on behalf of the Cardiac Disease in Pregnancy (CARPREG) InvestigatorsBackground-The maternal and neonatal risks associated with pregnancy in women with heart disease receiving comprehensive prenatal care have not been well defined. Methods and Results-We prospectively enrolled 562 consecutive pregnant women with heart disease and determined the outcomes of 599 pregnancies not ending in miscarriage. Pulmonary edema, arrhythmia, stroke, or cardiac death complicated 13% of pregnancies. Prior cardiac events or arrhythmia, poor functional class or cyanosis, left heart obstruction, and left ventricular systolic dysfunction independently predicted maternal cardiac complications; the cardiac event rate can be predicted using a risk index incorporating these predictors. Neonatal complications (20% of pregnancies) were associated with poor functional class or cyanosis, left heart obstruction, anticoagulation, smoking, and multiple gestations. Conclusions-Pregnancy in women with heart disease is associated with significant cardiac and neonatal complications, despite state-of-the-art obstetric and cardiac care. Maternal cardiac risk can be predicted with the use of a risk index.

In young, healthy people the alveolar-arterial P O 2 difference (A-aDO 2 ) is small at rest, but frequently increases during exercise. Previously, investigators have focused on ventilation/perfusion mismatch and diffusion abnormalities to explain the impairment in gas exchange, as significant physiological intra-pulmonary shunt has not been found. The aim of this study was to use a non-gas exchange method to determine if anatomical intra-pulmonary (I-P) shunts develop during exercise, and, if so, whether there is a relationship between shunt and increased A-aDO 2 . Healthy male participants performed graded upright cycling to 90%V O 2 max while pulmonary arterial (PAP) and pulmonary artery wedge pressures were measured. Blood samples were obtained from the radial artery, cardiac output (Q) was calculated by the direct Fick method and I-P shunt was determined by administering agitated saline during continuous 2-D echocardiography. A-aDO 2 progressively increased with exercise and was related toQ (r = 0.86) and PAP (r = 0.75). No evidence of I-P shunt was found at rest in the upright position; however, 7 of 8 subjects developed I-P shunts during exercise. In these subjects, point bi-serial correlations indicated that I-P shunts were related to the increased A-aDO 2 (r = 0.68),Q (r = 0.76) and PAP (r = 0.73). During exercise, intra-pulmonary shunt always occurred when A-aDO 2 exceeded 12 mmHg andQ was greater than 24 l min −1 . These results indicate that anatomical I-P shunts develop during exercise and we suggest that shunt recruitment may contribute to the widened A-aDO 2 during exercise.

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The aim of this study was to examine the effects of 12 weeks of supervised aerobic and strength training (SET) versus no-training (NT) on peak aerobic power (VO 2peak ), submaximal exercise left ventricular (LV) systolic function, peripheral vascular function, lean tissue mass and maximal strength in clinically stable heart transplant recipients (HTR). Forty-three HTR were randomly assigned to 12 weeks of SET (n = 22; age: 57 ± 10 years; time posttransplant: 5.4 ± 4.9 years) or NT (n = 21; age: 59 ± 11 years; time posttransplant: 4.4 ± 3.3 years). The change in VO 2peak (3.11 mL/kg/min, 95% CI: 1.2-5.0 mL/kg/min), leg and total lean tissue mass (0.78 kg, 95% CI: 0.31-1.3 kg and 1.34 kg, 95% CI: 0.34-2.3 kg, respectively), chest-press (10.4 kg, 95% CI: 5.2-15.5 kg) and leg-press strength (34.7 kg, 95% CI: 3.7-65.6 kg) were significantly higher after SET versus NT. No significant change was found for submaximal exercise LV systolic function or brachial artery endothelialdependent or -independent vasodilation. Supervised exercise training is an effective intervention to improve VO 2peak , lean tissue mass and muscle strength in HTR. This training regimen did not improve exercise LV systolic function or brachial artery endothelial function.

Subjects with greater aerobic fitness demonstrate better diastolic compliance at rest, but whether fitness modulates exercise cardiac compliance and cardiac filling pressures remains to be determined. On the basis of maximal oxygen consumption (VO2max), healthy male subjects were categorized into either low (LO: VO2max=43+/-6 ml.kg-1.min-1; n=3) or high (HI: VO2max=60+/-3 ml.kg-1.min-1; n=5) aerobic power. Subjects performed incremental cycle exercise to 90% Vo(2max). Right atrial (RAP) and pulmonary artery wedge (PAWP) pressures were measured, and left ventricular (LV) transmural filling pressure (TMFP=PAWP-RAP) was calculated. Cardiac output (CO) and stroke volume (SV) were determined by direct Fick, and LV end-diastolic volume (EDV) was estimated from echocardiographic fractional area change and Fick SV. There were no between-group differences for any measure at rest. At a submaximal workload of 150 W, PAWP and TMFP were higher (P<0.05) in LO compared with HI (12 vs. 8 mmHg, and 9 vs. 4 mmHg, respectively). At peak exercise, CO, SV, and EDV were lower in LO (P<0.05). RAP was not different at peak exercise, but PAWP (23 vs. 15 mmHg) and TMFP (12 vs. 6 mmHg) were higher in LO (P<0.05). Compared with less fit subjects, subjects with greater aerobic fitness demonstrated lower LV filling pressures during exercise, whereas SV and EDV were either similar (submaximal exercise) or higher (peak exercise), suggesting superior diastolic function and compliance.