Cardiac Manifestations of Preeclampsia

先兆子痫的心脏表现

• 批准号: 10631830
• 负责人: Natalie A Bello
• 金额: $ 38.86万
• 依托单位: CEDARS-SINAI MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-06-15 至 2024-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10631830
• 关键词: Affect; Ancillary Study; Angiogenic Proteins; Biological Markers; Blood Pressure; Cardiac; Cardiac health; Cardiovascular Abnormalities; Cardiovascular Diseases; Cessation of life; Child; Conceptions; Coronary; Coronary Angiography; Development; Discipline of obstetrics; Enrollment; Equation; Event; Female; Fibrosis; Funding; Future; Health Care Costs; Heart; Heart Abnormalities; Heart Diseases; Heart failure; Hypertension; Image; Incidence; Intervention; Interview; Ionizing radiation; Knowledge; Lead; Left Ventricular Function; Left Ventricular Hypertrophy; Left Ventricular Mass; Life; Longevity; Magnetic Resonance; Measures; Medical Records; Medical center; Methods; Microcirculation; Microvascular Dysfunction; Modeling; Modification; Monitor; Morbidity - disease rate; Mothers; Myocardial; Myocardial Infarction; Myocardial Ischemia; Myocardial perfusion; Nulliparity; Obesity; Outcome Study; Pathologic; Perinatal; Phenotype; Placenta; Play; Postpartum Period; Pre-Eclampsia; Pregnancy; Pregnancy Outcome; Pregnancy Proteins; Proteins; Proteinuria; Protocols documentation; Recording of previous events; Risk; Risk Factors; Role; Site; Stress; Structure; Sustainable Development; Telephone; Testing; Time; United States National Institutes of Health; Universities; Visit; Woman; cardiac magnetic resonance imaging; cardiovascular disorder risk; cardiovascular effects; cohort; coronary fibrosis; coronary perfusion; defined contribution; diagnostic accuracy; endothelial dysfunction; fetal; heart imaging; imaging modality; indexing; interstitial; mortality; novel; pathophysiology of preeclampsia; potential biomarker; pregnancy disorder; premature; prevent; recruit; risk sharing; risk stratification; sex; young woman

Preeclampsia, a hypertensive disorder affecting 5-8% of pregnancies, is associated with life-threatening maternal-fetal consequences and its incidence is on the rise. Long regarded as a temporary obstetrical condition with implications limited to pregnancy, it is now recognized that women with prior preeclampsia are at elevated risk for the development of sustained hypertension, premature cardiovascular disease (CVD) and a shortened lifespan. The pathophysiology of preeclampsia includes excessive placental release of anti- angiogenic proteins that lead to systemic manifestations of hypertension, proteinuria, and endothelial dysfunction. Preeclampsia is also associated with left ventricular (LV) hypertrophy and abnormal LV function, and growing body of evidence suggests that the cardiovascular abnormalities persist beyond the peripartum period. The mechanism of insult of preeclampsia’s cardiovascular effects are unknown. The central hypothesis of this proposal is that the anti-angiogenic state induced by preeclampsia increases future CVD risk by directly altering cardiac structure and function. We will employ state of the art cardiac magnetic resonance (CMR) stress imaging to quantify the coronary microcirculation and to provide deep cardiac phenotyping of the structural and functional changes after preeclampsia. We will perform a single site ancillary study in 120 women (40 with preeclampsia) followed at Columbia University in the Nulliparous Pregnancy Outcomes Study Monitoring Mothers-to-be Heart Health Study (nuMoM2b-HHS) to pursue the following specific aims: (1) To examine whether there are differences in the coronary microcirculation of women with a history of preeclampsia during their nuMoM2b index pregnancy compared to control women who did not have preeclampsia; (2) To determine the extent to which previous preeclampsia directly alters later cardiac structure by increasing LV mass and separately fibrosis; (3) To quantify the associations between circulating anti-angiogenic proteins of pregnancy with coronary perfusion and fibrosis 7 to 14 years after delivery. Comprehensive cardiac phenotyping of women with and without a history of preeclampsia will inform future studies examining CVD risk stratification and modification in women with a history of preeclampsia. Despite sharing many risk factors, including female predominance, obesity, and hypertension, the associations of preeclampsia with coronary microvascular disease and myocardial fibrosis have not been examined. This proposal is a crucial step towards better understanding the mechanisms through which preeclampsia alters future CVD risk in women. This knowledge will enable the development of novel, informed interventions to prevent or delay the incidence of CVD in women with a history of preeclampsia thereby decreasing premature morbidity and mortality and healthcare costs in a young and expanding subset of women.

先兆子痫是一种高血压疾病，影响5-8%的妊娠，与危及生命有关。 母婴后果，其发病率正在上升。长期以来被视为临时产科 目前，人们认识到，有先兆子痫病史的妇女， 发生持续性高血压、早发心血管疾病（CVD）和 寿命缩短先兆子痫的病理生理学包括胎盘过度释放抗- 血管生成蛋白，导致高血压、蛋白尿和内皮细胞增生的全身表现， 功能障碍先兆子痫还与左心室（LV）肥大和LV功能异常有关， 越来越多的证据表明，心血管异常持续超过围产期， 期先兆子痫对心血管影响的机制尚不清楚。核心假设 这一建议的一个重要方面是，先兆子痫诱导的抗血管生成状态直接增加了未来CVD的风险， 改变心脏结构和功能我们将采用最先进的心脏磁共振（CMR） 应力成像，以量化冠状动脉微循环，并提供深心脏表型的 先兆子痫后的结构和功能变化。我们将在120个研究中心进行单中心辅助研究 在哥伦比亚大学的未产妊娠结局研究中， 监测准妈妈心脏健康研究（nuMoM 2b-HHS）的具体目标如下：（1） 检查有先兆子痫病史的女性冠状动脉微循环是否存在差异 与没有先兆子痫的对照妇女相比，在nuMoM 2b指数妊娠期间;（2） 确定既往先兆子痫通过增加LV质量直接改变后期心脏结构的程度 （3）量化妊娠期循环中抗血管生成蛋白与血管生成的关系， 冠状动脉灌注和纤维化7至14年后交付。女性的综合心脏表型 有和没有先兆子痫病史将为未来的研究提供信息， 有先兆子痫病史的妇女中的变化。尽管有许多风险因素，包括女性 优势，肥胖，高血压，先兆子痫与冠状动脉微血管的关系 疾病和心肌纤维化尚未被检查。这一提议是朝着更好地 了解先兆子痫改变女性未来CVD风险的机制。这些知识 将使开发新的，知情的干预措施，以预防或延迟心血管疾病的发病率， 有先兆子痫病史的妇女，从而降低过早发病率和死亡率， 在年轻和不断扩大的女性子集中的成本。