Myocardial Native T1 Predicts Load-Independent Left Ventricular Chamber Stiffness In Patients With HFpEF

Omori, Taku; Nakamori, Shiro; Fujimoto, Naoki; Ishida, Masaki; Kitagawa, Kakuya; Ichikawa, Yasutaka; Kumagai, Naoto; Kurita, Tairo; Imanaka‐Yoshida, Kyoko; Hiroe, Michiaki; Sakuma, Hajime; M, Ito; Dohi, Kaoru

doi:10.1016/j.jcmg.2020.05.030

Cited by 14 publications

(18 citation statements)

References 32 publications

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“…Consistent with the common biological functions in the heart and adipose tissue, the interaction between PRKCD and F2R activates the biological process of positive regulation of the MAPK cascade. MAPK1 is closely related to the increased extracellular volume in the cerebral artery and adipose tissue, which is a characteristic in patients with HFpEF ( Omori et al, 2020 ). In the cerebral artery, the interaction between MAPK1 , FABP5 (recombinant human fatty acid-binding protein-5), and FN1 (fibronectin 1) was involved in the biological processes of response to wounding, which may accelerate the process of atherosclerosis ( Pintucci et al, 2002 ).…”

Section: Resultsmentioning

confidence: 99%

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

et al. 2021

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Heart failure with preserved ejection fraction (HFpEF) is a complex disease characterized by dysfunctions in the heart, adipose tissue, and cerebral arteries. The elucidation of the interactions between these three tissues in HFpEF will improve our understanding of the mechanism of HFpEF. In this study, we propose a multilevel comparative framework based on differentially expressed genes (DEGs) and differentially correlated gene pairs (DCGs) to investigate the shared and unique pathological features among the three tissues in HFpEF. At the network level, functional enrichment analysis revealed that the networks of the heart, adipose tissue, and cerebral arteries were enriched in the cell cycle and immune response. The networks of the heart and adipose tissues were enriched in hemostasis, G-protein coupled receptor (GPCR) ligand, and cancer-related pathway. The heart-specific networks were enriched in the inflammatory response and cardiac hypertrophy, while the adipose-tissue-specific networks were enriched in the response to peptides and regulation of cell adhesion. The cerebral-artery-specific networks were enriched in gene expression (transcription). At the module and gene levels, 5 housekeeping DEGs, 2 housekeeping DCGs, 6 modules of merged protein–protein interaction network, 5 tissue-specific hub genes, and 20 shared hub genes were identified through comparative analysis of tissue pairs. Furthermore, the therapeutic drugs for HFpEF-targeting these genes were examined using molecular docking. The combination of multitissue and multilevel comparative frameworks is a potential strategy for the discovery of effective therapy and personalized medicine for HFpEF.

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Section: Resultsmentioning

confidence: 99%

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

et al. 2021

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“… 8 Calibration offset was corrected by matching a conductance catheter signal at end diastole with LVEDV and that at end‐systole with LVESV measured by cardiac MRI. 9 …”

Section: Methodsmentioning

confidence: 99%

“…Real‐time pressure–volume diagram generation and analog/digital conversion (333 Hz) were performed using a 16‐bit microcomputer system (PC‐ 9801VX, NEC Co, Tokyo, Japan), as previously reported 8 . Calibration offset was corrected by matching a conductance catheter signal at end diastole with LVEDV and that at end‐systole with LVESV measured by cardiac MRI 9 …”

Section: Methodsmentioning

confidence: 99%

Comparison of haemodynamic response to muscle reflex in heart failure with reduced vs. preserved ejection fraction

et al. 2021

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Aims Isometric handgrip (IHG) training reduces the blood pressure in patients with hypertension. It is unclear how IHG exercise affects the haemodynamics and cardiovascular function through the muscle reflex in patients with heart failure (HF) with reduced (HFrEF) and preserved ejection fraction (HFpEF). Methods and results Twenty patients (HFrEF: n = 10, HFpEF: n = 10) underwent left ventricular (LV) pressure-volume assessments using a conductance catheter and microtip manometer to evaluate haemodynamics, LV and arterial function, and LV-arterial coupling during 3 min of IHG at 30% of maximal voluntary contraction (MVC), followed by 3 min of post-exercise circulatory arrest (PECA). Three minutes of IHG exercise produced significant and modest increases in the heart rate (HR) and LV end-systolic pressure (LVESP), respectively, in both HFpEF and HFrEF groups. In HFrEF, the increase in LVESP was caused by the variable increase in effective arterial elastance (Ea), which was counterbalanced by the increase in LV end-systolic elastance (Ees), resulting in a maintained Ees/Ea. In HFpEF, the increase in LVESP was not accompanied by changes in Ea, Ees, Ees/Ea, or LV end-diastolic pressure. LVESP during PECA was not maintained in HFpEF, suggesting smaller metabo-reflex activity in HFpEF. Conclusions The IHG exercise used in this study may increase the LVESP and LVEDP without detrimental effects on cardiac function or ventricular-arterial coupling, especially in HFpEF patients. The effects of IHG exercise on haemodynamics and ventricular-arterial coupling may be affected by the patient background and the type and intensity of the exercise.

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“…There is a relationship between CMR parameters, such as native myocardial T1 and ECV, and invasive parameters [ 55 ]. Omori et al performed a study including CMR with native Myocardial T1 and ECV, invasive evaluation of filling pressures and endomyocardial biopsy, in HFpEF patients [ 71 ]. They found that native T1 and especially ECV were higher in HFpEF than in the control group and that they are both reliable in determining the percentage of collagen volume fraction and the passive stiffness of the left ventricle, calculated invasively through the beta relaxation constant [ 71 ].…”

Section: The Pathophysiology Of Heart Failure With Preserved Ejection Fractionmentioning

confidence: 99%

“…Omori et al performed a study including CMR with native Myocardial T1 and ECV, invasive evaluation of filling pressures and endomyocardial biopsy, in HFpEF patients [ 71 ]. They found that native T1 and especially ECV were higher in HFpEF than in the control group and that they are both reliable in determining the percentage of collagen volume fraction and the passive stiffness of the left ventricle, calculated invasively through the beta relaxation constant [ 71 ]. ECV has a proven validation with the histopathology found through intraoperative biopsy studies performed at the time of aortic stenosis or heart transplant surgery [ 62 , 72 , 73 ].…”

Section: The Pathophysiology Of Heart Failure With Preserved Ejection Fractionmentioning

confidence: 99%

Myocardial Tissue Characterization in Heart Failure with Preserved Ejection Fraction: From Histopathology and Cardiac Magnetic Resonance Findings to Therapeutic Targets

Severino¹,

D’Amato²,

Prosperi³

et al. 2021

IJMS

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Heart failure with preserved ejection fraction (HFpEF) is a complex clinical syndrome responsible for high mortality and morbidity rates. It has an ever growing social and economic impact and a deeper knowledge of molecular and pathophysiological basis is essential for the ideal management of HFpEF patients. The association between HFpEF and traditional cardiovascular risk factors is known. However, myocardial alterations, as well as pathophysiological mechanisms involved are not completely defined. Under the definition of HFpEF there is a wide spectrum of different myocardial structural alterations. Myocardial hypertrophy and fibrosis, coronary microvascular dysfunction, oxidative stress and inflammation are only some of the main pathological detectable processes. Furthermore, there is a lack of effective pharmacological targets to improve HFpEF patients’ outcomes and risk factors control is the primary and unique approach to treat those patients. Myocardial tissue characterization, through invasive and non-invasive techniques, such as endomyocardial biopsy and cardiac magnetic resonance respectively, may represent the starting point to understand the genetic, molecular and pathophysiological mechanisms underlying this complex syndrome. The correlation between histopathological findings and imaging aspects may be the future challenge for the earlier and large-scale HFpEF diagnosis, in order to plan a specific and effective treatment able to modify the disease’s natural course.

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Myocardial Native T1 Predicts Load-Independent Left Ventricular Chamber Stiffness In Patients With HFpEF

Cited by 14 publications

References 32 publications

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

Comparison of haemodynamic response to muscle reflex in heart failure with reduced vs. preserved ejection fraction

Myocardial Tissue Characterization in Heart Failure with Preserved Ejection Fraction: From Histopathology and Cardiac Magnetic Resonance Findings to Therapeutic Targets

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