Key result
Pathogenic sequence variants and CNVs showed numerically higher adverse cardiovascular risks in ACHD, but lost significance after multiple-testing adjustment.
Why the study?
Genetic abnormalities contribute to the phenotypic heterogeneity of congenital heart disease, yet the prognostic significance of pathogenic sequence variants and copy number variants in adults with congenital heart disease remains incompletely understood.
Are pathogenic sequence variants and copy number variants associated with higher risks of adverse cardiovascular outcomes in adults with congenital heart disease?
Cohort (n=1,000)
No
Are pathogenic sequence variants and copy number variants associated with higher risks of adverse cardiovascular outcomes in adults with congenital heart disease?
Although pathogenic sequence variants and copy number variants were associated with numerically higher rates of adverse cardiovascular events in adults with congenital heart disease, their independent prognostic significance was not statistically established after adjustment for multiple testing.
Answers are grounded in this paper and cite their sources.
Does not support incorporating variants into risk models; leaves open their independent prognostic value in congenital heart disease.
Background: Genetic abnormalities contribute to the phenotypic heterogeneity of congenital heart disease, yet their prognostic significance in adults with congenital heart disease remains incompletely understood. We examined the associations of pathogenic sequence variants and copy number variants (CNVs) with cardiovascular and major clinical outcomes in ACHD. Methods: In this prospective observational cohort study, 1,000 adults with structurally confirmed CHD were recruited from a tertiary care center in Noida, India, between January 2022 and January 2026 and followed through August 2026. Participants underwent exome sequencing and chromosomal microarray analysis and were classified into four mutually exclusive groups: reference, sequence-variant-only, CNV-only, and dual-positive. The primary outcome was time to first occurrence of a composite of cardiovascular death, unplanned heart failure hospitalization, resuscitated cardiac arrest, sustained ventricular tachyarrhythmia, heart transplantation, or durable mechanical circulatory support. Associations were evaluated using multivariable Cox regression. Results: Of 1,000 participants, 800 comprised the reference group, 120 had sequence variants only, 60 had CNVs only, and 20 had both sequence variants and CNVs. Over a median follow-up of 4.2 years, the primary outcome occurred in 12.0%, 20.0%, 25.0%, and 30.0% of participants, respectively. In fully adjusted analyses, the sequence-variant-only group had a higher risk of the primary outcome versus the reference group (hazard ratio [HR], 1.65; 95% confidence interval [CI], 1.01?2.69; p=0.0455). The CNV-only group had an HR of 1.92 (95% CI, 1.04?3.52; p=0.0360). Neither association remained significant after Holm adjustment (adjusted p=0.072 for both). The dual-positive group had an HR of 2.12 (95% CI, 0.83?5.42; p=0.1182). Extracardiac congenital anomalies and neurological disorders were more prevalent among individuals with genetic variants, while secondary outcomes showed no significant associations. Conclusions: Pathogenic sequence variants and CNVs were associated with numerically higher risks of adverse cardiovascular outcomes in ACHD, but independent prognostic significance was not established after adjustment for multiple testing.
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Youssef et al. (2026) conducted a cohort in Congenital heart disease in adults (ACHD) (n=1,000). Pathogenic sequence variants and copy number variants (CNVs) vs. Reference group without pathogenic sequence variants or CNVs was evaluated on Composite of cardiovascular death, unplanned heart failure hospitalization, resuscitated cardiac arrest, sustained ventricular tachyarrhythmia, heart transplantation, or durable mechanical circulatory support (HR 1.65, 95% CI 1.01-2.69, p=0.0455 (adjusted p=0.072)). Pathogenic sequence variants and CNVs showed numerically higher adverse cardiovascular risks in ACHD, but lost significance after multiple-testing adjustment.
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