Coronary Microvascular Function Following Severe Preeclampsia

Author:

Honigberg Michael C.12ORCID,Economy Katherine E.3ORCID,Pabón Maria A.4ORCID,Wang Xiaowen4ORCID,Castro Claire1ORCID,Brown Jenifer M.45ORCID,Divakaran Sanjay45ORCID,Weber Brittany N.45ORCID,Barrett Leanne5ORCID,Perillo Anna5,Sun Anina Y.5,Antoine Tajmara1,Farrohi Faranak4,Docktor Brenda4,Lau Emily S.1ORCID,DeFaria Yeh Doreen1,Natarajan Pradeep12ORCID,Sarma Amy A.1,Weisbrod Robert M.6,Hamburg Naomi M.6ORCID,Ho Jennifer E.7ORCID,Roh Jason D.1ORCID,Wood Malissa J.18,Scott Nandita S.1ORCID,Di Carli Marcelo F.45ORCID

Affiliation:

1. Cardiology Division, Department of Medicine, Massachusetts General Hospital (M.C.H., C.C., T.A., E.S.L., D.D.Y., P.N., A.A.S., J.D.R., M.J.W., N.S.S.), Harvard Medical School, Boston.

2. Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA (M.C.H., P.N.).

3. Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology (K.E.E.), Brigham and Women’s Hospital, Harvard Medical School, Boston, MA.

4. Division of Cardiovascular Medicine, Department of Medicine (M.A.P., X.W., J.M.B., S.D., B.N.W., F.F., B.D., M.F.D.C.), Brigham and Women’s Hospital, Harvard Medical School, Boston, MA.

5. Cardiovascular Imaging Program, Departments of Radiology and Medicine and Division of Nuclear Medicine and Molecular Imaging, Department of Radiology (J.M.B., S.D., B.N.W., L.B., A.P., A.Y.S., M.F.D.C.), Brigham and Women’s Hospital, Harvard Medical School, Boston, MA.

6. Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (R.M.W., N.M.H.).

7. Division of Cardiovascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center (J.E.H.), Harvard Medical School, Boston.

8. Lee Health Heart Institute, Fort Myers, FL (M.J.W.).

Abstract

BACKGROUND: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating proangiogenic and antiangiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia-associated cardiovascular risk. METHODS: Women with singleton pregnancies complicated by severe antepartum-onset preeclampsia and a comparator group with normotensive deliveries underwent cardiac positron emission tomography within 4 weeks of delivery. A control group of premenopausal, nonpostpartum women was also included. Myocardial flow reserve, myocardial blood flow, and coronary vascular resistance were compared across groups. sFlt-1 (soluble fms-like tyrosine kinase receptor-1) and PlGF (placental growth factor) were measured at imaging. RESULTS: The primary cohort included 19 women with severe preeclampsia (imaged at a mean of 15.3 days postpartum), 5 with normotensive pregnancy (mean, 14.4 days postpartum), and 13 nonpostpartum female controls. Preeclampsia was associated with lower myocardial flow reserve (β, −0.67 [95% CI, −1.21 to −0.13]; P =0.016), lower stress myocardial blood flow (β, −0.68 [95% CI, −1.07 to −0.29] mL/min per g; P =0.001), and higher stress coronary vascular resistance (β, +12.4 [95% CI, 6.0 to 18.7] mm Hg/mL per min/g; P =0.001) versus nonpostpartum controls. Myocardial flow reserve and coronary vascular resistance after normotensive pregnancy were intermediate between preeclamptic and nonpostpartum groups. Following preeclampsia, myocardial flow reserve was positively associated with time following delivery ( P =0.008). The sFlt-1/PlGF ratio strongly correlated with rest myocardial blood flow ( r =0.71; P <0.001), independent of hemodynamics. CONCLUSIONS: In this exploratory cross-sectional study, we observed reduced coronary microvascular function in the early postpartum period following preeclampsia, suggesting that systemic microvascular dysfunction in preeclampsia involves coronary microcirculation. Further research is needed to establish interventions to mitigate the risk of preeclampsia-associated cardiovascular disease.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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