ST-segment elevation myocardial infarction (STEMI) caused by spontaneous coronary artery dissection (SCAD) in a patient with von Willebrand disease.

A postpartum woman in her early 40s, with a history of pre-eclampsia and von Willebrand disease (VWD), presented to the emergency room with chest pain suggestive of an acute coronary syndrome. Initial workup revealed an evolving anterior wall ST-segment elevation myocardial infarction on ECG and elevated cardiac biomarkers, confirming myocardial damage. Point-of-care ultrasound showed apical hypokinesis and coronary angiography revealed a distal dissection of the left anterior descending coronary artery. There was TIMI 3 flow and no evidence of plaque rupture. No percutaneous coronary intervention was performed and the patient was managed conservatively.Fibromuscular dysplasia was ruled out on screening CT angiography. Dual antiplatelet therapy was initiated for an amended course of 3 months given the history of VWD. Our patient had an uncomplicated course in the hospital with a downward trend in their cardiac biomarkers, resolving anterior ST elevation on serial ECGs, and no bleeding complications.

A Novel Frameshift Mutation, KCNH2 [p.Asp896ArgfsX79], Leading to Malignant Ventricular Arrhythmia, Identified After Treatment of Gastrointestinal Bleeding.

A novel frameshift mutation in the KCNH2 gene for long QT syndrome type 2 (LQTS2) was identified after torsades des pointes ventricular tachycardia in a 49-year-old patient managed with octreotide and nadolol for an acute variceal bleed. In spite of removal of offending medications, and correction of underlying electrolyte abnormalities, the patient's QT interval remained prolonged-at 521 ms-raising the suspicion of an underlying channelopathy. Genetic studies confirmed heterozygosity for a novel frameshift mutation for the KCNH2 gene, D896Rfs X79. We explore the pathogenicity and clinical impact of this variant mutation.

Une nouvelle mutation de changement de phase du gène KCNH2 impliqué dans le syndrome du QT long de type 2 (SQTL2) a été trouvée après une tachycardie ventriculaire à torsades de pointes chez un patient de 49 ans traité par octréotide et nadolol en raison d'un saignement variqueux en phase aiguë. En dépit du retrait des médicaments mis en cause et de la correction des anomalies électrolytiques sous-jacentes, l'intervalle du QT du patient qui demeurait prolongé (à 521 ms) a suscité la suspicion d'une canalopathie sous-jacente. Des études génétiques ont permis de confirmer l'hétérozygosité d'une nouvelle mutation de changement de phase du gène KCNH2, D896Rfs X79. Nous examinons la pathogénicité et les répercussions cliniques de cette mutation du variant.

Gemella morbillorum endocarditis and osteomyelitis in a patient with ankylosing spondylitis.

We report a rare case of Gemella morbillorum endocarditis of the native aortic and mitral valves, and native vertebral osteomyelitis, in a 49-year-old male with HLA-B27 negative ankylosing spondylitis (AKS). G. morbillorum is a rare cause of endocarditis; the incidence of which is unknown. AKS may predispose patients to endocarditis through chronic valvulitis. G. morbillorum bacteremia in patients with AKS should prompt consideration of infective endocarditis and a search for possible portals of entry.

Les auteurs déclarent un rare cas d'endocardite à Gemella morbillorum des valves aortiques et mitrales naturelles et une ostéomyélite des vertèbres naturelles chez un homme de 49 ans atteint de spondylite ankylosante négative au HLA-B27 (SAK). Le G. morbillorum est une rare cause d'endocardite dont on ne connaît pas l'incidence. La SAK peut prédisposer à l'endocardite par une valvulite chronique. La bactériémie à G. morbillorum chez des patients atteints de SAK devrait inciter à envisager rapidement une endocardite infectieuse et à rechercher les voies d'entrée possibles.