Abstract
Objectives The aim of the study was to determine carotid intima-media thickness (CIMT) values in patients who developed and did not develop preeclampsia (PE), and to determine whether CIMT values could be predictors of PE development. Methods The study included pregnant women who were examined by regular ultrasound examination at the Materno-Infantil Presidente Vargas Hospital (HMIPV) in Porto Alegre, Brazil, from April 2016 to September 2017. The examinations were performed every three months. Patients were divided into two groups. The first group included patients diagnosed with PE (n=21) and second group included patients who did not have PE (n=199). A high frequency ultrasound device (12MHz) with a semi-automatic method was used to estimate CIMT. Results CIMT was significantly higher in pregnant women with PE than in women without PE (55±0.11 vs. 0.44±0.06, respectively; p<0.001). Using a cut-off value of 0.51mm, CIMT had a specificity of 77.9% and sensitivity of 81% in the diagnosis of PE. With CIMT≥0.6mm, the probability of a patient developing PE was 44.4%; with CIMT >0.42mm, the probability was only 4.2%. Conclusions An increase in CIMT was associated with the onset of PE. CIMT values were significantly higher in patients who develop PE.
Highlights
Atherosclerosis is the primary cause of cardiovascular diseases [1]
Eikendal et al have concluded in 3,067 adult patients younger than 45 years of age without symptomatic cardiovascular disease that carotid intima-media thickness (CIMT) may be a marker for cardiovascular risk [20]
Mori et al have shown that pre-existing hypertension is a factor leading to an increase in CIMT, and concluded that endothelial dysfunction induced by enhanced oxidative stress is reversible in women with PE, and that vascular reactivity itself may be associated with earlier changes in hypertension [32]
Summary
The complication of atherosclerosis is atherothrombosis which can have fatal consequences (cerebrovascular and cardiovascular incidents). Preeclampsia (PE) is a multisystemic disease, complicating 3–8% of pregnancies, and is one of the largest causes of maternal mortality [4, 5]. It is defined as new onset hypertension after 20 weeks of gestation with systolic blood pressure (BP) >140 mmHg or diastolic BP ≥90 mmHg and significant proteinuria 300 mg of protein in 24 h [6, 7]. Endothelial dysfunction, the basis of the onset of atherothrombosis, is the process underlying the PE [11, 12]. Dysfunctional endothelium is characterized by reduced nitric oxide bioavailability and overproduction of endothelin one, which impairs vascular
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