Emerging tool for assessment of left ventricular–arterial coupling after pre‐eclampsia

History of pre-eclampsia (PE) is a cardiovascular (CV) risk factor, associated with the development of CV disease later in life, when compared with the general female population matched for age. In order to further analyze this epidemiological link, we enrolled 60 women with a pregnancy complicated by PE (30 with early-onset PE and 30 with late-onset PE), 6 months to 4 years after delivery, and 30 healthy controls. The major strength of our investigation was that a study cohort without CV risk factors was selected in order to avoid bias. Cases and controls were evaluated comprehensively and contemporaneously by peripheral arterial tonometry (EndoPAT-2000, Itamar Medical Ltd, Caesarea, Israel), vascular plethysmography (Vascular Explorer, Enverdis GmbH, Jena, Germany) and echocardiography (traditional tissue Doppler imaging, speckle tracking and integrated backscatter). To summarize, we demonstrated that women with a history of PE, particularly those who experienced early-onset disease, had an increased incidence of endothelial dysfunction (37–77%, depending on the method)1, arterial stiffness (10–57%, depending on the method)1, concentric left ventricular (LV) remodeling (60%) with abnormally high LV mass (52%)2, 3, diastolic dysfunction (10% Grade I)3, myocardial impairment (53% for LV global longitudinal strain (GLS), 23% for LV radial two-dimensional strain, 33% for LV circumferential two-dimensional strain, 20% for LV torsion, 10% for left atrial strain and 23% for right ventricular strain)3, 4 and LV and aortic fibrosis1. These findings led us to hypothesize that the CV sequelae of PE may be considered a phenotype of heart failure with preserved ejection fraction (HFpEF), as we have discussed elsewhere1. Indeed, as commonly seen in HFpEF patients, ventricular–arterial coupling (VAC), calculated by Chen's method5, was within the normal range in the early-onset PE group, although it was significantly greater than that in the late-onset PE group and controls3. Furthermore, both of its components (i.e. aortic elastance (Ea) and LV end-systolic elastance (Ees)) were abnormal in approximately half of the cases with previous early-onset PE (Table 1)3. Interestingly, Ikonomidis et al. proposed recently a new promising marker to assess VAC itself, namely the ratio of carotid–femoral pulse-wave velocity (cfPWV) to GLS6. The main advantage of this marker is that cfPWV and GLS are optimal markers with which to assess arterial stiffness and myocardial performance, respectively, and are prognostic factors for CV events. In addition, while Ea and Ees increase concomitantly in HFpEF, leading to a ‘normal’ ratio, cfPWV increases while GLS decreases (as an absolute value), resulting in a greater absolute value of their ratio6. On the other hand, this method could become more expensive and time-consuming because the use of two non-invasive devices would be required to obtain VAC. Applying the new formula to our cohort, we found significantly impaired VAC in the early-onset PE group compared with the late-onset PE group and controls (Table 1). In addition, the two methods to calculate VAC correlated with each other (r = 0.465; P < 0.001). On the contrary, cfPWV/GLS was correlated more strongly with several vascular, biventricular and left atrial parameters than was Ea/Ees (Table 2). These data are consistent with those reported by Ikonomidis et al., who found that cfPWV/GLS, but not Ea/Ees, is related to impaired carotid intima–media thickness, coronary-flow reserve and LV diastolic dysfunction6. Larger studies are needed to validate this novel and promising parameter, which underlines the complex interplay between the heart and the vascular system. Our data reinforce that women with a history of PE represent a high-risk group and may benefit from closer follow-up. Data available on request from the authors.

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