Myokardfibrose

Espeland, Torvald; Lunde, Ida G.; Amundsen, Brage H.; Gullestad, Lars; Aakhus, Svend

doi:10.4045/tidsskr.17.1027

Cited by 28 publications

(34 citation statements)

References 37 publications

(88 reference statements)

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“…This is supported by MRI studies in patients with pulmonary hypertension that have shown elevated T1 times in the entire LV, which is correlated with changes in the eccentricity index (Reiter et al, ). The aforementioned computational studies in our lab have suggested a potential mechanism by showing that increased RV pressure overload causes increased LV myocardial stress (Kheyfets et al, ), which is a biomechanical initiator for fibroblast activation (Espeland, Lunde, B, Gullestad, & Aakhus, ). However, these modeling studies were conducted on a human heart model and an actual estimate of myocardial stress was not available for the mice in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, while evidence of LV perivascular fibrosis may be a marker of elevated myocardial stress, there has been debate about its implication for function. Traditional thinking has suggested that myocardial fibrosis depresses electrical and mechanical function in the heart (Espeland et al., ), but some studies have suggested that fibrosis is both an adaptive and maladaptive response (Andersen et al, ). Therefore, it is unlikely that the minimal fibrosis we observed in the LV of PAB mice is somehow contributing to reduced torsion rate or EF, but is likely a benign response to biomechanical and biochemical stimuli.…”

Section: Discussionmentioning

confidence: 99%

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The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload

et al. 2020

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Pulmonary hypertension (PH) results in right ventricular (RV) pressure overload and eventual failure. Current research efforts have focused on the RV while overlooking the left ventricle (LV), which is responsible for mechanically assisting the RV during contraction. The objective of this study is to evaluate the biomechanical and gene expression changes occurring in the LV due to RV pressure overload in a mouse model. Nine male mice were divided into two groups: (a) pulmonary arterial banding (PAB, N = 4) and (b) sham surgery (Sham, N = 5). Tagged and steady-state free precision cardiac MRI was performed on each mouse at 1, 4, and 7 weeks after surgery.At/week7, the mice were euthanized following right/left heart catheterization with RV/LV tissue harvested for histology and gene expression (using RT-PCR) studies.Compared to Sham mice, the PAB group revealed a significantly decreased LV and RV ejection fraction, and LV maximum torsion and torsion rate, within the first week after banding. In the PAB group, there was also a slight but significant increase in LV perivascular fibrosis, which suggests elevated myocardial stress. LV fibrosis was also accompanied with changes in gene expression in the hypertensive group, which was correlated with LV contractile mechanics. In fact, principal component (PC) analysis of LV gene expression effectively separated Sham and PAB mice along PC2. Changes in LV contractile mechanics were also significantly correlated with unfavorable changes in RV contractile mechanics, but a direct causal relationship

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload

et al. 2020

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“…Myofibroblasts have an increased production of proteins that are deposited in the extracellular matrix. This increase in collagen between myocytes leads to an increased stiffness of the myocardium [18,19], and causes structural and electrical changes that predispose patients to arrhythmias, heart failure and ischemia. Increased myocardial stiffness is therefore a second clinical indicator of fibrosis.…”

Section: Myocardial Fibrosismentioning

confidence: 99%

“…Interstitial (or diffuse) fibrosis is characterized by diffuse spread of extracellular collagen and is believed to be reversible if treated early. This type is also seen in elderly people, and in diseases such aortic stenosis and coronary heart disease without infarction [19]. Fibrosis is currently diagnosed invasively with biomarkers measured in biopsies and blood tests, and non-invasively with MRI (with and without contrast), cardiac CT and echocardiography (by identifying areas of increased reflectivity).…”

Section: Myocardial Fibrosismentioning

confidence: 99%

Detection of Regional Mechanical Activation of the Left Ventricular Myocardium Using High Frame Rate Ultrasound Imaging

Kvåle

Bersvendsen²,

Remme

et al. 2019

IEEE Trans. Med. Imaging

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Ph.D. program, GE Vingmed Ultrasound for hosting me as an industrial Ph.D. student and the Department of Informatics at the University of Oslo for giving me the chance to pursue my Ph.D. It has been tremendously rewarding to be part of a multidisciplinary community and to experience the collaboration between industry and academia that I have had the opportunity to do during my research. I would also like to thank my team of supervisors. A special thanks goes to my main supervisor Prof. Eigil Samset for your insight, helpful discussions, your thorough reviews of my work, and for pushing me forward. Additionally, I would like to thank my co-supervisors Prof. Thor Edvardsen, Pål H. Brekke and Sebastien Salles for your insight, discussions and guidance during my research. In particular, I would like to thank Pål H. Brekke for sharing your clinical expertise, your enthusiasm and for always keeping cold beverages in your office, and Sebastien Salles for sharing your technical expertise and for your continuous help throughout my whole Ph.D project. I have been fortunate to have a large number of colleagues in a wide range of research groups. A special thanks goes to my former colleague at GE Vingmed Ultrasound, Jørn Bersvendsen, for your guidance in the early days of my project, my colleagues at the CCI, Espen W. Remme and John M. Aalen, for the collaboration on data collection and helpful discussions on theory and results, the ultrasound group at NTNU for providing me with data for my final article and for the fun times at conferences, and my fellow students at the University of Oslo for helpful discussions, coffee breaks and friendships. Finally, I would like to thank my family and friends for the continuous encouragement, motivation, patience, love and support throughout these years.

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“…Torvald Espeland og medarbeidere har skrevet en verdifull og interessant oversikt over myokardfibrose, men utelater å nevne et viktig kardiologisk fagfelt ved myokardfibrose, nemlig medfødte hjertefeil hos både barn og voksne (1). Medfødt hjertefeil forekommer hos ca.…”

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Myokardfibrose ved medfødt hjertefeil

Möller¹,

Lange²

2018

Tidsskriftet

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Charlotte de Lange er overlege ved Barneradiologisk seksjon, Klinikk for Radiologi og Nukleaermedisin, Oslo universitetssykehus. Ingen oppgitte interessekonflikter. Torvald Espeland og medarbeidere har skrevet en verdifull og interessant oversikt over myokardfibrose, men utelater å nevne et viktig kardiologisk fagfelt ved myokardfibrose, nemlig medfødte hjertefeil hos både barn og voksne (1). Medfødt hjertefeil forekommer hos ca. 1 % av nyfødte. Langtidskomplikasjoner hos undergrupper med medfødte hjertefeil rammer derfor et betydelig antall pasienter, ofte i relativt ung alder.I flere tiår har man hatt kunnskapen om fibroseutvikling som en bekymringsverdig langtidskomplikasjon tross kirurgisk reparasjon av hjertefeilen tidlig i livet (2). Fibroseutviklingen synes hos disse pasientene ikke kun å vaere knyttet til hjertefeilens alvorlighetsgrad eller cyanose, men også til genetiske faktorer. Myokardfibrose er en viktig medvirkende årsak til hjertesviktutvikling hos voksne med medfødte hjertefeil (3). Hos pasienter med enkel ventrikkel bidrar tidlig fibroseutvikling sannsynligvis til pumpesvikt i barnealder (4).MR-undersøkelse med T1-mapping og beregning av ekstracellulaert volum kan gi unik informasjon om myokard og grad av diffus fibrose, men er noe mer komplisert å bruke enn angitt i artikkelen. Metoden for T1-mapping er maskinspesifikk og ennå ikke helt standardisert for klinisk bruk. T1-relaksasjonstiden påvirkes av flere faktorer og forskjellige tekniske parametre, og ekstracellulaert volum anses som en mer robust parameter. Derfor er det anbefalt å etablere lokale referanseverdier for å oppnå reproduserbare målinger av god kvalitet (5). Økt diffus myokardfibrose er påvist med T1-mapping ved ulike typer hjertefeil som Fallots tetrade, medfødt aortastenose, enkel ventrikkel og transposisjon av de store arterier (6).Myokardfibrose er en viktig faktor for utvikling av nedsatt myokardfunksjon ved ervervede og medfødte hjertesykdommer. Korrekt anvendt kan MR-teknikker hjelpe med å forstå og kartlegge fibroseprosessen.

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Myokardfibrose

Cited by 28 publications

References 37 publications

The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload

The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload

Detection of Regional Mechanical Activation of the Left Ventricular Myocardium Using High Frame Rate Ultrasound Imaging

Myokardfibrose ved medfødt hjertefeil

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