P-SCAD patients had more acute presentations and high-risk features than women with NP-SCAD did. The highest frequency of P-SCAD occurred during the first postpartum month and P-SCAD patients less often had extracoronary vascular abnormalities. Hormonal, hemodynamic variations, and yet-undefined mechanisms might be significant contributors to P-SCAD. (The "Virtual" Multicenter Spontaneous Coronary Artery Dissection [SCAD] Registry [SCAD]; NCT01429727; Genetic Investigations in Spontaneous Coronary Artery Dissection [SCAD]; NCT01427179).

Spontaneous coronary artery dissection is a major cause of myocardial infarction in pregnancy and the postpartum period. It occurs predominantly in young women with few or no conventional risk factors for atherosclerosis and has been clinically underrecognized. Treatment differs from that of myocardial infarction as a result of atherosclerosis and the diagnosis should be considered in all parturient and postpartum patients with acute coronary syndrome. Complications of spontaneous coronary artery dissection include recurrence, congestive heart failure, and death. Thus, specialist obstetrician-gynecologists and maternal-fetal medicine specialists need to gain knowledge of spontaneous coronary artery dissection to improve outcomes.

Objective: To develop and validate criteria for the retrospective diagnoses of hypertensive disorders of pregnancy that would be amenable to the development of an electronic algorithm, and to compare the accuracy of diagnoses based on both the algorithm and diagnostic codes against the gold standard, i.e., physician-made diagnosis. Patients and Methods: An algorithm for hypertensive disorders of pregnancy was developed by first defining a set of criteria for retrospective diagnoses, which included relevant clinical variables and diagnosis of hypertension that required blood pressure elevations in greater than 50 % of readings (“the 50% rule”). The algorithm was validated using the Rochester Epidemiology Project (Rochester, MN, USA). A stratified-random sample of pregnancies and deliveries between January 1, 1976 and December 31, 1982 according to the algorithm-based diagnoses was generated for review and physician-made diagnoses (normotensive, gestational hypertension, and preeclampsia), which served as the gold standard; the targeted cohort for analysis was 25 per diagnosis category based on the gold standard. The agreements between i) the algorithm-based diagnoses and ii) diagnostic codes and the gold standard were analyzed. Results: Sensitivities of the algorithm for 25 normotensive, 25 gestational hypertension, and 25 preeclamptic pregnancies were 100%, 88%, and 100%, respectively. Specificities were 94%, 100%, and 100%, respectively. Diagnostic code sensitivities were 96% for normotensive, 32% for gestational hypertension and 96% for preeclampsia. Specificities were 78%, 96%, and 88%, respectively. Conclusion: Electronic diagnostic algorithm was highly sensitive and specific in identifying and classifying hypertensive disorders of pregnancy and was superior to diagnostic codes.

Spontaneous coronary artery dissection (SCAD) is an important etiology of myocardial infarction (MI) and sudden cardiac death in young women (1). Previously considered rare, substantial improvement in SCAD diagnosis and awareness has facilitated research of this disease. Many women with a history of SCAD have recurrent chest pain despite lack of demonstrable ischemia or coronary obstruction. Herein, we report the hypothesis-generating finding of women who experience chest pain that predictably occurs or worsens synchronous with menstruation. The objective was to describe the observation and treatment of cyclic chest pain associated with menstruation (catamenial chest pain) in SCAD.The Mayo Clinic Institutional Review Board approved the study. We reviewed the records of patients in the Mayo Clinic SCAD Registry enrolled from 2012 to 2016 and identified those who voluntarily described chest pain associated with menstruation. These patients were contacted by telephone and participated in a focused survey.A total of 11 women were identified (Table 1). Four had experienced post-partum SCAD, 2 had fibromuscular dysplasia, and 1 had Ehlers-Danlos syndrome type IV. Most (7 of 11, 64%) presented with ST-segment elevation MI at time of SCAD; 1 presented in cardiac arrest. The majority (7 of 11, 64%) had left anterior descending coronary artery SCAD.All women described onset of chest pain just prior to menstruation, usually 1 to 2 days before onset of bleeding. Symptoms persisted into menses in 4 (36%). Two women (18%) had coronary artery obstruction on coronary angiography (CA) (1 with persistent dissection and another with instent stenosis); these patients' catamenial chest pain persisted despite revascularization and negative subsequent stress studies. Six women (55%) had negative stress tests, 2 of whom had patent coronaries upon imaging. Of these, patient #5 had chronic troponin I elevations in the absence of electrocardiogram changes or left ventricular wall motion abnormalities. Two (18%) underwent CA without a preceding stress test with the finding of patent coronaries; another woman (9%) had an unremarkable coronary computed tomography angiography.

Patients with a history of peripartum cardiomyopathy who recover LV function are at risk for a transient minor decrease in LV ejection fraction during future pregnancies, but obstetric and neonatal outcomes are often favorable.

Recognizing the lack of clearly defined milestones in ultrasound training in OB-GYN residency, this study confirms the substantial heterogeneity in curricula between programs, highlighting a need for a standardized ultrasound curriculum.

Glomerular damage is common in preeclampsia (PE), but the extent and etiology of tubular injury are not well understood. The aim of this study was to evaluate tubular injury in patients with PE and to assess whether it predates clinical disease. We performed a prospective cohort study of 315 pregnant women who provided urine samples at the end of the second trimester and at delivery. This analysis included women who developed PE ( = 15), gestational hypertension (GH; = 14), and normotensive controls (NC; = 44). Urinary markers of tubular injury, α1-microglobulin (A1M), retinol-binding protein (RBP), kidney-injury molecule-1 (KIM1), complement C5b-9, tissue inhibitor metalloproteinase-2 (TIMP-2), and insulin-like growth factor binding protein-7 (IGFBP-7) were measured by enzyme-linked immunosorbent assay (ELISA) and reported in relation to urine creatinine concentration. Second-trimester concentrations of all markers were similar among groups. At delivery, A1M concentrations were higher in the PE group than in the GH and NC groups as an A1M/creatinine ratio >13 (66.7, 8.3, and 35%, respectively, = 0.01). Concentrations of C5b-9 were higher in the PE group than in the GH and NC groups (medians 9.85, 0.05, and 0.28 ng/mg, respectively, = 0.003). KIM1, RBP, TIMP-2, and IGFBP-7 concentrations did not differ among groups at delivery. In conclusion, proximal tubular dysfunction, as assessed by A1M and C5b-9, developed during the interval between the end of the second trimester and delivery in patients with PE. However, this was not matched by abnormalities in markers previously associated with tubular cell injury (KIM-1, IGFBP-7, and TIMP-2).

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