Poor maternal CV health increases CVD risk in offspring
Introduction and methods
An ideal cardiovascular health (CVH) according to the American Heart Association (AHA) is the simultaneous presence of four ideal modifiable health behaviors and three ideal health factors. These ideal modifiable behavior factors are non-smoking, normal BMI, physical activity and dietary pattern consistent with current guidelines. The ideal health factors are total cholesterol <200 mg/dL, blood pressure <120/<80 mm Hg, and fasting glucose <100 mg/dL . Adherence to a healthy lifestyle reduces the risk of cardiovascular disease (CVD) and increases life expectancy and numbers of years free of CVD [2-4].
Parental transmission of CVH to children occurs via genetic and shared environmental factors across generations [4,5]. Evidence has suggested that CVD risk factors aggregate in families and are transmitted from parents to offspring [6-10]. Also, families with long life expectancies are more likely to have lower CVD risks . And maternal exposure to negative health effects are transmitted to the offspring during the fetal life [12,13].
This study prospectively examined the association between parental CVH and time to onset of CVD in offspring, stratified to sex or education level, and compared paternal and maternal CVH to CVD-free survival in their offspring.
The Framingham Heart Study (FHS) is a long-term, multigenerational study, comprised of residents of Framingham, MA, USA and focusing on the epidemiology of CVD. For this study, the Original and Offspring cohorts from the FHS were used. Participants aged 28 to 62 years were in 1948 included in the Original cohort. The children (6 to 70 years at baseline exam) from the participants of the Original cohort were included in the Offspring cohort in 1971. Only offspring (n=1,989) with their father (n=1,989) and mother (n=1,989) participating in the Original cohort were included in this subanalysis. Primary endpoint was the first occurrence of a fatal or non-fatal CVD event among offspring. A CVD event included coronary heart disease, intermittent claudication, congestive heart failure, stroke or transient ischemic attack. The CVH score was calculated from the AHA metric guideline and parents were grouped into three categories: poor (0-4), intermediate (5-9), or ideal (10-14). Recorded incident CVD events were analyzed from 1971 to December 31th, 2017.
- The overall CVD incidence rate (IR) in offspring was 10 per 1000 person-years (95% CI: 9.3-10.7). Sons had a higher CVD IR compared to daughters (IR 12.9, 95% CI: 11.7-14.2 vs. IR 7.6, 95% CI: 6.8-8.5, respectively, P<0.001).
- Sons of mothers with a poor CVH had the highest IR for CVD compared to sons of fathers with poor CVH score (IR 34.7, 95% CI: 26.3-45.8 vs. IR 14.9 95% CI: 12.0-18.5, respectively). Similar results were obtained for daughters stratified by their maternal and paternal’s CVH (for those with a mother with poor CVH: IR 17.7, 95% CI: 11.9-26.5 and for those with a father with poor CVH: IR 10.3, 95% CI: 8.2-13.0).
- The offspring of mothers with an ideal as well as intermediate CVH pattern lived 9 more years CVD-free compared to offspring from mother with a poor CVH score (27 vs. 18 years, P<0.001). There was no significant difference in median time lived free of CVD for offspring by paternal CVH status.
- The offspring of mothers with a poor CVH score had a ~2 fold risk increase in CVD compared to children of mothers with an ideal health pattern (aHR 2.09, 95% CI: 1.50-2.92, P<0.001). Similar results were seen by sex-specific analyses, where sons and daughters of mothers with a poor CVH pattern had a ~2 fold increase in early onset of CVD compared to ideal CVH mothers (sons: aHR 2.14, 95% CI: 1.41-3.26, P<0.001 and daughters: aHR 2.10, 95% CI: 1.20-3.67, P=0.010).
Offspring of mothers with an ideal CVH score lived significantly longer CVD-free lives than children from mothers with a poor health pattern. Moreover, the incidence rate of CVD in children with a poor maternal CVH score was highest among sons. The maternal CVH score was a more robust predictor of onset CVD for sons and daughters than paternal CVH.