Background: As of 2016, ≈1.4 million people in the United States identify as transgender. Despite their growing number and increasing specific medical needs, there has been a lack of research on cardiovascular disease (CVD) and CVD risk factors in this population. Recent studies have reported that the transgender population had a significantly higher rate of CVD risk factors without a significant increase in overall CVD morbidity and mortality. These studies are limited by their small sample sizes and their predominant focus on younger transgender populations. With a larger sample size and inclusion of broader age range, our study aims to provide insight into the association between being transgender and cardiovascular risk factors, as well as myocardial infarction. Methods and Results: The Behavioral Risk Factor Surveillance System data from 2014 to 2017 were used to evaluate the cross-sectional association between being transgender and the reported history of myocardial infarction and CVD risk factors. A logistic regression model was constructed to study the association between being transgender and myocardial infarction after adjusting for CVD risk factors including age, diabetes mellitus, hypertension, hypercholesterolemia, chronic kidney disease, smoking, and exercise. Multivariable analysis revealed that transgender men had a >2-fold and 4-fold increase in the rate of myocardial infarction compared with cisgender men (odds ratio, 2.53; 95% CI, 1.14–5.63; P =0.02) and cisgender women (odds ratio, 4.90; 95% CI, 2.21–10.90; P <0.01), respectively. Conversely, transgender women had >2-fold increase in the rate of myocardial infarction compared with cisgender women (odds ratio, 2.56; 95% CI, 1.78–3.68; P <0.01) but did not have a significant increase in the rate of myocardial infarction compared with cisgender men. Conclusions: The transgender population had a higher reported history of myocardial infarction in comparison to the cisgender population, except for transgender women compared with cisgender men, even after adjusting for cardiovascular risk factors.

Breast arterial calcification (BAC) is a type of medial artery calcification that can be seen incidentally on mammography. Studies have suggested association of BAC with cardiovascular risk factors, coronary artery disease (CAD), and cardiovascular morbidity and mortality. Recently published studies have also suggested a modest correlation of BAC with coronary artery calcium (CAC) scoring. Roughly 40 million mammograms are already performed annually in the United States with overlap in patients that undergo CAD screening via CAC scoring. Thus, identification of cardiovascular risk by demonstrating an association between BAC and CAC may enable an instrumental sex-specific methodology to identify asymptomatic women at risk for CAD. The purpose of this article is to review the current state of the literature for BAC and its association with CAC, to review contemporary breast cancer screening guidelines, and to discuss the clinical implications of these findings.

The natriuretic peptide system plays an active role in the regulation of fluid balance and systemic vascular resistance. Advances in recombinant technology have provided the opportunity for the exogenous administration of a recombinant form of B-type natriuretic peptide (nesiritide). To date, reports of its use in the pediatric population are limited, with limited information regarding its use in patients less than 12 months of age. We retrospectively reviewed our experience with nesiritide in infants less than 12 months of age to determine its efficacy and adverse effect profile. The study cohort included 22 patients, ranging in age from 4 days to 12 months. The starting dose of the nesiritide infusion ranged from 0.01 to 0.05 microg/kg/min (0.015+/-0.01microg/ kg/min) and was administered for a total of 3 to 264 hours (85.2+/-75.0 hours). Nesiritide resulted in a significant increase in urine output even in the face of decreased fluid intake. Mean urine output increased from 3.1+/-2.5 mL/kg/h before nesiritide to 5.7+/-4.5 mL/kg/h (P = .03) during the initial 24 hours after starting the infusion. Fluid intake before and after the infusion were 126 +/- 60 mL/kg/d and 108+/-56 mL/kg/d, respectively. There were no statistically or clinically significant changes in hemodynamic parameters (heart rate, blood pressure, and central venous pressure) during the nesiritide infusion. No change in electrolytes, blood urea nitrogen, and creatinine were noted. No adverse effects of the nesiritide infusion were noted. No infusion was stopped due to adverse effects. These data suggest that nesiritide is a safe method of improving urine output in pediatrics patients less than 12 months of age and that the adverse effect profile does not appear to be different than that reported in older children.

A review of our first 21 cases demonstrated three important lessons: (1) the maximum diameter of the PDA suitable for coil occlusion is approximately 3 mm; (2) CFM must show complete obliteration of flow in the catheterization lab in order to ensure occlusion of the PDA at follow-up; and (3) the Jackson detachable system allows for precise placement of the coil, often within another coil.

The authors retrospectively reviewed their experience with nitric oxide (NO) in a pediatric ICU. Given its cost ($3000/d), ongoing evaluations are required to ensure its effective use and avoid inappropriate applications. NO use included 4 categories: (1) hypoxemic respiratory failure, (2) pulmonary hypertension following surgery for congenital heart disease (CHD), (3) intraoperatively for surgical procedures such BT shunt placement or 1-lung ventilation, and (4) during ECMO. In the 19 patients with respiratory failure, NO resulted in an increase in oxygenation in 15 of 19 patients (Pao2/Fio2 ratio increased from 83 +/- 60 mm Hg to 188 +/- 105 mm Hg, P = 0.0007). In 4 patients, NO did not improve oxygenation. The 15 patients that responded to NO survived, whereas the 4 patients who did not respond died (P = 0.0003). NO was used to treat pulmonary hypertension in 19 patients following cardiopulmonary bypass (CPB) and surgery for CHD. In 13 of 19 patients, a high pulmonary artery (PA) pressure was documented by direct measurement with a needle inserted into the PA while the chest was open (n = 9) or a postoperative transthoracic PA catheter (n = 4). NO resulted in a decrease in the PA pressure in 9 of 13 patients (37 +/- 5 mm Hg to 21 +/- 3 mm Hg, P < 0.0001). In the one patient in whom NO did not lower intraoperative PA pressure, it was not possible to wean from CPB. For the 10 patients in whom NO was started in the PICU, 4 had PA catheters in place and documented elevated PA pressure. NO resulted in a significant decrease in the PA pressure in only 1 of these 4 patients. The survival of responders was 9 of 9 versus 1 of 4 for nonresponders (P = 0.014). No significant adverse effects requiring therapy other than decreasing the inhaled NO concentration were noted. Potential interventions and practices to limit the unwarranted use of this costly agent are discussed.