Acute myopericarditis is primarily a pericarditic syndrome with variable myocardial involvement, as evidenced by elevated cardiac enzymes. It is a rare entity, exclusively seen in male adolescents and accounts for less than 2% of the cases of inpatient admissions for chest pain/pericarditis in the pediatric age group. The electrocardiographic changes of pericarditis include J point/ST segment elevation, which needs to be differentiated from the benign early repolarization pattern that is common in young adolescents and the subtle anterior ST segment elevation myocardial infarction. Differentiating acute myopericarditis from acute coronary syndromes can be challenging because they share the presenting triad of acute chest pain, ST segment changes, and elevated cardiac enzymes. The accurate distinction of myopericarditis from acute myocarditis or acute coronary syndrome is important because of their differences in risk for specific complications, prognosis, and treatment implications. We present a case of acute myopericarditis in an adolescent who presented with atypical precordial chest pain, accompanied by inferolateral focal electrocardiographic changes and significant elevation of cardiac enzymes. The differential diagnosis and management of myopericarditis is reviewed with a focus on electrocardiographic changes and troponin assays.

All placental abruptions begin as partial abruptions, which sometimes manifest as fetal bradycardia. The progression from partial to total abruption was mimicked by a new rabbit model of placental insufficiency, and we compared it, with sufficient statistical power, with the previous model mimicking total placental abruption. The previous model uses total uterine ischemia at E22 or E25 (70% or 79% term, respectively), in pregnant New Zealand white rabbits for 40 min (Full H‐I). The new model, Partial+Full H‐I, added a 30‐min partial ischemia before the 40‐min total ischemia. Fetuses were delivered either at E31.5 (full term) vaginally for neurobehavior testing, or by C‐section at E25 for ex vivo brain cell viability evaluation. The onset of fetal bradycardia was within the first 2 min of either H‐I protocol. There was no difference between Full H‐I (n = 442 for E22, 312 for E25) and Partial+Full H‐I (n = 154 and 80) groups in death or severely affected kits at E22 (76% vs. 79%) or at E25 (66% vs. 64%), or normal kits at E22 or E25, or any of the individual newborn neurobehavioral tests at any age. No sex differences were found. Partial+Full H‐I (n = 6) showed less cell viability than Full H‐I (n = 8) at 72‐hr ex vivo in the brain regions studied. Partial+Full H‐I insult produced similar cerebral palsy phenotype as our previous Full H‐I model in a sufficiently powered study and may be more suitable for testing of potential neuroprotectants.

Objective To determine normal four-extremity blood pressure (BP) in the NICU at birth and the utility of upper (UE) and lower extremity (LE) BP difference to screen for coarctation of aorta (Co-A) and interrupted aortic arch (IAA). Study Design Retrospective study of BP at birth (n=866), and case-control study of Co-A/IAA infants and matched controls (1:2). Results Although BP increased with gestational age (R2=0.3, p<0.0001), the pressure gradient between UE and LE did not change with gestation (p=0.68). Forty-six cases of Co-A/IAA were identified, with 92 controls. Pressure gradient was significantly higher in patients with Co-A/IAA (7.6±14.8 vs.0.4±10mmHg, p=0.004). However, there was overlap between cases and controls resulting in low sensitivity (41.3% with ≥10mmHg gradient cut-off). Conclusion Evaluation of UE-LE BP gradient at birth is a poor screening test for Co-A/IAA with low sensitivity. Repeating four-limb BP after ductal closure at 24–48h along with SpO2 screening for critical congenital heart disease may increase sensitivity.

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