Background Pacemaker recipients are predisposed to heart failure (HF), yet evidence guiding preventive pharmacotherapy in this population remains unexplored. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have redefined HF management across a broad spectrum of cardiometabolic phenotypes. This study evaluated the association between SGLT2i therapy and clinical outcomes after pacemaker implantation for atrioventricular block. Methods Patients receiving conventional pacemakers between 2016 and 2024 were retrospectively analyzed and stratified by baseline SGLT2i therapy. Exclusions included sinus node dysfunction or iatrogenic pacing indications, single-chamber devices, and estimated glomerular filtration rate < 20 mL/min/1.73m2. Events within 3 months post-implantation were omitted to reduce peri-procedural confounding. After propensity score matching, Cox regression assessed associations between SGLT2i use and all-cause mortality and HF hospitalization. Results Among 11,518 eligible patients, propensity score matching yielded two well-balanced cohorts of 1,226 SGLT2i users and non-SGLT2i users. Over three years, death occurred in 124 (10.1%) in the SGLT2i users and in 194 (15.8%) in the non-SGLT2i group (hazard ratio [HR], 0.62; 95% confidence interval [CI], 0.50 to 0.78; P < 0.001). HF hospitalization occurred in 132 (10.7%) in the SGLT2i group, and in 280 (22.8%) in the non-SGLT2i group (HR, 0.50; 95% CI, 0.41 to 0.62; P < 0.001). Subgroup analyses demonstrated consistent effects across strata. Conclusions SGLT2i therapy was associated with reduced risk of all-cause mortality and HF–related hospitalizations following pacemaker implantation. Future randomized studies are needed to confirm this association. Graphical abstract

A 77-year-old woman presented with interchangeable episodes of both fast and slow heart rate. Past history was notable for paroxysmal atrial fibrillation treated with eliquis and tambocor and atrial septal defect closure 35 years ago. Except for mild tachycardia, vitals and physical examination were unremarkable. The 12-lead electrocardiogram (Figure 1) showed narrow complex tachycardia at 106 beats/min without obvious P-waves. Verapamil (5 mg) was given by the emergency medical services prior to her admission. Subsequently, two rounds of intravenous metoprolol (5 mg each) were given in our facility, failing to slow her heart rate. There was no documented attempt to prefrom vagal maneuvers. Within 30 min, the emergency ward physician injected a low-dose (6 mg) intravenous adenosine. Some seconds later, prolonged complete atrioventricular block (AVB) occurred (Figure 2). The patient loss consciousness and cardiopulmonary resuscitation was commenced with chest compression and bag mask ventilation. The were no ventricular escape beats. The effect of adenosine lasted 40 s until atrioventricular conduction gradually recovered, and she became alert. The drug unmasked (atrial flutter, AFL), identified by its characteristic sawtooth waveform with atrial rate of 220 beats/min. The positive deflections in inferior leads II, III and aVF suggest the atypical form, the cavotricuspid isthmus-independent AFL. The cardiac rhythm post-adenosine was AFL with variable conduction at 90 beats/min. She was admitted to the cardiology unit, where continuous monitoring revealed tachycardia-bradycardia episodes, thus permanent dual-chamber pacemaker was implanted. As she spontaneously converted to sinus rhythm, we opted for follow-up of the atypical AFL. She was discharged with cardiloc 2.5 mg twice a day and increased tambocor 100 mg twice a day. During 12-months of follow-up including pacemaker interrogation, except several atrial high rate

Aortic stenosis (AS) is treated through transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement (SAVR), with diabetes being prevalent among these patients. Inflammation participates in the pathogenesis of AS, and emerging evidence suggests that TAVI may exert anti-inflammatory effects. Given the established link between diabetes and inflammation, we sought to evaluate the impact of aortic valve replacement (AVR) on glycemic control. Data from 10,129 consecutive patients undergoing either TAVI or SAVR between January 2010 and January 2022 were analyzed. Of these, 3,783 with diabetes had available pre- and post-procedural glycated hemoglobin (HbA1c) measurements. Analysis of 1,284 individuals with HbA1c ≥ 7 % was conducted. Propensity-score matching produced two well-matched cohorts of 266 TAVI and SAVR patients, enabling comparison of periprocedural HbA1c. In the total cohort (n = 1,284), HbA1c decreased from 8.15 ± 1.12 to 7.88 ± 1.38 (p < 0.001). After matching, the TAVI group showed a significant reduction from 8.31 ± 1.31 to 7.86 ± 1.56 (p < 0.001), while a modest decrease from 8.33 ± 1.33 to 8.15 ± 1.61 (p = 0.046) was observed in SAVR group. The TAVI group showed a trend toward a greater percentage change in HbA1c (p = 0.051). Clinically meaningful improvement in HbA1c (≥ 0.3 %) was similar between TAVI (53.1 %) and SAVR (45.6 %) patients (OR = 1.34, 95 % CI 0.93–1.95). Management of AS through either intervention improved post-procedural glycemia in patients with uncontrolled diabetes. The extent of glycemic improvement was more pronounced with TAVI. Further investigations through controlled and prospective studies could provide more conclusive insights into this matter.