Hemodynamic recovery after restoration of sinus rhythm after complete atrioventricular block during off-pump coronary artery bypass surgery: a case report

Abstract

Background

Off-pump coronary artery bypass (OPCAB) surgery is frequently chosen for high-risk patients to mitigate cardiopulmonary bypass–related complications. However, OPCAB is associated with significant intraoperative hemodynamic challenges, particularly in patients with impaired ventricular function and pre-existing conduction abnormalities. High-grade atrioventricular (AV) conduction disturbances during off-pump coronary artery bypass surgery are rare but can result in life-threatening hemodynamic collapse.

Case presentation

We report the case of a 75-year-old man with severe ischemic cardiomyopathy (LVEF 36%) and baseline left bundle branch block who underwent off-pump coronary artery bypass surgery for multivessel coronary artery disease with collateral-dependent coronary circulation. During right internal mammary artery harvesting, the patient developed progressive PR prolongation followed by transient complete atrioventricular block. Although the initial conduction disturbance was hemodynamically tolerated with vasoactive support, subsequent minimal cardiac displacement for left anterior descending artery exposure precipitated profound hemodynamic instability. The instability was refractory to ventricular pacing and maximal pharmacologic support but resolved immediately after spontaneous restoration of sinus rhythm, allowing completion of the procedure without conversion to cardiopulmonary bypass.

Conclusions

This case highlights the critical importance of atrioventricular synchrony in maintaining hemodynamic stability during off-pump coronary artery bypass surgery, particularly in patients with low ejection fraction, baseline conduction abnormalities, and collateral-dependent coronary circulation. Even surgical maneuvers considered relatively safe, such as right internal mammary artery harvesting or minimal cardiac displacement, may precipitate life-threatening hemodynamic collapse when AV synchrony is lost. Awareness of this interaction is essential for timely recognition and appropriate intraoperative decision-making in high-risk patients undergoing OPCAB.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s13019-026-04574-z.

Background

Off-pump coronary artery bypass (OPCAB) surgery has been widely adopted as an alternative to conventional on-pump coronary artery bypass grafting (ONCAB), as it avoids cardiopulmonary bypass–related systemic inflammatory responses and reduces perioperative complications such as stroke, acute kidney injury, transfusion, pulmonary complication and reoperation due to bleeding [1–5]. In particular, OPCAB is considered a favorable strategy for high-risk patients with reduced left ventricular ejection fraction (LVEF). Large observational studies and registry-based analyses have demonstrated that OPCAB is associated with lower early mortality and reduced major postoperative complications compared with ONCAB in patients with severely impaired ventricular function [6–12].

Despite these advantages, OPCAB is technically demanding and inherently carries a risk of intraoperative hemodynamic instability. Cardiac displacement and transient myocardial ischemia during target vessel exposure can compromise ventricular filling and cardiac output [13–16]. While tachyarrhythmias are common during OPCAB, high-grade conduction disturbances such as complete atrioventricular block (AVB) are uncommon but can lead to profound hemodynamic collapse [17].

Patients with ischemic cardiomyopathy and baseline conduction abnormalities, such as left bundle branch block (LBBB), are particularly vulnerable to the loss of atrioventricular synchrony. In these patients, the atrial contribution to ventricular filling (atrial kick) plays a crucial role in maintaining cardiac output. Consequently, the loss of AV synchrony can critically impair forward flow, even if the heart rate is maintained via ventricular pacing. Under such conditions, surgical manipulation—even steps considered relatively safe like right internal mammary artery (RIMA) harvesting—may precipitate severe and refractory hemodynamic deterioration.

We report a case of transient complete AV block that originated during right internal mammary artery (RIMA) harvesting in a patient with markedly reduced left ventricular function. Although the initial conduction disturbance was hemodynamically tolerated, subsequent minimal cardiac displacement for left anterior descending (LAD) artery exposure precipitated profound hemodynamic collapse. This instability was refractory to ventricular pacing and maximal pharmacologic support but resolved immediately upon the spontaneous restoration of sinus rhythm. This case highlights the critical importance of atrioventricular synchrony in preserving hemodynamic reserve against mechanical manipulation in high-risk patients undergoing OPCAB.

Case presentation

A 75-year-old man (height 166.9 cm, weight 55.1 kg) with a history of lumbar spinal stenosis under neurosurgical follow-up presented to the emergency department with a one-week history of progressive dyspnea, bilateral lower extremity pitting edema, and intermittent chest discomfort. Chest computed tomography performed at presentation demonstrated pulmonary edema with cardiomegaly and bilateral pleural effusion, and initial laboratory evaluation revealed markedly elevated NT-proBNP (N-terminal pro-B-type natriuretic peptide) (10,640 pg/mL) and elevated cardiac troponin T (0.20 ng/mL), raising concern for acute decompensated heart failure with concomitant myocardial ischemia. Given these findings, the patient was admitted for further evaluation and appropriate management.

Preoperative evaluation

Transthoracic echocardiography performed on January 13, 2026, revealed moderate left ventricular systolic dysfunction consistent with ischemic cardiomyopathy, with an M-mode (Teichholz)-derived left ventricular ejection fraction (LVEF) of 36%, a left ventricular end-diastolic dimension of 52 mm, an end-systolic dimension of 43 mm, an end-diastolic volume of 118 mL, and an end-systolic volume of 81.3 mL, suggesting no marked LV dilatation despite reduced systolic function. Regional wall motion abnormalities were noted, including akinesia of the entire anteroseptal, anterior, and apical segments, as well as hypokinesia of the mid-to-apical inferior wall. Additional findings included mild aortic stenosis (mean pressure gradient 18 mmHg), mild mitral regurgitation, concentric left ventricular hypertrophy, left atrial enlargement (left atrial volume index 43 mL/m²), grade II diastolic dysfunction, and mild pulmonary hypertension (estimated pulmonary artery systolic pressure 46 mmHg). Coronary angiography performed on the next day demonstrated two-vessel coronary artery disease, including chronic total occlusion (CTO) of the proximal left anterior descending artery (LAD), 90% ostial stenosis of the ramus intermedius with collateral flow from the right coronary artery (RCA), and 50% stenosis of the mid-RCA, indicating collateral-dependent coronary circulation (Fig. 1). Serial electrocardiograms obtained during hospitalization showed progressive conduction abnormalities. An initial electrocardiogram revealed sinus rhythm with a wide QRS complex, and subsequent tracings demonstrated gradual QRS prolongation, eventually evolving into complete left bundle branch block prior to surgery (Fig. 2).

Fig. 1.

Coronary angiography revealing Chronic Total Occlusion (CTO) of the Left Anterior Descending (LAD) artery and well-developed collateral circulation. (A, B) Left coronary angiography showing complete occlusion of the proximal LAD. (C, D) Right coronary angiography demonstrating retrograde collateral filling of the distal LAD from the RCA

Fig. 2.

Serial 12-lead electrocardiograms illustrating the progression of conduction disturbances from initial presentation to the postoperative period. (A) Baseline ECG on admission (Jan 12) showing sinus rhythm with intraventricular conduction delay (IVCD; QRS duration 140 ms). (B, C) Progressive widening of the QRS complex (168 ms and 165 ms, respectively) observed during the preoperative stabilization period (Jan 14–15). (D) Evolution to complete left bundle branch block (LBBB; QRS duration 172 ms) with anterior and lateral infarction patterns (Jan 19). (E) Preoperative ECG on the day before surgery (Feb 2). (F) Postoperative ECG following off-pump coronary artery bypass surgery (Feb 3)

Following coronary angiography, the case was discussed by a multidisciplinary Heart Team involving cardiologists and cardiac surgeons. Although percutaneous coronary intervention (PCI) was considered, surgical revascularization was favored due to the presence of complex coronary anatomy, including a chronic total occlusion (CTO) of the proximal left anterior descending artery with collateral-dependent circulation and significant stenosis of the ramus intermedius, which raised concerns regarding the feasibility of achieving complete and durable revascularization with PCI. Although dedicated myocardial viability imaging, such as positron emission tomography, cardiac magnetic resonance imaging, or dobutamine stress echocardiography, was not performed, the collateral-dependent retrograde filling of the LAD territory and the patient’s ongoing angina were considered clinically suggestive of viable, jeopardized myocardium.

In addition, current guidelines, including the 2021 ACC/AHA/SCAI guideline for coronary artery revascularization, support the use of CABG in patients with multivessel disease and reduced left ventricular function to improve survival [18].

The clinical course was complicated by acute kidney injury (AKI) secondary to the left renal infarction, with creatinine levels rising from 0.86 mg/dL to 2.15 mg/dL (eGFR 29.05 mL/min/1.73m²). This necessitated the postponement of the scheduled surgery. Under multidisciplinary management, heart failure medications, including ARNI (Angiotensin receptor-neprilysin inhibitor), beta blocker, SGLT2 (sodium glucose co-transporter 2) inhibitor, and diuretics including MRA (mineralocorticoid receptor antagonist), were carefully titrated or temporarily held due to episodes of hypotension and renal dysfunction. After stabilization of renal function (Cr 1.16 mg/dL) and optimization of respiratory status with umeclidinium/vilanterol for underlying emphysema, the patient was cleared for surgery on February 3, 2026. Given the patient’s recent acute kidney injury secondary to renal infarction, there was concern that the use of cardiopulmonary bypass (CPB) could further aggravate renal dysfunction. In addition, the presence of newly diagnosed chronic obstructive pulmonary disease raised concern for postoperative pulmonary complications associated with CPB. Therefore, an off-pump coronary artery bypass grafting (OPCAB) strategy was selected to minimize the risk of perioperative organ dysfunction.

Anesthetic management and intraoperative course

On February 3, 2026, the patient underwent off-pump coronary artery bypass grafting (OPCAB) with left internal mammary artery (LIMA) to distal left anterior descending artery (LAD) and right internal mammary artery (RIMA) to ramus intermedius via Y-graft configuration. A total arterial revascularization strategy using a LIMA–RIMA Y-graft was chosen because the radial artery was unsuitable as a conduit. This configuration also allowed avoidance of manipulation of the ascending aorta, which was considered important given the patient’s systemic vascular disease, including severe peripheral arterial occlusive disease and recent renal infarction. Both internal mammary arteries were harvested in a skeletonized fashion to preserve sternal perfusion and mitigate the risk of sternal wound complications.

Upon arrival in the operating room, standard monitors including 5-lead electrocardiography (leads II and V5), Patient State Index (PSI), and cerebral oximetry were applied. Due to a high risk of infection, a previously placed peripherally inserted central catheter (PICC) had been removed the day before surgery. Consequently, peripheral venous access was challenging; an 18-gauge intravenous line was secured in the right arm, and a right radial arterial line was established before induction. Anesthesia was induced cautiously to minimize hemodynamic depression. Considering the patient’s severely reduced ventricular function, a reduced dose of midazolam (2.5 mg) and sufentanil (40 mcg) was administered, along with lidocaine (40 mg, administered routinely to attenuate rocuronium-associated injection discomfort) and rocuronium (60 mg). During induction, transient hypotension was managed with repeated boluses of vasopressin (0.2 IU × 4 times) and ephedrine (4 mg × 2 times) with continuous infusion of norepinephrine. Maintenance was achieved with sevoflurane and continuous infusions of sufentanil and rocuronium. A multi-lumen access (MAC) catheter was inserted via the right internal jugular vein, through which a pulmonary artery catheter was advanced; an additional 16-gauge line was secured in the left external jugular vein. Following catheter placement, the pulmonary artery pressure was 33/13 mmHg (mean 21 mmHg) with a cardiac index of 2.4 L/min/m². Intraoperative transesophageal echocardiography (TEE) corroborated preoperative findings, showing a severely depressed LVEF (approximately 20%) with near-akinesis of the anterior and anteroseptal walls. Hemodynamic stability was initially maintained with norepinephrine (0.09 mcg/kg/min) and milrinone (0.35 mcg/kg/min). The initial rhythm remained sinus with an LBBB morphology, and the clinical course was stable through sternotomy and left internal mammary artery (LIMA) harvesting.

Intraoperative atrioventricular block and recovery

During left internal mammary artery (LIMA) harvesting, the patient remained in sinus rhythm with a wide QRS complex consistent with baseline conduction abnormalities; hemodynamics was stable with norepinephrine and milrinone support. No significant changes in transesophageal echocardiography (TEE) findings were observed at that time. However, during harvesting of the right internal mammary artery (RIMA), a progressive prolongation of the PR interval was noted, followed by the sudden development of complete atrioventricular (AV) block with AV dissociation. The ventricular escape rhythm dropped to approximately 40 beats per minute. Immediate TEE evaluation ruled out overt right ventricular (RV) free-wall compression, RV in-flow obstruction, or RV outflow tract compromise. In response to this bradyarrhythmia, milrinone infusion was escalated to 0.6 mcg/kg/min, and dobutamine was initiated at 2.9 mcg/kg/min. Despite the administration of glycopyrrolate (0.2 mg) and ephedrine (8 mg), the heart rate remained refractory. Norepinephrine was increased to 0.12 mcg/kg/min, which managed to maintain systemic arterial pressure within an acceptable range despite the persistent AV dissociation. Temporary external ventricular pacing (VOO mode, 72–80 bpm) was attempted but yielded only intermittent and inconsistent capture (Video S1). AV sequential pacing using a temporary epicardial atrial wire was also attempted; however, reliable atrial capture could not be achieved. The AV dissociation persisted even after the completion of RIMA harvesting and the return of the heart to a neutral position.

As RIMA harvesting neared completion, heparin (80 IU/kg, 5,000 IU) was administered according to our institutional protocol for OPCAB. The activated clotting time (ACT) was monitored every 40 min to maintain a target of > 250 s, with a total of 10,000 IU administered throughout the procedure. During the construction of the LIMA–RIMA Y-graft, an arterial blood gas analysis excluded a significant metabolic or electrolyte cause, with normal potassium and ionized calcium (pH 7.43, K⁺ 3.3 mmol/L, iCa²⁺ 1.31 mmol/L, lactate 0.90 mmol/L). Following Y-graft construction, the heart was prepared for the distal anastomosis to the LAD. To optimize surgical exposure while minimizing further hemodynamic compromise in this highly vulnerable state, posterior pericardial gauze padding was placed underneath the heart to elevate the target site. This maneuver was performed carefully to avoid apical suction, which could have exacerbated the already precarious cardiac displacement. Despite these strategic adjustments and maximal pharmacologic support—including norepinephrine (0.3 mcg/kg/min), vasopressin (4 IU/hr), and ventricular pacing—the mean arterial pressure remained marginal, with systolic blood pressure hovering in the 90 mmHg range. As hemodynamic instability persisted despite the escalation of pharmacologic and mechanical support, the surgical team remained on high alert for potential conversion to cardiopulmonary bypass (CPB). Unexpectedly, spontaneous restoration of sinus rhythm with a wide QRS morphology occurred shortly thereafter, with the heart rate increasing to 87 bpm. This rhythm conversion was accompanied by immediate hemodynamic recovery, allowing for the rapid de-escalation of inotropic and vasopressor support (Fig. 3). Following the successful completion of the distal anastomosis to the LAD, a deep pericardial stitch was placed to facilitate better exposure of the lateral wall. An epicardial stabilizer was then applied to secure the heart in preparation for the next target. During cardiac manipulation to access the ramus intermedius branch, a brief recurrence of atrioventricular (AV) dissociation was observed; however, it resolved spontaneously within seconds as the heart was stabilized. Once sinus rhythm was restored, the anastomosis to the ramus intermedius (RI) was initiated and completed uneventfully. Immediately following the completion of the RI grafting, a transient period of ventricular ectopy, consistent with short runs of bigeminy, occurred before the rhythm subsequently reverted to a stable sinus morphology. After confirming satisfactory graft flow via transit-time flowmetry in both the LAD and RI territories, 40 mg of protamine was administered for heparin reversal. The baseline ACT was 118 s, and the post-protamine ACT was 105 s, confirming successful reversal. Hemodynamics remained stable at the end of surgery (pulmonary artery pressure 33/14 mmHg, mean 22 mmHg, cardiac index 2.3 L/min/m²). The patient was transferred to the intensive care unit in stable condition with no further arrhythmic events.

Fig. 3.

Sequential hemodynamic and electrocardiographic changes during off-pump coronary artery bypass surgery culminating in transient complete atrioventricular block. (A) Baseline recordings showing stable sinus rhythm and hemodynamics. (B, C) Transition to complete atrioventricular block with associated hemodynamic instability. (D) Subsequent recovery of sinus rhythm and hemodynamic stabilization

Postoperative course and follow-up

The patient’s postoperative recovery was uneventful. Serial cardiac troponin T levels showed only a modest perioperative rise (0.20 ng/mL on admission; 0.30 ng/mL on the day of surgery; a peak of 0.40 ng/mL on postoperative day 1; declining to 0.20 ng/mL and subsequently 0.10 ng/mL), consistent with expected surgical myocardial injury rather than a major perioperative infarction. No further episodes of atrioventricular block or other significant arrhythmias were observed during the intensive care unit stay or throughout the remainder of the hospitalization. Transthoracic echocardiography performed on February 9, 2026, demonstrated a left ventricular ejection fraction (LVEF) of 36%, which was consistent with the preoperative value. Regional wall motion abnormalities persisted, including hypokinesia of the entire anteroseptal, anterior, and apical walls, as well as the mid-to-apical inferior wall. The patient was discharged on February 12, 2026 in stable condition without further cardiac events. At outpatient follow-up on March 5, 2026, the patient was clinically stable without symptoms of heart failure. At a subsequent outpatient visit on April 6, 2026, the patient reported significant improvement in chest pain compared to the preoperative state, with no new cardiac-related complaints. At the most recent follow-up (June 4, 2026), the LVEF was 38%, with comparable LV dimensions and volumes: end-diastolic dimension 52.9 mm, end-systolic dimension 43.1 mm, end-diastolic volume 135 mL, and end-systolic volume 83.5 mL.

Discussion and conclusions

Off-pump coronary artery bypass (OPCAB) surgery is inherently associated with significant hemodynamic challenges, particularly in patients with impaired ventricular function and pre-existing conduction abnormalities [6–12]. We report a case of transient complete atrioventricular block (AVB) during OPCAB that resulted in catastrophic hemodynamic collapse despite ventricular pacing and maximal pharmacologic support. The immediate restoration of hemodynamic stability after the spontaneous recovery of sinus rhythm suggests a reversible physiological disturbance rather than irreversible myocardial injury.

This patient had multiple baseline factors predisposing to hemodynamic intolerance, including severe ischemic cardiomyopathy with a reduced LVEF, diastolic dysfunction, and underlying LBBB. In such patients, cardiac output is highly dependent on preload and atrioventricular synchrony, rendering them particularly vulnerable to both rhythm disturbances and mechanical perturbations during beating-heart surgery.

The most plausible mechanism underlying the transient complete AV block is ischemia involving the conduction system, specifically triggered during the RIMA harvesting phase. Preoperative angiography revealed a collateral-dependent coronary circulation, with the right coronary artery (RCA) supplying critical retrograde flow to the left anterior descending (LAD) territory. During RIMA harvesting, a sternal-lift internal mammary artery harvesting retractor was used. This lever-type device elevates and rotates the hemisternum using a blade placed beneath the hemisternum and another blade applied to the sternum, thereby improving exposure of the internal mammary artery. However, this maneuver can also cause significant cardiac rotation, rightward displacement, and transient right-sided cardiac compression. Such mechanical effects may kink or compress the RCA—which in this patient was collateral-supplying and carried a 50% mid-vessel stenosis—thereby jeopardizing AV-nodal and septal perfusion. Given the patient’s dependence on RCA collaterals for septal perfusion, even a brief reduction in RCA flow could trigger significant septal ischemia affecting the AV node and bundle branches. A similar phenomenon has been reported where complete AV block occurred during IMA harvesting, which was attributed to transient coronary ischemia and successfully managed by restoring perfusion [19].

Notably, in our case, the AV block did not resolve immediately upon returning the heart to a neutral position; it persisted through the Y-graft anastomosis and the initial placement of gauze pads for LAD exposure. This delayed recovery suggests that the conduction system may have experienced a period of transient stunning or that a certain duration was required for the washout of ischemic metabolites after the initial mechanical-ischemic insult. The eventual spontaneous restoration of sinus rhythm, following the removal of the RIMA-specific retraction stress, reinforces the hypothesis of a reversible physiological disturbance rather than a permanent electrophysiological injury.

An autonomic or vagally mediated mechanism may also have contributed. Surgical manipulation during IMA harvesting can stimulate cardiac autonomic plexuses, potentially increasing vagal tone. Additionally, ischemia related to RCA compromise may trigger reflex-mediated responses, such as the Bezold–Jarisch reflex [20, 21]. However, the lack of response to anticholinergic and sympathomimetic agents suggests that a purely vagal mechanism was unlikely to be the primary cause of the sustained AV dissociation.

Coronary vasospasm represents another potential contributor, particularly given the substantial vasopressor requirements and previous reports of perioperative coronary spasm during OPCAB, including reports from East Asian centers [22, 23]. However, several features argued against vasospasm as the primary mechanism in this case: the absence of clear evolving ischemic ST-segment changes, the lack of new global wall-motion deterioration on TEE, and—most notably—the restoration of sinus rhythm and hemodynamic stability while vasopressor support was still ongoing. A transient spastic component nonetheless cannot be entirely excluded.

A critical finding in this case was the failure of ventricular pacing to restore hemodynamics. In patients with severe LV dysfunction and LBBB, the loss of the atrial kick can reduce cardiac output by up to 30% [13, 15, 17]. Ventricular pacing could support ventricular rate intermittently but failed to restore AV synchrony, and therefore could not compensate for the lost atrial contribution. Furthermore, mechanical displacement during surgery has been shown to cause direct right ventricular deformation and impaired filling [13, 14, 16]. In this case, even minimal cardiac displacement for LAD exposure likely exacerbated the diastolic limitation, creating a vicious cycle of low output that only resolved when AV synchrony was restored. Positional adjuncts such as Trendelenburg positioning with rightward table rotation, and right pleural opening in selected cases, can augment venous return and reduce right-heart compression during OPCAB; in our case, exposure and preload were managed with posterior pericardial gauze packing, a deep pericardial stitch, and avoidance of apical suction.

In retrospect, restoration of atrioventricular synchrony—rather than ventricular rate alone—was the physiologically appropriate therapeutic target. We attempted atrioventricular sequential pacing using a temporary epicardial atrial wire; however, reliable atrial capture could not be achieved, possibly because of atrial ischemia and underlying atrial remodeling, as suggested by left atrial enlargement (left atrial volume index, 43 mL/m²). We were therefore limited to asynchronous ventricular pacing (VOO), which restored ventricular rate but failed to restore AV synchrony and consequently did not reverse the hemodynamic collapse. This observation underscores the central message of this report: in patients with severe LV dysfunction and LBBB, ventricular pacing without atrial synchrony may be hemodynamically insufficient, and right ventricular pacing alone may further impair ventricular synchrony. In such high-risk OPCAB candidates, reliable atrial—and ideally left ventricular or biventricular—epicardial pacing capability should be considered in advance so that AV sequential or resynchronization pacing can be immediately deployed if needed.

The clinical decision to avoid immediate conversion to cardiopulmonary bypass (CPB) was supported by the absence of persistent ST changes on other leads, normal electrolytes, and the rapid recovery of stability following rhythm normalization. This illustrates that in selected situations, careful hemodynamic support and observation may allow time for spontaneous recovery from transient conduction disturbances. Intra-aortic balloon pump support was considered as a potential bailout but was relatively contraindicated by the patient’s severe peripheral arterial occlusive disease; the abrupt restoration of sinus rhythm ultimately obviated the need for either mechanical support or CPB conversion.

In conclusion, this case highlights the potential interplay between cardiac rhythm, coronary perfusion (specifically collateral flow), and mechanical positioning during OPCAB. In patients with LBBB and low EF, maintaining AV synchrony appears to be as important as maintaining heart rate. Anesthesiologists and surgeons should be aware that RIMA harvesting may potentially precipitate life-threatening arrhythmias in patients with collateral-dependent anatomy.

Limitations of this report include the inferential nature of the proposed mechanism, as direct measurements of coronary blood flow were not performed. Additionally, while the baseline ECG showed LBBB, the exact electrophysiological mechanism of the transient block cannot be definitively confirmed without an electrophysiology study. Likewise, formal myocardial viability imaging was not performed. Nevertheless, the temporal relationship between the surgical maneuver, rhythm disturbance, and hemodynamic collapse provides valuable clinical insight.

Supplementary Information

Below is the link to the electronic supplementary material.

Abbreviations

OPCAB

Off-pump coronary artery bypass

ONCAB

On-pump coronary artery bypass grafting

LVEF

Left ventricular ejection fraction

AVB

Atrioventricular block

RIMA

Right internal mammary artery

LAD

Left anterior descending

RCA

Right coronary artery

RI

Ramus intermedius

LBBB

Left bundle branch block

CTO

Chronic total occlusion

NT-proBNP

N-terminal pro-B-type natriuretic peptide

AKI

Acute kidney injury

ARNI

Angiotensin receptor-neprilysin inhibitor

SGLT2

Sodium glucose co-transporter 2

MRA

Mineralocorticoid receptor antagonist

TEE

Transesophageal echocardiography

CPB

Cardiopulmonary bypass

Author contributions

S.M.S. was responsible for conceptualization, data curation, formal analysis, and writing the original draft. J.W.P and W.H.C. contributed to data curation. All authors read and approved the final manuscript.

Funding

This work was supported by the Soonchunhyang University Research Fund (2026-0014).

Data availability

The datasets generated and/or analysed during the current study are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

The study was conducted in accordance with the Declaration of Helsinki, and approved by the Institutional Review Board of Soonchunhyang University Seoul Hospital (IRB No. SCHUH 2026-02-002).

Consent for publication

Written informed consent has been obtained from the patient for publication of this case report and any accompanying images.

Competing interests

The authors declare no competing interests.