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Malignant Arrhythmic Mitral Valve Prolapse: a Continuum of Clinical Challenges from Diagnosis to Risk Stratification and Patient Management

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Malignant Arrhythmic Mitral Valve Prolapse: a Continuum of Clinical Challenges from Diagnosis to Risk Stratification and Patient Management Journal of Cardiovascular Development and Disease Case Report Malignant Arrhythmic Mitral Valve Prolapse: A Continuum of Clinical Challenges from Diagnosis to Risk Stratification and Patient Management Idit Yedidya 1,2 , Aniek L. van Wijngaarden 1 and Nina Ajmone Marsan 1,* 1 Department of Cardiology, Leiden University Medical Center, Leiden, 2300RC Zuid-Holland, The Netherlands; [email protected] (I.Y.); [email protected] (A.L.v.W.) 2 Department of Cardiology, Rabin Medical Center, Petah-Tikva 49372, Israel * Correspondence: [email protected]; Tel.: +31-71-5262020; Fax: +31-71-5266809 Abstract: Mitral valve prolapse (MVP) is a common valvular disease, which may remain a benign condition for a long period of time. However, some patients experience malignant ventricular arrhythmias and sudden cardiac death (SCD). It is still largely unknown how to risk-stratify these patients, and no specific recommendations have been proposed to help the clinical decision-making. We present the case of a young man whose first clinical presentation was an out-of-hospital cardiac arrest and was subsequently diagnosed with MVP. We highlighted the possible risk factors for SCD and the challenges in the clinical management of these patients. Keywords: mitral valve prolapse; sudden cardiac death; risk factors 1. Introduction Citation: Yedidya, I.; van Mitral valve prolapse (MVP) is one of the most common valvular heart diseases, which Wijngaarden, A.L.; Ajmone Marsan, may remain a benign condition for a long period of time, unless accompanied by severe N. Malignant Arrhythmic Mitral mitral regurgitation (MR) which requires surgical treatment when patients develop symp- Valve Prolapse: A Continuum of toms or the left ventricle (LV) begins to dilate and dysfunction. However, some patients, Clinical Challenges from Diagnosis to usually young and without any significant comorbidities, experience malignant ventricular Risk Stratification and Patient arrhythmias (VA) and sudden cardiac death (SCD), estimated in 0.2–0.4% per year, and Management. J. Cardiovasc. Dev. Dis. up to 1.8% per year in the presence of a flail leaflet [1,2]. Several studies have identified 2021, 8, 2. https://doi.org/10.3390/ some risk factors associated with malignant arrhythmias and SCD in MVP patients, mainly jcdd8010002 (i) female sex, (ii) bi-leaflet prolapse, (iii) mitral annulus abnormalities such as dilatation and disjunction (defined as a separation between the left atrial (LA) wall at the level of the Received: 30 October 2020 valve junction with the LV free wall), (iv) electrocardiographic repolarization abnormalities Accepted: 24 December 2020 specifically on the inferolateral leads [3–5], (v) frequent and complex premature ventricular Published: 29 December 2020 contractions (PVCs), and (vi) presence of myocardial fibrosis at the level of the papillary Publisher’s Note: MDPI stays neu- muscles [6,7]. However, it is still largely unknown how to risk-stratify these patients and tral with regard to jurisdictional claims no specific recommendations have been proposed to help the clinical decision-making. in published maps and institutional We present the case of a young man whose first clinical presentation was an out- affiliations. of-hospital cardiac arrest and was subsequently diagnosed with MVP, with the aim of highlighting the diagnostic tests performed to exclude other causes of SCD and to identify possible specific risk factors in MVP, and of creating further awareness of the challenges in the clinical management of these patients. Copyright: © 2020 by the authors. Li- censee MDPI, Basel, Switzerland. This 2. Case Report article is an open access article distributed A 44-year-old man was admitted to the hospital after an out-of-hospital cardiac under the terms and conditions of the arrest, with a successful resuscitation including nine shocks for ventricular tachycar- Creative Commons Attribution (CC BY) dia/ventricular fibrillation (VT/VF). Retrospectively, it was discovered that he had hyper- license (https://creativecommons.org/ tension and hyperlipidemia and had been treated with an angiotensin-converting enzyme licenses/by/4.0/). J. Cardiovasc. Dev. Dis. 2021, 8, 2. https://doi.org/10.3390/jcdd8010002 https://www.mdpi.com/journal/jcdd J. Cardiovasc. Dev. Dis. 2021, 8, 2 2 of 6 inhibitor and a statin. His family medical history included early coronary heart disease (father’s side) and SCD in his mother’s family, which was never further explored. Before the event, he had no specific cardiac complaints. Upon arrival to the emergency room, he was hemodynamically unstable with a blood pressure of 80/50 mmHg, and on physical examination, a grade II/III systolic murmur was noted at the apex. The electrocardiogram (ECG) showed a junctional rhythm without signs of acute coronary syndrome, but the patient was brought immediately to the catheterization- laboratory, where no significant coronary artery disease was found, and a temporarily LV support device was positioned (Impella, Abiomed). The blood tests did not show any abnormalities except a peak troponin T of 1392 ng/L. After hemodynamic stabilization, the J. Cardiovasc. Dev. Dis. 2021, 8, x FOR PEERLV support REVIEW device was removed, and at the fourth day of hospitalization he was weaned2 of 7 from ventilation support. The ECG then showed a sinus rhythm with T wave inversion on lead III and AVF (Figure1); at the telemetry, several PVCs could be observed but without non-sustained VT. A complete echocardiogram was performed, which showed a dilated 2. Case Report LV (end-diastolic diameter = 63 mm) with normal systolic function, a moderate-severe late- systolicA 44-year-old MR by a bi-leaflet man was prolapse admitted (Barlow’s to the hospital MVP) with after a mildan out-of-hospital mitral annulus cardiac disjunction ar- rest,(<5 mm)with a but successful no evidence resuscitation of flail or including rupture chordae nine shocks (Figure for2 ),ventricular enlarged LA tachycardia/ven- (volume index tricular= 61 mL/m fibrillation2), and (VT/VF). right ventricle Retrospectively, systolic pressure it was withindiscovered normal that range. he had hypertension and hyperlipidemiaA contrast-enhanced and had cardiac been treated magnetic with resonance an angiotensin-converting (CMR) imaging wasenzyme performed inhib- itoron and the a eighth statin. day His offamily admission medical to history exclude included cardiomyopathy, early coronary and heart showed disease a dilated (father’s LV side)(end-diastolic and SCD in volume his mother’s index family, = 137 mL/m which2 )was with never no regional further explored. wall motion Before abnormalities, the event, hegood had systolicno specific function cardiac (ejection complaints. fraction = 56%) and no presence of myocardial fibrosis; the presenceUpon arrival of the to bi-leafletthe emergency prolapse room, was he confirmed was hemodynamically with mild mitral unstable annular with disjunction a blood pressure(Figure2 of). The80/50 lack mmHg, of late and gadolinium on physical enhancement examination, (myocardial a grade II/III scar systolic or fibrosis) murmur on CMR, was notedtogether at the with apex. the absenceThe electrocardiogram of regional wall (ECG) motion showed abnormalities, a junctional of significant rhythm coronarywithout signsartery of disease acute coronary by coronary syndrome, angiography but the and patient of dynamic was brought ECG abnormalities, immediately confirmedto the cathe- the terization-laboratory,exclusion of ischemic where heart diseaseno significant as a cause coronary for the artery cardiac disease arrest. was found, and a tem- porarilyConsidering LV support the device out-of-hospital was positioned cardiac (Impella, arrest without Abiomed). clear The reversible blood tests cause, did an not im- showplantable any abnormalities cardioverter defibrillator except a peak (ICD) troponin was implanted, T of 1392 andng/L. the After patient hemodynamic was discharged. sta- bilization,Before discharge, the LV support genetic device counseling was removed, was performed and at accordingthe fourth today standard of hospitalization practice in- hecluding was weaned whole exomefrom ventilation sequencing. support. Firstly, The 522 ECG genes then associated showed witha sinus cardiovascular rhythm with de-T wavevelopment inversion and on disease lead III were and evaluated, AVF (Figure with 1); special at the telemetry, attention to several the genes PVCs know could to be be observedassociated but with without mitral non-sustained valve prolapse VT. (Dachsous A complete Cadherin-Related echocardiogram 1(DCHS1), was performed, Filamin A which(FLNA), showed Phospholipase a dilated D1LV (PLD1), (end-diastolic and DAZ diameter interacting = 63 protein mm) with 1(DZIP1) normal [7 ].systolic Furthermore, func- tion,family a moderate-severe screening was advised, late-systolic and MR his sisterby a bi-leaflet also underwent prolapse echocardiography (Barlow’s MVP) with (which a mildrevealed mitral also annulus a Barlow’s disjunction MVP with (<5 mildmm) MR)but no and evidence genetic of testing. flail or So rupture far, no knownchordae genetic (Fig- uremutations 2), enlarged have beenLA (volume found, but index the comparison= 61 mL/m of2), theand whole right exome ventricle analysis systolic of the pressure brother withinand sister normal is still range. ongoing to try to find new pathogenic variants. FigureFigure 1. 1. ComparisonComparison of electrocardiogram (ECG)(ECG) before before and and after after mitral mitral valve valve repair. repair. Panel Panel (A): ( ECGA):
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