We describe a case of a 60 year-old man after inferior wall myocardial infarction with intermittent preexcitation syndrome. In ECG, the pathologic Q waves in the inferior leads were masked by the intermittent preexcitation. In this patient, paroxysmal asymptomatic second-degree atrioventicular block coexists with inconstant atrioventricular conduction maintained by the accessory pathway, periodically 2:1.
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J Electrocardiol
January 2025
Division of Pediatric Cardiology, Department of Pediatrics, Medical University Graz, Graz, Austria.
We report wide QRS complexes appearing in conjunction with prolonged R-R intervals in a 5- year old patient with situs ambiguous and mirror image dextrocardia, who had undergone ASD and VSD closure at of the age of one. We present differential diagnoses of intermittent spontaneous QRS widening and refer to ECG lead positioning in mirror image dextrocardia patients.
View Article and Find Full Text PDFInt J Cardiol Heart Vasc
December 2024
Telemedico Srl-Telecardiology Center, Genova, Italy.
Europace
October 2024
Paediatric Cardiology and Cardiac Arrhythmias Unit, Bambino Gesù Children's Hospital, IRCCS, Piazza S. Onofrio 4, Rome 00165, Italy.
J Vet Cardiol
August 2024
Clinica Veterinaria Malpensa, Viale Marconi, 27, 21017, Samarate, VA, Italy; College of Veterinary Medicine, Cornell University, 930 Campus Road, 14853, Ithaca, NY, USA.
A four-year-old Labrador Retriever was presented for intermittent tachycardia. The electrocardiogram showed sinus rhythm conducted with ventricular pre-excitation and short runs of orthodromic atrioventricular reciprocating tachycardia. Four months later, the rhythm degenerated into a symptomatic sustained tachycardia, suspected to be pre-excited atrial fibrillation, a potentially life-threatening rhythm in the presence of an accessory pathway with a short refractory period.
View Article and Find Full Text PDFJ Pediatr Hematol Oncol
August 2024
Department of Pediatric Allergy and Immunology.
Agammaglobulinemia represents the most profound primary antibody deficiency, stemming from early cessation of B-cell development. Deficiency in folliculin-interacting protein 1 (FNIP1) is a novel inborn error of immunity characterized by a severe defect in B-cell development, agammaglobulinemia, variable neutropenia, and hypertrophic cardiomyopathy. FNIP1 plays a critical role in B-cell development and metabolic homeostasis, establishing a metabolic checkpoint that ensures pre-B cells possess sufficient metabolic capacity to undergo division while concurrently limiting lymphogenesis due to abnormal growth.
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