Atrioventricular block after reperfusion: A reflection on early beta-blocker therapy for acute myocardial infarction

To the Editor,

Early coronary reperfusion achieved by primary percutaneous coronary intervention (pPCI) significantly reduces the occurrence of complete atrioventricular block (CAVB) in acute myocardial infarction (AMI) patients. The reported incidence of high-degree AVB was 7% and 1% in patients with right coronary artery (RCA) and left anterior descending artery (LAD) culprit lesion, respectively (1). We report a case of late-onset CAVB after successful pPCI, highlighting the potential risk of early beta-blocker therapy in ST segment elevation myocardial infarction (STEMI) patients.

A 43-year-old man with hypertension had chest pain lasting for 3 h. Electrocardiography revealed Q wave and ST segment elevation in leads V1 through V5 and occasional ventricular premature beats. Troponin T level was 47.3 ng/L. Coronary angiography showed total occlusion at the proximal LAD and severe stenosis in the mid-of RCA. Thrombus aspiration and stent implantation was successfully performed in LAD. Post-stent angiography revealed TIMI grade 3 blood flow of LAD with no septal branch occlusion. Drug regimen included aspirin, clopidogrel, tirofiban, perindopril, and atorvastatin. The use of beta-blocker was deferred, as large areas of infarction might put the patient at risk of heart failure and cardiogenic shock. Twenty hours after the PCI, the patient had a syncope attack. Electrocardiography revealed CAVB with no escape rhythm, which was followed by ventricular fibrillation. With external cardiac compression 60 s later, normal atrioventricular conduction was restored. No ST segment deviation was detected on electrocardiography. Such CAVB repeatedly occurred without electrolyte disturbance. Emergency coronary angiography showed that the lesion in RCA was not aggravated and also confirmed the patency of the LAD stent. With a transvenous temporary pacemaker, the patient was pacing dependent. Nine hours later, normal atrioventricular conduction was restored. Two days later, additional stenting was performed for the RCA lesion. Cardiac magnetic resonance performed 7 days later demonstrated a near transmural infarction of the septum, with a hypodense core signifying microvascular obstruction (MVO) in this region. The patient was discharged without beta-blocker considering the risk of bradycardia. At follow-up, repeated Holter monitoring showed no conduction defects and left ventricular ejection fraction was 60%; bisoprolol 2.5 mg qd was then added to his drug regimen.

Even after successful pPCI, patients are still at risk of problems such as reperfusion injury. Our patient’s late-onset CAVB may be related to MVO (2), which is a type of myocardial reperfusion injury. Current clinical guidelines recommend the initiation of oral beta-blockers within 24 h in STEMI patients with no contraindications (3). However, it also cautions against early use in patients with risk factors for hemodynamic instability. However, data from an observational study showed that beta-blocker use after the first 24 h of hospitalization was associated with a 56% decreased risk of in-hospital mortality compared with early oral administration. While hemodynamically stable STEMI patients were favorable to receive early beta-block therapy, early oral beta-blocker users still experienced an increase in short-term mortality, despite reductions in the rate of cardiogenic shock (4). Severe bradyarrhythmias such as CVAB may explain the excess in mortality. Further reflection on early beta-blocker therapy in secondary prevention after AMI is therefore necessary.