Faculty Profiles - AKAGI Satoshi

Papers - AKAGI Satoshi

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Feasibility of Treat and Repair Strategy in Congenital Heart Defects With Pulmonary Arterial Hypertension. Reviewed International journal

Satoshi Akagi, Shingo Kasahara, Teiji Akagi, Kentaro Ejiri, Toshiharu Mitsuhashi, Koji Nakagawa, Kazufumi Nakamura, Hiroshi Ito

JACC. Advances 3 ( 4 ) 100887 - 100887 2024.4

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: A treatment strategy for congenital heart defects with moderate to severe pulmonary arterial hypertension (PAH) has not been established. OBJECTIVES: The purpose of this study was to identify patients in whom a treat and repair strategy was considered and to examine pretreatment variables associated with successful defect repair. METHODS: Patients with atrial or ventricular septal defect and PAH (pulmonary vascular resistance [PVR] ≥ 5 Wood units) eligible for the treat and repair strategy were included. Hemodynamics among pretreatment, pre-repair, and post-defect repair were compared. Clinical outcomes in patients with or without defect repair were also compared. Clinical outcomes included all-cause death, hospitalization for worsening pulmonary hypertension, and lung transplantation. RESULTS: Among 25 eligible for the treat and repair strategy, 20 underwent successful repair (repaired group) and 5 did not have a repair (unrepaired group). In the repaired group, PVR significantly decreased from 9.6 ± 2.6 WU at pretreatment to 5.0 ± 3.4 pre-repair (ß coefficient -4.6 [95% CI: -5.9 to -3.3]). The pulmonary to systemic blood flow ratio (Qp/Qs) increased from 1.5 ± 0.6 at pretreatment to 2.4 ± 1.3 pre-repair (ß coefficient 0.9 [95% CI: 0.4-1.38]). In the unrepaired group, pretreatment PVR decreased with treatment; however, PVR remained elevated. Qp/Qs did not change between pretreatment and post-treatment. The repaired group had a better prognosis than the unrepaired group (HR 0.092 [95% CI: 0.009-0.905]). Pretreatment mean pulmonary artery pressure, PVR, Qp/Qs, and arterial oxygen saturations were associated with undergoing defect repair. CONCLUSIONS: In this small cohort, a treat and repair strategy was successfully used in a significant proportion of the patients with congenital heart defects with moderate to severe PAH.

DOI： 10.1016/j.jacadv.2024.100887

Modern treatment to reduce pulmonary arterial pressure in pulmonary arterial hypertension. Invited Reviewed International journal

Satoshi Akagi, Hiromi Matsubara, Kazufumi Nakamura, Hiroshi Ito

Journal of cardiology 72 ( 6 ) 466 - 472 2018.12

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

Treatment goals in pulmonary arterial hypertension (PAH) include improved quality of life and exercise capacity as well as improved life prognosis. In our experience, only remarkable reductions in pulmonary arterial pressure (PAP) improve long-term survival. Lowering PAP could contribute to reverse remodeling by reducing hemodynamic stress. Proper and prompt use of PAH-specific drugs lowers PAP in patients with PAH. Upfront combination therapy with different PAH-specific drugs and quickly establishing high-dose epoprostenol lowers PAP sufficiently to improve prognosis in patients with PAH. PAH is often a comorbidity with other diseases including congenital heart defect, connective tissue diseases, and pulmonary arterial aneurysm. It is essential in these conditions to lower PAP to allow the next treatment strategy. In this report, we review modern treatments to lower PAP in patients with PAH.

DOI： 10.1016/j.jjcc.2018.04.014

Treat-and-repair strategy is a feasible therapeutic choice in adult patients with severe pulmonary arterial hypertension associated with a ventricular septal defect: case series. Reviewed International journal

Satoshi Akagi, Shingo Kasahara, Toshihiro Sarashina, Kazufumi Nakamura, Hiroshi Ito

European heart journal. Case reports 2 ( 2 ) yty033 2018.6

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

Introduction: Recent advances in pulmonary arterial hypertension (PAH)-specific drugs have dramatically changed the therapeutic strategy for PAH. A strategy that includes 'treatment' with PAH-specific drugs initially and then 'repair' by closure of the cardiac defect (i.e. 'treat and repair') was devised, and has been attempted, in patients with PAH associated with a cardiac defect. Case presentation: We present three cases of severe PAH associated with a ventricular septal defect (VSD) in adult patients who were initially treated with PAH-specific drugs followed by VSD closure. Two of the patients were treated with a combination of an endothelin receptor antagonist (ERA), phosphodiesterase type 5 inhibitor, and intravenous prostacyclin before VSD closure. The third patient was treated with an ERA and pulmonary artery banding before VSD closure. After 12 months of anti-PAH treatment, the pulmonary vascular resistance index and the ratio of the pulmonary vascular index to the systemic vascular resistance index decreased to levels that allowed VSD closure. At the mid- and long-term follow-up measurements after surgical closure of the VSD, the mean pulmonary artery pressure had markedly decreased. Discussion: Our case series suggests that the treat-and-repair strategy is a promising approach for adult patients with severe PAH associated with VSD.

DOI： 10.1093/ehjcr/yty033

Prostaglandin I2 induces apoptosis via upregulation of Fas ligand in pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension. Reviewed International journal

Satoshi Akagi, Kazufumi Nakamura, Hiromi Matsubara, Kengo Fukushima Kusano, Noriyuki Kataoka, Takahiro Oto, Katsumasa Miyaji, Aya Miura, Aiko Ogawa, Masashi Yoshida, Hatsue Ueda-Ishibashi, Chikao Yutani, Hiroshi Ito

International journal of cardiology 165 ( 3 ) 499 - 505 2013.5

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Pulmonary vascular remodeling with idiopathic pulmonary arterial hypertension (IPAH) is associated with impaired apoptosis of pulmonary artery smooth muscle cells (PASMCs). We have reported that high-dose prostaglandin I2 (PGI2) therapy markedly improved hemodynamics in IPAH patients. The therapy is thought to reverse vascular remodeling, though the mechanism is unclear. The aim of this study is to assess proapoptotic effects of PGI2 on PASMCs obtained from IPAH patients. METHODS: We investigated proapoptotic effects of PGI2 in PAH-PASMCs by TUNEL assays, caspase-3,-7 assays and transmission electron microscopy. We examined the expression of Fas ligand (FasL), an apoptosis-inducing member of the TNF cytokine family, in PAH-PASMCs. We measured the serum FasL levels in IPAH patients treated with PGI2. RESULTS: TUNEL-positive, caspase-3, 7-active cells and fragmentation of the nucleus were detected in PAH-PASMCs treated with PGI2. The percentage of apoptotic cells induced by PGI2 at a high concentration was higher than that induced by PGI2 at a low concentration. PCR-array analysis revealed that PGI2 upregulated the FasL gene in PAH-PASMCs, and we measured the FasL expression by quantitative RT-PCR and Western blotting. PGI2 significantly increased the mRNA level of FasL by 3.98 fold and the protein level of FasL by 1.70 fold. An IP receptor antagonist inhibited the induction of apoptosis, elevation of cyclic AMP and upregulation of FasL by PGI2. Serum FasL level had a significant positive correlation with PGI2 dose in IPAH patients treated with PGI2. CONCLUSIONS: PGI2 has proapoptotic effects on PAH-PASMCs via the IP receptor and upregulation of FasL.

DOI： 10.1016/j.ijcard.2011.09.004

Marked hemodynamic improvements by high-dose epoprostenol therapy in patients with idiopathic pulmonary arterial hypertension. Reviewed

Satoshi Akagi, Kazufumi Nakamura, Katsumasa Miyaji, Aiko Ogawa, Kengo Fukushima Kusano, Hiroshi Ito, Hiromi Matsubara

Circulation journal : official journal of the Japanese Circulation Society 74 ( 10 ) 2200 - 5 2010.10

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: The appropriate dose range of epoprostenol is thought to be 25-40 ng · kg(-1) · min(-1) based on the results of previous studies showing that epoprostenol therapy reduced mean pulmonary artery pressure (mPAP) by 12-22% and pulmonary vascular resistance (PVR) by 32-53% compared with baseline values in patients with idiopathic pulmonary arterial hypertension (IPAH). However, the efficacy of treatment of IPAH patients with epoprostenol >40 ng · kg(-1) · min(-1) has not been determined and this was the aim of the present study. METHODS AND RESULTS: The study group comprised 16 consecutive patients, none of whom died; 2 dropped out because they could not be titrated up as needed to the highest effective epoprostenol dose. Hemodynamics were evaluated in 14 IPAH patients who received high-dose epoprostenol monotherapy. The mean epoprostenol dosage was 107 ± 40 ng · kg(-1) · min(-1) (range, 54-190 ng · kg(-1) · min(-1)) and the mean duration of high-dose epoprostenol therapy was 1,355 ± 627 days (range, 582-2,410 days). Significant decreases from baseline values were seen in mPAP (from 66 ± 16 to 47 ± 12 mmHg, P<0.001) and PVR (from 21.6 ± 8.3 to 6.9 ± 2.9 Wood units, P<0.001). Compared with the baseline state, high-dose epoprostenol therapy reduced mPAP by 30% and PVR by 68%. CONCLUSIONS: The present study suggests high-dose epoprostenol therapy is a new treatment strategy for IPAH.

Induced Pluripotent Stem Cells in Cardiomyopathy: Advancing Disease Modeling, Therapeutic Development, and Regenerative Therapy. International journal

Quan Duy Vo, Kazufumi Nakamura, Yukihiro Saito, Satoshi Akagi, Toru Miyoshi, Shinsuke Yuasa

International journal of molecular sciences 26 ( 11 ) 2025.5

Language：English Publishing type：Research paper (scientific journal)

Cardiomyopathies are a heterogeneous group of heart muscle diseases that can lead to heart failure, arrhythmias, and sudden cardiac death. Traditional animal models and in vitro systems have limitations in replicating the complex pathology of human cardiomyopathies. Induced pluripotent stem cells (iPSCs) offer a transformative platform by enabling the generation of patient-specific cardiomyocytes, thus opening new avenues for disease modeling, drug discovery, and regenerative therapy. This process involves reprogramming somatic cells into iPSCs and subsequently differentiating them into functional cardiomyocytes, which can be characterized using techniques such as electrophysiology, contractility assays, and gene expression profiling. iPSC-derived cardiomyocyte (iPSC-CM) platforms are also being explored for drug screening and personalized medicine, including high-throughput testing for cardiotoxicity and the identification of patient-tailored therapies. While iPSC-CMs already serve as valuable models for understanding disease mechanisms and screening drugs, ongoing advances in maturation and bioengineering are bringing iPSC-based therapies closer to clinical application. Furthermore, the integration of multi-omics approaches and artificial intelligence (AI) is enhancing the predictive power of iPSC models. iPSC-based technologies are paving the way for a new era of personalized cardiology, with the potential to revolutionize the management of cardiomyopathies through patient-specific insights and regenerative strategies.

DOI： 10.3390/ijms26114984

Anticoagulant effects of edoxaban in cancer and noncancer patients with venous thromboembolism. Reviewed International journal

Masashi Yoshida, Kentaro Ejiri, Naoaki Matsuo, Takanori Naito, Kazuhiro Kuroda, Koji Tokioka, Kunihiko Hatanaka, Ryohei Fujimoto, Hidenaru Yamaoka, Yutaka Kajikawa, Kazuki Suruga, Hiroki Sugiyama, Tsuyoshi Miyaji, Yoshimasa Morimoto, Nobuhiro Okamura, Toshihiro Sarashina, Satoshi Akagi, Toru Miyoshi, Kazufumi Nakamura, Hiroshi Ito, Shinsuke Yuasa

Thrombosis journal 23 ( 1 ) 36 - 36 2025.4

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Edoxaban, a direct oral anticoagulant (DOAC), is a first-line treatment for venous thromboembolism (VTE) and the suppression of VTE recurrence. In patients with cancer, however, recurrent VTE after DOAC treatment may be more common than in noncancer patients. To evaluate our hypothesis that the anticoagulation effect of edoxaban is lower in VTE patients with cancer than in noncancer patients. METHODS: This study was a prospective, multicenter, observational study including patients treated with edoxaban for VTE in Japan. The primary outcome was the difference in the prothrombin time (PT), activated partial thromboplastin time (APTT), and D-dimer level at 5 h after initial edoxaban administration between the cancer and noncancer groups. An additional outcome was the longitudinal change in PT and APTT from 5 h to overnight after edoxaban administration. The incidence of adverse events was further investigated. RESULTS: PT and APTT at 5 h after initial edoxaban administration were not significantly different between the cancer (n = 84) and noncancer groups (n = 138) (e.g., log-transformed APTT 3.55 vs. 3.55, p = 0.45). However, D-dimer in the cancer groups was significantly greater than that in the noncancer groups (log-transformed 1.83 vs. 1.79, p = 0.009). PT and APTT significantly decreased from 5 h to overnight after edoxaban, but a similar pattern was observed in each group. All adverse events after edoxaban administration were also similar between patients with cancer and noncancer. CONCLUSION: PT and APTT after edoxaban administration were similar between VTE patients with cancer and noncancer groups, suggesting that edoxaban has anticoagulation effects on cancer-associated VTE similar to those of noncancer patients. TRIAL REGISTRATION: UMIN000041973; Registration Date: 2020.10.5.

DOI： 10.1186/s12959-025-00720-0

Pathophysiology of Group 3 Pulmonary Hypertension Associated with Lung Diseases and/or Hypoxia. International journal

Kazufumi Nakamura, Satoshi Akagi, Kentaro Ejiri, Satoshi Taya, Yukihiro Saito, Kazuhiro Kuroda, Yoichi Takaya, Norihisa Toh, Rie Nakayama, Yuki Katanosaka, Shinsuke Yuasa

International journal of molecular sciences 26 ( 2 ) 2025.1

Language：English Publishing type：Research paper (scientific journal)

Pulmonary hypertension associated with lung diseases and/or hypoxia is classified as group 3 in the clinical classification of pulmonary hypertension. The efficacy of existing selective pulmonary vasodilators for group 3 pulmonary hypertension is still unknown, and it is currently associated with a poor prognosis. The mechanisms by which pulmonary hypertension occurs include hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, a decrease in pulmonary vascular beds, endothelial dysfunction, endothelial-to-mesenchymal transition, mitochondrial dysfunction, oxidative stress, hypoxia-inducible factors (HIFs), inflammation, microRNA, and genetic predisposition. Among these, hypoxic pulmonary vasoconstriction and subsequent pulmonary vascular remodeling are characteristic factors involving the pulmonary vasculature and are the focus of this review. Several factors have been reported to mediate vascular remodeling induced by hypoxic pulmonary vasoconstriction, such as HIF-1α and mechanosensors, including TRP channels. New therapies that target novel molecules, such as mechanoreceptors, to inhibit vascular remodeling are awaited.

DOI： 10.3390/ijms26020835

iPSC-Derived Biological Pacemaker—From Bench to Bedside

Quan Duy Vo, Kazufumi Nakamura, Yukihiro Saito, Toshihiro Iida, Masashi Yoshida, Naofumi Amioka, Satoshi Akagi, Toru Miyoshi, Shinsuke Yuasa

Cells 13 ( 24 ) 2045 - 2045 2024.12

Publishing type：Research paper (scientific journal) Publisher：MDPI AG

Induced pluripotent stem cell (iPSC)-derived biological pacemakers have emerged as an alternative to traditional electronic pacemakers for managing cardiac arrhythmias. While effective, electronic pacemakers face challenges such as device failure, lead complications, and surgical risks, particularly in children. iPSC-derived pacemakers offer a promising solution by mimicking the sinoatrial node’s natural pacemaking function, providing a more physiological approach to rhythm control. These cells can differentiate into cardiomyocytes capable of autonomous electrical activity, integrating into heart tissue. However, challenges such as achieving cellular maturity, long-term functionality, and immune response remain significant barriers to clinical translation. Future research should focus on refining gene-editing techniques, optimizing differentiation, and developing scalable production processes to enhance the safety and effectiveness of these biological pacemakers. With further advancements, iPSC-derived pacemakers could offer a patient-specific, durable alternative for cardiac rhythm management. This review discusses key advancements in differentiation protocols and preclinical studies, demonstrating their potential in treating dysrhythmias.

DOI： 10.3390/cells13242045

Fenestrated GORE® CARDIOFORM ASD occluder for transcatheter atrial septal defect closure in a geriatric patient. Reviewed

Mitsutaka Nakashima, Teiji Akagi, Takashi Miki, Rie Nakayama, Yoichi Takaya, Koji Nakagawa, Satoshi Akagi, Norihisa Toh, Kazufumi Nakamura

Journal of cardiology cases 30 ( 2 ) 31 - 34 2024.8

Language：English Publishing type：Research paper (scientific journal)

UNLABELLED: An 82-year-old man with a secundum atrial septal defect (ASD) underwent transcatheter closure. The patient had a wide area of aortic and superior rim deficiency, with left ventricular diastolic dysfunction and moderate mitral regurgitation. These findings suggested the risk of both cardiac erosion and increased left atrial pressure after closure. To avoid cardiac erosion, a GORE® CARDIOFORM ASD (GCA) occluder (W.L. Gore & Associates, Flagstaff, AZ, USA) was considered an appropriate device in this patient. However, the possibility of excessively high left atrial pressure due to complete defect closure was a concern. Thus, we created a 4.5-mm fenestration using a surgical punch in the fabric membrane of a 44-mm GCA. The device was deployed in an appropriate position, and no significant elevation of pulmonary capillary wedge pressure was observed. One month after the closure, marked improvement in clinical symptoms and continuous flow through the fenestration were observed. This novel fenestration technique may contribute to expansion of the indications for transcatheter ASD closure in patients who require a GCA owing to an anatomically high risk of erosion accompanied by left ventricular diastolic dysfunction. LEARNING OBJECTIVE: In elderly patients with left ventricular diastolic dysfunction, transcatheter atrial septal defect (ASD) closure is difficult because rapid resolution of an ASD shunt can cause an increase in left atrial pressure. Previous reports described the creation of a fenestration in the closure device. The use of a GORE® CARDIOFORM ASD (GCA) occluder can reduce the erosion risk; however, creating a stable fenestration is difficult. We developed a novel technique to create a stable fenestration in a GCA.

DOI： 10.1016/j.jccase.2024.04.001

Prognostic Implications of Insulin Resistance in Heart Failure in Japan Reviewed International journal

Keiichiro Iwasaki, Kazufumi Nakamura, Satoshi Akagi, Yoichi Takaya, Hironobu Toda, Toru Miyoshi, Shinsuke Yuasa

Nutrients 16 ( 12 ) 1888 - 1888 2024.6

Language：English Publishing type：Research paper (scientific journal) Publisher：MDPI AG

Diabetes mellitus (DM) is a major risk and prognostic factor for heart failure (HF). Insulin resistance (IR) is an important component of DM, but the relationship between IR and HF prognosis has not yet been established across a wide variety of HF populations. We retrospectively evaluated the relationship between IR and clinical outcomes of HF patients at our hospital between 2017 and 2021. IR was defined as a homeostatic model assessment of IR (HOMA-IR) index ≥ 2.5, calculated from fasting blood glucose and insulin concentrations. The primary outcome was a composite of all-cause death and hospitalisation for HF (HHF). Among 682 patients included in the analyses, 337 (49.4%) had IR. The median age was 70 [interquartile range (IQR): 59–77] years old, and 66% of the patients were men. Among the patients, 41% had a left ventricular ejection fraction below 40%, and 32% had DM. The median follow-up period was 16.5 [IQR: 4.4–37.3] months. IR was independently associated with the primary outcome (HR: 1.91, 95% CI: 1.39–2.62, p < 0.0001), death (hazard ratio [HR]: 1.86, 95% confidence interval [CI]: 1.28–2.83, p < 0.01), and HHF (HR: 1.91, 95% CI: 1.28–2.83, p < 0.01). HOMA-IR is an independent prognostic factor of HF in a wide variety of HF populations.

DOI： 10.3390/nu16121888

Risk Assessment in Pulmonary Arterial Hypertension. Invited Reviewed

Satoshi Akagi

Circulation journal : official journal of the Japanese Circulation Society 2024.3

Catheter-directed thrombolysis for critical hand ischemia with failed distal venous arterialization. Reviewed

Mitsutaka Nakashima, Hironobu Toda, Kentaro Ejiri, Susumu Ozawa, Satoshi Akagi, Kazufumi Nakamura

Cardiovascular intervention and therapeutics 39 ( 1 ) 95 - 96 2023.8

Woman in Her 50s With Pulmonary Hypertension Associated With Takayasu Arteritis. Reviewed International journal

Kentaro Ejiri, Satoshi Akagi, Hiroshi Ito

JAMA cardiology 8 ( 8 ) 792 - 792 2023.8

Evidence for Hypoxia-Induced Shift in ATP Production from Glycolysis to Mitochondrial Respiration in Pulmonary Artery Smooth Muscle Cells in Pulmonary Arterial Hypertension. Reviewed International journal

Satoshi Akagi, Kazufumi Nakamura, Megumi Kondo, Satoshi Hirohata, Heiichiro Udono, Mikako Nishida, Yukihiro Saito, Masashi Yoshida, Toru Miyoshi, Hiroshi Ito

Journal of clinical medicine 12 ( 15 ) 2023.7

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: The metabolic state of pulmonary artery smooth muscle cells (PASMCs) from patients with pulmonary arterial hypertension (PAH) is not well understood. In this study, we examined the balance between glycolysis and mitochondrial respiration in non-PAH-PASMCs and PAH-PASMCs under normoxia and hypoxia. METHODS: We investigated the enzymes involved in glycolysis and mitochondrial respiration, and studied the two major energy-yielding pathways (glycolysis and mitochondrial respiration) by measuring extracellular acidification rate (ECAR) and cellular oxygen consumption rate (OCR) using the Seahorse extracellular flux technology. RESULTS: Under both normoxia and hypoxia, the mRNA and protein levels of pyruvate dehydrogenase kinase 1 and pyruvate dehydrogenase were increased in PAH-PASMCs compared with non-PAH-PASMCs. The mRNA and protein levels of lactate dehydrogenase, as well as the intracellular lactate concentration, were also increased in PAH-PASMCs compared with non-PAH-PASMCs under normoxia. However, these were not significantly increased in PAH-PASMCs compared with non-PAH-PASMCs under hypoxia. Under normoxia, ATP production was significantly lower in PAH-PASMCs (59 ± 5 pmol/min) than in non-PAH-PASMCs (70 ± 10 pmol/min). On the other hand, ATP production was significantly higher in PAH-PASMCs (31 ± 5 pmol/min) than in non-PAH-PASMCs (14 ± 3 pmol/min) under hypoxia. CONCLUSIONS: There is an underlying change in the metabolic strategy to generate ATP production under the challenge of hypoxia.

DOI： 10.3390/jcm12155028

Immunosuppressive Treatment for an anti-U1 Ribonucleoprotein Antibody-positive Patient with Pulmonary Arterial Hypertension: A Case Report. Reviewed

Kazuya Matsumoto, Yoshia Miyawaki, Takayuki Katsuyama, Takato Nakadoi, Kenta Shidahara, Kei Hirose, Shoichi Nawachi, Yosuke Asano, Yu Katayama, Eri Katsuyama, Mariko Takano-Narazaki, Yoshinori Matsumoto, Atsushi Mori, Satoshi Akagi, Ken-Ei Sada, Jun Wada

Internal medicine (Tokyo, Japan) 63 ( 5 ) 671 - 676 2023.7

Language：English Publishing type：Research paper (scientific journal)

A 34-year-old woman with pulmonary arterial hypertension (PAH) was admitted to the hospital. She had been diagnosed with PAH three years earlier and treated with triple vasodilator therapy. She was positive for anti-U1 ribonucleoprotein antibodies but did not show any other symptoms associated with autoimmune diseases. Corticosteroid and cyclophosphamide therapy was administered, suspecting the involvement of immunological pathophysiology. After 3 weeks, the mean pulmonary artery pressure decreased from 50 to 38 mmHg without any change in the vasodilators. Immunosuppressive therapy was effective in this patient with PAH with an anti-U1 ribonucleoprotein-antibody-positive response and might be an option for patients with these specific features.

DOI： 10.2169/internalmedicine.1407-22

A successful bridge to recovery with Impella 5.0 and subsequent hybrid cardiac resynchronization therapy in systemic right ventricle failure: a case report. Reviewed International journal

Keiichiro Iwasaki, Nobuhiro Nishii, Satoshi Akagi, Hiroshi Ito

European heart journal. Case reports 7 ( 5 ) ytad214 2023.5

Language：English

BACKGROUND: Impella 5.0 is currently used as a temporary mechanical circulatory support device in cardiogenic shock (CS). However, Impella 5.0 implantation for the systemic right ventricle (sRV) has not been well documented. CASE SUMMARY: A 50-year-old man with atrial switch for dextro-transposition of the great arteries was transferred to our hospital for the treatment of embolic acute myocardial infarction of the left main trunk lesion with CS. To stabilize haemodynamics, we implanted Impella 5.0 via the left subclavian artery in the sRV. After optimal medical therapy initiation and gradual weaning of Impella 5.0, Impella 5.0 was successfully explanted. An electrocardiogram was obtained, which showed complete right branch block with a QRS duration of 172 ms. Acute invasive haemodynamic evaluation of cardiac resynchronization therapy (CRT) pacing showed that dP/dt increased from 497 to 605 mmHg/s (21.7% improvement), and hybrid cardiac resynchronization therapy defibrillator (CRTD) with a sRV epicardial lead was subsequently implanted. The patient was discharged without inotropic support. DISCUSSION: Coronary artery embolism is a rare but serious complication of dextro-transposition of the great arteries after atrial switch operations. Impella 5.0 implantation is a feasible bridge strategy for refractory CS due to sRV failure. Although CRT implantation in patients with sRV is controversial, an acute invasive haemodynamic evaluation can help assess its potential benefits.

DOI： 10.1093/ehjcr/ytad214

Pulmonary arteriovenous fistula in a rare location: The importance of excluding patent foramen ovale. Reviewed

Mitsutaka Nakashima, Takashi Miki, Yoichi Takaya, Rie Nakayama, Koji Nakagawa, Satoshi Akagi, Norihisa Toh, Teiji Akagi, Hiroshi Ito

Journal of cardiology cases 27 ( 3 ) 124 - 127 2023.3

Language：English

UNLABELLED: A 46-year-old woman with a history of repeated thromboembolic stroke and anti-phospholipid antibody syndrome was referred to our hospital. Saline contrast transthoracic echocardiography showed that microbubbles appeared in the left atrium within 4 heartbeats. Thus, she was initially suspected as having a patent foramen ovale with associated paradoxical embolism. However, no evidence of patent foramen ovale or atrial septal defect could be found using transesophageal echocardiography. Saline contrast transesophageal echocardiography showed that microbubbles flowed into the left atrium through the left superior pulmonary vein. Ultimately, she was diagnosed as having a pulmonary arteriovenous malformation located at the upper left pulmonary lobe using contrast computed tomography and pulmonary artery angiography. Pulmonary arteriovenous malformations are typically located in the lower lobe of either lung and, in bubble studies, contrast appears in the left atrium after 4 heartbeats. Here, the pulmonary arteriovenous malformation was in the upper lobe, and contrast appeared in the left atrium at an earlier time point: one associated with patent foramen ovale. These findings made it difficult to differentiate the two diseases initially. This case suggests that pulmonary arteriovenous malformation should be carefully considered, even if microbubbles appear in the left atrium early on a saline contrast transthoracic echocardiograph. LEARNING OBJECTIVE: Pulmonary arteriovenous malformation occasionally appears in the upper lobe. In these cases, microbubbles may appear in the left atrium after detection in the right atrium with a time-course that is suggestive of a patent foramen ovale. Therefore, diagnosis should be carefully confirmed by using other multimodal imaging tests, such as transesophageal echocardiography, contrast computed tomography, or pulmonary artery angiography.

DOI： 10.1016/j.jccase.2022.11.005

Association between Cardiovascular Disease and Liver Disease, from a Clinically Pragmatic Perspective as a Cardiologist. Reviewed International journal

Mitsutaka Nakashima, Kazufumi Nakamura, Takahiro Nishihara, Keishi Ichikawa, Rie Nakayama, Yoichi Takaya, Norihisa Toh, Satoshi Akagi, Toru Miyoshi, Teiji Akagi, Hiroshi Ito

Nutrients 15 ( 3 ) 2023.2

Language：English Publishing type：Research paper (scientific journal)

Cardiovascular diseases and liver diseases are closely related. Non-alcoholic fatty liver disease has the same risk factors as those for atherosclerotic cardiovascular disease and may also be a risk factor for atherosclerotic cardiovascular disease on its own. Heart failure causes liver fibrosis, and liver fibrosis results in worsened cardiac preload and congestion. Although some previous reports regard the association between cardiovascular diseases and liver disease, the management strategy for liver disease in patients with cardiovascular diseases is not still established. This review summarized the association between cardiovascular diseases and liver disease. In patients with non-alcoholic fatty liver disease, the degree of liver fibrosis progresses with worsening cardiovascular prognosis. In patients with heart failure, liver fibrosis could be a prognostic marker. Liver stiffness assessed with shear wave elastography, the fibrosis-4 index, and non-alcoholic fatty liver disease fibrosis score is associated with both liver fibrosis in patients with liver diseases and worse prognosis in patients with heart failure. With the current population ageing, the importance of management for cardiovascular diseases and liver disease has been increasing. However, whether management and interventions for liver disease improve the prognosis of cardiovascular diseases has not been fully understood. Future investigations are needed.

DOI： 10.3390/nu15030748

Microcalcification and 99mTc-Pyrophosphate Uptake without Increased Bone Metabolism in Cardiac Tissue from Patients with Transthyretin Cardiac Amyloidosis. Reviewed International journal

Atsushi Mori, Yukihiro Saito, Kazufumi Nakamura, Toshihiro Iida, Satoshi Akagi, Masashi Yoshida, Makiko Taniyama, Toru Miyoshi, Hiroshi Ito

International journal of molecular sciences 24 ( 3 ) 2023.1

Language：English Publishing type：Research paper (scientific journal)

Transthyretin cardiac amyloidosis (ATTR-CA) is characterized by high 99mTc-labeled bone tracer uptake in the heart. However, the mechanism of bone tracer uptake into the heart remains controversial. Since bone tracer uptake into metastatic bone tumors is thought to be associated with increased bone metabolism, we examined 99mTc-pyrophosphate (PYP) scintigraphy findings, endomyocardial biopsy (EMB) tissue findings, and the expression of bone metabolism-related genes in the EMB tissues in patients with ATTR-CA, amyloid light-chain cardiac amyloidosis (AL-CA), and noncardiac amyloidosis (non-CA) in this study. The uptake of 99mTc-PYP in the heart was significantly higher in the ATTR-CA patients than in the AL-CA and non-CA patients. A higher percentage of ATTR-CA EMB tissue showed von Kossa-positive microparticles: ATTR-CA, 62%; AL-CA, 33%; and non-CA, 0%. Calcified microparticles were identified using transmission electron microscopy. However, none of the osteogenic marker genes, osteoclastic marker genes, or phosphate/pyrophosphate-related genes were upregulated in the EMB samples from ATTR-CA patients compared to those from AL-CA and non-CA patients. These results suggest that active calcification-promoting mechanisms are not involved in the microcalcification observed in the heart in ATTR-CA. The mechanisms explaining bone tracer uptake in the heart, which is stronger than that in the ribs, require further investigation.

DOI： 10.3390/ijms24031921

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