Subclinical cardiac stiffness is associated with arterial stiffness in healthy young nulligravid women: Potential links to preeclampsia.

OBJECTIVES: Preeclampsia is an independent risk factor for subsequent cardiovascular disease and diastolic dysfunction and has been linked to arterial stiffness. We hypothesized that arterial stiffness would be associated with echocardiographic markers of diastolic dysfunction in healthy nulligravid women. STUDY DESIGN: 31 healthy nulligravid women underwent assessment of peripheral arterial stiffness via aorto-femoral pulse wave velocity, popliteal distensibility and ß stiffness measures as well as hemodynamic response to volume challenge. 22 underwent cardiac assessment via conventional and stress echocardiography with a focus on diastolic function utilizing tissue/pulse wave Doppler imaging and 3D speckle tracking. Bivariate associations between variables were evaluated using correlation coefficients (Pearson r) and Student's t-tests. RESULTS: No participants had echocardiographic values meeting criteria for overt diastolic dysfunction. Baseline global circumferential strain was significantly correlated with distensibility and ß stiffness (n = 18, r = -0.61, p = 0.007, n = 18, r = 0.56, p = 0.01). Peak deceleration time was correlated with ßstiffness (n = 9; r = 0.80, p = 0.01). Pulse wave velocity was not significantly correlated with cardiac measures (p > 0.05). Family history of a first or second degree relative with myocardial infarction or hypertension was associated with decreased popliteal artery distensibility (p = 0.02 and p = 0.03, respectively). CONCLUSIONS: In healthy nulligravid women there is evidence that markers of decreased left ventricular relaxation are associated with increased peripheral vascular stiffness as is a family history of myocardial infarction or hypertension. These findings raise the possibility that the diastolic dysfunction and arterial stiffness observed in the setting of preeclampsia are driven by underlying properties present prior to pregnancy and contribute to lifetime cardiovascular risk.

The Independent Contribution of Uterine Blood Flow to Birth Weight and Body Composition in Smoking Mothers.

OBJECTIVE: This study aims to evaluate the relationship of maternal smoking to uterine artery hemodynamics and examine independent contributions to birth weight and fetal body composition. STUDY DESIGN: Women were enrolled in a prospective randomized controlled study targeting smoking abstinence. Uterine artery Doppler ultrasound was performed and volumetric blood flow was calculated. Third trimester ultrasound estimates of fetal body composition were performed and birth weight was recorded. RESULTS: Uterine artery volumetric flow and resistance index (RI) were significantly correlated with birth weight adjusted for gestational age (R = 0.35, p = 0.002; R = - 0.27, p = 0.02). Volumetric flow was significantly associated with fetal fat mass (R = 0.30, p = 0.018). Smoking status did not have significant effects on lean body mass (t [61] = 0.60, p = 0.55), fat mass (t [61] = 1.67, p = 0.10), or volumetric flow (t = 0.86, df = 87, p = 0.39). Stepwise regression identified volumetric flow (ß = 0.81, 95% confidence interval [CI]: 0.35-1.27, p < 0.001), maternal prepregnancy body mass index (ß = 16.04, 95% CI: 2.57-29.50, p = 0.02), and fetal sex (ß = 346.28, 95% CI: -532.64 to 159.91, p < 0.001, where male = 0 and female = 1) as independent contributors to birth weight adjusted for gestational age. CONCLUSION: No direct relationship of smoking to uterine artery hemodynamics was demonstrated. Volumetric flow was an independent contributor to birth weight and was associated with fetal fat deposition, while smoking was not independently associated with either outcome.

ACTA2 mutation and postpartum hemorrhage: a case report.

BACKGROUND: ACTA2 encodes smooth muscle specific α-actin, a critical component or the contractile complex of vascular smooth muscle. Mutations in ACTA2 are the most common genetic cause of thoracic aortic aneurysm, and are also the cause of other disorders, including Moyamoya disease, coronary artery disease and stroke as well as Multisystemic Smooth Muscle Dysfunction Syndrome. We note that ACTA2 is also expressed in uterine smooth muscle, and this raises the possibility that women harboring ACTA2 mutations might exhibit uterine smooth muscle dysfunction. CASE PRESENTATION: We present a young woman whose ACTA2 mutation was ascertained during pregnancy because of her father's history of dissecting aneurysms. She was delivered at full term by cesarean section and subsequently had severe uterine hemorrhage due to uterine atony. Although her atony was successfully treated with uterotonic medications, she required blood transfusion. CONCLUSIONS: This case raises the possibility that women with ACTA2 mutations may be at risk of uterine muscle dysfunction and hemorrhage. Obstetricians should be alerted to and prepared for this possibility.