Intestinal tuberculosis (TB) typically presents with gastrointestinal symptoms, and cardiac conduction abnormalities associated with isolated intestinal TB have rarely been reported. We describe a 37-year-old male presenting with abdominal pain, constipation, and significant weight loss, with epidemiological exposure to cattle and raw milk. During hospitalization, he developed sinus bradycardia with a lowest corrected heart rate of approximately 46 beats per minute. The bradycardia persisted despite treatment with propantheline and atropine. Colonoscopy revealed terminal ileitis, and histopathology demonstrated nonspecific chronic ileitis without granuloma formation. Cardiac evaluation including echocardiography, troponin levels, electrolytes, and serum cortisol was unremarkable. Hydrocortisone administration was temporally associated with improvement in heart rate within 48 hours. Empirical anti-tuberculosis therapy was subsequently initiated, and the patient demonstrated sustained clinical improvement. Although causality cannot be definitively established, this case illustrates a rare temporal association between presumptive intestinal tuberculosis and steroid-responsive bradycardia. The report highlights the importance of considering systemic inflammatory processes in unexplained bradycardia, particularly in tuberculosis-endemic settings.

The heme oxygenase/carbon monoxide system is well-established as a critical regulator of contractile cardiomyocyte development. Although the heme oxygenase/carbon monoxide system is known to have protective effects against arrhythmias by reducing oxidative stress and preserving mitochondrial function in general myocardium, its specific impact on components of the cardiac conduction system, such as the sinoatrial and atrioventricular nodes, is unclear. On the one hand, the antioxidant and anti-inflammatory properties of the heme oxygenase/carbon monoxide system are believed to help maintain normal electrical conduction and prevent arrhythmias. On the other hand, pathological conditions such as age-related sick sinus syndrome have been linked to dysfunction of the heme oxygenase/carbon monoxide system, even though carbon monoxide is detrimental at toxic levels. This review synthesizes the current evidence on the dual nature of the heme oxygenase/carbon monoxide system in the cardiac conduction system. This review highlights the critical need for further investigation of the heme oxygenase/carbon monoxide system's physiological roles and therapeutic potential for conduction pathologies. JOURNAL/mgres/04.03/01612956-990000000-00091/figure1/v/2026-04-13T130436Z/r/image-tiff.

Atrial fibrillation (AF) and atrial flutter (AFL) are common arrhythmias, with incidence increasing with age. Catheter ablation and left atrial appendage closure (LAAC) are guideline-recommended treatments for patient with AF and high thromboembolic risk of stroke. We report the case of a patient with paroxysmal AF/AFL at high thromboembolic risk who developed paroxysmal rapid AF with sinus arrest following combined pulmonary vein isolation (PVI) and LAAC. Notably, both the arrhythmia and sinus node dysfunction gradually resolved over three months without pacemaker implantation. We propose that a watchful waiting strategy may be appropriate in similar clinical scenarios.

Left bundle branch area pacing (LBBAP) is a physiological pacing modality that preserves ventricular synchrony. In patients with sinus node dysfunction, who frequently exhibit delayed intrinsic atrioventricular conduction, the optimal postimplant programming strategy remains uncertain. Minimal ventricular pacing algorithms prioritize intrinsic conduction but may permit nonphysiological atrioventricular (AV) prolongation, potentially contributing to left atrial remodeling and atrial tachyarrhythmias. This is a prospective, single-center, randomized, open-label trial with blinded endpoint assessment (PROBE design). A total of 216 patients with sinus node dysfunction and successful LBBAP implantation will be randomized 1:1 to either a fixed optimized AV delay strategy (paced AV 150 ms; sensed AV 120 ms; minimal ventricular pacing algorithms disabled) or a minimal ventricular pacing strategy using device-specific algorithms (paced AV 200 ms; sensed AV 150 ms). The primary endpoint is the change in left atrial volume from baseline to 12 months, evaluated in a noninferiority comparison. Secondary endpoints include device-detected atrial high-rate episodes and atrial fibrillation burden (AF burden). In conclusion, this trial is designed to determine whether active optimization of AV synchrony after LBBAP implantation is noninferior to a conventional minimal ventricular pacing strategy in preventing left atrial remodeling and whether it may reduce atrial arrhythmia burden.