implant a permanent pacemaker for AV or intraventricular conduction block complicating acute MI depends on the type of conduction disturbance, the location of the infarction and the relation of the electrical disturbance to infarct time. Indications for percutaneous catheter interventions in acute MI include presentation within 12 hours or persisting symptoms at the time of presentation.6 In cases of cardiogenic shock, a window of time up to 18 hours from the onset of the shock is considered appropriate if the shock occurred within 36 hours after MI. Beyond the above time frames, persistent advanced AV block complicating acute MI, by itself, is not a traditional indication for percutaneous coronary intervention (PCI). We describe a patient with inferior MI in whom persistent complete AV block was reversed by PCI, which suggests that such a block could be an indicator of ongoing ischemia. Case Report. A 67-year-old male with diabetes and hypertension was admitted to our hospital for permanent pacemaker implantation with a referral diagnosis of complete heart block (CHB). A careful history revealed that 10 days prior to admission, the patient had a brief episode of acute chest pain and syncope at rest. Two days later, the patient sought medical consultation from a local physician who diagnosed complete heart block and advised permanent pacemaker implantation. The electrocardiograms (ECG) done at that time showed third-degree AV block with wide QRS escape complexes of left bundle-branch block (LBBB) morphology at a rate of about 50/min (Figure 1). On reviewing the ECG, we found ST-elevation in inferior leads of Discussion. Atrioventricular block in patients with acute inferior MI is postulated to occur by a variety of mechanisms. Increased parasympathetic activity, acute ischemia and ischemic metabolites such as adenosine and extracellular potassium have been implicated in the development of complete heart block in patients with inferior wall acute MI.7–10 CHB in inferior MI usually involves the supra-Hisian AV junction5 due to hypoperfusion of the AV nodal artery. Differences in physiology of the contractile and conducting myocardial fibers make their vulnerability to ischemia follow different paths. The conducting fibers are less dependent on oxidative phosphorylation than are the contractile elements. Hence, there may be a possibility of recovery of conductive function, even with late revascularization. In the context of inferior MI, though most advanced AV blocks are transient, the persistence of CHB beyond the hospital course is an indication for permanent pacing.11 This implies that the possibility of spontaneous reversal of CHB beyond this period is remote. Earlier studies in the thrombolytic era suggest that early reperfusion in patients with complete AV block and MI may help hasten restoration to sinus rhythm. In the study by Harpaz et al,4 a comparison of prethrombolytic and thrombolytic eras revealed a lower incidence of complete AV block in the latter period (5.3 vs. 3.7%). However, this is only an indirect indicator of the possible beneficial effect of thrombolysis in restoring sinus rhythm. Furthermore, the data were not exclusive for inferior MI. In another study by Kimura et al12 involving 21 patients with inferior MI and complete AV block, sinus rhythm was restored spontaneously in 2, after atropine in 3 and after reperfusion (thrombolysis or PCI) in the remaining patients. Restoration to sinus rhythm following reperfusion occurred as rapidly as within 3 minutes (13 patients) to within 1 hour (3 patients) after reperfusion. This study, however, relates to those patients who received reperfusion within 6 hours of infarction. Therefore, although reperfusion appears to have facilitated restoration of sinus rhythm in these patients, the possibility of delayed spontaneous reversion to sinus rhythm, at least in some of them, cannot be ruled out. In our patient, however, complete AV block had persisted for 2 weeks following the infarction, making the likelihood of spontaneous reversion to sinus rhythm remote. The benefit of revascularization and reperfusion in restoring sinus rhythm is therefore clearly established in this instance. Further thrombolytic therapy may be ineffective in achieving adequate reperfusion, especially in patients presenting late with AV block when the thrombus is relatively resistant to thrombolytics.13,14 This may be one of the reasons for the development of CHB following thrombolysis, as reported earlier and as shown in one of the studies confirming this fact by coronary angiography.14 PCI, however, accomplishes complete revascularization with certainty and may be more useful in reestablishing flow in these patients. Present-day guidelines do not recommend reperfusion strategies for conduction abnormalities complicating MI. This is evidently due to the lack of data supporting such strategies. Our case report exemplifies the fact that PCI could benefit patients with acute inferior MI and persistent CHB, even in the absence of other indications for invasive management. In particular, some patients who would otherwise be regarded as candidates for permanent pacemaker insertion may not require it after successful reperfusion. If a larger study confirms our findings, it would imply that: 1) all such patients should be considered for PCI before advising permanent pacemaker insertion; 2) complete or high-grade AV block complicating inferior MI could become an independent indication for an early invasive strategy, with PCI being directed at reversing the conduction defect. References 1. Harpaz D, Behar S, Gottlieb S, et al. Complete atrioventricular block complicating acute myocardial infarction in the thrombolytic era. SPRINT Study Group and the Israeli Thrombolytic Survey Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial. J Am Coll Cardiol 1999;15;34:1721–1728. 2. Clemmensen P, Bates ER, Califf RM, et al. Complete atrioventricular block complicating inferior wall acute myocardial infarction treated with reperfusion therapy. Am J Cardiol 1991;67:225–230. 3. Berger PB, Ruocco NA Jr, Ryan TJ, et al and the TIMI Investigators. Incidence and prognostic implications of heart block complicating inferior myocardial infarction treated with thrombolytic therapy: Results from TIMI II. J Am Coll Cardiol 1992;20:533– 540. 4. Harpaz D, Behar S, Gottlieb S, et al. Complete atrioventricular block complicating acute myocardial infarction in the thrombolytic era. J Am Coll Cardiol 1999;34:1721–1728. 5. Gregoratos G, Abrams J, Epstein AE, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines/North American Society for Pacing and Electrophysiology Committee to Update the 1998 Pacemaker Guidelines. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: Summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation 2002;106:2145–2161. 6. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:E1–E211. 7. Kosuge M, Kimura K, Ishikawa T, et al. Clinical features of patients with reperfused inferior wall acute myocardial infarction complicated by early complete atrioventricular block. Am J Cardiol 2001;88:1187–1191. 8. Feigl D, Ashkenazy J, Kishon Y. Early and late atrioventricular block in acute inferior myocardial infarction. J Am Coll Cardiol 1984;4:35–38. 9. Sclarovsky S, Strasberg B, Hirshberg A, et al. Advanced early and late atrioventricular block in acute inferior wall myocardial infarction. Am Heart J 1984;108:19–24. 10. Strasberg B, Bassevich R, Mager A, et al. Effects of aminophylline on atrioventricular conduction in patients with late atrioventricular block during inferior wall acute myocardial infarction. Am J Cardiol 1991; 67:527–528. 11. Antman EM. ST elevation myocardial infarction: Management In: Zipes DP, Libby P, Braunwald E and Bonow RO (eds). Heart disease: A textbook of cardiovascular medicine. 7th ed. Philadelphia: W.B. Saunders, 2004:pp:1167–1226. 12. Kimura K, Kosuge M, Ishikawa T. Comparison of results of early reperfusion in patients with inferior wall acute myocardial infarction with and without complete atrioventricular block. Am J Cardiol 1999;84:731–733. 13. Clemmensen P, Bates ER, Califf RM, et al. Complete atrioventricular block complicating inferior wall acute myocardial infarction treated with reperfusion therapy. TAMI Study Group. Am J Cardiol 1991;67:225–230. 14. Berger PB, Ruocco NA Jr, Ryan TJ, et al. Incidence and prognostic implications of heart block complicating inferior myocardial infarction treated with thrombolytic therapy: Results from TIMI II. J Am Coll Cardiol 1992;20:533–540.