INTRODUCTION
Increasing evidence demonstrates an association between offspring size at birth and maternal cardiovascular disease (CVD) risk. A meta-analysis of six studies, published in 2007, showed an inverse relationship between offspring weight at birth and maternal CVD mortality (pooled adjusted hazard ratio (aHR) of 0.75 (95% confidence interval (CI): 0.67 to 0.84) for 1-standard deviation (SD) increase in offspring birthweight)1. A subsequent study of 1,400,383 women showed 1.8 times higher risk of mortality from CVD among women who gave birth to low birth weight (LBW, birthweight <2500g) infants compared to those who gave birth to normal birthweight (2500-3999g) infants (aHR: 1.85; 95% CI 1.57 to 2.18)2. Recent studies have shown similar associations for women who give birth to infants diagnosed as small for gestational age (SGA) at birth compared to women who give birth to average for gestational age (AGA) infants3, 4. The terms “LBW” and “SGA” are both used to define infants considered small at birth. Although many infants classified as SGA or LBW have intrauterine growth restriction (IUGR) and many growth restricted infants are born with LBW or are classified as SGA, the three terms are not synonymous5. LBW simply means birthweight < 2.5 kg and at present, the definition is mostly used in developing countries where gestational age is often uncertain, and reliable population centiles let alone customized centiles are not available. SGA means birthweight < 10th centile for a given gestational age. Population centiles use birthweight centiles on a whole population, irrespective of maternal ethnicity, height and weight and customized centiles provide birthweight centiles customized for maternal ethnicity, height, weight and parity. Infants with IUGR are those that do not achieve fullin utero growth potential because of genetic or environmental factors and are at increased risk for significant morbidity and mortality compared to infants with normal in utero growth. Infants born growth restricted are at increased risk of CVD and type 2 diabetes mellitus in adulthood and “programming in response to an adverse intrauterine environment” as well as genetic and environmental influences are proposed to contribute to the risk. However, associations between offspring SGA/LBW and maternal CVD risk cannot be explained to a large extent by programming. This, however, can be explained by the presence of genetic polymorphisms that influence both fetal growth and CVD as well as by adverse environmental influences that operate across the parental life course and affect both offspring and adult health. To our knowledge there is no systematic review and meta-analysis that has assessed maternal risk for CVD using data from studies reporting on the three common classifications of offspring size at birth. Therefore, the aim of this study was to identify the relationship between offspring size at birth and maternal CVD risk based on different classifications of offspring size at birth.