Article Text
Abstract
Objective Cardiac disease is the leading cause of indirect maternal mortality. The aim of this study was to analyse to what extent socioeconomic factors influence the outcome of pregnancy in women with heart disease.
Methods The Registry of Pregnancy and Cardiac disease is a global prospective registry. For this analysis, countries that enrolled ≥10 patients were included. A combined cardiac endpoint included maternal cardiac death, arrhythmia requiring treatment, heart failure, thromboembolic event, aortic dissection, endocarditis, acute coronary syndrome, hospitalisation for cardiac reason or intervention. Associations between patient characteristics, country characteristics (income inequality expressed as Gini coefficient, health expenditure, schooling, gross domestic product, birth rate and hospital beds) and cardiac endpoints were checked in a three-level model (patient–centre–country).
Results A total of 30 countries enrolled 2924 patients from 89 centres. At least one endpoint occurred in 645 women (22.1%). Maternal age, New York Heart Association classification and modified WHO risk classification were associated with the combined endpoint and explained 37% of variance in outcome. Gini coefficient and country-specific birth rate explained an additional 4%. There were large differences between the individual countries, but the need for multilevel modelling to account for these differences disappeared after adjustment for patient characteristics, Gini and country-specific birth rate.
Conclusion While there are definite interregional differences in pregnancy outcome in women with cardiac disease, these differences seem to be mainly driven by individual patient characteristics. Adjustment for country characteristics refined the results to a limited extent, but maternal condition seems to be the main determinant of outcome.
- pregnancy
- global health
- congenital heart disease
- valvular heart disease
- heart failure
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Footnotes
Contributors Conception and design: IMvH, LT, APPM, MRJ, RH, JWR-H. Acquisition: IMvH, KS-H, NT, ML, MRJ, RH, JWR-H, ROPAC investigators. Analysis and interpretation: IMvH, SB, RFSK, KS-H, NM, RF, JWR-H. Drafting: IMvH, SB, JWR-H. Critical revision: IMvH, SB, RFSK, KS-H, NT, ML, LT, APPM, MRJ, NM, RF, RH, JWR-H. Final approval: IMvH, SB, RFSK, KS-H, NT, ML, LT, APPM, MRJ, NM, RF, RH, JWRH. Agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved: IMvH, SB, RFSK, KS-H, NT, ML, LT, APPM, MRJ, NM, RF, RH, JWRH.
Funding Since the start of EORP, the following companies have supported the programme: Abbott Vascular Int. (2011–2014), Amgen Cardiovascular (2009–2018), AstraZeneca (2014–2017), Bayer (2009–2018), Boehringer Ingelheim (2009–2016), Boston Scientific (2009–2012), The Bristol Myers Squibb and Pfizer Alliance (2011–2016), The Alliance Daiichi Sankyo Europe GmbH and Eli Lilly and Company (2011–2017), Edwards (2016–2019), Gedeon Richter Plc (2014–2017), Menarini Int. Op. (2009–2012), MSD-Merck and Co. (2011–2014), Novartis Pharma AG (2014–2017), ResMed (2014–2016), Sanofi (2009–2011) and SERVIER (2010–2018). The companies that support EORP were not involved in any part of the study or this report.
Competing interests APPM reports grants from Novartis, Cardiorentis and Bayer outside the submitted work. LT reports personal fees from Servier, CVIE Therapeutics, Cardiorentis, Boston Scientific and Medtronic outside the submitted work.
Provenance and peer review Not commissioned; externally peer reviewed.