Modifiable risk factors and risk of myocardial infarction in offspring with parental disease

Author:

Møller Amalie Lykkemark12ORCID,Larson Martin G34,Xanthakis Vanessa134ORCID,Vasan Ramachandran S1356ORCID,Andersson Charlotte7ORCID

Affiliation:

1. Section of Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine , 72 E Concord Street, Boston, 02118 MA , USA

2. Department of Cardiology, Nordsjællands Hospital , Dyrehavevej 29, 3400 Hillerød , Denmark

3. Boston University’s and National Heart, Lung, and Blood Institute’s Framingham Heart Study , 73 Mt Wayte Avenue, Framingham, 01702 MA , USA

4. Department of Biostatistics, Boston University School of Public Health , 801 Massachusetts Avenue, Boston, 02118 MA , USA

5. University of Texas School of Public Health San Antonio , 8403 Floyd Curl Drive, San Antonio, 78229 TX , USA

6. Departments of Medicine and Population Health Sciences, University of Texas Health Science Center , 7703 Floyd Curl Drive, San Antonio, 78229 TX , USA

7. Center for Advanced Heart Disease, Brigham and Women’s Hospital, Harvard Medical School , 75 Francis Street, Boston, 02115 MA , USA

Abstract

Abstract Aims Children of patients with early-onset myocardial infarction (MI) are at increased risk, but the importance of concordant vs. discordant parent–offspring risk factor profiles on MI risk is largely unknown. We quantified the long-term absolute risk of MI according to shared risk factors in adulthood. Methods and results We sampled data on familial predisposed offspring and their parents from the Framingham Heart Study. Early MI was defined as a history of parental MI onset before age 55 in men or 65 in women. Individuals were matched 3:1 with non-predisposed offspring. Cardiovascular risk factors included obesity, smoking, hypertension, high cholesterol, and diabetes. We estimated the absolute 20-year incidence of MI using the Aalen–Johansen estimator. At age 40, the 20-year risk of MI varied by cholesterol level [high cholesterol 25.7% (95% confidence interval 11.2–40.2%) vs. non-high cholesterol 3.4% (0.5–6.4)] among predisposed individuals, and this difference was greater than in controls [high cholesterol 9.3% (1.5–17.0) vs. non-high cholesterol 2.5% (1.1–3.8)]. Similar results were observed for prevalent hypertension [26.7% (10.8–42.5) vs. 4.0% (0.9–7.1) in predisposed vs. 10.8% (3.2–18.3) and 2.1% (0.8–3.4) in controls]. Among offspring without risk factors, parental risk factors carried a residual impact on 20-year MI risk in offspring [0% (0–11.6) for 0–1 parental risk factors vs. 3.3% (0–9.8) for ≥2 parent risk factors at age 40, vs. 2.9% (0–8.4) and 8.5% (0–19.8) at age 50 years]. Conclusion Children of patients with early-onset MI have low absolute risks of MI in the absence of midlife cardiovascular risk factors, especially if the parent also had a low risk factor burden prior to MI.

Funder

National Heart, Lung and Blood Institute

Evans Medical Foundation

Jay and Louis Coffman Endowment

Department of Medicine, Boston University School of Medicine

Danish Heart Foundation

Direktør Ib Henriksens Foundation

William Demant Foundation

Knud Højgaards Foundation

Aalborg University

Publisher

Oxford University Press (OUP)

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1. Does risk factor control beat familial predisposition for myocardial infarction?;European Journal of Preventive Cardiology;2024-06-06

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