Peri-partum cardiomyopathy (PPCM) is a frequently fatal disease that affects women near delivery, and occurs more frequently in women with pre-eclampsia and/or multiple gestation. The etiology of PPCM, or why it associates with pre-eclampsia, remains unknown. We show here that PPCM is associated with a systemic angiogenic imbalance, accentuated by pre-eclampsia. Mice that lack cardiac PGC-1α, a powerful regulator of angiogenesis, develop profound PPCM. Importantly, the PPCM is entirely rescued by pro-angiogenic therapies. In humans, the placenta in late gestation secretes VEGF inhibitors like soluble Flt1 (sFlt1), and this is accentuated by multiple gestation and pre-eclampsia. This anti-angiogenic environment is accompanied by sub-clinical cardiac dysfunction, the extent of which correlates with circulating levels of sFlt1. Exogenous sFlt1 alone caused diastolic dysfunction in wildtype mice, and profound systolic dysfunction in mice lacking cardiac PGC-1α. Finally, plasma samples from women with PPCM contained abnormally high levels of sFlt1. These data strongly suggest that PPCM is in large part a vascular disease, caused by excess anti-angiogenic signaling in the peri-partum period. The data also explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.

The presence of perioperative diastolic dysfunction as assessed with Vp is an independent predictor of postoperative CHF and prolonged length of stay after major vascular surgery. Patient age, gender, type of surgery, and renal failure were also predictors of outcome. Perioperative systolic function was not a predictor of postoperative outcome in our patients.

The use of vasopressors during microsurgery is still debated. General anesthesia often induces hypotension, but microsurgeons are reluctant to use intraoperative vasopressors with the potential risks of vasoconstriction. A retrospective review was performed on 187 consecutive patients undergoing 258 deep inferior epigastric perforator flaps, free transverse rectus abdominis myocutaneous flap, and muscle-sparing free transverse rectus abdominis myocutaneous flap operations. A total of 102 patients (140 flaps) received intraoperative ephedrine and/or phenylephrine and 85 patients (118 flaps) did not. The administration of vasopressors did not affect the rates of reoperation, complete flap loss, partial flap loss, or fat necrosis. Patients receiving vasopressors had no differences in operative time, number of perforators, or number of rows of perforators harvested. There was no statistically significant association between dosage, timing, and complications. Although we do not recommend routine vasopressor use during microsurgery, administration does not seem to increase complications in microsurgical breast reconstruction.

Postoperative glycemic variability is associated with MAEs after cardiac surgery. Glycemic variability is only measured when the patient leaves the intensive care unit, and there is no opportunity to intervene earlier. Preoperative HbA1C identifies risk for postoperative glycemic variability and may provide a more rational guide for targeting measures to reduce variability.

An incomplete understanding of the molecular mechanisms responsible for myometrial activation from the quiescent pregnant state to the active contractile state during labor has hindered the development of effective therapies for preterm labor. Myometrial stretch has been implicated clinically in the initiation of labor and the etiology of preterm labor, but the molecular mechanisms involved in the human have not been determined. We investigated the mechanisms by which gestation-dependent stretch contributes to myometrial activation, by using human uterine samples from gynecologic hysterectomies and Cesarean sections. Here we demonstrate that the Ca requirement for activation of the contractile filaments in human myometrium increases with caldesmon protein content during gestation and that an increase in caldesmon phosphorylation can reverse this inhibitory effect during labor. By using phosphotyrosine screening and mass spectrometry of stretched human myometrial samples, we identify 3 stretch-activated focal adhesion proteins, FAK, p130Cas, and alpha actinin. FAK-Y397, which signals integrin engagement, is constitutively phosphorylated in term human myometrium whereas FAK-Y925, which signals downstream ERK activation, is phosphorylated during stretch. We have recently identified smooth muscle Archvillin (SmAV) as an ERK regulator. A newly produced SmAV-specific antibody demonstrates gestation-specific increases in SmAV protein levels and stretch-specific increases in SmAV association with focal adhesion proteins. Thus, whereas increases in caldesmon levels suppress human myometrium contractility during pregnancy, stretch-dependent focal adhesion signaling, facilitated by the ERK activator SmAV, can contribute to myometrial activation. These results suggest that focal adhesion proteins may present new targets for drug discovery programs aimed at regulation of uterine contractility.

A simulation-based TEE curriculum can teach knowledge and technical skills to echo-naive learners. Kinematic measures can objectively evaluate the progression of manual TEE skills.

Background Patients with preeclampsia are at risk for cardiovascular disease. Changes in cardiac function are subtle in preeclampsia and are difficult to quantify with conventional imaging. Strain measurements using speckle-tracking echocardiography have been used to sensitively quantify abnormalities in other disease settings. Methods and Results We evaluated the feasibility and sensitivity of strain imaging using speckle-tracking echocardiography in women with preeclampsia. Forty-seven women were enrolled in this pilot study and 39 were analyzed: 11 with preeclampsia, 17 without a hypertensive disorder and 11 with nonproteinuric hypertension. Echocardiographic ejection fraction and global peak longitudinal, radial and circumferential strain were measured. Longitudinal strain was significantly worsened in women with preeclampsia compared to women without a hypertensive disorder (P=0.0009). Similar results were observed for radial strain (P=0.007) and circumferential strain (P=0.04). Women with preeclampsia also had significantly worsened longitudinal (P=0.04), radial (P=0.01) and circumferential (P=0.002) strain compared with women with nonproteinuric hypertension. Women with preeclampsia did not have a significantly different ejection fraction compared with women without a hypertensive disorder (P=0.52) and women with nonproteinuric hypertension (P=0.44). Conclusions Myocardial strain imaging using speckle tracking is more sensitive than left ventricular ejection fraction to detect differences in left ventricular systolic function in women with and without preeclampsia.

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