There is often a diagnostic dilemma in pediatric patients presenting with depressed ventricular function, as myocarditis and dilated cardiomyopathy (DCM) of other etiologies can appear very similar. Accurate identification is critical to guide treatment and to provide families with the most accurate expectation of long-term outcomes. The objective of this study was to identify patterns of clinical presentation and to assess non-invasive measures to differentiate patients with acute myocarditis from other forms of DCM. We identified all children (< 18 years) from our institution with a diagnosis of idiopathic DCM or myocarditis based on endomyocardial biopsy or explant pathology (1996-2015). Characteristics at the time of presentation were compared between patients with a definite diagnosis of myocarditis and those with idiopathic DCM. Data collected included clinical and laboratory data, radiography, echocardiography, and cardiac catheterization data. A total of 58 patients were included in the study; 46 (79%) with idiopathic DCM and 12 (21%) with acute myocarditis. Findings favoring a diagnosis of myocarditis included a history of fever (58 vs. 15%, p = 0.002), arrhythmia (17 vs. 0%, p = 0.003), higher degree of cardiac enzyme elevation, absence of left ventricular dilation (42 vs. 7%, p = 0.002), segmental wall motion abnormalities (58 vs. 13%, p = 0.001), lower left ventricular dimension z-score (3.7 vs. 5.2, p = 0.031), and less severe depression of left ventricular systolic function. There are notable differences between patients with myocarditis and other forms of DCM that can be detected non-invasively at the time of presentation without the need for endomyocardial biopsy. These data suggest that it may be possible to develop a predictive model to differentiate myocarditis from other forms of DCM using non-invasive measures.
Respiratory morbidity may not always associate with PH at 36 weeks among ELGANs. However, components of nitric oxide metabolism are potential biologic markers of PH in need of further study.
Pulmonary vein stenosis (PVS) has emerged as a critical problem in premature infants with persistent respiratory diseases, particularly bronchopulmonary dysplasia (BPD). As a parenchymal lung disease, BPD also influences vascular development with associated pulmonary hypertension recognized as an important comorbidity of both BPD and PVS. PVS is commonly detected later in infancy, suggesting additional postnatal factors that contribute to disease development, progression, and severity. The same processes that result in BPD, some of which are inflammatory-mediated, may also contribute to the postnatal development of PVS. Although both PVS and BPD are recognized as diseases of inflammation, the link between them is less well-described. In this review, we explore the relationship between parenchymal lung diseases, BPD, and PVS, with a specific focus on the epidemiology, clinical presentation, risk factors, and plausible biological mechanisms in premature infants. We offer an algorithm for early detection and prevention and provide suggestions for research priorities.
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