Key result
Desmoplakin variants linked to ~3-fold higher heart failure risk in arrhythmogenic cardiomyopathy.
Why the study?
Improved arrhythmic risk stratification and therapies have enhanced survival in arrhythmogenic cardiomyopathy, making heart failure an increasingly relevant clinical issue requiring characterization and risk factor identification.
Observational (n=657)
No
Odds Ratio: 3.08
p-value: p=0.01
Heart failure in arrhythmogenic cardiomyopathy is associated with a more severe phenotype, and its occurrence can be predicted by specific genetic (DSP), electrocardiographic, and imaging markers.
BACKGROUND: Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease primarily associated with life-threatening ventricular arrhythmias. Improved arrhythmic risk stratification and therapies have enhanced survival, making heart failure (HF) an increasingly relevant clinical issue. This study aims to characterize HF in ACM patients and identify variables associated with its occurrence. METHODS: This retrospective, single-center study included 657 ACM patients diagnosed according to the 2010 Revised Task Force Criteria and Padua criteria. HF was defined as hospitalization due to HF symptoms. Clinical, electrocardiographic, imaging and genetic data were compared between patients with and without HF. RESULTS: HF occurred in 48 patients (7.3%). Those with HF were more often probands (p = 0.007) and showed more ECG abnormalities, including T-wave inversions in right (p = 0.004) and lateral leads (p < 0.001) and low QRS voltages in precordial and peripheral leads (p < 0.001). Genetic analysis revealed a higher prevalence of Desmoplakin (DSP) (p = 0.03) and Desmin (p = 0.002) genetic variants. Imaging showed increased ventricular volumes and reduced biventricular systolic function (p < 0.001). The arrhythmic burden was also higher (p = 0.022). Variables associated with HF occurrence were DSP genetic variants (OR = 3.08, p = 0.01), low QRS voltages in peripheral leads (OR = 3.76, p = 0.002), and reduced left ventricular ejection fraction (EF) (OR = 0.89, p < 0.001) and right ventricular EF (OR = 0.93, p < 0.001). CONCLUSIONS: HF in ACM reflects a more severe phenotype with biventricular dysfunction and high arrhythmic burden. Genetic (DSP), electrocardiographic, and imaging markers may contribute to early identification of patients at higher risk and support earlier intervention strategies.
No takes yet. Share an insight, caveat, or question.
Martini et al. (2026) conducted an observational in Arrhythmogenic cardiomyopathy (n=657). Desmoplakin (DSP) genetic variants and electrocardiographic/imaging abnormalities vs. Absence of these variants and abnormalities was evaluated on Heart failure (hospitalization due to HF symptoms) (OR 3.08, p=0.01). Desmoplakin genetic variants were significantly associated with heart failure occurrence in patients with arrhythmogenic cardiomyopathy (OR 3.08, p=0.01).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: