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While left-sided congenital heart defects have been well described in females with Turner syndrome (45, X), the literature is scarce regarding arrhythmias in this patient population.

A full-term neonate referred to cardiology was found to have a non-apex forming left ventricle and partial anomalous pulmonary venous return. During the echocardiogram, she developed atrial flutter, followed by orthodromic reentrant supraventricular tachycardia (SVT). She was started on propranolol and eventually switched to sotalol due to breakthrough SVT. A genetics evaluation revealed Turner syndrome with complete monosomy X (45, X). The patient is now 18 months old and has not had any further arrhythmias.

We present a rare case of atrial flutter followed by supraventricular tachycardia in a neonate with Turner syndrome and left-sided heart defects. This case highlights the importance of early and precise investigation of cardiac abnormalities in neonatal patients, especially among females with Turner syndrome given their relatively higher risk of cardiovascular disease compared to the general population.
We present a rare case of atrial flutter followed by supraventricular tachycardia in a neonate with Turner syndrome and left-sided heart defects. This case highlights the importance of early and precise investigation of cardiac abnormalities in neonatal patients, especially among females with Turner syndrome given their relatively higher risk of cardiovascular disease compared to the general population.
An 82-year-old female with a history of atrial fibrillation and repeated episodes of major bleeding on direct oral anticoagulant therapy, with a high risk for thromboembolism and was referred for left atrial appendage closure.

During the procedure, an unrecognized puncture of the aorta by the transseptal puncture (TSP) needle and inadvertent advancement of the sheath resulted in ascending aorta perforation. This perforation was closed percutaneously using an Amplatzer™ Duct Occluder (ADO). Reversal of heparinization with protamine sulphate was given to avoid intractable bleeding. However, this resulted in thrombus formation and subsequent embolization causing an ST-elevation myocardial infarction. This was treated with balloon dilatation and thrombus aspiration with subsequent Thrombolysis in Myocardial Infarction 3 flow.

Inadvertent ascending aorta perforation is a rare yet serious complication that can occur during TSP. Percutaneous closure using an ADO is a viable management option. Brivudine The reversal of heparin carries a risk of thrombus formation and should be avoided in cases where there is no evidence of overt bleeding.
Inadvertent ascending aorta perforation is a rare yet serious complication that can occur during TSP. Percutaneous closure using an ADO is a viable management option. The reversal of heparin carries a risk of thrombus formation and should be avoided in cases where there is no evidence of overt bleeding.
An acute single leaflet device attachment (SLDA) may occur during transcatheter mitral valve edge-to-edge repair (TMVr), if an inadequate grasping of the target leaflet and/or a leaflet injury are concomitant. The bail-out TMVr often fails due to the complex pathophysiology.

We report a case of an acute SLDA after TMVr with the PASCAL Repair System for severe mitral regurgitation (MR) with mixed aetiology, i.e., a thin-appeared posterior leaflet and pseudo-prolapse of the anterior mitral leaflet due to mitral annular dilatation. An acute SLDA occurred 2 min after the deployment, with device detachment of the posterior leaflet. A bail-out TMVr with the MitraClip XTR system led to an optimal MR reduction with the PASCAL stabilized. Despite an adequate leaflet insertion of the 1st device achieved, the posterior leaflet was tear due to its fragile tissue characteristics. At discharge, echocardiography confirmed an optimal MR reduction to mild grade with both devices stabilized.

The pathology of the mitral valve leaflet is essential to achieve successful TMVr procedure using edge-to-edge repair device. Since the mechanical stress to the target leaflet appears to vary according to the edge-to-edge repair devices, the leaflet tissue characteristics should be respected during device selection.
The pathology of the mitral valve leaflet is essential to achieve successful TMVr procedure using edge-to-edge repair device. Since the mechanical stress to the target leaflet appears to vary according to the edge-to-edge repair devices, the leaflet tissue characteristics should be respected during device selection.
A subset of patients with takotsubo cardiomyopathy will develop significant dynamic left ventricular outflow tract (LVOT) obstruction leading to cardiogenic shock. However, traditional therapies for cardiogenic shock that focus on increased inotropy and afterload reduction can be detrimental in this situation.

We describe a 71-year-old woman who presented to the emergency department with typical, substernal chest pain found to be hypotensive with ST-elevations in the lateral leads. Coronary angiography showed no significant coronary artery disease, but a left ventriculogram demonstrated takotsubo cardiomyopathy. Right heart catheterization revealed cardiogenic shock and elevated filling pressures. Haemodynamics and symptoms worsened with the initiation of dopamine and placement of intra-aortic balloon pump but improved with the initiation of phenylephrine. Follow-up echocardiogram demonstrated dynamic LVOT obstruction with concomitant severe mitral regurgitation (MR). The patient recovered in the intensive care unit for 5 days after successful weaning of phenylephrine and initiation of low-dose beta-blocker. Repeat echocardiogram 3 weeks later showed complete resolution of apical akinesis, LVOT obstruction, and MR.

Elucidating whether dynamic LVOT obstruction is contributing to cardiogenic shock physiology is paramount since the management radically differs depending on the presence or absence of obstruction. Corrective therapy focuses on reducing the LVOT gradient and includes fluid administration to improve preload, beta-blocker therapy to increase diastolic filling time, and vasopressors to raise afterload.
Elucidating whether dynamic LVOT obstruction is contributing to cardiogenic shock physiology is paramount since the management radically differs depending on the presence or absence of obstruction. Corrective therapy focuses on reducing the LVOT gradient and includes fluid administration to improve preload, beta-blocker therapy to increase diastolic filling time, and vasopressors to raise afterload.
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