Delayed Complete Heart Block Secondary to Jailed First
Septal Perforator

Lisa M. Nee, MD, Brian Guttormsen, MD, Giorgio Gimelli, MD
Lisa M. Nee, MD, Brian Guttormsen, MD, Giorgio Gimelli, MD

Complete heart block (CHB) due to the loss of a first septal perforator (FSP) following left anterior descending artery (LAD) stenting is uncommon, with few reported cases in the literature.1,2 It usually occurs at the time of the procedure and is transient, typically resolving within 72 hours. This report describes the case of an elderly female who developed unheralded syncope secondary to CHB 2 days after uneventful percutaneous coronary angioplasty and stenting of the LAD.

Case Report. A 76-year-old female with hypertension and dyslipidemia presented to an outside hospital with a 2-hour history of chest pain. An electrocardiogram (ECG) revealed an acute infero-posterior myocardial infarction. She was transported to our facility via helicopter and was taken emergently to the cardiac catheterization laboratory. Diagnostic angiography demonstrated a right dominant system with multivessel disease consisting of an acutely occluded obtuse marginal (OM) branch of the left circumflex artery, a 90% proximal-to-mid LAD lesion and a 50% lesion of the mid right coronary artery (RCA). The patient underwent successful stenting of the OM with placement of 2 baremetal stents dilated to 18 atm (3.0 x 28 mm and 2.5 x 18 mm Vision Cobalt Chromium stents, Boston Scientific, Natick, Massachusetts). A follow-up ECG revealed a posterior infarct pattern with left anterior fascicular block (LAFB) (Figure 1). Post-catheterization the patient did well and was discharged home after 48 hours with recommendation for a staged elective percutaneous coronary intervention on the LAD lesion.

The patient returned 2 weeks later, and 2 drug-eluting Cypher stents (3.0 x 23 mm and 2.75 x 18 mm, Cordis Corp., Miami Lakes, Florida) were deployed with subsequent jailing of the first septal perforator (FSP), resulting in TIMI 2 flow down this branch (Figure 2). She remained symptom-free and hemodynamically stable while in the cardiac catheterization laboratory, and given the small-to-medium size of the septal perforator, no intervention was performed on this vessel. At the end of the procedure, no collateral flow to the septal perforator branch was noted. During the hospital stay, she continued to remain completely asymptomatic and without ECG changes, and was discharged home the following day.
Two days following the procedure, the patient experienced a syncopal episode while at home, with loss of consciousness for approximately 2 minutes. She was taken to her local emergency room where was noted to be in complete heart block (CHB) with a low junctional escape rhythm at a rate of 30 bpm (Figure 3). The QRS morphology demonstrated a right bundle-branch block in addition to the previously noted LAFB. A transvenous pacemaker was placed with good capture and clinical stabilization. Upon arrival to our facility, she was noted to have an elevated troponin I at 9 ng/mL and was taken back to the cardiac catheterization laboratory. Left coronary angiography revealed patent stents in the OM and LAD with complete occlusion of the FSP (Figure 4); the RCA remained unchanged. The patient continued to be pacemaker-dependent for the next 48 hours with a low junctional escape rhythm at a rate of 20 bpm. She underwent placement of a permanent pacemaker the following day. The patient was later discharged home and has continued to do well 2 months later.


Discussion. Blood supply to the atrio-ventricular (AV) node, the His bundle and its proximal left and right bundles emanates from two sources: the AV nodal artery and the FSP.3 Despite this dual supply, however, CHB can occur in up to 44% of hypertrophic cardiomyopathy (HCM) patients who undergo alcohol septal ablation for treatment of left ventricular outflow tract obstruction.4 In particular, patients with preexisting conduction system disease are more prone to the development of CHB following alcohol septal ablation.5 It is, therefore, somewhat surprising that CHB does not occur more frequently when the FSP branch is compromised during LAD percutaneous coronary interventions. In this case, the time course of the presentation and the troponin leak are consistent with hypoperfusion and subsequent necrosis of the conduction tissue supplied by the FSP. The original ECG (Figure 1) demonstrates conduction disease in the left anterior fascicle, with further damage to the right bundle occurring after jailing of the FSP. We postulate that the location of the patient’s block is infra-Hisian, given the right bundle configuration on the escape rhythm.
Side branch occlusion (SBO) is a known complication of percutaneous coronary stenting occurring in up to 18% of patients.6 The mechanism is thought to be plaque shifting or “snow plowing” into the side branch.7 Although SBO is typically associated with a benign prognosis, operators will occasionally wire or predilate sizable side branches before stenting of the main branch, especially when the side branch is ≥ 2.5 mm in diameter and its ostium is diseased. In our practice, however, we have not felt the need to routinely protect septal perforator branches during LAD interventions.7,8
Although prior reports have documented transient CHB immediately following jailing of the FSP during coronary intervention, the case presented here is unusual in that its occurrence was delayed and its duration prolonged, thus requiring permanent pacing.1,2 We find the delayed presentation especially worrisome, since in our institutions, patients are usually discharged the day after uncomplicated percutaneous intervention. Although we do not advocate routine prolonged observation after LAD stenting with jailing of and residual disease in the septal perforator, this may need to be considered for those patients with preexisting conduction abnormalities. Additionally, one may consider protecting the FSP during LAD interventions in this group of patients.
In conclusion, FSP compromise can have significant clinical consequences in certain patients undergoing LAD interventions. For those with preexisting conduction abnormalities, protection of this branch or more prolonged observation following the procedure may be considered.




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3. Frink RJ, James TN. Normal blood supply to the human His bundle and proximal bundle branches. Circulation 1973;47:8–18.

4. Nagueh SF, Ommen SR, Lakkis NM, et al. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38:1701–1706.

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6. Cho GY, Lee CW, Hong MK, et al. Effects of stent design on side branch occlusion after coronary stent placement. Catheter Cardiovasc Interv 2001;52:18–23.

7. Aliabadi D, Tilli FV, Bowers TR, et al. Incidence and angiographic predictors of side branch occlusion following high-pressure intracoronary stenting. Am J Cardiol 1997;80:994–997.

8. Poerner TC, Kralev S, Voelker W, et al. Natural history of small and mediumsized side branches after coronary stent implantat ion. Am Heart J 2002;143:627–635.