Usefulness of three-dimensional spherical index to assess different types of left ventricular remodeling

Zeng, Decai; Chen, Hui; Jiang, Chun Lan; Wu, Jianzhong

doi:10.1097/md.0000000000007968

Cited by 3 publications

(3 citation statements)

References 28 publications

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“…Use of the sphericity index (SI) has been an effort to simply assess LV shape and function. An increased SI is associated with eccentric remodeling following myocardial injury, volume or pressure overload and a worse outcome after AVR ( 23 , 24 ). LV-Hemodynamic forces and Intraventricular Pressure Gradients (IVPG) are modern techniques to detect clinically inapparent myocardial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Assessment of 10-Year Left-Ventricular-Remodeling by CMR in Patients Following Aortic Valve Replacement

Rank

Stoiber

Nasser

et al. 2021

Front. Cardiovasc. Med.

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Aims: Aortic valve replacement (AVR) may result in reverse cardiac remodeling. We aimed to assess long-term changes in the myocardium following AVR by Cardiac Magnetic Resonance Imaging (CMR).Methods: We prospectively observed the long-term left ventricular (LV) function and structure of 27 patients with AVR [n = 19 with aortic stenosis (AS); n = 8 with aortic regurgitation (AR)] by CMR. Patients underwent CMR before, as well as 1, 5, and 10 years after AVR. We evaluated clinical parameters, LV volumes, mass, geometry, ejection fraction (EF), global myocardial longitudinal strain (MyoGLS), global myocardial circular strain (MyoGCS), hemodynamic forces (HemForces), and Late Gadolinium Enhancement (LGE).Results: The median of LVMI, EDVI, and ESVI decreased in both groups. Patients with AR had higher initial values of EDVI and ESVI and showed a more prominent initial reduction. In AS, MyoGLS improved already after 1 year and remained constant afterward, whereas, in AR no improvement of MyoGLS was found. MyoGCS remained unchanged in the AS group but deteriorated in the AR group over 10 years. Ejection fraction (EF) was higher in AS patients compared to AR 10 years post-AVR. Late gadolinium enhancement (LGE) could be found more frequently in AS patients.Conclusion: CMR was well suited to investigate myocardial changes over a 10-year follow up period in patients with aortic valve disease. Regarding the long-term functional changes following AVR, patients with AR seemed to benefit less from AVR compared to AS patients. Fibrosis was more common in AS, but this did not reflect functional evolution in these patients. Close monitoring seems indispensable to avoid irreversible structural damage of the heart and to perform AVR at an appropriate stage.

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Section: Introductionmentioning

confidence: 99%

Assessment of 10-Year Left-Ventricular-Remodeling by CMR in Patients Following Aortic Valve Replacement

Rank

Stoiber

Nasser

et al. 2021

Front. Cardiovasc. Med.

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“…To dissect if macrophage expression of these biomarkers was responsible for the dilation status, we calculated the spherical index that reflects LV eccentric remodeling in post-MI patients. [30] Spherical index negatively correlated with macrophage numbers, indicating that macrophages prevented LV dilation (Figure 7B). Mice with fewer macrophages had increased spherical index signifying a larger, rounder LV.…”

Section: Macrophage Highly Expressed Mip-1γ and Correlated With Spher...mentioning

confidence: 90%

Identifying the molecular and cellular signature of cardiac dilation following myocardial infarction

Lindsey

Flynn

et al. 2019

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Pressure overload induced by TAC has become a classical animal model in rodents to simulate cardiac damage caused by pressure overload in humans [ 1 ]. Continuous exposure to increased pressure gradually transforms the initially compensatory response into pathological cardiac remodelling, manifested as increased cardiomyocyte mass, sarcomere rearrangement, extracellular matrix deposition, and immune cell activation, which eventually lead to terminal-stage heart failure [ 2 , 3 ]. The heart mainly relies on mitochondria to manufacture the energy used for its contractile function; these account for over 30% of the volume of myocardial cells and provide 90% of cellular ATP energy via oxidative phosphorylation and fatty acid oxidation [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

Shao

et al. 2022

Oxidative Medicine and Cellular Longevity

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The pathological mechanisms underlying cardiac remodelling and cardiac dysfunction caused by pressure overload are poorly understood. Mitochondrial damage and functional dysfunction, including mitochondrial bioenergetic disorder, oxidative stress, and mtDNA damage, contribute to heart injury caused by pressure overload. Mitophagy, an important regulator of mitochondrial homeostasis and function, is triggered by mitochondrial damage and participates in the pathological process of cardiovascular diseases. Recent studies indicate that mitophagy plays a critical role in the pressure overload model, but evidence on the causal relationship between mitophagy abnormality and pressure overload-induced heart injury is inconclusive. This review summarises the mechanism, role, and regulation of mitophagy in the pressure overload model. It also pays special attention to active compounds that may regulate mitophagy in pressure overload, which provide clues for possible clinical applications.

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Usefulness of three-dimensional spherical index to assess different types of left ventricular remodeling

Abstract: 3D SpI can be widely used to assess LV remodeling in patients with eccentric remodeling, but has limitations in predicting concentric hypertrophy and regional or chronic myocardial injury.

Cited by 3 publications

References 28 publications

Assessment of 10-Year Left-Ventricular-Remodeling by CMR in Patients Following Aortic Valve Replacement

Assessment of 10-Year Left-Ventricular-Remodeling by CMR in Patients Following Aortic Valve Replacement

Identifying the molecular and cellular signature of cardiac dilation following myocardial infarction

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

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