Background: Mitral valve prolapse (MVP) is a common condition, typically benign, but in a small subset of patients, it may lead to life-threatening arrhythmias and sudden cardiac death (SCD). This arrhythmogenic MVP phenotype is often associated with bileaflet prolapse, mitral annular disjunction (MAD), and myocardial fibrosis identified via late gadolinium enhancement (LGE) on cardiac MRI.Case Summary: Our patient is a 49-year-old man presented with monomorphic ventricular tachycardia and near-syncope. Echocardiography showed bileaflet MVP, MAD and mild mitral regurgitation. Cardiac MRI revealed fibrosis in the papillary muscle. Electrophysiological study (EPS) confirmed inducible ventricular fibrillation (VF) triggered by papillary muscle PVCs. Catheter ablation was successfully performed, eliminating the arrhythmic focus. Despite successful ablation, an implantable cardioverter-defibrillator (ICD) was implanted for secondary prevention, given the high-risk structural substrate. The patient remained arrhythmia-free over 2 years of follow-up.Discussion: This case highlights critical diagnostic markers—bileaflet prolapse and LGE—associated with arrhythmogenic MVP. While ablation may suppress triggers, it does not completely eliminate the underlying substrate. Current expert consensus supports ICD implantation in patients with sustained VT/VF or sudden cardiac arrest, regardless of ablation success. Management should be individualized based on risk profile, imaging findings, and clinical presentation.Conclusion: Malignant MVP warrants comprehensive evaluation with echocardiography, cardiac MRI, and EPS. Catheter ablation is effective in eliminating arrhythmic foci, but ICD therapy remains essential for secondary prevention. Future high-quality trials and clear guidelines for diagnosis, risk stratification, and management are essential to avoid both over- and under-treatment, ensuring optimal outcomes for the patients with MVP.

Background and Objectives: Selection for implantable cardioverter-defibrillator (ICD) therapy anchored in left ventricular ejection fraction (LVEF) may miss at-risk patients with LVEF > 35%. We tested whether a simple electrocardiogram (ECG) burden adds discrimination for appropriate ICD therapy beyond clinical factors and LVEF. Methods Single-center retrospective cohort of 237 ICD recipients. Six routinely reported ECG abnormalities were prespecified and summed as an ECG burden (0–6), then categorized as 0–1, 2–3, or ≥ 4 abnormalities. Logistic regression estimated odds ratios (OR) with 95% CIs for appropriate ICD therapy. Multivariable models included LVEF category (≤ 35% vs > 35%), ischemic vs non-ischemic cardiomyopathy, ICD indication (secondary vs primary prevention), and ECG burden category. Discrimination of the clinical + LVEF model with and without ECG burden was assessed by the C-statistic and DeLong test. Results Mean age was 62.1 ± 16.2 years; 71% male; 61% ischemic; 72% primary prevention; follow-up 7.6 ± 2.9 years. High ECG burden (≥ 4) independently predicted appropriate therapy (OR 3.6, 95% CI 1.8–7.2; p < 0.001). Adding ECG burden to a clinical + LVEF model improved discrimination, increasing the C-statistic from 0.67 to 0.75 (DeLong p = 0.01). Kaplan–Meier curves showed graded separation across burden categories (log-rank p < 0.001). Among patients with LVEF > 35%, observed therapy was higher with high burden (~ 26.3%) than with low burden (~ 6.2%). Conclusions An ECG burden based on six routine abnormalities provides independent and incremental prognostic value beyond LVEF, including in patients with preserved LVEF. This approach uses routinely available measures and may help refine risk-aligned ICD decisions. Prospective multicenter validation is warranted.

On 4 September 2026, the Lp(a)HORIZON trial reported that pelacarsen did not reduce its primary composite endpoint in 8,323 patients with established atherosclerotic cardiovascular disease and lipoprotein(a) of at least 70 mg/dL. The full dataset has not been presented. This commentary argues that the topline result should neither be dismissed nor allowed to erase the genetic and epidemiologic evidence preceding it, because the two bodies of evidence answer different questions. Mendelian randomization describes lifelong exposure and cannot be translated directly into the effect of a finite-duration drug. Imaging associates Lp(a) with plaque burden and, in one post hoc analysis, independently with focal vulnerable plaque; neither is a clinical outcome. Intensive LDL-C lowering itself modifies plaque vulnerability, so no exclusive division of labor between the two lipoproteins is supportable. The most parsimonious reading of a negative trial remains that the intervention does not work, and that possibility is held open here. Five parameters are proposed — achieved absolute concentration, the prespecified ≥90 mg/dL population, coronary endpoint components, follow-up distribution with event-time curves, and background lipid-lowering therapy and adherence — that determine what the trial actually tested, whatever the direction of the result.