Pregnancy as a cardiac stress model.
Cardiac hypertrophy occurs during pregnancy as a consequence of both volume overload and hormonal changes. Both pregnancy- and exercise-induced cardiac hypertrophy are generally thought to be similar and physiological. Despite the fact that there are shared transcriptional responses in both forms of cardiac adaptation, pregnancy results in a distinct signature of gene expression in the heart. In some cases, however, pregnancy can induce adverse cardiac events in previously healthy women without any known cardiovascular disease. Peripartum cardiomyopathy is the leading cause of non-obstetric mortality during pregnancy. To understand how pregnancy can cause heart disease, it is first important to understand cardiac adaptation during normal pregnancy. This review provides an overview of the cardiac consequences of pregnancy, including haemodynamic, functional, structural, and morphological adaptations, as well as molecular phenotypes. In addition, this review describes the signalling pathways responsible for pregnancy-induced cardiac hypertrophy and angiogenesis. We also compare and contrast cardiac adaptation in response to disease, exercise, and pregnancy. The comparisons of these settings of cardiac hypertrophy provide insight into pregnancy-associated cardiac adaptation.
Department of Health, Exercise, and Sport Sciences, Texas Tech University, Lubbock, TX 79409, USA.
Eunhee
E
Chung
Leslie A
LA
Leinwand
D000818:Animals; D015444:Exercise; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006331:Heart Diseases / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology; D013312:Stress, Physiological
Hormones; Molecular signatures; Physiological cardiac hypertrophy; Pregnancy; Signalling pathways