Background: Manifest nodofascicular/ventricular (NFV) pathways are rare.
Methods And Results: From 2008 to 2013, 4 cases were identified with manifest NFV pathways from 3 centers. The clinical findings and ablation sites are reported. All 4 cases presented with a wide complex tachycardia but with different QRS morphologies. Case 1 showed a left bundle branch block/superior axis, case 2 showed a right bundle branch block/inferior axis, case 3 showed a left bundle branch block/inferior axis, and case 4 showed a narrow QRS tachycardia and a wide complex tachycardia with a left bundle branch block/inferior axis. Three of the 4 tachycardias had atrioventricular dissociation ruling out extranodal accessory pathways, including atriofascicular pathways. Programmed extrastimuli showed evidence of a decremental accessory pathway in 3 of the 4 cases. Coexisting tachycardia mechanisms were seen in 3 of the 4 cases (atrioventricular nodal reentry tachycardia [2] and atrioventricular reentrant tachycardia [1]). Ablation in the slow pathway region eliminated the NFV pathway in 3 (transient in 1) with the other responding to surgical closure of a large atrial septal defect. The NFV pathway was a critical part of the tachycardia circuit in 1 and proved to be a bystander in the other 3 cases.
Conclusions: Manifest NFV pathways presented with variable QRS expression dependent on the ventricular insertion site and often coexisted with other tachycardia mechanisms (atrioventricular nodal reentry tachycardia and atrioventricular reentrant tachycardia). In most cases, the atrial insertion of the pathway was in or near the slow pathway region. The NFV pathways were either critical to the tachycardia circuit or served as bystanders.
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http://dx.doi.org/10.1161/CIRCEP.114.001924 | DOI Listing |
Cancers (Basel)
December 2021
Experimental Pathology Unit, Department of Pathology, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC H3A 2B4, Canada.
High-grade serous ovarian cancer (HGSOC) is a significant cause of mortality among women worldwide. Traditional treatment consists of platinum-based therapy; however, rapid development of platinum resistance contributes to lower life expectancy, warranting newer therapies to supplement the current platinum-based protocol. Repurposing market-available drugs as cancer therapeutics is a cost- and time-effective way to avail new therapies to drug-resistant patients.
View Article and Find Full Text PDFCancer
July 2021
Division of Gynecology Oncology, Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Pharm Res
June 2020
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, 8000 Utopia Parkway, Queens, New York, 11439, USA.
Purpose: Nelfinavir (NFV), a FDA approved antiretroviral drug, has been reported to exhibit cancer cells growth inhibition and increased apoptosis. However, it requires a higher dose leading to toxicity, thus limiting its potential clinical translation. We aim to develop biodegradable (poly (lactic-co-glycolic acid)) PLGA nanoparticles of nelfinavir and determine their efficacy to treat non-small cell lung cancer (NSCLC).
View Article and Find Full Text PDFCirc Arrhythm Electrophysiol
September 2019
Cardiology Division (T.E.W., B.K.L., E.P.G., M.M.S.), University of California San Francisco.
Background: Nodofascicular and nodoventricular (NFV) accessory pathways connect the atrioventricular node and the Purkinje system or ventricular myocardium, respectively. Concealed NFV pathways participate as the retrograde limb of supraventricular tachycardia (SVT). Manifest NFV pathways can comprise the anterograde limb of wide-complex SVT but are quite rare.
View Article and Find Full Text PDFCirculation
October 2019
Veterans Affairs Palo Alto Health Care System, CA (W.T, X.J., Y.K.S., E.S., A.B.T., G.P., Y.K., P.Z., S.P., P.D., M.R.N.).
Background: (bone morphogenetic protein receptor 2) mutations are critical risk factors for hereditary pulmonary arterial hypertension (PAH) with approximately 20% of carriers developing disease. There is an unmet medical need to understand how environmental factors, such as inflammation, render mutants susceptible to PAH. Overexpressing 5-LO (5-lipoxygenase) provokes lung inflammation and transient PAH in mice.
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