Le paradoxe cardiovasculaire de la grossesse

The cardiovascular paradox of pregnancy

Centre de recherche, CHU Sainte-Justine, Département d’obstétrique et gynécologie, Faculté de médecine, Université de Montréal, 3175, chemin de la Côte Sainte- Catherine, Montréal (Québec), H3T 1C5 Canada

^* jean.st-louis@umontreal.ca
^* michele.brochu@umontreal.ca

Résumé

Malgré l’accès plus généralisé aux soins prénataux dans les pays développés, on connaît très peu les mécanismes qui régissent l’adaptation maternelle à l’état physiologique qu’est la grossesse. Deux études récentes nous rappellent que certains phénomènes se manifestent très tôt lors de la grossesse et que le succès de leur mise en place assurerait la poursuite d’une grossesse en santé. Ces études concernent respectivement la fonction du corps jaune de gestation et le réajustement du système rénine - angiotensine - aldostérone (SRAA) favorisant les actions minéralocorticoïdes de l’angiotensine II aux dépens de ses effets vasculaires. Ainsi, malgré l’activation du SRAA, on observerait une vasodilatation périphérique importante et une augmentation compensatoire du volume sanguin. On présume que les stéroïdes sexuels joueraient un rôle dans ces adaptations hémodynamiques propres à la grossesse.

Abstract

Despite widespread accessibility to prenatal care, little is known on the mechanisms initiating early maternal adaptation to pregnancy. Moreover, preeclampsia and intrauterine growth retardation remain the most frequent and serious complications of pregnancy. Recent studies, both in humans and in laboratory animals, have shown that very early events in gestation may be important determinants for the continuation of healthy pregnancy. Certain of these early adaptations appear to be linked to the corpus luteum of pregnancy, as ovarian steroid hormones (especially progesterone) would set the basic hemodynamic conditions, more specifically, generalized vasodilation. This new hemodynamic setup initiates a vicious cycle in which the renin - angiotensin - aldosterone system is activated, together with the resetting of the control of antidiuretic hormone secretion relative to plasma osmolality. This leads to a gradual and substantial increase in plasma volume and a parallel increase in cardiac function (both heart rate and stroke volume) with the goal of maintaining blood pressure in the face of the generalised vasodilation. This includes the creation of a functional arterio-venous shunt represented by the utero-placental circulation. By the end of the first trimester, the decrease in peripheral vascular resistance is marked relative to the increase in cardiac output, resulting in a significant decrease in blood pressure that will be maintained until the third trimester. It is proposed that in preeclampsia, these very early events (vasodilation - increased plasma volume) fail to occur, resulting in an absence of the usual decrease in blood pressure, which is normally seen in the second trimester of pregnancy, and hypertension in the third trimester. Experimental animals, especially the rat, are suitable models to study this early maternal adaptation to pregnancy, since both endocrine and hemodynamic changes appear to be similar to humans.