Arrhythmogenic Mitral Valve Prolapse and Sudden Cardiac Death: An Update and Current Perspectives

Battaglia, Valeria; Santangelo, Gloria; Bursi, Francesca; Simeoli, P; Guazzi, Marco

doi:10.1016/j.cpcardiol.2023.101724

Cited by 9 publications

(6 citation statements)

References 81 publications

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“…Finally, mitral valve prolapse is known to be associated with sudden cardiac death from VT, an entity termed arrhythmogenic mitral valve pro-lapse. 27 – 31 Myocardial fibrosis is known to occur in one-third of patients with mitral valve prolapse. An imaging study from 2020 examined 20 patients with mitral valve prolapse and ventricular ectopy using simultaneous cardiac 18F FDG-PET and magnetic resonance imaging with late gadolinium enhance-ment: 85% of patients had evidence of PET positive lesions, and 70% of patients had PET positive lesions which also had late gadolinium enhancement.…”

Section: Surgical Ablation For Ventricular Tachycardiamentioning

confidence: 99%

Surgery for Cardiac Arrhythmias: Past, Present, Future

Waterford,

2024

Rambam Maimonides Med J

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There is a rich history of surgery for cardiac arrhythmias, spanning from atrial fibrillation and Wolff–Parkinson–White syndrome to inappropriate sinus tachycardia and ventricular tachycardia. This review describes the history of these operations, their evolution over time, and the current state of practice. We devote considerable time to the discussion of atrial fibrillation, the most common cardiac arrhythmia addressed by surgeons. We discuss ablation of atrial fibrillation as a stand-alone operation and as a concomitant operation performed at the time of cardiac surgery. We also discuss the emergence of newer procedures to address atrial fibrillation in the past decade, such as the convergent procedure and totally thoracoscopic ablation, and their outcomes relative to historic approaches such as the Cox maze procedure.

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Section: Surgical Ablation For Ventricular Tachycardiamentioning

confidence: 99%

Surgery for Cardiac Arrhythmias: Past, Present, Future

Waterford,

2024

Rambam Maimonides Med J

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“…MVP is defined as the systolic displacement of one or both mitral valve (MV) leaflets more than 2 mm above the mitral annular plane in the sagittal view of the MV at echocardiography [ 1 ]. The main etiologies are (1) myxomatous MVP or Barlow’s disease, (2) fibroelastic deficiency (FED), and (3) syndromic MVP in the context of connective tissue diseases such as Marfan syndrome, Loeys–Dietz syndrome, and Ehlers–Danlos syndrome [ 4 , 5 ]. Mitral annular disjunction (MAD) is a mitral annular abnormality that may not necessarily be associated with MVP and is described as a systolic separation or detachment of the basal left ventricular (LV) myocardium and the mitral annulus supporting the mitral leaflet (most commonly, the posterior leaflet), with a consequent abnormal systolic displacement of the leaflet hinge point into the left atrium (LA) [ 5 , 6 ].…”

Section: Introduction and Epidemiologymentioning

confidence: 99%

Arrhythmic Mitral Valve Prolapse and Sports Activity: Pathophysiology, Risk Stratification, and Sports Eligibility Assessment

Compagnucci,

Selimi,

Cipolletta

et al. 2024

JCM

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Although mitral valve prolapse (MVP) is the most prevalent valvular abnormality in Western countries and generally carries a good prognosis, a small subset of patients is exposed to a significant risk of malignant ventricular arrhythmias (VAs) and sudden cardiac death (SCD), the so-called arrhythmic MVP (AMVP) syndrome. Recent work has emphasized phenotypical risk features of severe AMVP and clarified its pathophysiology. However, the appropriate assessment and risk stratification of patients with suspected AMVP remains a clinical conundrum, with the possibility of both overestimating and underestimating the risk of malignant VAs, with the inappropriate use of advanced imaging and invasive electrophysiology study on one hand, and the catastrophic occurrence of SCD on the other. Furthermore, the sports eligibility assessment of athletes with AMVP remains ill defined, especially in the grey zone of intermediate arrhythmic risk. The definition, epidemiology, pathophysiology, risk stratification, and treatment of AMVP are covered in the present review. Considering recent guidelines and expert consensus statements, we propose a comprehensive pathway to facilitate appropriate counseling concerning the practice of competitive/leisure-time sports, envisioning shared decision making and the multidisciplinary “sports heart team” evaluation of borderline cases. Our final aim is to encourage an active lifestyle without compromising patients’ safety.

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“…Mitral valve prolapse (MVP) is a common valvular disease, affecting 2-3% of the adult human population [1]. MVP can arise with a syndromic condition like Marfan's syndrome, but it more commonly manifests as a non-syndromic condition [2], such as myxomatous mitral valve prolapse.…”

Section: Introductionmentioning

confidence: 99%

Defining the Role of the miR-145—KLF4—αSMA Axis in Mitral Valvular Interstitial Cell Activation in Myxomatous Mitral Valve Prolapse Using the Canine Model

Yang,

Moyer,

Zhou

et al. 2024

IJMS

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Mitral valve prolapse (MVP) is a common valvular disease, affecting 2–3% of the adult human population and is a degenerative condition. A total of 5–10% of the afflicted will develop severe mitral regurgitation, cardiac dysfunction, congestive heart failure, and sudden cardiac death. Naturally occurring myxomatous MVP in dogs closely resembles MVP in humans structurally, and functional consequences are similar. In both species, valvular interstitial cells (VICs) in affected valves exhibit phenotype consistent with activated myofibroblasts with increased alpha-smooth muscle actin (αSMA) expression. Using VICs collected from normal and MVP-affected valves of dogs, we analyzed the miRNA expression profile of the cells and their associated small extracellular vesicles (sEV) using RNA sequencing to understand the role of non-coding RNAs and sEV in MVP pathogenesis. miR-145 was shown to be upregulated in both the affected VICs and sEV, and overexpression of miR-145 by mimic transfection in quiescent VIC recapitulates the activated myofibroblastic phenotype. Concurrently, KLF4 expression was noted to be suppressed by miR-145, confirming the miR-145—KLF4—αSMA axis. Targeting this axis may serve as a potential therapy in controlling pathologic abnormalities found in MVP valves.

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Arrhythmogenic Mitral Valve Prolapse and Sudden Cardiac Death: An Update and Current Perspectives

Cited by 9 publications

References 81 publications

Surgery for Cardiac Arrhythmias: Past, Present, Future

Surgery for Cardiac Arrhythmias: Past, Present, Future

Arrhythmic Mitral Valve Prolapse and Sports Activity: Pathophysiology, Risk Stratification, and Sports Eligibility Assessment

Defining the Role of the miR-145—KLF4—αSMA Axis in Mitral Valvular Interstitial Cell Activation in Myxomatous Mitral Valve Prolapse Using the Canine Model

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