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The carotid bifurcation is a common site of atherosclerotic plaque. Plaque development is thought to occur preferentially at geometrically predisposed areas such as arterial branch points. The aim of this study was to investigate the geometric and anatomical variables that contribute to the development of carotid plaque using three-dimensional (3D) ultrasound. Sixty-seven consecutive outpatients referred for elective coronary angiography underwent 3D carotid ultrasound scans for the purpose of carotid plaque quantification. Geometric quantification of the left and right carotid bulbs were performed retrospectively on this study population. Geometric values such as angle, area and length of the carotid bulb and the bifurcation were determined using QLAB software (Philips Healthcare). Plaque volume within the carotid bulb and artery branches was quantified using the stacked contour method. Pearson's correlation and linear regression analysis were used to determine the relationship between anatomical variables and plaque volume. The mean age for the total patient population was 65.9 ± 11.5 years. Carotid bulb inflow area (BIA) (r = 0.28, p = 0.001), bulb volume (BV) (r = 0.21, p = 0.01) and bifurcation angle (BifA) (r = 0.18, p = 0.04) showed a positive linear relationship with plaque volume. In contrast, internal carotid artery angle (ICAA) (r = - 0.18, p = 0.04) and bulb flare (r = - 0.20, p = 0.02) displayed a negative linear relationship with plaque volume. When adjusting for age and sex, only the BIA remained significant (β = 0.18, p = 0.04). Geometric variables were identified as potential risk factors associated with plaque volume in the carotid bulb. Further analysis of the evolution of the BIA as well as the relationship to other geometric variables could create a stronger predictive model of atherosclerosis as well as assist in preoperative planning.

Pregnancy induces cardiovascular adaptations in response to increased volume overload. Aside from the hemodynamic changes that occur during pregnancy, the maternal heart also undergoes structural changes. However, cardiac modulation in pregnancies complicated by gestational hypertension is incompletely understood. The objectives of the current investigation were to determine the role of the natriuretic peptide (NP) system in pregnancy and to assess alterations in pregnancy-induced cardiac hypertrophy between gestationally hypertensive and normotensive dams. Previously we have shown that mice lacking the expression of atrial NP (ANP; ANP(-/-)) exhibit a gestational hypertensive phenotype. In the current study, female ANP(+/+) and ANP(-/-) mice were mated with ANP(+/+) males. Changes in cardiac size and weight were evaluated across pregnancy at Gestational Days 15.5 and 17.5 and Postnatal Days 7, 14, and 28. Nonpregnant mice were used as controls. Physical measurement recordings and histological analyses demonstrated peak cardiac hypertrophy occurring at 14 days postpartum in both ANP(+/+) and ANP(-/-) dams with little to no change during pregnancy. Additionally, left ventricular expression of the renin-angiotensin system (RAS) and NP system was quantified by real-time quantitative polymerase chain reaction. Up-regulation of Agt and AT(1a) genes was observed late in pregnancy, while Nppa and Nppb genes were significantly up-regulated postpartum. Our data suggest that pregnancy-induced cardiac hypertrophy may be influenced by the RAS throughout gestation and by the NP system postpartum. Further investigations are required to gain a complete understanding of the mechanistic aspects of pregnancy-induced cardiac hypertrophy.

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ContextPhosphate has gained recognition as a risk factor for adverse cardiovascular outcomes, potentially due to accelerated vascular calcification. Fibroblast growth factor-23 (FGF-23) is a counter-regulatory hormone that increases renal phosphate excretion to maintain normal levels.ObjectiveThe purpose of the study was to determine the association of phosphate and FGF-23 to atherosclerosis.Design and SettingA prospective cohort study (n = 204) of outpatients referred for coronary angiography over of a 1-year recruitment period at the Kingston General Hospital.InterventionBlood was collected, and a focused carotid ultrasound was performed.Main Outcome MeasureDegree of angiographic coronary artery disease was scored. Carotid maximum plaque height, total area, grayscale median, and tissue pixel distribution were measured. Plasma phosphate was assessed by mineral assay and FGF-23 by ELISA.ResultsCarotid plaque burden [total plaque area (TPA)] was associated with higher levels of phosphate (TPA, r = 0.20, P < 0.01) and FGF-23 (r = 0.19, P < 0.01). FGF-23 was associated with increased plaque % calcium-like tissue. Participants with no coronary artery disease had significantly lower phosphate levels. Phosphate was associated with higher grayscale median (GSM) in male subjects but with lower GSM in female subjects. FGF-23 was associated with increased plaque % fat in male subjects but increased plaque % calcium in female subjects.ConclusionsPhosphate was independently associated with the severity of atherosclerosis in terms of plaque burden and composition. FGF-23 was associated with plaque calcification. These findings suggest that abnormal phosphate homeostasis may play an under-recognized but potentially modifiable role in cardiovascular disease.