Preterm Birth, Maternal Blood Pressure, and IMT (page 641)
Preterm birth was thought to have no longterm consequences for mothers; however, emerging evidence indicates that women who deliver before 37 weeks gestation have excess cardiovascular disease (CVD). Mechanisms that link these conditions are not understood, and whether this association is due to hypertension during pregnancy is equivocal. We studied 916 women (46% black) with 1181 live births between enrollment in the Coronary Artery Risk Development in Young Adults study (CARDIA) and 20 years later. Blood pressure trajectories, inflammatory markers, and carotid intima-media thickness were compared in women with and without preterm births. Blood pressure was moderately higher in women before pregnancies delivered preterm compared to term, and they accumulated risk factors (increasing systolic and diastolic blood pressure and higher BMI) across 20 years of follow-up independent of hypertension during pregnancy. Our results differ from those assessed in European cohorts, perhaps due to different predisposing risks for both preterm birth and CVD. Preterm birth occurs in 4-5% of European births compared to 12% in the United States. There are persistent race disparities in preterm birth and hypertension in the United States, and white women have preterm birth rates twice as high as their European counterparts. Thus, preterm birth may mark women at excess risk of higher blood pressure in the years after pregnancy. These women may benefit from closer surveillance after pregnancy in order to prevent or delay onset of hypertension.
Aortic Calcification and Stiffening (page 609)
Aortic stiffness is an important predictor of cardiovascular events, including atherosclerotic coronary events. It has been assumed that it is a marker of atherosclerosis along the aorta. However, the mechanism through which it relates to cardiovascular events remains uncertain. We used combined computed tomography and magnetic resonance imaging to characterize noncalcified (Figure, A) and calcified aortic plaque (Figure, B) and to identify aortic calcification in the absence of plaque (Figure, C) in asymptomatic postmenopausal women from the Twins UK cohort. A substantial proportion of women with absent or low calcification scores had a relatively high plaque burden, suggesting that atherosclerosis and calcification are unlikely to be interchangeable measures of atherosclerosis. Higher heritability of calcification compared to atherosclerosis suggests that vascular calcification has an important genetic component distinct from atherosclerosis and that calcification and atherosclerosis are, at least in part, driven by separate processes. Arterial stiffness related to calcification rather than atherosclerotic plaque and the association of arterial stiffness with calcification was explained by common genes. The prognostic importance of arterial stiffness is unlikely to be explained by it being a marker of atherosclerosis, but because of adverse hemodynamic consequences of stiffening, such as increased pulsatility that may increase load on the left ventricle and predispose to plaque rupture in coronary, carotid, and cerebral arteries.
23Na-MRI in age and hypertension (page 635)
A widely accepted theory suggests that body sodium content is maintained constant within narrow limits. Otherwise, sodium ions would exert osmotic activity and induce extracellular volume expansion. Recent findings in animals suggest that sodium additionally can be stored in muscle and skin. The interpretation of these findings is controversial. Questions such as how extracellular sodium ions may escape equilibrium or how intracellular sodium concentrations could increase without deleterious effects on membrane potential are unanswered.
A burning question for clinician-scientists is whether this storage phenomenon is an animal-research curiosity or whether it exists in humans. To address this question, we have implemented 23NaMRI technology to quantitatively and noninvasively visualize sodium reservoirs in humans. We find sodium storage in muscle and skin, which increases with age, is more pronounced in men than in women and is directly associated with blood pressure levels. This association leads to the hypothesis that tissue sodium storage characterizes a disruption of internal environment composition, which may be causally linked to essential hypertension.
The emerging concept of sodium storage opens new questions for basic researchers and clinician-scientists. Some straightforward clinical questions are whether humans with increased sodium storage are at risk for developing cardiovascular disease and whether tissue sodium content can be modified by life-style changes or medical treatment. Seeing the sodium in humans is a new conceptual approach to provide answers.
- © 2013 American Heart Association, Inc.