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Arrhythmias and electrophysiology
Published in Nicholas Green, Steven Gaydos, Hutchison Ewan, Edward Nicol, Handbook of Aviation and Space Medicine, 2019
Nicholas Green, Steven Gaydos, Hutchison Ewan, Edward Nicol
Supraventricular tachycardia (SVT) consists of: AV nodal re-entrant tachycardia (AVNRT).AV re-entrant tachycardia (AVRT).Atrial tachycardia.
Supraventricular tachyarrhythmias in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Jason T. Jacobson, Sei Iwai, Ali Ahmed, Wilbert S. Aronow
PSVT is usually caused by reentry but may be caused by abnormal automaticity or by triggered activity. AV nodal reentrant tachycardia (AVNRT) accounts for 60% of episodes of PSVT (250). Discrete P waves are not seen on the 12-lead ECG in two thirds of these patients. Retrograde P waves (inverted in leads II, III, and aVF) following the QRS complex occur in approximately 30% of these patients. In approximately 10% of patients, the reentry circuit is reversed, with anterograde conduction over the fast pathway and retrograde conduction over the slow pathway (250). This type of PSVT is referred to as atypical AVNRT, and the RP interval is longer than the PR interval.
Fundamentals of cardiac electrophysiology
Published in Ever D. Grech, Practical Interventional Cardiology, 2017
Sunil Kapur, William G Stevenson, Roy M John
Re-entry is probably the most common and best-defined arrhythmia mechanism in the human heart, re-entrant tachycardias are due to repetitive propagation of an excitatory wave around a fixed anatomical or a functional barrier, returning to its site of origin to reactivate that site (Figure 37.4). A re-entrant circuit usually has an area of slow conduction and re-entry is initiated by a premature beat that cause unidirectional block in a part of the circuit. AVN-dependent supraventricular tachycardias such as AV nodal re-entrant tachycardia, atrio-ventricular reciprocating tachycardias due to accessory pathways are typical examples of large re-entry circuits (macro-re-entry). Other examples include common right atrial flutter that involves a circuit revolving along the tricuspid valve annulus.
Lysozyme amyloidosis—a report on a large German cohort and the characterisation of a novel amyloidogenic lysozyme gene variant
Published in Amyloid, 2022
Sophie Anker, Katrin Hinderhofer, Julian Baur, Christian Haupt, Christoph Röcken, Jörg Beimler, Martin Zeier, Markus Weiler, Elke Wühl, Christoph Kimmich, Stefan Schönland, Ute Hegenbart
The presenting feature in patient 10 with the W112R variant was spasmodic abdominal pain associated with diarrhoea at the age of 36 as already published by Röcken et al. [45]. After developing renal insufficiency, the patient reached ESRD at the age of 43 and underwent allogeneic kidney transplantation at the age of 44. As the transplant failed within one year, the kidney was explanted and dialysis was restarted. Histology revealed chronic allograft nephropathy, whereas no amyloid deposits were found in the explanted transplant. Shortness of breath upon physical strain and orthostatic dizziness were additional clinical features the patient suffered from since he was 46 years old. Because of an AV nodal re-entrant tachycardia and progressive dyspnoea, the patient was admitted for further cardiac diagnostics including a myocardial biopsy. Immunohistochemical analysis of heart tissue revealed amyloid deposits confirming a cardiac involvement of ALys amyloidosis. Sensory disturbances in both toes indicated peripheral polyneuropathy. Patient 10 is the only one who does not have any relatives with biopsy-proven amyloidosis or amyloidosis-related symptoms.
Atypical tachycardia mimicking typical reentry: what is the mechanism?
Published in Acta Cardiologica, 2022
Hussam Ali, Guido De Ambroggi, Pierpaolo Lupo, Sara Foresti, Carmine De Lucia, Riccardo Cappato
While 2:1 AV block during the ongoing tachycardia ruled out orthodromic AV re-entry via an accessory AV pathway, the reproducible paradoxical delay in atrial activation by ventricular extrastimuli made atrial tachycardia unlikely as a mechanism. Based on these features, adenosine sensibility, and the presence of dual nodal physiology the most likely mechanism was atypical (fast-slow) AV nodal re-entrant tachycardia (AVNRT). Ventricular entrainment is another useful pacing manoeuvre to differentiate between AVNRT and orthodromic AV re-entry using a septal accessory pathway. During this manoeuvre, longer postpacing intervals (>115 ms compared to tachycardia cycle length), and stimulus-atrium intervals (>85 ms compared to tachycardia VA interval) favour the diagnosis of AVNRT. However, para-Hisian pacing manoeuvre performed in our patient at fast rates (280 ms) during the basal study, showed a nodal response with the same retrograde atrial activation supporting the diagnosis of AVNRT (Figure 1C).
Supraventricular tachycardia with the use of phentermine: case report and review of literature
Published in Postgraduate Medicine, 2021
Sundeep Kumar, Akhil Mogalapalli, Ruthvik Srinivasamurthy, Sayed T. Hussain, Philip L. Mar
AV nodal reentrant tachycardia (AVNRT) is a type of SVT originating from above the bundle of His. It results from a reentry circuit in or around the AV node, produced by two distinct pathways, designated as a slow and fast pathway. The slow-fast or typical AVNRT is the most common form of this arrhythmia. The circuit consists of anterograde conduction down the slow pathway with retrograde conduction up the fast pathway. Under normal circumstances (sinus rhythm), the impulse progresses down both pathways, but the impulse propagating down the fast pathway will reach the end of the AV node first, rendering the end of the slow pathway refractory before progressing into the bundle of His. AVNRT can occur because of differences in the rate of recovery for each pathway (refractory period). While the slow pathway conducts slower than the fast pathway, it ‘recharges’ or repolarizes faster than the fast pathway. Thus, this arrhythmia can be initiated if a critically timed premature atrial contraction sends an impulse down the slow pathway while the fast pathway is still refractory. In this scenario, when the impulse conducts down the slow pathway only, it can conduct retrogradely up the fast pathway once it reaches the end of the AV node if the fast pathway has recovered, setting up a reentry loop back down the slow pathway, all within the AV node, until something perturbs the cycle, such as carotid massage, Valsalva maneuvers, or IV adenosine [21].