For the past three decades, rates of gestational hypertension, preeclampsia, and chronic hypertension have been increasing [1]. Recently, the literature has reported increased rates of pregnancy-related hypertensive disorders during the COVID pandemic in the overall population, regardless of COVID infection or COVID symptoms [2], [3]. While one study showed that the rates of hypertensive disorders of pregnancy during the COVID pandemic did not differ significantly in those testing positive for COVID-19 compared to those testing negative, studies comparing the rates of hypertensive disorders during pregnancy prior to and during the COVID pandemic are lacking [4]. It is thus difficult to determine whether the increase in gestational hypertensive disorders is a direct consequence of COVID-19 infection, the stress of the pandemic, or some other explanation.

The first case of COVID-19 in the United States was documented on January 20, 2020 [5]. There have since been over 2.5 million deaths and over 113 million cases of COVID worldwide, and the effects of this pandemic have persisted into 2021 [6]. During the pandemic, there have been documented increases in psychological conditions such as depression, anxiety, and stress which have occurred via multifactorial mechanisms including isolation from family, changes in employment status, and relationship status [7]. These drivers may be responsible for a broad-stroke effect on blood pressure notwithstanding to one’s COVID-19 infection status.

Some individuals with baseline normal blood pressures are noted to have an increase in blood pressure during events with heightened psychological stress resulting in an increased likelihood to develop essential hypertension in the future [8]. It has also been shown that the more prolonged a stress response is, the more likely an individual is to experience an increase in blood pressure [9]. Proposed pathophysiology includes increased allostatic load leading to chronic inflammation and activation of the sympathetic nervous system, chronic stress increasing corticosteroid and catecholamine release, acute stress increasing synthesis of endothelin-1 resulting in endothelial dysfunction, and several others [10]. Increased corticosteroids and catecholamine release may be the cause of stress-induced hypertension which could explain the potentially increased likelihood of preeclampsia during periods of prolonged stress. In preeclampsia, there are lower levels of 11B-hydroxysteroid dehydrogenase type 2 (11B-HSD2) [11]. This enzyme’s normal function is to protect the fetus from elevated levels of circulating cortisol within the mother [11]. A high percentage of placental tissue in preeclamptic mothers had detectable cortisol present, while over 90 % of placental tissue in normotensive mothers had undetectable cortisol levels [11].

According to the current research, the COVID-19 pandemic represents a period of prolonged stress for many individuals [7]. We therefore suggest that the increase in hypertensive disorders during pregnancy is not specific to COVID-19 infection among mothers but would apply to all individuals who had been pregnant during this period. Moreover, other studies have shown that COVID-19 may be implicated in the development of hypertensive disorders in pregnancy, specifically pre-eclampsia, in other ways. COVID-19 has been shown to bind to angiotensin converting enzyme 2 (ACE-2) to gain entrance into cells, and decreased ACE-2 expression has been shown to be associated with pre-eclampsia [12], [13], [14]. Therefore, our study hypothesizes that via several potential mechanisms, an increased incidence of hypertensive disorders during pregnancy will be evident in all pregnant individuals since the beginning of the COVID-19 pandemic, regardless of individual COVID-19 infective status. In addition, we anticipate the increased stress experienced during the pandemic will impact racial groups differently due to known disparities in the experiences of chronic stress among certain populations.