Dilated cardiomyopathy (DCM) is characterized by ventricular dilation and impaired cardiac function, often leading to heart failure and arrhythmias [1]. Complete left bundle branch block (CLBBB) in patients with DCM is associated with a worse prognosis due to its impact on ventricular synchrony and overall cardiac function [2]. The standard treatment for DCM includes angiotensin-converting enzyme inhibitors (ACEIs), beta-blockers, and mineralocorticoid receptor antagonists (MRAs), which have been shown to improve mortality and morbidity [3]. However, the reversal of CLBBB using these treatments is rare and not well-documented.

This case report was approved by the Jeju National University Hospital (IRB No. 2024-06-010) ethics committee, which waived the requirement for informed consent.

A 76-year-old man with a history of hypertension presented with worsening dyspnea, fatigue, palpitations, and chest pain. At the time of presentation, he was well-oriented and had a blood pressure of 118/68 mmHg, heart rate of 81 beats/min, respiratory rate of 16/min, and body temperature of 37.2℃. Electrocardiography (ECG) showed a QRS duration of 150 ms and a broad notched or slurred R wave in leads I, aVL, V5, and V6 with no Q waves in leads I, V5, and V6, findings indicative of CLBBB (Fig. 1). Echocardiography showed a left ventricular ejection fraction (LVEF) of 38%, left ventricular end-diastolic dimension (LVEDD) of 62 mm, left ventricular end-systolic dimension (LVESD) of 46 mm, left ventricular (LV) mass index of 151 g/m², left atrial (LA) dimension of 51 mm, and LA end-systolic volume index (LAESVI) of 54 mL/m² consistent with DCM (Fig. 2A, B). Laboratory examinations revealed the following: N-terminal pro B-type natriuretic peptide (NT-proBNP), 1,021.0 pg/mL (normal range, 0.0-100.0); troponin, 0.10 ng/mL (normal range, 0.00-0.05); white blood cell count, 4.4×10³/µL (normal range, 4.0×103 -10.0×10³/µL); hemoglobin, 13.8 g/dL (normal range, 13.0-17.0); platelet count, 301×10 3 /µL (normal range, 150×10³-450×10³/µL); blood urea nitrogen, 17.2 mg/dL (normal range, 8.0-20.0); and serum creatinine, 0.96 mg/dL (normal range, 0.90-1.30). Coronary angiography revealed no significant coronary stenosis.

The patient was initiated on a standard heart failure regimen consisting of an ACEI (enalapril, titrated to 5 mg/day), a beta-blocker (nebivolol, titrated to 5 mg/day), and an MRA (aldosterone, titrated to 25 mg/day). Over the following 3 months, the patient’s symptoms gradually improved. A follow-up echocardiogram performed at 3 months post-treatment revealed a slightly improved LVEF (46.1%). This improvement became more pronounced after 1 year, with the LVEF increasing significantly to 63.6%. Concurrently, parameters indicating LV reverse remodeling showed substantial enhancement on a 1-year follow-up echocardiogram. The LVEDD decreased from 62 to 47 mm, while the LVESD decreased from 46 to 30 mm. Additionally, the LV mass index decreased from 151 to 101 g/m², LA dimension decreased from 51 to 34 mm, and LAESVI decreased from 54.0 to 29.7 mL/m² (Fig. 2C, D). Interestingly, ECG repeated at 1 year (Fig. 3A) and 3 years (Fig. 3B) post-treatment revealed resolution of the CLBBB with a normal QRS duration, while the NT-proBNP levels showed significant reduction (524 and 260 pg/mL, respectively). The follow-up period lasted 5 years, and the patient continued to undergo intermittent reexaminations and follow the prescribed medication regimen.

Here we described resolution of the CLBBB in a patient with DCM after heart failure management. DCM is often considered a distinct form of heart failure with reduced ejection fraction due to its specific characteristics [3]. In this context, left bundle branch block (LBBB) may be causative of or secondary to the underlying disease. Indeed, LBBB can cause non-ischemic cardiomyopathy; in selected patients, resynchronization is often associated with disease control and LVEF normalization [4]. On the other hand, a conduction system impairment and intraventricular conduction delay, often leading to LBBB, are frequently observed in DCM patients [5]. New-onset LBBB during follow-up for DCM has been associated with worse outcomes as a result of progressive cardiac remodeling [6]. LBBB is an independent predictor of adverse clinical events and outcomes of DCM, including sudden cardiac death, mortality due to myocardial infarction, and heart failure [2]. The resolution of CLBBB in this patient suggests that optimized medical therapy can lead to significant electrical remodeling in DCM.

The mechanisms by which ACEIs, beta-blockers, and MRAs may facilitate this improvement include ACEIs inhibiting the angiotensin-converting enzyme, which converts angiotensin I to angiotensin II, a potent vasoconstrictor. A reduction in angiotensin II levels leads to vasodilation, decreases afterload, and enables the heart to pump more efficiently. By lowering the afterload and mitigating the effects of angiotensin II, ACEIs reduce stress on the heart muscle, thereby preventing or reversing hypertrophy. Moreover, ACEIs diminish the fibrotic effects of angiotensin II on the heart, aiding in the maintenance of cardiac structure and function. Beta-blockers inhibit sympathetic nervous system activity and prevent adverse cardiac remodeling. This decreases heart rate and myocardial contractility, reducing the overall workload and oxygen demand of the heart and preventing cardiac remodeling.

Recent guidelines recommend the prioritized use of another important class of medications used for treating DCM. MRAs block the mineralocorticoid receptors, reducing aldosterone’s effects on sodium retention and potassium excretion, decreasing blood volume and lowering blood pressure [7]. Studies have shown that ACEIs, beta-blockers, and MRAs improve heart failure symptoms, decrease hospitalizations, reduce mortality, and lower the risk of arrhythmias in patients with DCM [3,8]. Recent guidelines recommend the prioritized use of angiotensin receptor-neprilysin inhibitor (ARNI)/ACEI/angiotensin receptor blocker, beta-blockers, MRAs, and sodium-glucose cotransporter-2 inhibitors as the optimal management of patients with symptomatic heart failure with reduced ejection fraction [7]. There was a reported case of DCM and LBBB that improved following 9 months of ARNI treatment, which significantly enhanced cardiac function and resolved the LBBB, suggesting the effectiveness of ARNI therapy in such complex cardiac conditions [9]. Unlike previous reports, in this case, the patient’s cardiac function, CLBBB, and heart failure symptoms improved following treatment with an ACEI, beta-blocker, and MRA. This case involved a long-term 5-year follow-up, which provided valuable insight into the sustained benefits of extend-ed medical treatment.

Reverse cardiac remodeling is defined as an improved LVEF, decreased chamber size, and reduced LV mass. Reverse cardiac remodeling is a complex process involving LV remodeling and various other cardiac structures. It is considered a crucial prognostic instrument for DCM treatment [8,10]. In this case, resolution of the CLBBB was concomitant with improved heart failure symptoms, decreased chamber size, and improved LVEF.

In summary, the present case demonstrated that optimized heart failure management led to reverse cardiac remodeling and significantly improved cardiac function, which resolved the patient’s symptoms and CLBBB.