.-Increased cardiac output in pregnancy is associated with cardiac remodeling and possible reduction in contractility, which may worsen in preeclampsia. Left ventricular (LV) geometry and function were compared between nonpregnant controls (n ϭ 12) and normotensive (n ϭ 44) and preeclamptic (n ϭ 15) pregnant women using echocardiography. Loadindependent comparisons of LV systolic function compared end-systolic stress (ESS) and rate-corrected velocity of circumferential fiber shortening (V CFC). Mean arterial pressures were 101 Ϯ 14 mmHg in preeclampsia, 76 Ϯ 6 mmHg in normotensive pregnancy, and 78 Ϯ 6 mmHg in controls (P Ͻ 0.005 vs. preeclampsia). LV mass increased during normotensive pregnancy (66 Ϯ 13 to 76 Ϯ 16 g/m 2 ; P Ͻ 0.05; controls, 65 Ϯ 10 g/m 2 ; P Ͻ 0.05) and was greater in preeclampsia (90 Ϯ 18 g/m 2 ; P Ͻ 0.05). In normotensive pregnancy, ESS decreased (59 Ϯ 9 to 52 Ϯ 11 g/cm 2 ; P Ͻ 0.05; controls, 66 Ϯ 14 g/cm 2 ; P Ͻ 0.005). ESS was greater in preeclampsia (60 Ϯ 14 g/cm 2 ; P Ͻ 0.05). In controls, there was an inverse relationship between ESS and V CFC (r ϭ Ϫ0.78). The ESS-V CFC relationships in normotensive and preeclamptic pregnancy were unchanged from controls. We conclude that LV hypertrophy in normotensive and preeclamptic pregnancy matches changes in cardiac work, and LV contractility is preserved. preeclampsia; echocardiography; ventricular function; myocardial contractility; hypertension PREGNANCY IS ASSOCIATED WITH hemodynamic and hormonal changes that can affect the heart. From the first trimester, there is an increase in cardiac output that places a volume load on the heart. Hormonal changes include increased circulating estrogen and relaxin, which may directly or indirectly affect the heart. During pregnancy, the heart undergoes remodeling similar to that observed in athletes (9, 13) with increases in chamber dimensions, left ventricular (LV) wall thickness, and mass (2, 13, 24) that is consistent with a process of eccentric hypertrophy (15).More controversial is whether myocardial contractile function also changes in pregnancy. Ejection-phase indices of LV function, including systolic fractional shortening (FS) and mean velocity of circumferential fiber thickening (V CFC ), have been variously reported to increase (26), remain constant (15), or decrease (24) during pregnancy. The use of these indices is limited by the changes in ventricular loading conditions that occur during pregnancy. The inverse relationship between ventricular end-systolic stress (ESS) and V CFC has been described as a load-independent measure of contractility (5). The results of one study (21) that used the ESS-V CFC relationship suggest that myocardial contractility is actually reduced during pregnancy. There are even less data about changes in LV diastolic function during pregnancy. Hypertrophy of the left ventricle may result in reduced diastolic compliance (20), whereas hormonal influences such as nitric oxide may have the opposite effect (22).A change in myocardial contractility during pregnancy has impo...

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Right ventricular contractile response to pharmacological stress in pulmonary arterial hypertension (PAH) has not been characterised. We evaluated right ventricular contractile reserve in adults with PAH using dobutamine stress echocardiography.16 PAH patients and 18 age-matched controls underwent low-dose dobutamine stress echocardiography. Contractile reserve was assessed by the change (Δ; peak stress minus rest value) in tricuspid annular plane systolic excursion (TAPSE) and tricuspid annular systolic velocity (S′). A subgroup of 13 PAH patients underwent treadmill cardiopulmonary exercise testing for peak oxygen uptake (V′O 2 peak).At rest, TAPSE and S′ were reduced in the PAH group compared with controls (1.7±0.4 versus 2.4±0.2 cm and 9.7±2.6 versus 12.5±1.2 cm·s −1 , respectively; p<0.05). Contractile reserve was markedly attenuated in PAH compared to controls (ΔTAPSE 0.1±0.2 versus 0.6±0.3 cm and ΔS′ 4.6±2.8 versus 11.2±3.6 cm·s −1 ; p<0.0001). In the sub-group of PAH patients with preserved right ventricular systolic function at rest, contractile reserve remained depressed compared to controls. V′O 2 peak was significantly correlated with ΔS′ (r=0.87, p=0.0003) and change in stroke volume (r=0.59, p=0.03).Dobutamine stress can reveal sub-clinical reduction in right ventricular contractile reserve in patients with PAH. A correlation with exercise capacity suggests potential clinical value beyond resting measurements. @ERSpublications Dobutamine-induced right ventricular contractile reserve is impaired in PAH and correlates with exercise capacity

Aims. We compared the demographic profile and clinical characteristics of individuals with new onset steroid-induced diabetes (NOSID) to Type 2 diabetes (T2DM) patients with and without steroid treatment. Methods. The demographic profile and clinical characteristics of 60 individuals who developed NOSID were examined and matched to 60 type 2 diabetes patients receiving steroid therapy (T2DM+S) and 360 diabetic patients not on steroids (T2DM) for age, duration of diabetes, HbA1c, gender, and ethnicity. Results. Patients who developed NOSID had less family history of diabetes (P ≤ 0.05) and were less overweight (P ≤ 0.02). NOSID was more commonly treated with insulin. Despite a matching duration of diabetes and glycaemic control, significantly less retinopathy was found in the group of patients with NOSID (P < 0.03). Conclusions. It appears that steroid treatment primarily precipitated diabetes in a group of individuals otherwise less affected by risk factors of diabetes at that point in time, rather than just opportunistically unmasking preexisting diabetes. Furthermore, the absence of retinopathy suggests that patients with NOSID had not been exposed to long periods of hyperglycaemia. However, the impact of the underlying conditions necessitating steroid treatment and concomitant medications such as immunosuppressants on diabetes development remain to be defined.