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      Deterioration in cardiac systolic and diastolic function late in normal human pregnancy

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          Abstract

          The aim of the present study was to undertake a longitudinal study of systolic and diastolic cardiac function during normal pregnancy. At a median of 16 weeks of gestation, 100 primiparous women underwent echocardiography, including tissue Doppler imaging, determining left ventricular mass, cardiac output, systolic and diastolic velocities, and wall stress. A total of 32 were assessed again at a median of 37 weeks of gestation. Non-pregnant control estimates (n=9) were obtained by averaging four separate measures over two menstrual cycles. Initially, the pregnant women had significantly higher pulse rates than controls, associated with greater ventricular wall stress (two-tailed P value=0.015), and systolic (two-tailed P value=0.005) and diastolic (two-tailed P value=0.018) lateral wall myocardial velocities, but no differences in systolic blood pressure, left ventricular mass or cardiac output. By 37 weeks of gestation, increased blood pressure (two-tailed P value <0.001) and left ventricular mass (two-tailed P value=0.002) were associated with a significant increase in ventricular wall stress (two-tailed P value <0.001), and reductions in septal systolic (two-tailed P value=0.004) and septal and lateral early diastolic (two-tailed P value <0.001) myocardial velocities. The diastolic velocities at 37 weeks correlated inversely with maternal weight and age. In conclusion, by term pregnancy, an increase in ventricular wall stress is accompanied by a deterioration in cardiac function.

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          Most cited references44

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          Alterations of left ventricular myocardial characteristics associated with obesity.

          Obesity is associated with heart failure, but an effect of weight, independent of comorbidities, on cardiac structure and function is not well established. We sought whether body mass index (BMI) and insulin levels were associated with subclinical myocardial disturbances. Transthoracic echocardiography, myocardial Doppler-derived systolic (sm) and early diastolic velocity (em), strain and strain rate imaging and tissue characterization with cyclic variation (CVIB), and calibrated integrated backscatter (cIB) were obtained in 109 overweight or obese subjects and 33 referents (BMI 35) had reduced LV systolic and diastolic function and increased myocardial reflectivity compared with referents, evidenced by lower average long-axis strain, sm, cIB, lower CVIB, and reduced em, whereas LV ejection fraction remained normal. Differences in regional or global strain, sm, and em were identified between the severely obese (BMI >35) and the referent patients (P<0.001). Similar but lesser degrees of reduced function by sm, em, and basal septal strain and increased reflectivity by cIB were present in overweight (BMI, 25 to 29.9) and mildly obese (BMI, 30 to 35) groups (P<0.05). Although tissue Doppler measures were not associated with duration of obesity, they did correlate with fasting insulin levels and reduced exercise capacity. BMI was independently related to average LV strain (beta=0.40, P=0.02), sm (beta=-0.36, P=0.002), and em (beta=-0.41, P<0.001). Overweight subjects without overt heart disease have subclinical changes of LV structure and function even after adjustment for mean arterial pressure, age, gender, and LV mass.
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            The prevalence and impact of overweight and obesity in an Australian obstetric population.

            To assess the prevalence and impact of overweight and obesity in an Australian obstetric population. The Mater Mother's Hospital (MMH), South Brisbane, is an urban tertiary referral maternity hospital. We reviewed data for the 18 401 women who were booked for antenatal care at the MMH, delivered between January 1998 and December 2002, and had a singleton pregnancy. Of those women, 14 230 had an estimated pre-pregnancy body mass index (BMI) noted in their record; 2978 women with BMI 40 kg/m(2)). Prevalence of overweight and obesity in an obstetric population; maternal, peripartum and neonatal outcomes associated with raised BMI. Of the 14 230 women, 6443 (45%) were of normal weight, and 4809 (34%) were overweight, obese or morbidly obese. Overweight, obese and morbidly obese women were at increased risk of adverse outcomes (figures represent adjusted odds ratio [AOR] [95% CI]): hypertensive disorders of pregnancy (overweight 1.74 [1.45-2.15], obese 3.00 [2.40-3.74], morbidly obese 4.87 [3.27-7.24]); gestational diabetes (overweight 1.78 [1.25-2.52], obese 2.95 [2.05-4.25], morbidly obese 7.44 [4.42-12.54]); hospital admission longer than 5 days (overweight 1.36 [1.13-1.63], obese 1.49 [1.21-1.86], morbidly obese 3.18 [2.19-4.61]); and caesarean section (overweight 1.50 [1.36-1.66], obese 2.02 [1.79-2.29], morbidly obese 2.54 [1.94-3.32]). Neonates born to obese and morbidly obese women had an increased risk of birth defects (obese 1.58 [1.02-2.46], morbidly obese 3.41 [1.67-6.94]); and hypoglycaemia (obese 2.57 [1.39-4.78], morbidly obese 7.14 [3.04-16.74]). Neonates born to morbidly obese women were at increased risk of admission to intensive care (2.77 [1.81-4.25]); premature delivery (< 34 weeks' gestation) (2.13 [1.13-4.01]); and jaundice (1.44 [1.09-1.89]). Overweight and obesity are common in pregnant women. Increasing BMI is associated with maternal and neonatal outcomes that may increase the costs of obstetric care. To assist in planning health service delivery, we believe that BMI should be routinely recorded on perinatal data collection sheets.
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              Impact of glucose intolerance and insulin resistance on cardiac structure and function: sex-related differences in the Framingham Heart Study.

              Although insulin resistance has been implicated in the pathogenesis of left ventricular (LV) hypertrophy, previous studies have yielded inconsistent results and are limited by referral bias. We examined the relations between echocardiographic LV measurements and glucose tolerance status in 2623 Framingham Study subjects (1514 women, mean age 53 years) free of myocardial infarction and heart failure. We also evaluated the relations of insulin resistance (homeostasis model, HOMA-IR) and LV and left atrial (LA) measures within the normal and abnormal glucose tolerance categories (the latter included impaired glucose tolerance, impaired fasting glucose, and newly diagnosed diabetes). LV mass (adjusted for age, height, heart rate, and systolic blood pressure) increased across categories of worsening glucose tolerance; the trend was more striking in women (P<0.001) compared with men (P=0.054). In subjects with normal (n=2022) and abnormal glucose tolerance (n=327), covariate-adjusted LV mass and LV wall thickness increased across HOMA-IR quartiles in women (P<0.001) but not men. In contrast, covariate-adjusted LA size increased with worsening glucose tolerance and across HOMA-IR quartiles in the normal and abnormal glucose tolerance groups in both sexes. Adjustment for body mass index considerably attenuated the relations of LV/LA measures and HOMA-IR, rendering them statistically nonsignificant in the normal glucose tolerance group. In our large community-based sample, LV mass and wall thickness increased with worsening glucose intolerance, an effect that was more striking in women compared with men. Insulin resistance was associated with increased LV mass in women alone, but this relation was largely accounted for by obesity.
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                Author and article information

                Journal
                Clinical Science
                Portland Press Ltd.
                0143-5221
                1470-8736
                April 01 2009
                March 02 2009
                April 01 2009
                : 116
                : 7
                : 599-606
                Affiliations
                [1 ]Department of Physiology, University of Melbourne, Parkville, VIC 3010, Australia
                [2 ]Department of Cardiology, The Royal Melbourne Hospital, Grattan St, Parkville, VIC 3050, Australia
                [3 ]Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, VIC 3010, Australia
                [4 ]Royal Women's Hospital, Flemington Rd, Parkville, VIC 3052, Australia
                Article
                10.1042/CS20080142
                18855763
                ba820511-9daa-4732-9d02-c215114031d4
                © 2009
                History

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