Maternal cardiovascular profile is altered in the preclinical phase of normotensive early and late intrauterine growth restriction.

BACKGROUND: The maternal cardiovascular profile of patients who develop late fetal growth restriction has yet to be well characterized, however, a subclinical impairment in maternal hemodynamics and cardiac function may be present before pregnancy and may become evident because of the hemodynamic alterations associated with pregnancy. OBJECTIVE: This study aimed to investigate if maternal hemodynamics and the cardiovascular profile might be different in the preclinical stages (22-24 weeks' gestation) in cases of early and late fetal growth restriction in normotensive patients. STUDY DESIGN: This was a prospective echocardiographic study of 1152 normotensive nulliparous pregnant women at 22 to 24 weeks' gestation. The echocardiographic evaluation included morphologic parameters (left ventricular mass index and relative wall thickness, left atrial volume index) and systolic and diastolic maternal left ventricular function (ejection fraction, left ventricular global longitudinal strain, E/A ratio, and E/e' ratio). Patients were followed until the end of pregnancy to note the development of normotensive early or late fetal growth restriction. RESULTS: Of the study cohort, 1049 patients had no complications, 73 were classified as having late fetal growth restriction, and 30 were classified as having early fetal growth restriction. In terms of left ventricular morphology, the left ventricular end-diastolic diameter was greater in uneventful pregnancies (4.84±0.28 cm) than in late (4.67±0.26 cm) and in early (4.55±0.26 cm) (P<.001) fetal growth restriction cases, whereas left ventricular end-systolic diameter was smaller in uneventful pregnancies (2.66±0.39 cm) than in late (2.83±0.40 cm) and in early (2.82±0.38 cm) (P<.001) fetal growth restriction cases. The relative wall thickness was slightly higher in early (0.34±0.05) and late (0.35±0.04) fetal growth restriction cases than in uneventful pregnancies (0.32±0.05) (P<.05). In terms of systolic left ventricular function, at 22 to 24 weeks' gestation, cardiac output was higher in uneventful pregnancies (6.58±1.07 L/min) than in late (5.40±0.97 L/min) and in early (4.76±1.05 L/min) (P<.001) fetal growth restriction cases with the lowest values in the early-onset group. Left ventricular global longitudinal strain was lower in appropriate for gestational age neonates (-21.6%±2.0%) and progressively higher in late (-20.1%±2.2%) and early (-18.5%±2.3%) (P<.001) fetal growth restriction cases. In terms of diastolic left ventricular function, the E/e' ratio showed intermediate values in the late fetal growth restriction group (7.90±2.73) when compared with the appropriate for gestational age group (7.24±2.43) and with the early fetal growth restriction group (10.76±3.25) (P<.001). The total peripheral vascular resistance was also intermediate in the late fetal growth restriction group (1300±199 dyne·s·cm-5) when compared with the appropriate for gestational age group (993±175 dyne·s·cm-5) and the early fetal growth restriction group (1488±255 dyne.s.cm-5) (P<.001). CONCLUSION: Early and late fetal growth restriction share similar maternal hemodynamic and cardiovascular profiles with a different degree of expression. These features are already present at 22 to 24 weeks' gestation and are characterized by a hypodynamic state. The degree of these cardiovascular changes may influence the timing of the manifestation of the disease; a hypovolemic, high resistance, low cardiac output state might be associated with early-onset fetal growth restriction, whereas a milder hypovolemic state seems to favor the development of the disease in the final stages of pregnancy.

NO donors on top of anti-hypertensive therapy reduces complications in chronic hypertensive pregnancies with hypodynamic circulation.

OBJECTIVES: Chronic hypertension is associated with significant adverse maternal and fetal outcomes that appear to be often associated to a hypodynamic circulation. Treatment of hypertensive disorders of pregnancy tailored on maternal hemodynamics might reduce or mitigate these complications. Our purpose was to assess the hemodynamic modifications induced by the addition of NO donors and increased oral fluid intake on top of standard antihypertensive therapy in hypodynamic chronic hypertensive patients. We further evaluated if the possible hemodynamic modification induced by NO donors and increased oral fluid intake might be associated to a reduction of the severity and rate of complications vs. patients on antihypertensive standard treatment. STUDY DESIGN: This was a case-control study of 321 chronic hypertensive patients with a hypodynamic circulation at the echocardiographic evaluation at 24 weeks' gestation. We included 160 controls (standard antihypertensive therapy) and 161 cases (standard therapy + NO donor patches + increased oral fluid intake). Student T test for paired and unpaired data, univariate logistic regression analysis, ROC curve analysis, and Cox Hazards Regression analysis were used as appropriate. RESULTS: At enrollment the hemodynamic parameters were similar between the two groups. After 3-4 weeks stroke volume (77 ± 19 mL vs. 69 ± 19 mL; p < 0.001), and cardiac output (6.2 ± 1.7 L vs. 5.0 ± 1.6 L; p < 0.001) were higher and total peripheral vascular resistance (1465 ± 469 dyne·s·cm-5 vs. 1814 ± 524 dyne·s·cm-5; p < 0.001) was lower in the cases vs controls. Superimposed preeclampsia, preterm delivery before 34 weeks, abruptio placentae, HELLP Syndrome, fetal growth restriction, and perinatal death were more represented in the standard treatment group vs NO treated patients (81% vs 53%; p < 0.001). In particular, the standard treatment group showed 48% fetal growth restriction vs 34% in the NO treated group (p < 0.011). The Cox proportional-hazards regression showed a lower proportion of event-free pregnancies in controls on standard treatment (HR 2.6; 95% CI 2.0-3.5; p < 0.0001), and a prolongation of pregnancies in CH cases complicated by fetal growth restriction taking NO donors (HR 0.29; 95% CI 0.19-0.43; p = 0.0001). CONCLUSIONS: The tailored treatment with NO donors and oral fluids of hypodynamic CH might have positive effects on the reduction or mitigations of adverse outcomes.

Diagnosis and management of cerebral venous sinus thrombosis in children: a single-center retrospective analysis.

PURPOSE: Cerebral venous thrombosis (CVT) is a rare disease in children, characterized by partial or total occlusion of blood flow in the cerebral venous system. The aim of this study is to describe clinical presentation, neuroimaging features, therapeutic management, and outcome of children with CVT. METHODS: We retrospectively analyzed the data, including clinical manifestations, laboratory data, neurological findings, and treatment of children with radiologically confirmed CVT, admitted between January 2010 and March 2020 to our hospital. Cases of CVT complicating brain surgery were excluded. RESULTS: We enrolled 24 children with CVT. Infection was the main etiology (58.3%), followed by trauma in 16.7% of cases. In the remaining 25% of cases, the cause was identified only in one patient presenting a thrombophilic factor. The most frequent site of thrombosis was the superficial venous system (86.8%), with multiple localizations disclosed in 79% of patients. All children received anticoagulant therapy with low molecular weight heparin (LMWH). One patient died for systemic complications of an underlying disease. No patient developed hemorrhagic events during the therapy, lasting from 35 to 360 days (mean 86 days). In all but one surviving patients (22 out of 24), recanalization of the sinus was observed at AngioMRI performed during follow-up. No neurological complications of CVT were recorded (mean follow-up: 1.5 year). CONCLUSIONS: CVT may present with subtle and unspecific clinical manifestations in children. High level of suspicion should be kept in trauma and sinusitis. Anticoagulation treatment is safe and effective and should be promptly started to improve outcome.