Preeclampsia: a gestational cardiorenal syndrome

Abstract

It is generally accepted today that there are two different types of preeclampsia: an early‐onset or placental type and a late‐onset or maternal type. In the latent phase, the first one presents with a low output/high resistance circulation eventually leading in the late second or early third trimester to an intense and acutely aggravating systemic disorder with an important impact on maternal and neonatal mortality and morbidity; the other type presents initially as a high volume/low resistance circulation, gradually evolving to a state of circulatory decompensation usually in the later stages of pregnancy, with a less severe impact on maternal and neonatal outcome. For both processes, numerous dysfunctions of the heart, kidneys, arteries, veins and interconnecting systems are reported, most of them presenting earlier and more severely in early‐ than in late‐onset preeclampsia; however, some very specific dysfunctions exist for either type. Experimental, clinical and epidemiological observations before, during and after pregnancy are consistent with gestation‐induced worsening of subclinical pre‐existing chronic cardiovascular dysfunction in early‐onset preeclampsia, and thus sharing the pathophysiology of cardiorenal syndrome type II, and with acute volume overload decompensation of the maternal circulation in late‐onset preeclampsia, thus sharing the pathophysiology of cardiorenal syndrome type 1. Cardiorenal syndrome type V is consistent with the process of preeclampsia superimposed upon clinical cardiovascular and/or renal disease, alone or as part of a systemic disorder. This review focuses on the specific differences in haemodynamic dysfunctions between the two types of preeclampsia, with special emphasis on the interorgan interactions between heart and kidneys, introducing the theoretical concept that the pathophysiological processes of preeclampsia can be regarded as the gestational manifestations of cardiorenal syndromes.

Preeclampsia: the role of persistent endothelial cells in uteroplacental arteries. Brosens I, Brosens JJ, Muter J, Puttemans P, Benagiano G. Am J Obstet Gynecol 2019;221:219-26.

“…2 (4) Similarly, risk factors for cardiovascular disease predispose to the development of preeclampsia. 3 (5) In formerly preeclamptic women, the recurrence rate of preeclampsia is increased when left ventricular and diastolic dysfunction is present before conception. 4 (6) Pregnant women with prepregnancy cardiovascular disease (essential hypertension, congenital heart disease) are more likely to experience preeclampsia.…”

Intra‐abdominal pressure as an ignored parameter in the pathophysiology of preeclampsia

“…1 However, recent work into cardiovascular maladaptation of the pregnancy-induced expansion of body water volume has gained interest as a novel explanation of the hemodynamic mechanisms behind early-onset and late-onset PE. 2 Specifically, increasing evidence supports the critical role of diastolic cardiac dysfunction and venous congestion in PE-related organ dysfunction. 2 Venous congestion is a well-known phenomenon during intra-abdominal hypertension (IAH) triggering arterial hypertension, hypoperfusion, and multiple organ dysfunctions.…”

“…2 Specifically, increasing evidence supports the critical role of diastolic cardiac dysfunction and venous congestion in PE-related organ dysfunction. 2 Venous congestion is a well-known phenomenon during intra-abdominal hypertension (IAH) triggering arterial hypertension, hypoperfusion, and multiple organ dysfunctions. 3 Interestingly, PE is associated with increased intra-abdominal pressure (IAP), irrespective of gestational age or birthweight, and correlates with maternal intestinal permeability and oliguria.…”

“…This sequence of events unfolds similarly in cardiorenal syndrome and preeclampsia (PE), but also occurs at other internal organs, including the uterus and placenta of pregnant women. 2 Microcirculatory dysfunction in PE is clinically indicated by increased serum concentration of uric acid and albuminuria >300 mg/24 h. Renal dysfunction proceeds to oliguria and eventually to renal failure pressure cut off will lead to increased surveillance and diagnosis of PE, which increases the importance of having an excellent understanding of the pathophysiologic basis of disease and of the ability to accurately identify patients at the highest risk of suffering adverse effects from high IAP. In the present study, there was some overlap between the two groups as the mean arterial pressure in the normotensive group was around 93 mm Hg.…”

Efficacy of Diltiazem for the Control of Blood Pressure in Puerperal Patients with Severe Preeclampsia: A Randomized, Single-Blind, Controlled Trial

“…Although these two pregnancy-related disorders have been widely studied, their cause remains unknown. Pathophysiological mechanisms involve the reduction of maternal placental blood flow as of week 20 of gestation, with an increase in peripheral vascular resistance that predominantly takes place in the kidney, liver, and brain [4][5][6][7][8][9]. It has been reported that placenta plays a key role in the pathogenesis of preeclampsia, and it was assumed that, after delivery, its influence in the maternal cardiovascular system would be over.…”