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Parental history of cardiovascular events and atherosclerosis among stroke patients and partners – The first and second generation in the Norwegian Stroke in the Young Study

Parental cardiovascular events and arteries in offspring

Beenish Nawaz
Neurological department, Haukeland university hospital, Bergen, Norway
Sahrai Saeed
Cardiology department, Oslo university hospital, Ullevaal, Oslo, Norway
Jörg Assmus
Centre for clinical research, Haukeland university hospital, Bergen, Norway
Annette Fromm
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Halvor Øygarden
Department of Neurology, Sørlandet Hospital, Kristiansand, Norway
Solveig Boland
Department of Medicine, Sykehuset Innlandet, Hamar, Norway
Halvor Næss
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Ulrike Waje-Andreassen
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Keywords:
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Copyright (c) 2026 MD, PhD, Consultant Beenish Nawaz, MD, PhD, Associate professor, Consultant Sahrai Saeed, Mr Jörg Assmus, MD, Phd, Consultant Annette Fromm, MD, PhD, Associate Professor, Consultant Halvor Øygarden, MD Solveig Boland, MD, Phd, Professor, Senior Consultant Halvor Næss, MD, PhD, Professor, Senior Consultant Ulrike Waje-Andreassen

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Abstract

Introduction: Age, sex and family history of cardiovascular disease (CVD) are non-modifiable risk factors of CVD in offspring. Our aim was to relate parental CVD (pCVD) to artery vessel-wall measurements in offspring.
Patients and methods: Offspring consisted of acute ischaemic stroke patients (15-60 years) and their partners. Young offspring was defined as ≤45 years old. Arterial wall changes were assessed as intima-media thickness of carotid and femoral arteries (cIMT/fIMT), abdominal aortic plaques (AAP), and ankle-arm index (AAI). Any offspring reported parental coronary artery disease (pCAD) and parental peripheral artery disease (pPAD). In addition, pCAD and pPAD were also verified by standardized questionnaires for living parents, or by medical records for deceased parents.
Results: Reported vs. verified pCVD was present for around 90% vs. 50% of parents. Reported pCAD/pPAD was positive for 227/67 offspring and verified pCAD/pPAD was positive for 148/36 offspring, respectively.
Reported and verified pCAD and pPAD were related to higher cIMT and fIMT. Reported and verified pCAD was also related to AAP and reported pPAD to AAI. The effect attenuated after adjusting for age, hypertension, dyslipidemia, diabetes mellitus and smoking. Among young offspring, reported pCAD was associated with higher cIMT and fIMT, even though the total number of young offspring was 4-fold lower compared to middle-aged offspring.
Conclusions: Parental CVD is related to artery wall changes in offspring, particularly in young offspring. Regarding CVD risk assessment, extensive parental verification of CVD might not be necessary as many young patients and partners seem to be well-orientated about their parental CVD. Primary prevention from young age should get more attention.

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