Observational studyClinical cardiology2019
Titin-truncating variants are associated with heart failure events in patients with left ventricular non-compaction cardiomyopathy.
Observational study in Clinical cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Histopathological and epigenetic changes in myocardium associated with cancer therapy-related cardiac dysfunction.ESC heart failure · 2022Article
- Left Ventricular Noncompaction in Children: The Role of Genetics, Morphology, and Function for Outcome.Journal of cardiovascular development and disease · 2022Review
- Discerning the Ambiguous Role of MissenseJournal of personalized medicine · 2022Article
- Shared Genetic Risk Factors Between Cancer and Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2022Article
- Molecular Diagnosis of Inherited Cardiac Diseases in the Era of Next-Generation Sequencing: A Single Center's Experience Over 5 Years.Molecular diagnosis & therapy · 2021Article
- Reduced Systolic Function and Not Genetic Variants Determine Outcome in Pediatric and Adult Left Ventricular Noncompaction Cardiomyopathy.Frontiers in pediatrics · 2021Article
- Human Induced Pluripotent Stem-Cell-Derived Cardiomyocytes as Models for Genetic Cardiomyopathies.International journal of molecular sciences · 2019Review
- Titin-truncating variants are associated with heart failure events in patients with left ventricular non-compaction cardiomyopathy.Clinical cardiology · 2019Observational
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundTitin-truncating variants (TTNtv) have been recognized as the most prevalent genetic cause of dilated cardiomyopathy. However, their effects on phenotypes of left ventricular non-compaction cardiomyopathy (LVNC) remain largely unknown. HYPOTHESIS: The presence of TTNtv may have an effect on the phenotype of LVNC.
methodsTTN was comprehensively screened by targeted sequencing in a cohort of 83 adult patients with LVNC. Baseline and follow-up data of all participants were collected. The primary endpoint was a composite of death and heart transplantation. The secondary endpoint was heart failure (HF) events, a composite of HF-related death, heart transplantation, and HF hospitalization.
resultsOverall, 13 TTNtv were identified in 13 patients, with 9 TTNtv located in the A-band of titin. There was no significant difference in baseline characteristics between patients with and without TTNtv. During a median follow-up of 4.4 years, no significant difference in death and heart transplantation between the two groups was observed. However, more HF events occurred in TTNtv carriers than in non-carriers (P = 0.006). Multivariable analyses showed that TTNtv were associated with an increased risk of HF events independent of sex, age, and baseline cardiac function (hazard ratio: 3.25, 95% confidence interval: 1.50-7.01, P = 0.003). Sensitivity analysis excluding non-A-band TTNtv yielded similar results, but with less strength.
conclusionsThe presence of TTNtv may be a genetic modifier of LVNC and confer a higher risk of HF events among adult patients. Studies of larger cohorts are needed to confirm our findings.
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