Julie Damp1, Michael M Givertz2, Marc Semigran3, Rami Alharethi4, Gregory Ewald5, G Michael Felker6, Biykem Bozkurt7, John Boehmer8, Jennifer Haythe9, Hal Skopicki10, Karen Hanley-Yanez11, Jessica Pisarcik11, Indrani Halder11, John Gorcsan11, Sarosh Rana12, Zoltan Arany13, James D Fett11, Dennis M McNamara11. 1. Division of Cardiovascular Medicine, Vanderbilt University, Nashville, Tennessee. Electronic address: julie.boyd@vanderbilt.edu. 2. Division of Cardiology, Brigham and Women's Hospital, Boston, Massachusetts. 3. Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts. 4. Division of Cardiology, Intermountain Medical Center, Salt Lake City, Utah. 5. Division of Cardiology, Washington University in St. Louis, St. Louis, Missouri. 6. Division of Cardiology, Duke University, Durham, North Carolina. 7. Section of Cardiovascular Medicine, Baylor College of Medicine, Houston, Texas. 8. Division of Cardiology, Penn State Hershey Medical Center, Hershey, Pennsylvania. 9. Division of Cardiology, Columbia University, New York, New York. 10. Division of Cardiology, Stony Brook Medical Center, Stony Brook, New York. 11. Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, Pennsylvania. 12. Department of Obstetrics and Gynecology, University of Chicago, Chicago, Illinois. 13. Division of Cardiology, University of Pennsylvania, Philadelphia, Pennsylvania.
Abstract
OBJECTIVES: This study explored the association of vascular hormones with myocardial recovery and clinical outcomes in peripartum cardiomyopathy (PPCM). BACKGROUND: PPCM is an uncommon disorder with unknown etiology. Angiogenic imbalance may contribute to its pathophysiology. METHODS: In 98 women with newly diagnosed PPCM enrolled in the Investigation in Pregnancy Associated Cardiomyopathy study, serum was obtained at baseline for analysis of relaxin-2, prolactin, soluble fms-like tyrosine kinase 1 (sFlt1), and vascular endothelial growth factor (VEGF). Left ventricular ejection fraction (LVEF) was assessed by echocardiography at baseline and 2, 6, and 12 months. RESULTS: Mean age was 30 ± 6 years, with a baseline of LVEF 0.35 ± 0.09. Relaxin-2, prolactin, and sFlt1 were elevated in women presenting early post-partum, but decreased rapidly and were correlated inversely with time from delivery to presentation. In tertile analysis, higher relaxin-2 was associated with smaller left ventricular systolic diameter (p = 0.006) and higher LVEF at 2 months (p = 0.01). This was particularly evident in women presenting soon after delivery (p = 0.02). No relationship was evident for myocardial recovery and prolactin, sFlt1 or VEGF levels. sFlt1 levels were higher in women with higher New York Heart Association functional class (p = 0.01) and adverse clinical events (p = 0.004). CONCLUSIONS: In women with newly diagnosed PPCM, higher relaxin-2 levels soon after delivery were associated with myocardial recovery at 2 months. In contrast, higher sFlt1 levels correlated with more severe symptoms and major adverse clinical events. Vascular mediators may contribute to the development of PPCM and influence subsequent myocardial recovery. (Investigation in Pregnancy Associate Cardiomyopathy [IPAC]; NCT01085955).
OBJECTIVES: This study explored the association of vascular hormones with myocardial recovery and clinical outcomes in peripartum cardiomyopathy (PPCM). BACKGROUND: PPCM is an uncommon disorder with unknown etiology. Angiogenic imbalance may contribute to its pathophysiology. METHODS: In 98 women with newly diagnosed PPCM enrolled in the Investigation in Pregnancy Associated Cardiomyopathy study, serum was obtained at baseline for analysis of relaxin-2, prolactin, soluble fms-like tyrosine kinase 1 (sFlt1), and vascular endothelial growth factor (VEGF). Left ventricular ejection fraction (LVEF) was assessed by echocardiography at baseline and 2, 6, and 12 months. RESULTS: Mean age was 30 ± 6 years, with a baseline of LVEF 0.35 ± 0.09. Relaxin-2, prolactin, and sFlt1 were elevated in women presenting early post-partum, but decreased rapidly and were correlated inversely with time from delivery to presentation. In tertile analysis, higher relaxin-2 was associated with smaller left ventricular systolic diameter (p = 0.006) and higher LVEF at 2 months (p = 0.01). This was particularly evident in women presenting soon after delivery (p = 0.02). No relationship was evident for myocardial recovery and prolactin, sFlt1 or VEGF levels. sFlt1 levels were higher in women with higher New York Heart Association functional class (p = 0.01) and adverse clinical events (p = 0.004). CONCLUSIONS: In women with newly diagnosed PPCM, higher relaxin-2 levels soon after delivery were associated with myocardial recovery at 2 months. In contrast, higher sFlt1 levels correlated with more severe symptoms and major adverse clinical events. Vascular mediators may contribute to the development of PPCM and influence subsequent myocardial recovery. (Investigation in Pregnancy Associate Cardiomyopathy [IPAC]; NCT01085955).
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