Early SGLT2 inhibitor use is associated with improved left atrial strain following acute coronary syndrome.

AIM: Left atrial (LA) strain, a novel marker of LA function, reliably predicts diastolic dysfunction. SGLT2 inhibitors improve heart failure outcomes, but limited data exists regarding their use in the immediate aftermath of acute coronary syndrome (ACS). We studied the effect of empagliflozin on LA strain in patients with type 2 diabetes (T2D) and ACS. METHODS: Patients with ACS and T2D were identified and empagliflozin was initiated in eligible patients prior to discharge. Patients not initiated on empagliflozin were analysed as a comparator group. A blinded investigator assessed LA strain using baseline and 3-6 month follow-up echocardiograms. RESULTS: Forty-four participants (n = 22 each group) were included. Baseline characteristics and LA strain were similar in the two groups. LA reservoir, conduit and contractile strain increased in empagliflozin group (28.0 ± 8.4% to 34.6 ± 12.2% p < 0.001, 14.5 ± 5.4% to 16.7 ± 7.0% p = 0.034, 13.5 ± 5.2% to 17.9 ± 7.2% p = 0.005, respectively) but remained unchanged in comparison group (29.2 ± 6.7% to 28.8 ± 7.0%, 12.8 ± 4.2% to 13.3 ± 4.7%, 16.7 ± 5.3% to 15.5 ± 4.5%, respectively, p = NS). The difference in change between groups was significant for LA reservoir (p = 0.003) and contractile strain (p = 0.005). CONCLUSION: In patients with ACS and T2D, addition of empagliflozin to standard ACS therapy prior to discharge is associated with improved LA function.

A novel RDS/peripherin gene mutation associated with diverse macular phenotypes.

Pattern dystrophy is a heterogeneous group of retinal dystrophies of which butterfly-shaped pattern dystrophy (BPD) and adult-onset foveomacular dystrophy (AOFMD) are the two most common forms. BPD is characterized by a butterfly-shaped, irregular, depigmented lesion at the level of the retinal pigment epithelium. In contrast, AOFMD is characterized by the presence of slightly elevated, symmetric, solitary, round to oval, yellow lesions at the level of the retinal pigment epithelium. We identified three independent kindreds with pattern dystrophy, one with four patients affected with BPD and the other two with 14 affected patients with AOFMD. We performed complete ophthalmic examination, fluorescein angiography, linkage mapping, and mutational screening in the RDS/peripherin gene in the affected patients. Patients affected with BPD had a best-corrected vision of 20/20 to 20/25, whereas vision in the eyes of patients with AOFMD ranged from 20/20 to 20/400. In all three kindreds, sequence analysis identified an A-to-G change at nucleotide position 422 of the RDS/peripherin gene, predicting a novel Tyr-141-Cys substitution. A haplotype analysis revealed that these three kindreds shared an identical disease haplotype at the RDS/peripherin locus, indicating that the mutation reflects a founder effect. The sequence change that segregated with the disease phenotype was not observed in 200 control chromosomes. Our results identified a novel mutation in the RDS/ peripherin gene that can cause diverse macular phenotypes. Genetic and clinical investigation of pattern dystrophy may provide useful diagnostic tools and new treatment strategies for this disorder.