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.

卫生症是一种高血压疾病，影响了5-8％的怀孕，与威胁生命有关 母亲的后果及其事件正在上升。长期以来被视为临时产科 有含义的病情仅限于怀孕，现在已经认识到，先前的先兆子痫的妇女处于 持续高血压，心血管疾病（CVD）和A的风险升高 寿命缩短。子痫前期的病理生理学包括额外的抗释放 导致高血压，蛋白尿和内皮的全身表现的血管生成蛋白 功能障碍。 precamia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，心血管异常持续了 时期。侵害前峰心血管效应的机制尚不清楚。中心假设 该提议是，先兆子痫诱导的抗血管生成状态通过直接提高了未来的CVD风险 改变心脏结构和功能。我们将采用ART心脏磁共振状态（CMR） 压力成像以量化冠状动脉微循环并提供深度心脏表型 先兆子痫后的结构和功能变化。我们将在120中进行单个站点辅助研究 妇女（40岁的先兆子痫）在哥伦比亚大学进行了无效的妊娠结局研究 监测准母亲健康研究（NUMOM2B-HHS）以购买以下特定目的：（1） 检查具有先兆子痫史的女性的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NUMOM2B指数期间妊娠期间； （2）至 通过增加LV质量来确定先前先前的先前前晶状体直接改变后来的心脏结构的程度 并分别纤维化； （3）量化妊娠循环抗血管生成蛋白之间的关联 分娩后7到14年，冠状动脉灌注和纤维化。女性的全面心脏表型 在有或没有学位前的史上，将为未来研究CVD风险分层和 具有先兆子痫史的女性的修改。尽管分享了许多风险因素，包括女性 先兆子痫与冠状动脉微血管的关联，肥胖和高血压 尚未检查疾病和心肌纤维化。该提议是迈向更好的关键一步 了解先兆子痫会改变女性未来CVD风险的机制。这个知识 将能够开发新颖，知情的干预措施，以防止或延迟CVD的事​​件 具有先兆子痫病史的妇女，从而降低了过早的发病率，死亡率和医疗保健 年轻且不断扩大的妇女的成本。