Basal Left Ventricular Dilatation and Reduced Contraction in Patients With Mitral Valve Prolapse Can Be Secondary to Annular Dilatation

Fukuda, Shota; Song, Jae‐Kwan; Mahara, Keitaro; Kuwaki, Hiroshi; Jang, Jeong Yoon; Takeuchi, Masaaki; Sun, Byung Joo; Kim, Yun Jeong; Miyamoto, Tetsu; Oginosawa, Yasushi; Sonoda, Shinjo; Eto, Masataka; Nishimura, Yuichi; Takanashi, Shuichiro; Levine, Robert A.; Otsuji, Yutaka

doi:10.1161/circimaging.115.005113

Cited by 30 publications

(13 citation statements)

References 33 publications

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“…been reported. MV annular dilation is known to cause regional LV base dilatation, leading to localized, reduced contraction of the LV base by increased wall tension with Laplace's law (9). The present study demonstrated a novel MV annulus-LV interaction.…”

Section: Discussionsupporting

confidence: 52%

Possible mechanism of late systolic mitral valve prolapse: systolic superior shift of leaflets secondary to annular dilatation that causes papillary muscle traction

Hei

Iwataki

Jang

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Progressive superior shift of the mitral valve (MV) during systole is associated with abnormal papillary muscle (PM) superior shift in late systolic MV prolapse (MVP). The causal relation of these superior shifts remains unclarified. We hypothesized that the MV superior shift is related to augmented MV superiorly pushing force by systolic left ventricular pressure due to MV annular dilatation, which can be corrected by surgical MV plasty, leading to postoperative disappearance of these superior shifts. In 35 controls, 28 patients with holosystolic MVP, and 28 patients with late systolic MVP, the MV coaptation depth from the MV annulus was measured at early and late systole by two-dimensional echocardiography. The PM tip superior shift was monitored by echocardiographic speckle tracking. MV superiorly pushing force was obtained as MV annular area × (systolic blood pressure − 10). Measurements were repeated after MV plasty in 14 patients with late systolic MVP. Compared with controls and patients with holosystolic MVP, MV and PM superior shifts and MV superiorly pushing force were greater in patients with late systolic MVP [1.3 (0.5) vs. 0.9 (0.6) vs. 3.9 (1.0) mm/m2, 1.3 (0.5) vs. 1.2 (1.0) vs. 3.3 (1.3) mm/m2, and 487 (90) vs. 606 (167) vs. 742 (177) mmHg·cm2·m−2, respectively, means (SD), P < 0.001]. MV superior shift was correlated with PM superior shift ( P < 0.001), which was further related to augmented MV superiorly pushing force ( P < 0.001). MV and PM superior shift disappeared after surgical MV plasty for late systolic MVP. These data suggest that MV annulus dilatation augmenting MV superiorly pushing force may promote secondary superior shift of the MV (equal to late systolic MVP) that causes subvalvular PM traction in patients with late systolic MVP. NEW & NOTEWORTHY Late systolic mitral valve prolapse (MVP) is associated with mitral valve (MV) and papillary muscle (PM) abnormal superior shifts during systole, but the causal relation remains unclarified. MV and PM superior shifts were correlated with augmented MV superiorly pushing force by annular dilatation and disappeared after surgical MV plasty with annulus size and MV superiorly pushing force reduction. This suggests that MV annulus dilatation may promote secondary superior shifts of the MV (late systolic MVP) that cause subvalvular PM traction.

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Section: Discussionsupporting

confidence: 52%

Possible mechanism of late systolic mitral valve prolapse: systolic superior shift of leaflets secondary to annular dilatation that causes papillary muscle traction

Hei

Iwataki

Jang

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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“…Fukuda and colleagues also showed reduced basal LV strain in MVP, possibly due to increased valve-related forces opposing basal longitudinal shortening. 39 Interestingly, they showed basal strain was normalized after MV repair; in another study, repair also normalized the exaggerated superior PM displacement that parallels leaflet prolapse. 26 , 40 Regarding the double-peak strain pattern, we can hypothesize a mechanism illustrated in Figure 5 : in early systole (left), myocardial contraction and shortening is expected to be normal in MVP.…”

Section: Discussionmentioning

confidence: 94%

Abnormal Mechanics Relate to Myocardial Fibrosis and Ventricular Arrhythmias in Patients With Mitral Valve Prolapse

Nagata

Bertrand

Baliyan

et al. 2023

Circ: Cardiovascular Imaging

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Background: The relation between ventricular arrhythmia and fibrosis in mitral valve prolapse (MVP) is reported, but underlying valve-induced mechanisms remain unknown. We evaluated the association between abnormal MVP-related mechanics and myocardial fibrosis, and their association with arrhythmia. Methods: We studied 113 patients with MVP with both echocardiogram and gadolinium cardiac magnetic resonance imaging for myocardial fibrosis. Two-dimensional and speckle-tracking echocardiography evaluated mitral regurgitation, superior leaflet and papillary muscle displacement with associated exaggerated basal myocardial systolic curling, and myocardial longitudinal strain. Follow-up assessed arrhythmic events (nonsustained or sustained ventricular tachycardia or ventricular fibrillation). Results: Myocardial fibrosis was observed in 43 patients with MVP, predominantly in the basal-midventricular inferior-lateral wall and papillary muscles. Patients with MVP with fibrosis had greater mitral regurgitation, prolapse, and superior papillary muscle displacement with basal curling and more impaired inferior-posterior basal strain than those without fibrosis ( P <0.001). An abnormal strain pattern with distinct peaks pre–end-systole and post–end-systole in inferior-lateral wall was frequent in patients with fibrosis (81 versus 26%, P <0.001) but absent in patients without MVP with basal inferior-lateral wall fibrosis (n=20). During median follow-up of 1008 days, 36 of 87 patients with MVP with >6-month follow-up developed ventricular arrhythmias associated (univariable) with fibrosis, greater prolapse, mitral annular disjunction, and double-peak strain. In multivariable analysis, double-peak strain showed incremental risk of arrhythmia over fibrosis. Conclusions: Basal inferior-posterior myocardial fibrosis in MVP is associated with abnormal MVP-related myocardial mechanics, which are potentially associated with ventricular arrhythmia. These associations suggest pathophysiological links between MVP-related mechanical abnormalities and myocardial fibrosis, which also may relate to ventricular arrhythmia and offer potential imaging markers of increased arrhythmic risk.

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“…Среди причин появления локального фиброза левого желудочка и эктопических фокусов в волокнах Пуркинье, определяемых у многих пациентов с ПМК и желудочковыми аритмиями, вероятно, следует отметить структурные нарушения [32]. В качестве фактора риска оценивалась механическая дисперсия, значение которой оказалось значительно выше у пациентов с «аритмическим» ПМК.…”

Section: механизмы аритмогенезаunclassified

"Arrhythmic" Mitral Valve Prolapse

Трисветова¹,

Ушакова²

2023

Кардиология В Беларуси

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Пролапс митрального клапана описан в 70-х годах прошлого века как доброкачественное заболевание, вместе с тем в последующие годы исследователи сообщали о случаях желудочковых нарушений ритма сердца и внезапной сердечной смерти у пациентов с пролабированием створок митрального клапана. В настоящее время описан фенотип «аритмического», или «злокачественного», пролапса митрального клапана с характерными демографическими, электрокардиографическими и выявленными при визуализации сердца признаками. «Аритмический» пролапс митрального клапана часто возникает у женщин молодого возраста с нарушениями реполяризации на электрокардиограмме, с дизъюнкцией и систолическим скручиванием (curling) митрального кольца, фиброзом папиллярных мышц и задне- или нижнебазальной стенки левого желудочка, являющихся морфологическим субстратом желудочковых аритмий. Среди патофизиологических механизмов, обусловливающих появление электрической нестабильности сердца, выделяют вызванные механическим стрессом изменения рефрактерных периодов желудочков, электрофизиологические изменения в волокнах Пуркинье, гипермобильность фиброзного кольца и аномальную тракцию папиллярных мышц. Знание о факторах риска развития жизнеугрожающих аритмий и внезапной сердечной смерти и их своевременное выявление позволит выбрать эффективные методы лечения и улучшить прогноз пациентов с «аритмическим» пролапсом митрального клапана. Mitral valve prolapse was described in the 1970s as a benign disease, however, in subsequent years researchers reported cases of ventricular arrhythmias and sudden cardiac death in patients with mitral valve prolapse. A phenotype of "arrhythmic" or "malignant" mitral valve prolapse has now been described, with characteristic demographic, electrocardiographic, and cardiac imaging features. "Arrhythmic" mitral valve prolapse often occurs in young women with repolarization disorders on the electrocardiogram, with disjunction and systolic "curling" (twisting) of the mitral ring, fibrosis of the papillary muscles and the posterior or inferior basal wall of the left ventricle, which are the morphological substrate of ventricular arrhythmias. Among pathophysiological mechanisms responsible for electrical instability in the heart are mechanical stress-induced changes in ventricular refractory periods, electrophysiological changes in Purkinje fibers, hypermobility of the fibrous ring and abnormal traction of papillary muscles. Awareness of risk factors for life-threatening arrhythmias and sudden cardiac death and their timely detection should allow choosing effective treatment methods and improving the prognosis for patients with "arrhythmic" mitral valve prolapse.

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Basal Left Ventricular Dilatation and Reduced Contraction in Patients With Mitral Valve Prolapse Can Be Secondary to Annular Dilatation

Cited by 30 publications

References 33 publications

Possible mechanism of late systolic mitral valve prolapse: systolic superior shift of leaflets secondary to annular dilatation that causes papillary muscle traction

Possible mechanism of late systolic mitral valve prolapse: systolic superior shift of leaflets secondary to annular dilatation that causes papillary muscle traction

Abnormal Mechanics Relate to Myocardial Fibrosis and Ventricular Arrhythmias in Patients With Mitral Valve Prolapse

"Arrhythmic" Mitral Valve Prolapse

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