Diastolic Dysfunction of Hypertrophic Cardiomyopathy Genotype‐Positive Subjects Without Hypertrophy Is Detected by Tissue <scp>D</scp>oppler Imaging: A Systematic Review and Meta‐analysis

Li, Wen; Sun, Dandan; Jun, Yang

doi:10.1002/jum.14250

Cited by 12 publications

(12 citation statements)

References 55 publications

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“…Generally, diastolic dysfunction with slowed relaxation and compromised ventricular filling (e.g., reviewed in Reference [173]), but not always found [173].…”

Section: Diastolic Dysfunctionmentioning

confidence: 99%

“…Later studies reported somewhat variable results, e.g., some studies reported no clear differences in TDI-based assessment of diastolic function between mutation carriers and a control group [201,202]. More recently, a meta-analysis [173] involving the three mentioned studies and seven more suggested statistically significantly lower Ea value at the septum in mutation carriers than among individuals in the control group implying that mutation carriers generally exhibit diastolic dysfunction. The latter effect would be compatible with often (but not invariably) increased calcium-sensitivity of contraction (see above).…”

Section: Whole Hearts and Cardiac Imagingmentioning

confidence: 99%

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Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy

Ušaj¹,

Moretto²,

Månsson³

2022

IJMS

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Hereditary hypertrophic cardiomyopathy (HCM), due to mutations in sarcomere proteins, occurs in more than 1/500 individuals and is the leading cause of sudden cardiac death in young people. The clinical course exhibits appreciable variability. However, typically, heart morphology and function are normal at birth, with pathological remodeling developing over years to decades, leading to a phenotype characterized by asymmetric ventricular hypertrophy, scattered fibrosis and myofibrillar/cellular disarray with ultimate mechanical heart failure and/or severe arrhythmias. The identity of the primary mutation-induced changes in sarcomere function and how they trigger debilitating remodeling are poorly understood. Support for the importance of mutation-induced hypercontractility, e.g., increased calcium sensitivity and/or increased power output, has been strengthened in recent years. However, other ideas that mutation-induced hypocontractility or non-uniformities with contractile instabilities, instead, constitute primary triggers cannot yet be discarded. Here, we review evidence for and criticism against the mentioned hypotheses. In this process, we find support for previous ideas that inefficient energy usage and a blunted Frank–Starling mechanism have central roles in pathogenesis, although presumably representing effects secondary to the primary mutation-induced changes. While first trying to reconcile apparently diverging evidence for the different hypotheses in one unified model, we also identify key remaining questions and suggest how experimental systems that are built around isolated primarily expressed proteins could be useful.

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“…Generally, diastolic dysfunction with slowed relaxation and compromised ventricular filling (e.g., reviewed in Reference [173]), but not always found [173].…”

Section: Diastolic Dysfunctionmentioning

confidence: 99%

Section: Whole Hearts and Cardiac Imagingmentioning

confidence: 99%

Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy

Ušaj¹,

Moretto²,

Månsson³

2022

IJMS

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“…Синдром дисфункции ЛЖ Диастолическая функция ЛЖ может быть нарушена уже у носителей мутации, в догипертрофической стадии ГКМП -генотип (+)/фенотип (-) [91].…”

Section: этиология и патогенез заболевания или состояния (группы заболеваний или состояний)unclassified

“…По мере прогрессирования гипертрофии, развития фиброза, нарастания степени митральной регургитации (МР), присоединения ишемии миокарда диастолические нарушения нарастают, приводя к увеличению давления в ЛП (соответственно, и к увеличению конечнодиастолического давления (КДД) ЛЖ). Также выраженная диастолическая дисфункция может приводить к развитию легочной гипертензии у некоторых пациентов (у 50% симптомных пациентов) [91][92][93][94][95][96].…”

Section: этиология и патогенез заболевания или состояния (группы заболеваний или состояний)unclassified

“…• Всем пациентам с ГКМП рекомендуется тщательная оценка диастолической функции ЛЖ, включая трансмитральный кровоток, в легочных венах, тканевую допплерографию, измерение размера и объема ЛП для стратификации риска ВСС [91,94,95,98,108,137,195,205].…”

Section: еок Ib (удд 4 уур с)unclassified

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2020 Clinical practice guidelines for Hypertrophic cardiomyopathy

Габрусенко¹,

Гудкова²,

Козиолова³

et al. 2021

Russ J Cardiol

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Russian Society of Cardiology (RSC)With the participation: Russian Association of Cardiovascular SurgeonsEndorsed by: Research and Practical Council of the Ministry of Health of the Russian Federation Task Force: Gabrusenko S.A. (Chairman), Gudkova A.Ya.* (Chairman), Koziolova N.A. (Chairman), Alexandrova S.A., Berseneva M.I., Gordeev M.L., Dzemeshkevich S.L., Zaklyazminskaya E.V., Irtyuga O.B., Kaplunova V.Yu., Kostareva A.A., Krutikov A.N., Malenkov D.A., Novikova T.N., Saidova M.A., Sanakoev M.K., Stukalova O.V.

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Mechanisms and prognostic impact of myocardial ischaemia in hypertrophic cardiomyopathy

Coleman

Ashkir

Raman

et al. 2023

Int J Cardiovasc Imaging

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Despite the progress made in risk stratification, sudden cardiac death and heart failure remain dreaded complications for hypertrophic cardiomyopathy (HCM) patients. Myocardial ischaemia is widely acknowledged as a contributor to cardiovascular events, but the assessment of ischaemia is not yet included in HCM clinical guidelines. This review aims to evaluate the HCM-specific pro-ischaemic mechanisms and the potential prognostic value of imaging for myocardial ischaemia in HCM. A literature review was performed using PubMed to identify studies with non-invasive imaging of ischaemia (cardiovascular magnetic resonance, echocardiography, and nuclear imaging) in HCM, prioritising studies published after the last major review in 2009. Other studies, including invasive ischaemia assessment and post-mortem histology, were also considered for mechanistic or prognostic relevance. Pro-ischaemic mechanisms in HCM reviewed included the effects of sarcomeric mutations, microvascular remodelling, hypertrophy, extravascular compressive forces and left ventricular outflow tract obstruction. The relationship between ischaemia and fibrosis was re-appraised by considering segment-wise analyses in multimodal imaging studies. The prognostic significance of myocardial ischaemia in HCM was evaluated using longitudinal studies with composite endpoints, and reports of ischaemia-arrhythmia associations were further considered. The high prevalence of ischaemia in HCM is explained by several micro- and macrostructural pathological features, alongside mutation-associated energetic impairment. Ischaemia on imaging identifies a subgroup of HCM patients at higher risk of adverse cardiovascular outcomes. Ischaemic HCM phenotypes are a high-risk subgroup associated with more advanced left ventricular remodelling, but further studies are required to evaluate the independent prognostic value of non-invasive imaging for ischaemia.

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Diastolic Dysfunction of Hypertrophic Cardiomyopathy Genotype‐Positive Subjects Without Hypertrophy Is Detected by Tissue Doppler Imaging: A Systematic Review and Meta‐analysis

Abstract: Tissue Doppler imaging-derived diastolic dysfunction can be found in HCM genotype-positive subjects without hypertrophy.

Cited by 12 publications

References 55 publications

Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy

Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy

2020 Clinical practice guidelines for Hypertrophic cardiomyopathy

Mechanisms and prognostic impact of myocardial ischaemia in hypertrophic cardiomyopathy

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