Sung-Hee Shin

Tricuspid regurgitation (TR) is related to a poor prognosis in atrial fibrillation (AF). Although right atrial (RA) structural remodeling contributes to TR progression, the impact of RA functional remodeling on the progression of TR remains unclear. We investigated whether RA function influences TR progression in AF. Among 664 AF patients with baseline and follow-up echocardiography, 484 (mean 68 ± 12 years, 38% female) with insignificant (mild or less) TR at baseline were included. Patients with prior cardiac surgery, cardiac implantable electronic devices, significant (at least moderate) valvular diseases, LVEF < 50%, suboptimal images for strain analysis, or follow-up echocardiography < 6 months were excluded. A cut-off value for RA reservoir strain was 12.6%, as determined by ROC analysis. Over a mean 3.6 ± 2.7 years, 46 (9.5%) patients developed significant TR. Patients with RA reservoir strain < 12.6% were older, had more persistent AF, higher E/e’ and pulmonary artery systolic pressure (PASP), larger left atrium (LA) and RA, and lower LA strain. On multivariable regression, RA reservoir strain < 12.6% was independently associated with TR progression after adjustment for age, sex, and RA volume (p = 0.027), and remained significant after further adjustment for E/e’ or PASP. Impaired RA reservoir strain was independently associated with TR progression in AF patients with initially insignificant TR, suggesting that RA functional assessment may provide additional information complementary to RA structural remodeling and help identify patients at higher risk of TR progression.

Shin SH. Korean Circ J. 2025 Nov;56:e34. https://doi.org/10.4070/kcj.2025.0402

Background: In young patients presenting with Wolff-Parkinson-White (WPW) syndrome and left ventricular hypertrophy (LVH), a genetic aetiology should be considered, particularly when cardiovascular risk factors such as hypertension or valvular heart disease are not present, or when there is a suggestive family history of cardiomyopathy. PRKAG2 syndrome is a rare genetic disorder characterised by cardiac glycogen storage, ventricular pre-excitation, and hypertrophy, often mimicking hypertrophic cardiomyopathy (HCM). Case Summary: A 22-year-old male with a history of WPW syndrome presented with recurrent palpitations and wide QRS tachycardia. Post-cardioversion electrocardiography (ECG) revealed persistent pre-excitation, and transthoracic echocardiography (TTE) confirmed LVH with preserved systolic function. Cardiac magnetic resonance imaging (MRI) demonstrated normal myocardial mass without late gadolinium enhancement. Genetic testing, prompted by a family history of sudden cardiac death (SCD), using a targeted panel sequencing including sarcomere protein gene mutations and other cardiomyopathy-related genes, identified a heterozygous PRKAG2 mutation. Given the high risk of SCD, implantable cardioverter-defibrillator (ICD) placement was recommended but declined. The patient subsequently experienced a fatal cardiac arrest eight days after the last clinic visit. Discussion: This case highlights the importance of genetic evaluation in young patients with unexplained arrhythmias and hypertrophy. PRKAG2 mutations, often overlooked in standard HCM panels, can lead to misdiagnosis and inadequate risk stratification. Clinicians should maintain a high index of suspicion for PRKAG2 syndrome, particularly in patients with conduction abnormalities, ventricular arrhythmias, and LVH. Early identification using genetic tests, risk assessment, and family screening are crucial to preventing adverse outcomes, including SCD.

Background: Tricuspid regurgitation (TR) severity is associated with poor prognosis in patients with atrial fibrillation (AF). Recently, right ventricular–pulmonary arterial (RV‐PA) coupling has been shown to be related to clinical outcomes in patients with TR. However, data on the relationship of RV‐PA coupling to the progression of significant TR are limited. This study aimed to investigate whether RV‐PA coupling affects the progression of significant TR in patients with AF. Methods: Among 664 patients with AF who underwent follow‐up echocardiography at least 6 months after the initial assessment, 484 consecutive patients with AF (mean age 68±12 years, 38% women) with insignificant TR were included. RV‐PA coupling was assessed by the ratio of RV 4‐chamber strain measured through speckle tracking echocardiography to pulmonary artery systolic pressure (PASP). Results: Over a mean 3.6±2.7 years of follow‐up, 46 (9.5%) patients have progressed to significant TR, at least a moderate degree. Patients who progressed to significant TR were older, more likely to be women, had higher E/eꞋ and PASP, lower RV4CSL and RV 4‐chamber strain /PASP compared with patients without TR progression. RV‐PA coupling, reflected by RV 4‐chamber strain/PASP, was independently associated with the progression of TR even after adjusting for age, sex, and E/eꞋ ( P P <0.001). Conclusions: In patients with AF, RV‐PA coupling was independently associated with the progression of TR, suggesting that it may be helpful in monitoring this population.

Background: Sodium glucose cotransporter 2 (SGLT2) inhibitors improve clinical outcomes in several populations including type 2 diabetes (T2D), chronic renal insufficiency, and heart failure (HF). However, limited data exist on their effects on atrial fibrillation (AF). Methods: We conducted a retrospective cohort study using the National Health Insurance Service database. A total of 4,771 patients with T2D and AF who were newly prescribed SGLT2 inhibitors or DPP4 inhibitors were selected and matched in a 1:2 ratio by propensity score with 37 confounding variables. We assessed the effect of SGLT2 inhibitors on the composite outcome of either HF hospitalization or death. Results: Over a median follow-up of 31 months, patients on SGLT2 inhibitors were associated with a lower risk of hospitalizations for HF or mortality compared to those on DPP4 inhibitors (HR 0.61; 95% CI 0.44–0.85; P = 0.004). SGLT2 inhibitor use was also associated with a lower risk of mortality (HR 0.61; 95% CI 0.39–0.94; P = 0.025) and CV mortality (HR 0.43; 95% CI 0.21–0.86; P = 0.018), but not of MI (HR 1.22 [95% CI 0.72–2.09]; P = 0.461) or stroke (HR 1.00 [95% CI 0.75–1.33]; P = 0.980). The incidence of hospitalizations for HF, although statistically insignificant, tended to be lower in the SGLT2 inhibitor group (HR 0.63 [95% CI 0.39–1.02]; P = 0.062). Conclusion: In a nationwide cohort of patients with T2D and AF, SGLT2 inhibitor was associated with a lower risk of mortality, which may suggest that SGLT2 inhibitors may be considered as the first-line antidiabetic medication in patients with T2D and AF.

Shin SH. Korean Circ J. 2025 Jun;55:e106. https://doi.org/10.4070/kcj.2025.0165

Lee SM, et al. Int J Heart Fail. 2025 Jan;7(1):32-46. https://doi.org/10.36628/ijhf.2024.0069

Background Acute dyspnoea is common in acute care settings. However, identifying the origin of dyspnoea in the emergency department (ED) is often challenging. We aimed to investigate whether our artificial intelligence (AI)-powered ECG analysis reliably distinguishes between the causes of dyspnoea and evaluate its potential as a clinical triage tool for comparing conventional heart failure diagnostic processes using natriuretic peptides. Methods A retrospective analysis was conducted using an AI-based ECG algorithm on patients ≥18 years old presenting with dyspnoea at the ED from February 2006 to September 2023. Patients were categorised into cardiac or pulmonary origin groups based on initial admission. The performance of an AI-ECG using a transformer neural network algorithm was assessed to analyse standard 12-lead ECGs for accuracy, sensitivity, specificity and area under the receiver operating characteristic curve (AUC). Additionally, we compared the diagnostic efficacy of AI-ECG models with N-terminal probrain natriuretic peptide (NT-proBNP) levels to identify cardiac origins. Results Among the 3105 patients included in the study, 1197 had cardiac-origin dyspnoea. The AI-ECG model demonstrated an AUC of 0.938 and 88.1% accuracy for cardiac-origin dyspnoea. The sensitivity, specificity and positive and negative predictive values were 93.0%, 79.5%, 89.0% and 86.4%, respectively. The F1 score was 0.828. AI-ECG demonstrated superior diagnostic performance in identifying cardiac-origin dyspnoea compared with NT-proBNP. True cardiac origin was confirmed in 96 patients in a sensitivity analysis of 129 patients with a high probability of cardiac origin initially misdiagnosed as pulmonary origin predicted by AI-ECG. Conclusions AI-ECG demonstrated superior diagnostic accuracy over NT-proBNP and showed promise as a clinical triage tool. It is a potentially valuable tool for identifying the origin of dyspnoea in emergency settings and supporting decision-making.

BACKGROUND: The morbidity and mortality rates of patients with heart failure (HF) and functional mitral regurgitation (MR) remain substantial despite guideline-directed medical therapy for HF. We evaluated the efficacy of ertugliflozin for reduction of functional MR associated with HF with mild to moderately reduced ejection fraction. METHODS: The EFFORT trial (Ertugliflozin for Functional Mitral Regurgitation) was a multicenter, double-blind, randomized trial to examine the hypothesis that the sodium-glucose cotransporter 2 inhibitor ertugliflozin is effective for improving MR in patients with HF with New York Heart Association functional class II or III, 35%≤ejection fraction0.1 cm ² on baseline echocardiography. We randomly assigned 128 patients to receive either ertugliflozin or placebo in addition to guideline-directed medical therapy for HF. The primary end point was change in effective regurgitant orifice area of functional MR from baseline to the 12-month follow-up. Secondary end points included changes in regurgitant volume, left ventricular (LV) volume indices, left atrial volume index, LV global longitudinal strain, and NT-proBNP (N-terminal pro-B-type natriuretic peptide). RESULTS: The treatment groups were generally well-balanced with regard to baseline characteristics: mean age, 66±11 years; 61% men; 13% diabetes; 51% atrial fibrillation; 43% use of angiotensin receptor-neprilysin inhibitor; ejection fraction, 42±8%; and effective regurgitant orifice area, 0.20±0.12 cm ² . The decrease in effective regurgitant orifice area was significantly greater in the ertugliflozin group than in the placebo group (−0.05±0.06 versus 0.03±0.12 cm ² ; P P =0.009), left atrial volume index by 6.0 mL/m ² (95% CI, −12.16 to 0.15; P =0.005), and LV global longitudinal strain by 1.44% (95% CI, −2.42% to −0.46%; P =0.004). There were no significant between-group differences regarding changes in LV volume indices, ejection fraction, or NT-proBNP levels. Serious adverse events occurred in one patient (1.6%) in the ertugliflozin group and 6 (9.2%) in the placebo group ( P =0.12). CONCLUSIONS: Among patients with functional MR associated with HF, ertugliflozin significantly improved LV global longitudinal strain and left atrial remodeling, and reduced functional MR. Sodium-glucose cotransporter 2 inhibitors may be considered for patients with functional MR. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04231331.