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Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study.

Arnott C, Skilton MR, Ruohonen S, Juonala M, Viikari JS, Kähönen M, Lehtimäki T, Laitinen T, Celermajer DS, Raitakari OT - Open Heart (2015)

Bottom Line: Impaired fetal growth is associated with increased cardiovascular morbidity and mortality in adulthood.LV stroke volume was greater in those born AGA (74.5 mL SGA vs 78.8 mL AGA, p<0.01), with no significant difference in cardiac output (5 L/min SGA vs 5.2 L/min AGA, p=0.06), heart rate, diastolic indices or sphericity index.Adults born SGA have some statistically significant but subtle changes in cardiac structure and function, which are less marked than have been described in childhood, and are unlikely to play a pathogenic role in their elevated cardiovascular risk.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medicine , University of Sydney , Sydney , Australia ; Department of Cardiology , Royal Prince Alfred Hospital , Sydney , Australia ; Department of Cardiology , Prince of Wales Hospital , Sydney , Australia.

ABSTRACT

Background and objectives: Impaired fetal growth is associated with increased cardiovascular morbidity and mortality in adulthood. We sought to determine whether adults born with intrauterine growth restriction have primary maladaptive changes in cardiac structure.

Methods: Study participants were adults (34-49 years) who attended the 31-year follow-up of the Cardiovascular Risk in Young Finns Study (longitudinal cohort). Transthoracic echocardiograms and demographic and cardiovascular risk surveys were completed for 157 adults born small for gestational age (SGA, birth weight <10th population centile) and 627 born average for gestational age (average for gestational age (AGA), birth weight 50th-90th population centile).

Results: Those born growth restricted had subtly enlarged hearts with indexed left ventricular (LV) end-systolic and end-diastolic diameters slightly greater in the SGA individuals than the AGA group (LVESD 18.7 mm/m(2) SGA vs 18.1 mm/m(2) AGA, p<0.01; LVEDD 27.5 mm/m(2) SGA vs 26.6 mm/m(2) AGA, p<0.01); LV base-to-apex length (47.4 mm/m(2) SGA vs 46.0 mm/m(2) AGA, p<0.01); LV basal diameter (26.4 mm/m(2) SGA vs 25.7 mm/m(2) AGA, p<0.01); and right ventricular base-to-apex length (40.1 mm/m(2) SGA vs 39.2 mm/m(2) AGA, p=0.02). LV stroke volume was greater in those born AGA (74.5 mL SGA vs 78.8 mL AGA, p<0.01), with no significant difference in cardiac output (5 L/min SGA vs 5.2 L/min AGA, p=0.06), heart rate, diastolic indices or sphericity index.

Conclusions: Adults born SGA have some statistically significant but subtle changes in cardiac structure and function, which are less marked than have been described in childhood, and are unlikely to play a pathogenic role in their elevated cardiovascular risk.

No MeSH data available.


Related in: MedlinePlus

Dimensions indexed to body surface area (AGA, appropriate birth weight for gestational age; SGA, small for gestational age; LVED, left ventricular end-diastolic; LVES, left ventricular end-systolic; RV, right ventricular). All data shown as means (95% CI) and adjusted for age, sex, blood pressure, physical activity levels and socioeconomic status.
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OPENHRT2015000265F2: Dimensions indexed to body surface area (AGA, appropriate birth weight for gestational age; SGA, small for gestational age; LVED, left ventricular end-diastolic; LVES, left ventricular end-systolic; RV, right ventricular). All data shown as means (95% CI) and adjusted for age, sex, blood pressure, physical activity levels and socioeconomic status.

Mentions: After indexing for BSA, indexed RV longitudinal base-to-apex length was significantly greater for the SGA versus AGA adults (40.1 mm/m2 SGA vs 39.2 mm/m2 AGA, p=0.02), with no difference noted in the indexed basal diameter or volumes. Despite the differences in indexed dimensions between the two groups, there was no difference in LV or RV sphericity index (tables 2 and 3; figure 2).


Subtle increases in heart size persist into adulthood in growth restricted babies: the Cardiovascular Risk in Young Finns Study.

Arnott C, Skilton MR, Ruohonen S, Juonala M, Viikari JS, Kähönen M, Lehtimäki T, Laitinen T, Celermajer DS, Raitakari OT - Open Heart (2015)

Dimensions indexed to body surface area (AGA, appropriate birth weight for gestational age; SGA, small for gestational age; LVED, left ventricular end-diastolic; LVES, left ventricular end-systolic; RV, right ventricular). All data shown as means (95% CI) and adjusted for age, sex, blood pressure, physical activity levels and socioeconomic status.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555072&req=5

OPENHRT2015000265F2: Dimensions indexed to body surface area (AGA, appropriate birth weight for gestational age; SGA, small for gestational age; LVED, left ventricular end-diastolic; LVES, left ventricular end-systolic; RV, right ventricular). All data shown as means (95% CI) and adjusted for age, sex, blood pressure, physical activity levels and socioeconomic status.
Mentions: After indexing for BSA, indexed RV longitudinal base-to-apex length was significantly greater for the SGA versus AGA adults (40.1 mm/m2 SGA vs 39.2 mm/m2 AGA, p=0.02), with no difference noted in the indexed basal diameter or volumes. Despite the differences in indexed dimensions between the two groups, there was no difference in LV or RV sphericity index (tables 2 and 3; figure 2).

Bottom Line: Impaired fetal growth is associated with increased cardiovascular morbidity and mortality in adulthood.LV stroke volume was greater in those born AGA (74.5 mL SGA vs 78.8 mL AGA, p<0.01), with no significant difference in cardiac output (5 L/min SGA vs 5.2 L/min AGA, p=0.06), heart rate, diastolic indices or sphericity index.Adults born SGA have some statistically significant but subtle changes in cardiac structure and function, which are less marked than have been described in childhood, and are unlikely to play a pathogenic role in their elevated cardiovascular risk.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Medicine , University of Sydney , Sydney , Australia ; Department of Cardiology , Royal Prince Alfred Hospital , Sydney , Australia ; Department of Cardiology , Prince of Wales Hospital , Sydney , Australia.

ABSTRACT

Background and objectives: Impaired fetal growth is associated with increased cardiovascular morbidity and mortality in adulthood. We sought to determine whether adults born with intrauterine growth restriction have primary maladaptive changes in cardiac structure.

Methods: Study participants were adults (34-49 years) who attended the 31-year follow-up of the Cardiovascular Risk in Young Finns Study (longitudinal cohort). Transthoracic echocardiograms and demographic and cardiovascular risk surveys were completed for 157 adults born small for gestational age (SGA, birth weight <10th population centile) and 627 born average for gestational age (average for gestational age (AGA), birth weight 50th-90th population centile).

Results: Those born growth restricted had subtly enlarged hearts with indexed left ventricular (LV) end-systolic and end-diastolic diameters slightly greater in the SGA individuals than the AGA group (LVESD 18.7 mm/m(2) SGA vs 18.1 mm/m(2) AGA, p<0.01; LVEDD 27.5 mm/m(2) SGA vs 26.6 mm/m(2) AGA, p<0.01); LV base-to-apex length (47.4 mm/m(2) SGA vs 46.0 mm/m(2) AGA, p<0.01); LV basal diameter (26.4 mm/m(2) SGA vs 25.7 mm/m(2) AGA, p<0.01); and right ventricular base-to-apex length (40.1 mm/m(2) SGA vs 39.2 mm/m(2) AGA, p=0.02). LV stroke volume was greater in those born AGA (74.5 mL SGA vs 78.8 mL AGA, p<0.01), with no significant difference in cardiac output (5 L/min SGA vs 5.2 L/min AGA, p=0.06), heart rate, diastolic indices or sphericity index.

Conclusions: Adults born SGA have some statistically significant but subtle changes in cardiac structure and function, which are less marked than have been described in childhood, and are unlikely to play a pathogenic role in their elevated cardiovascular risk.

No MeSH data available.


Related in: MedlinePlus