Developmental.Diseases.of.the.Hip.Diagnosis.[taliem.ir]

Introductory Chapter: Five-Dimensional Approach to the Developmental Dysplasia of the Hip

Developmental dysplasia of the hip (DDH) is not a specifc disorder; it is rather a scale of overlapping and transforming conditions. It ranges from occult dysplasia seen on ultrasound screening of newborns, neonatal hip instability and dislocated hip whether reducible by orthopaedic manipulation or not. The hallmark of DDH is acetabular dysplasia—abnormality in size, shape or orientation of acetabulum. A thoughtful elucidation regarding DDH is that it is ‘a common and preventable cause of childhood disability’ . Complications and consequences of DDH make this time interval much longer, though. The incidence of many faces of DDH is fortunately distributed: it is reported to be as much as 8% for dysplasia, 1–3% for neonatal hip instability and <0.2% for frank dislocation . These epidemiological data are greatly influenced by both diagnostic criteria and diagnostic methods used . They evolve not only due to demographic changes of population, predominantly through migrations and genetic mixing, but also due to changes in nutrition . DDH is not a disease of modern age. It was recognised and described by Hippocrates as a congenital dislocation of the hip. Dysplastic hips and presence of false acetabulum were found in skeletons from medieval times .
EHRA.Book.of.Interventional.Electrophysiology.Case-based.learning.[taliem.ir]

The EHRA Book of Interventional Electrophysiology

Orthodromic atrioventricular re-entrant tachycardia using dual anterograde nodal conduction Te underlying mechanism is orthodromic atrioventricular re-entrant tachycardia (AVRT) (anterograde nodal conduction, retrograde via lef-sided bypass tract). Conventionally, LBBB during orthodromic AVRT over a lef-sided bypass tract usually is associated with prolongation of the atrial cycle length (due to the larger circuit). In the present case, the shorter cycle length during LBBB is somewhat paradoxical (‘accelerating LBBB’) and needs explaining. In the lef part, rate-dependent LBB aberrancy is present. Most likely, LBB aberrancy perpetuates via concealed trans-septal retrograde conduction until this phenomenon is interrupted by retrograde invasion of a lef-sided premature ventricular complex (PVC) into the lef bundle. Moreover, this His-refractory PVC resets the atrium (excluding AT and proving active participation of the bypass tract). Te resulting shorter A–A interval causes a shif in anterograde conduction from the fast to the slow pathway. Together with peeling back refractoriness of the lef bundle, cycle length prolongation results in normal infra-Hisian conduction. Afer ablation of the lef-sided bypass tract, the patient was not inducible for atrioventricular nodal re-entrant tachycardia (AVNRT). Note: In this setting, measurement of the ventriculoatrial (VA) interval from QRS onset to the earliest atrial electrogram, instead of the cycle length, is less ambiguous. VA prolongation of >40ms provides strong evidence of a free wall accessory pathway in ipsilateral bundle branch block in the absence of a pre-existing underlying fascicular block.