A case report: mechanical mitral valve thrombosis in pregnancy.

BACKGROUND: Pregnancy in women with mechanical valves has a high risk of both valve thrombosis and bleeding as well as adverse effects on the foetus. There is limited data on achieving optimal anticoagulation in pregnancy and management of valve thrombosis, to achieve a successful foetal outcome, while prioritizing the mother's health. While warfarin may carry a lower risk of valve thrombosis, warfarin is teratogenic in the first trimester and is associated with increased foetal loss throughout the pregnancy. Heparin does not cross the placenta but is associated with increased maternal morbidity and mortality. CASE SUMMARY: We describe the case of a pregnant patient with thrombosis of a mechanical mitral valve presenting with an embolic stroke at 22 weeks of pregnancy. The stroke was treated with clot retrieval and resulted in no residual neurological deficit. Two previous pregnancies had been managed with low molecular weight heparin, and both resulted in foetal loss. The patient was determined to continue this pregnancy. She was treated with intravenous unfractionated heparin during the remainder of the pregnancy. She developed worsening heart failure due to persisting valve thrombosis despite maintenance of therapeutic anticoagulation. The patient deteriorated rapidly prior to a planned early elective delivery. Emergency Caesarean section was required followed by valve replacement using extracorporeal membrane oxygenation support with an ultimately successful maternal and foetal outcome. Anticoagulation regimes and treatment of mechanical valve thrombosis in pregnancy are discussed. DISCUSSION: The management of pregnant patients with mechanical valves is complex, especially when valve thrombosis and other complications occur. A multidisciplinary approach is essential and in this case led to successful outcome.

Nitric oxide does not mediate the vasodilation of early human pregnancy.

BACKGROUND: In early pregnancy, a substantial drop in arterial blood pressure occurs, that might be attributed to enhanced vascular nitric oxide synthesis. We investigated whether nitric oxide mediates the vasodilation that occurs in early human pregnancy. METHODS: Resting and stimulated forearm vascular resistance were measured (venous occlusion plethysmograph) in six women at 10 +/- 3 weeks of uncomplicated pregnancy and in the same women 7 +/- 5 weeks after elective termination of pregnancy. Forearm vascular resistance was also measured in six non-pregnant, healthy controls. RESULTS: Resting forearm vascular resistance was similar during pregnancy (33 +/- 16 arbitrary units (AU)), after pregnancy (31 +/- 10 AU) and in controls (41 +/- 13 AU, P > 0.05). The decreases in forearm vascular resistance to intrabrachial infusions of acetylcholine (2 and 20 microg/min), serotonin (10 and 100 ng/min) and sodium nitroprusside (1 and 2.5 microg/min) were similar in all groups. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (16 micromol/min) produced similar increases in vascular resistance in pregnant women (38 +/- 17 AU), after pregnancy (36 +/- 14 AU) and in control subjects (42 +/- 8 AU, P = NS). CONCLUSIONS: These results indicate that neither basal nor stimulated nitric oxide levels are altered in the forearm circulation during first trimester pregnancy.

Structural and functional changes in left ventricle during normotensive and preeclamptic pregnancy.

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 = 12) and normotensive (n = 44) and preeclamptic (n = 15) pregnant women using echocardiography. Load-independent 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 +/- 14 mmHg in preeclampsia, 76 +/- 6 mmHg in normotensive pregnancy, and 78 +/- 6 mmHg in controls (P < 0.005 vs. preeclampsia). LV mass increased during normotensive pregnancy (66 +/- 13 to 76 +/- 16 g/m(2); P < 0.05; controls, 65 +/- 10 g/m(2); P < 0.05) and was greater in preeclampsia (90 +/- 18 g/m(2); P < 0.05). In normotensive pregnancy, ESS decreased (59 +/- 9 to 52 +/- 11 g/cm(2); P < 0.05; controls, 66 +/- 14 g/cm(2); P < 0.005). ESS was greater in preeclampsia (60 +/- 14 g/cm(2); P < 0.05). In controls, there was an inverse relationship between ESS and V(CFC) (r = -0.78). 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.

Doppler tissue velocity, strain, and strain rate imaging with transesophageal echocardiography in the operating room: a feasibility study.

OBJECTIVE: Transesophageal echocardiography (TEE) is increasingly used to monitor regional myocardial function during cardiac operation. Doppler myocardial imaging (DMI) indices can potentially provide new information on regional radial and longitudinal myocardial motion and local deformation. This study examined the feasibility of TEE acquisition of regional radial and longitudinal velocity, displacement (D), strain, and strain rate data during cardiac operation and evaluated the effects of sternotomy and pericardial opening on these indices. METHODS: After a baseline transthoracic echocardiographic study, TEE was performed in 22 patients (age 64 +/- 7 years) before sternotomy, after sternotomy with intact pericardium, and after pericardial opening. Regional DMI velocity analysis was performed for the transgastric anterior and inferior walls midpapillary segment (radial function) and the 4-chamber septum and 2-chamber inferior walls basal, mid, and apical segments (longitudinal function). For each segment, systolic and diastolic velocity were derived and D, strain, and strain rate calculated. RESULTS: Transthoracic echocardiographic study and TEE provided similar data from an equivalent number of interpretable segments. In the basal and mid septum, maximum longitudinal systolic D decreased with pericardial opening (basal septum pericardium closed: 6.6 +/- 1.5 mm, open: 4.6 +/- 1.8 mm, P =.007; midseptum pericardium closed: 4.7 +/- 2.5 mm, open: 2.7 +/- 1.5 mm, P =.028). No changes were evident in systolic or diastolic DMI indices in all other segments. CONCLUSION: DMI with TEE is feasible during cardiac operation. During pericardial opening, longitudinal D decreases in the septum, but not in the inferior wall. DMI requires further evaluation in the assessment of ventricular function and the detection of ischemia in the operating room.