This case describes a clinically important progression of conduction disturbances following occlusion of a major SA supplying collateral flow to a chronically occluded RCA. The baseline ECG showed normal sinus rhythm without conduction abnormalities or ST–T changes. Immediately after SA occlusion, serial ECGs demonstrated abrupt development of a bifascicular block pattern—CRBBB with right axis deviation consistent with left posterior fascicular block (LPFB). This pattern persisted throughout the first three postoperative days, indicating persistent infranodal conduction involvement rather than a transient infarction-related vectorial shift.

At 62 h post-PCI, the patient developed complete AV block, while the CRBBB and right axis deviation remained unchanged. The persistence of a bifascicular block pattern (CRBBB and LPFB) prior to complete AV block strongly supports progressive ischemic injury to the His–Purkinje system. Laboratory parameters, including electrolytes and renal function, were unremarkable, excluding metabolic or reversible causes. Clinically, the appearance of a new bifascicular block pattern in the setting of myocardial infarction is a high-risk conduction profile and warrants prolonged rhythm surveillance and readiness for permanent pacing.

A notable early post-PCI finding was the presence of Qr morphology in leads V₁ and V₃, rather than the classical rSR′ configuration expected in CRBBB. This pattern reflects altered septal depolarization caused by septal infarction, supporting the diagnosis of ischemic injury to the interventricular septum.

Despite the abrupt loss of collateral flow to the chronically occluded RCA, no inferior ST-segment elevation was observed. The preserved inferior wall motion on baseline TTE suggests that the inferior myocardium remained viable under collateral supply before PCI. After the SA was lost, the patient developed acute hypokinesia of the inferior and inferolateral walls, with pathological Q waves and T-wave inversion in the inferior leads. The presence of new Q waves without ST elevation is consistent with non-transmural but clinically meaningful infarction. These findings underscore that loss of a collateral-supplying SA can cause silent yet significant ischemia in territories distal to a CTO.

Several reports over the past three decades have described late-onset high-grade or complete AV block following SA occlusion during PCI (Supplementary Table S1), most commonly involving the first SA and frequently necessitating permanent pacemaker implantation (2–12). In these reports, conduction disturbances often evolve with temporal delay after the procedure (2–10), although recovery of AV conduction has been documented in a minority of cases, either spontaneously (2, 3) or after successful SA revascularization (5, 10).

Beyond PCI-related mechanisms, non–PCI-associated compromise of SAs due to atherosclerotic stenosis, acute occlusion, or vasospasm has also been reported to precipitate complete AV block (Supplementary Table S2), reinforcing the critical role of septal branches in sustaining His–Purkinje system perfusion (13–16).

Against this background, the present case adds an incremental anatomical–clinical perspective by involving a collateral-supplying major SA responsible for perfusion of a chronically occluded RCA. Unlike previously reported cases that primarily focused on conduction outcomes, our patient exhibited a combined electromechanical presentation characterized by late-onset complete AV block together with marked left ventricular systolic dysfunction affecting the septal, inferior, and inferolateral territories. This observation broadens the clinical perspective on SA occlusion beyond conduction-only complications and highlights the importance of considering both conduction and myocardial consequences when SAs with collateral function are at risk during LAD PCI.

The main coronary contributors to the cardiac conduction system are the RCA and the LAD. The AV nodal artery most commonly arises from the RCA, which also supplies the His bundle and the proximal left posterior fascicle. SAs arising from the LAD provide the dominant blood supply to the right bundle branch and to the left anterior fascicle, and may also contribute variably to portions of the left posterior fascicle depending on coronary dominance. This anatomical configuration explains why isolated SA occlusion rarely results in complete AV block in most previously reported cases.

SAs display considerable anatomical heterogeneity, and current PCI guidelines do not provide specific recommendations regarding their protection during LAD interventions. However, accumulating case-based evidence—including the present report and the literature summarized in Supplementary Tables 1, 2 suggests that certain SAs may warrant particular attention. First, the first septal perforator emerges repeatedly across published cases as the vessel most frequently implicated in conduction disturbances following occlusion, consistent with its dominant perfusion of the proximal His–Purkinje system. Second, in line with the present observation, SAs that supply collateral flow to territories affected by CTO may have disproportionately greater functional significance; loss of such collateral-supplying SAs can compromise both conduction tissue perfusion and large myocardial regions that had remained viable through collateral support. Third, large-caliber or deeply intramyocardial SAs may be mechanically more vulnerable during PCI and more difficult to rescue if occluded. Taken together, these observations indicate that although routine SA protection is not standard practice, LAD PCI in patients with a dominant, proximal, or collateral-supplying SA may merit a more deliberate protective strategy, informed by pre-procedural angiographic assessment and intravascular imaging.

The mechanisms of side branch ostial occlusion after main vessel PCI include carina shift, plaque shift, ostial dissection, thrombus formation, and vasospasm, with carina and plaque shift being the most common. In our case, intravascular ultrasound (IVUS) demonstrated complete ostial occlusion secondary to plaque and carina shift, without evidence of thrombus or dissection. Despite multiple rewiring attempts and intracoronary nitroglycerin administration, mechanical occlusion persisted.

From a procedural standpoint, management of LAD–SA bifurcations requires recognition of the small caliber, deep intramyocardial course, and limited bailout options of septal branches. In the present case, a jailed-wire strategy was selected based on IVUS findings demonstrating a narrow septal takeoff angle and low ostial plaque burden. The jailed balloon technique—shown to reduce side-branch compromise in conventional epicardial bifurcations (17)—is often impractical in SAs, where incomplete balloon expansion, difficulty in device retrieval, and the risk of stent-edge distortion or entrapment limit its safety. Despite appropriate strategy selection and contemporary rescue attempts, the SA was ultimately lost, illustrating that even optimal protection techniques may fail due to intrinsic anatomical vulnerability rather than procedural error.

Although the SA was lost, one could hypothesize that antegrade recanalization of the RCA CTO before LAD PCI might have preserved collateral flow to dependent myocardium, potentially attenuating the subsequent electromechanical consequences. In this patient presenting with NSTEMI, the close temporal association between loss of a major collateral-supplying SA and the subsequent development of conduction disturbances and new regional wall-motion abnormalities supports a mechanistically plausible relationship rather than definitive causality. Retrospective consideration of alternative revascularization sequencing is therefore speculative and intended solely to highlight the potential vulnerability of collateral-dependent anatomies.

Taken together, the persistence of complete AV block requiring pacing support and the development of marked left ventricular systolic dysfunction following SA occlusion prompted consideration of an individualized permanent pacing strategy. Current ESC and AHA/HRS guidelines support consideration of cardiac resynchronization therapy (CRT) with defibrillator capability in patients with ischemic cardiomyopathy, reduced LVEF, and persistent complete AV block requiring permanent pacing after myocardial infarction (18, 19). In this case, CRT-D was preferred over CRT with a pacemaker, as the patient exhibited persistent complete AV block lasting more than five days, an ischemic etiology of conduction disturbance suggesting advanced infranodal conduction involvement, together with a markedly reduced LVEF (32%) associated with an increased arrhythmic risk.

Although the patient met the formal guideline criteria for CRT-D, the timing of implantation in the early post–MI period remains an area of clinical uncertainty. Both the 2021 ESC and 2023 AHA/HRS documents emphasize that early CRT (<40 days post-MI) should generally be deferred because conduction disturbances or left ventricular systolic dysfunction may recover after optimal revascularization and medical therapy (18, 19). Nevertheless, in this patient, complete AV block persisted for over five days despite metabolic stability with new septal and inferior–inferolateral wall-motion abnormalities and severely reduced left ventricular systolic function. Under these conditions, deferring device therapy could have resulted in prolonged bradyarrhythmia, progressive heart failure, or sudden cardiac death. Accordingly, early CRT-D implantation was considered an individualized and pragmatic clinical decision in this specific context.

With respect to device selection and pacing strategy, conventional biventricular CRT was preferred over conduction system pacing (CSP) approaches such as left bundle branch area pacing (LBBAP) or left bundle branch pacing–optimized CRT (LOT-CRT). This choice was primarily influenced by the presence of a broad septal infarction—an area essential for lead fixation and capture stability in CSP techniques. In the acute phase of septal injury, lead placement in necrotic or markedly edematous tissue carries an increased risk of septal perforation, lead instability, and unreliable or fluctuating capture thresholds. Furthermore, the substantial septal fibrosis anticipated during healing could jeopardize long-term CSP performance. By contrast, conventional biventricular CRT provides more predictable lead stability and resynchronization efficacy in this context and avoids additional mechanical manipulation of the infarcted septum during the vulnerable early post-MI period.

Overall, this case illustrates that in rare and highly selected scenarios characterized by persistent complete AV block and severely reduced left ventricular systolic function, early individualized consideration of CRT-D implantation may be clinically appropriate despite general guideline caution.