Introduction
Hypertensive disorders of pregnancy (HDP) are a risk factor for both peripartum cardiomyopathy (PPCM)1–3 and cardiomyopathy in later life.4 Indeed, the levels of cardiac biomarkers, such as brain natriuretic peptide (BNP) and troponin I, are increased in women with HDP compared with those with normotensive control pregnancy (NCP).5–7 These observations suggest that somewhat pathological cardiac remodelling, that is, relative lack of capillary density and replacement with fibrosis,8 9 is more likely to occur in HDP than in NCP.
Blood volume increases physiologically by approximately 40% in pregnancy,10 and this volume expansion is associated with morphofunctional cardiac changes in pregnancy, such as increased left ventricular (LV) mass,11–13 increased left atrial (LA) volume,11 12 decreased systemic vascular resistance (SVR)13 and significantly reduced ratio of early to late diastolic transmitral flow velocity.11–13 As the maximal cardiac changes in morphology occur within 1 week after childbirth,14 pathological remodelling may be likely to occur around childbirth. Troponin I reflects cardiac remodelling8 and predicts the outcome of patients with heart failure.8 15 PPCM is characterised by reduced LV ejection fraction (LVEF) and is accompanied by persistent LV diastolic dysfunction. If this is indeed the case, perinatal troponin I would predict a sustained decrease in LV relaxation monitored by early diastolic mitral annular velocity in pregnant women.
The degree of volume expansion is lower in HDP, especially in pregnancies complicated by preeclampsia,16 while LV preloading monitored by LA volume is increased to a greater extent11 in HDP compared with NCP. Preeclampsia is characterised by sympathetic overactivity17 and a marked increase in SVR.13 Splanchnic organs constitute 10% of the body weight, but contain 25% of the total blood volume, and thus the splanchnic vasculature serves as an important blood reservoir for the circulatory system.18 19 Sympathetic activation expels blood from splanchnic capacitance vessels, producing a rapid increase in venous return up to 800 mL.18 19 If this is the case in HDP, the inferior vena cava (IVC) diameter and LA volume would be increased in women with HDP, resulting in increased risk of heart failure compared with those with NCP.
This study was performed to better characterise the heart in HDP in relation to various cardiac biomarkers, using longitudinally prospectively collected data on simultaneous echocardiography and blood variables from women with HDP.