Primary mitral valve regurgitation: Update and review

Apostolidou, Eirini; Maslow, Andrew; Poppas, Athena

doi:10.21542/gcsp.2017.3

Cited by 31 publications

(17 citation statements)

References 109 publications

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“…The natural course of degenerative mitral valve disease, including FED and Barlow’s disease, varies significantly and is influenced by several factors such as mitral regurgitant volume, LV function and pulmonary pressures [ 69 ]. Asymptomatic patients with only mild mitral regurgitation often remain stable for several years, and only a small proportion of the patients develop severe mitral regurgitation [ 69 ].…”

Section: Outcomementioning

confidence: 99%

Characterization of Degenerative Mitral Valve Disease: Differences between Fibroelastic Deficiency and Barlow’s Disease

Wijngaarden

Kruithof

Vinella

et al. 2021

JCDD

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Degenerative mitral valve disease causing mitral valve prolapse is the most common cause of primary mitral regurgitation, with two distinct phenotypes generally recognized with some major differences, i.e., fibroelastic deficiency (FED) and Barlow’s disease. The aim of this review was to describe the main histological, clinical and echocardiographic features of patients with FED and Barlow’s disease, highlighting the differences in diagnosis, risk stratification and patient management, but also the still significant gaps in understanding the exact pathophysiology of these two phenotypes.

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Section: Outcomementioning

confidence: 99%

Characterization of Degenerative Mitral Valve Disease: Differences between Fibroelastic Deficiency and Barlow’s Disease

Wijngaarden

Kruithof

Vinella

et al. 2021

JCDD

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“…Primary MR is associated with degeneration of the valve apparatus or with annular dilatation. Even though patients with a severe primary MR remain asymptomatic for a remarkably long period of time with preserved LV function (2)(3)(4)(5), an increased risk for cardiovascular morbidity and mortality is described (2,4,6). Therefore, early surgical mitral valve repair (MVR) is strongly recommended in experienced surgical center by current guidelines (7) due to the lack of effective pharmacological treatments.…”

Section: Introductionmentioning

confidence: 99%

Late plasma exosome microRNA-21-5p depicts magnitude of reverse ventricular remodeling after early surgical repair of primary mitral valve regurgitation

Pizzino

Furini

Casieri

et al. 2022

Front. Cardiovasc. Med.

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IntroductionPrimary mitral valve regurgitation (MR) results from degeneration of mitral valve apparatus. Mechanisms leading to incomplete postoperative left ventricular (LV) reverse remodeling (Rev–Rem) despite timely and successful surgical mitral valve repair (MVR) remain unknown. Plasma exosomes (pEXOs) are smallest nanovesicles exerting early postoperative cardioprotection. We hypothesized that late plasma exosomal microRNAs (miRs) contribute to Rev–Rem during the late postoperative period.MethodsPrimary MR patients (n = 19; age, 45–71 years) underwent cardiac magnetic resonance imaging and blood sampling before (T0) and 6 months after (T1) MVR. The postoperative LV Rev–Rem was assessed in terms of a decrease in LV end-diastolic volume and patients were stratified into high (HiR-REM) and low (LoR-REM) LV Rev–Rem subgroups. Isolated pEXOs were quantified by nanoparticle tracking analysis. Exosomal microRNA (miR)-1, –21–5p, –133a, and –208a levels were measured by RT-qPCR. Anti-hypertrophic effects of pEXOs were tested in HL-1 cardiomyocytes cultured with angiotensin II (AngII, 1 μM for 48 h).ResultsSurgery zeroed out volume regurgitation in all patients. Although preoperative pEXOs were similar in both groups, pEXO levels increased after MVR in HiR-REM patients (+0.75-fold, p = 0.016), who showed lower cardiac mass index (–11%, p = 0.032). Postoperative exosomal miR-21-5p values of HiR-REM patients were higher than other groups (p < 0.05). In vitro, T1-pEXOs isolated from LoR-REM patients boosted the AngII-induced cardiomyocyte hypertrophy, but not postoperative exosomes of HiR-REM. This adaptive effect was counteracted by miR-21-5p inhibition.Summary/ConclusionHigh levels of miR-21-5p-enriched pEXOs during the late postoperative period depict higher LV Rev–Rem after MVR. miR-21-5p-enriched pEXOs may be helpful to predict and to treat incomplete LV Rev–Rem after successful early surgical MVR.

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“…Ventricular remodeling secondary to MR has been studied at the organ level in preclinical rodent and dog models, and in humans (5)(6)(7)(8)(9). At the organ level, rapid and profound chamber dilation occurs upon the onset of MR, with a gradual decline in cardiac function, in animal models and in patients.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural Adaptation of the Cardiomyocyte to Chronic Mitral Regurgitation

Corporan

Segura²,

Padala

2021

Front. Cardiovasc. Med.

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Introduction: Mitral regurgitation (MR) imposes volume overload on the left ventricle (LV) and elevates wall stress, triggering its adverse remodeling. Pronounced LV dilation, minimal wall thinning, and a gradual decline in cardiac ejection fraction (EF) are observed. The structural changes in the myocardium that define these gross, organ level remodeling are not known. Cardiomyocyte elongation and slippage have both been hypothesized, but neither are confirmed, nor are the changes to the cardiomyocyte structure known. Using a rodent model of MR, we used immunohistochemistry and transmission electron microscopy (TEM) to describe the ultrastructural remodeling of the cardiomyocyte.Methods: Twenty-four male Sprague-Dawley rats (350–400 g) were assigned to two groups: group (1) rats induced with severe MR (n = 18) and group (2) control rats that were healthy and age and weight matched (n = 6). MR was induced in the beating heart using a 23-G ultrasound-guided, transapical needle to perforate the anterior mitral leaflet, and the rats were followed to 2, 10, and 20 weeks (n = 6/time-point). Echocardiography was performed to quantify MR severity and to measure LV volume and function at each time-point. Explanted myocardial tissue were examined with TEM and immunohistochemistry to investigate the ultrastructural changes.Results: MR induced rapid and significant increase in end-diastolic volume (EDV), with a 50% increase by 2 weeks, compared with control. Rise in end-systolic volume (ESV) was more gradual; however, by 20 weeks, both EDV and ESV in MR rats were increased by 126% compared with control. A significant decline in EF was measured at 10 weeks of MR. At the ultrastructural level, as early as 2 weeks after MR, cardiomyocyte elongation and increase in cross-sectional area were observed. TEM depicted sarcomere shortening, with loss of Z-line and I-band. Desmin, a cytoskeletal protein that is uniformly distributed along the length of the cardiomyocyte, was disorganized and localized to the intercalated disc, in the rats induced with MR and not in the controls. In the rats with MR, the linear registry of the mitochondrial arrangement along the sarcomeres was lost, with mitochondrial fragmentation, aggregation around the nucleus, and irregularities in the cristae.Discussion: In the setting of chronic mitral regurgitation, LV dilatation occured by cardiomyocyte elongation, which manifests at the subcellular level as distinct ultrastructural alterations of the sarcomere, cytoskeleton, and mitochondria. Since the cytoskeleton not only provides tensegrity but has functional consequences on myocyte function, further investigation into the impact of cytoskeletal remodeling on progressive heart failure or recovery of function upon correcting the valve lesion are needed.

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Primary mitral valve regurgitation: Update and review

Cited by 31 publications

References 109 publications

Characterization of Degenerative Mitral Valve Disease: Differences between Fibroelastic Deficiency and Barlow’s Disease

Characterization of Degenerative Mitral Valve Disease: Differences between Fibroelastic Deficiency and Barlow’s Disease

Late plasma exosome microRNA-21-5p depicts magnitude of reverse ventricular remodeling after early surgical repair of primary mitral valve regurgitation

Ultrastructural Adaptation of the Cardiomyocyte to Chronic Mitral Regurgitation

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