Survival and Risk Factors for Mortality in Infants With Congenital Heart Disease in South Korea.

BACKGROUND/AIM: The survival of patients with congenital heart disease (CHD) has dramatically improved over recent decades. However, a disparity exists depending on the country and medical system. This study aimed to analyze the survival of infants with CHD until the age of 18 years using large-scale population data in South Korea and investigate the effect of neonatal conditions at birth. PATIENTS AND METHODS: We retrospectively extracted the Korean National Health Insurance Service claims data from January 2002 to December 2020. We included patients diagnosed with CHD who were less than one year of age. The follow-up duration was until their death or until they were censored before the age of 18 years. The CHD lesions were classified hierarchically (conotruncal, severe non-conotruncal, coarctation of the aorta, ventricular septal defect, atrial septal defect, and others). Several neonatal conditions were adopted as risk factors. RESULTS: Overall, 127,958 infants had been diagnosed with CHD and 2,275 died before the age of 18 years. The survival rate of infants with CHD during childhood was 97.9%. The highest childhood mortality rate was associated with non-conotruncal defects (19.7%), followed by conotruncal defects (10.2%). The significant risk factors for childhood mortality were complex CHD, pulmonary hypertension, birth asphyxia, small for gestational age, respiratory distress, pulmonary hemorrhage, bronchopulmonary dysplasia, and convulsions. CONCLUSION: The survival of infants with CHD has been favorable in South Korea. Several neonatal conditions are risk factors for childhood mortality. Individualized risk assessment and optimal treatment strategies may help improve their survival rate.

Morphometric assessment of tibial nerve and its branches around the ankle.

It is essential to understand the considerable variations in bifurcation patterns of the tibial nerve (TN) and its peripheral nerves at the level of the tarsal tunnel to prevent iatrogenic nerve injury during surgical nerve release or nerve block. A total of 16 ankles of 8 human cadavers were dissected to investigate the branching patterns of the TN, using 2 imaginary lines passing through the tip of the medial malleolus (MM) as reference lines. Bifurcation patterns and detailed information on the relative locations of the medial plantar, lateral plantar, medial calcaneal, and inferior calcaneal nerves to the reference lines were recorded. The most common bifurcation pattern was Type 1 in 12 ankles (75%), followed by Type 2 in 2 ankles (13%). One medial calcaneal nerve (MCN) was seen in 11 (69%) specimens and 2 MCN branches were seen in 5 (31%) specimen. 88% of the MCN branches bifurcated from the TN, whereas 6% originated from both TN and lateral plantar nerve (LPN). At the level of the tip of the MM, 2 of 7 parameters showed statistically significant difference between both sexes (P < .05). There was a statistically significant difference between left and right ankles in 2 of 7 measurements (P < .05). Further morphometric analysis of the width, distance, and angle between the TN branches and the tip of MM showed a highly variable nature of the location of the peripheral nerve branches.

Electrodiagnostic Findings Using Radial Motor Segmental Conduction Study and Inching Test in Patients with Radial Neuropathy.

OBJECTIVE: The aim of this study was to characterize the electrodiagnostic findings of radial neuropathy using motor segmental conduction study (RMSCS), and to determine the utility of subsequent inching test in precise lesion localization. DESIGN: Twenty-three patients with radial neuropathy were evaluated using RMSCS with three-point stimulation. The pathomechanism of the lesions according to the RMSCS was classified into three groups: conduction block (CB), mixed lesion (combination of CB and axonal degeneration), and axonal degeneration. Inching test was performed in patients with CB to localize the lesion site, and needle EMG identified the most proximal radial nerve-innervated muscles affected. RESULTS: Out of twenty-three cases, the RMSCS demonstrated probable partial CB in 10, mixed lesions in 2, and axonal degeneration in 10. One case could not be categorized with RMSCS alone. As determined by RMSCS and inching test, the most common cause of CB was compression, while the most common cause of axonal degeneration was iatrogenic. In the CB group, the lesion locations identified by RMSCS and inching test were consistent with needle EMG localization. CONCLUSION: The combined RMSCS and inching test technique can precisely localize radial motor nerve injuries and provide detailed information on electrodiagnostic characteristics of radial mononeuropathy.

Perspectives from clinical trials: is geographic atrophy one disease?

Geographic atrophy (GA) is currently an untreatable condition. Emerging evidence from recent clinical trials show that anti-complement therapy may be a successful treatment option. However, several trials in this therapy area have failed as well. This raises several questions. Firstly, does complement therapy work for all patients with GA? Secondly, is GA one disease? Can we assume that these failed clinical trials are due to ineffective interventions or are they due to flawed clinical trial designs, heterogeneity in GA progression rates or differences in study cohorts? In this article we try to answer these questions by providing an overview of the challenges of designing and interpreting outcomes of randomised controlled trials (RCTs) in GA. These include differing inclusion-exclusion criteria, heterogeneous progression rates of the disease, outcome choices and confounders.

Sub-toxic levels of Co2+ are anti-inflammatory and protect cartilage from degradation caused by IL-1ß.

BACKGROUND: Cobalt ions from some orthopaedic implants induce a dose-dependent cytotoxic and pro-inflammatory response. Recent studies show that sub-toxic levels of cobalt influence actin organisation regulating fibroblasts and macrophages behaviour. However little is known about the influence of sub-toxic levels of cobalt on articular cartilage biology and biomechanics. Previously, we have reported that IL-1ß signalling in chondrocytes, is regulated by primary cilia and associated intraflagellar transport. Since primary cilia expression is modulated by actin organisation, we set out to test the hypothesis that sub-toxic levels of cobalt regulate cilia expression and IL-1ß signalling thereby influencing articular cartilage degradation. METHODS: Isolated chondrocytes and bovine cartilage explants were subjected to Co2+ in the presence and absence of IL-1ß. Primary cilia were monitored by confocal immunofluorescence. Nitric oxide and PGE2 release were used to monitor IL-1ß signalling. Degradation of cartilage matrix was assessed by the release of sGAG and the biomechanical properties of the tissue in uniaxial unconfined compression. FINDINGS: Sub-toxic levels of Co2+ (50 µM) blocked IL-1ß-induced primary cilia elongation in isolated chondrocytes. This was associated with disruption of pro-inflammatory signalling in both isolated chondrocytes and cartilage explants, and inhibition of cartilage matrix degradation and loss of biomechanical properties. INTERPRETATION: This study reveals that low levels of cobalt ions are anti-inflammatory, preventing cartilage degradation in response to IL-1ß. This mechanism is associated with regulation of primary cilia elongation. These observations provide new insight into the potential beneficial role of cobalt and may lead to novel mechanisms for controlling cartilage inflammation.