Effects of Baroreceptor Activation Therapy on 24-Hour Ambulatory Blood Pressure (p 701)
The European Society for Hypertension/European Society of Cardiology recommends that in patients with truly therapy–refractory hypertension with clinic blood pressure (BP) values >160 mm Hg systolic or >110 mm Hg diastolic, invasive procedures such as renal denervation and baroreceptor stimulation should be considered (evidence class IIb). Despite the ongoing debate on whether renal denervation is effective in BP reduction, the Symplicity-HTN3 study has clearly shown that ambulatory blood pressure monitoring (ABPM) is an indispensable end point for evaluating the effectiveness of an invasive BP therapy. In the pivotal studies for baroreceptor activation therapy, office BP measured with an automated system averaging 6 brachial cuff measurements at 1-minute intervals was used for end points. This measurement method is more precise compared with sole office measurement, but its informative value is clearly below ABPM. ABPM is relatively immune to regression to the mean, and BP changes seen on ABPM are almost assuredly a treatment effect. ABPM data were available only in the minority of patients of the Device Based Therapy in Hypertension (DEBuT-HT) Trial using the first-generation Rheos device with bilateral electrodes placed on both carotid sinus with a significant BP decrease after 1 (n=15) and 2 years (n=8). The prospective observational study from Wallbach et al is the first demonstrating a significant 24-hour, day-, and night-time BP reduction in ABPM in patients treated with the second-generation baroreceptor activation therapy Barostim neo device using an unilateral electrode placed on 1 carotid sinus. Despite its limitations, this study adds valuable information for treatment of patients with therapy–refractory hypertension.
Cardiac Dysfunction in Recurrent Preeclampsia (p 748)
Women with a previous early preeclampsia showing a peculiar left ventricular geometry and diastolic dysfunction after pregnancy are at increased risk for cardiovascular disease later in life. This study tested the hypothesis that in these women in the nonpregnant state and before a second pregnancy, cardiac dysfunction and hemodynamic and left ventricular structural alterations might be signs to identify patients at risk for recurrent preeclampsia in the second pregnancy.
Patients with recurrent preeclampsia showed signs of left ventricular diastolic dysfunction, a hypertrophied ventricle, and high total vascular resistance, suggesting an underfilled cardiovascular system with pressure overload. Patients with nonrecurrent preeclampsia showed a geometric pattern of the left ventricle (left ventricular mass index and relative wall thickness) similar to those with recurrent preeclampsia, an intermediate pattern of diastolic function (E/E′ ratio) when compared with recurrent preeclamptic patients and controls, and hemodynamic characteristics (total vascular resistance) similar to controls.
In women with previous early preeclampsia, echocardiography performed in-between pregnancies may help in identifying those patient at risk for recurrent preeclampsia through the evidence of an impaired left ventricular diastolic function and specific hemodynamic and left ventricular geometric patterns in the nonpregnant state. If these data are confirmed by larger studies, echocardiography might become part of the counseling of women with previous early preeclampsia planning a second pregnancy, to identify patients at risk for recurrent preeclampsia. The early identification of these women might help in developing new strategies to follow and eventually treat these patients before and during the next pregnancy.
Placental Growth Factor Abolishes Placental Ischemia Hypertension (p 740)
Preeclampsia is a disorder of pregnancy characterized by new-onset hypertension during or after the 20th week of gestation accompanied by dysfunction of cardiovascular, cerebral, visual, or renal systems. Although preeclampsia is one of the leading causes of maternal and fetal morbidity and mortality, the only effective treatment is early delivery of the fetus and the ischemic placenta. Therefore, identifying novel therapeutic targets and agents against this maternal disorder is the subject of intensive investigation. The antiangiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1), which antagonizes and reduces bioavailable vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), is elevated in placental ischemic rats and in women with preeclampsia. Although PlGF and VEGF are both natural ligands for sFlt-1, VEGF also has high affinity to Flk1 (VEGFR2) causing side effects, such as edema. In contrast to VEGF, PlGF is specific for sFlt-1. In this issue of Hypertension, Spradley et al examined the effects of chronic administration of PlGF in a rat model of preeclampsia induced by placental ischemia. Administration of purified recombinant human PlGF abolished hypertension and the reductions in glomerular filtration rate in the placental ischemic model of preeclampsia. There was no effect on maternal weights or fetal health, as assessed by fetal/placental weights and fetal absorption rates in response to placental ischemia. They also showed that PlGF administration in placental ischemic rats dramatically reduced the rise in bioavailable levels of free sFlt-1, postulated to be a major pathogenic mediator of antiangiogenic state in preeclampsia. The finding that rhPlGF abolishes placental ischemia–induced hypertension without major adverse consequences suggests a strong therapeutic potential for this growth factor in preeclampsia.
- © 2016 American Heart Association, Inc.