Bio

Honors & Awards


  • Young Investigator Award, Clinical Research, Japanese Association of Cardiovascular Intervention and Therapeutics (July 2017)
  • Young Researcher Award, ESC, Working Group on Pulmonary Circulation and Right Ventricular Function (Aug. 2016)
  • Young Investigator Award, Basic Science, European Society of Cardiology (Aug. 2016)
  • Young Investigator Award, Clinical Research, Japanese Association of Cardiovascular Intervention and Therapeutics (Aug. 2016)
  • Top Score Poster AwardTop Score Poster Award, European Society of Cardiology (Aug. 2014)

Boards, Advisory Committees, Professional Organizations


  • Fellow, Japanese Society of Internal Medicine (2018 - Present)

Professional Education


  • Doctor of Philosophy, Kyushu University (2018)
  • Board Certification, Board Certified Echocardiographer for Structural Heart Disease, Japanese Society of Echocardiography, Cardiology (2018)
  • Board Certification, Board of Japanese Circulation Society, Cardiology (2017)
  • Board Certification, Japanese Board of Perioperative Transesophageal Echocardiography, Cardiology (2016)
  • Clinical Fellow, Aso Iizuka Hospital, Cardiovascular Medicine (2013)
  • Board Certification, Board of the Japanese Society of Internal Medicine, Internal Medicine (2012)
  • Clinical Fellow, Aso Iizuka Hospital, Emergency Medicine (2011)
  • Residency, Aso Iizuka Hospital (2010)
  • Doctor of Medicine, Kyushu University (2008)

Publications

All Publications


  • Nanoparticle-Mediated Targeting of Pitavastatin to Small Pulmonary Arteries and Leukocytes by Intravenous Administration Attenuates the Progression of Monocrotaline-Induced Established Pulmonary Arterial Hypertension in Rats. International heart journal Ichimura, K., Matoba, T., Koga, J. I., Nakano, K., Funamoto, D., Tsutsui, H., Egashira, K. 2018; 59 (6): 1432–44

    Abstract

    Statins are known to improve pulmonary arterial hypertension (PAH) by their anti-inflammatory and anti-proliferative effects in animal models. However, recent clinical studies have reported that clinically approved statin doses failed to improve clinical outcomes in patients with PAH. We therefore hypothesized that nanoparticle (NP) -mediated targeting of pitavastatin could attenuate the progression of established PAH.We induced PAH by subcutaneously injecting monocrotaline (MCT) in Sprague-Dawley rats. On day 14 after the MCT injection, animals that displayed established PAH on echocardiography were included. On day 17, they were randomly assigned to the following 5 groups: daily intravenous administration of (1) vehicle, (2) fluorescein-isothiocyanate-NP, (3) pitavastatin, (4) pitavastatin-NP, or (5) oral sildenafil. Intravenous NP was selectively delivered to small pulmonary arteries and circulating CD11b-positive leukocytes. On day 21, pitavastatin-NP attenuated the progression of PAH at lower doses than pitavastatin alone. This was associated with the inhibition of monocyte-mediated inflammation, proliferation, and remodeling of the pulmonary arteries. Interestingly, sildenafil attenuated the development of PAH, but had no effects on inflammation or remodeling of the pulmonary arteries. In separate experiments, only treatment with pitavastatin-NP reduced the mortality rate at day 35.NP-mediated targeting of pitavastatin to small pulmonary arteries and leukocytes attenuated the progression of established MCT-induced PAH and improved survival. Therapeutically, pitavastatin-NP was associated with anti-inflammatory and anti-proliferative effects on small pulmonary arteries, which was completely distinct from the vasodilatory effect of sildenafil. Pitavastatin-NP can be a novel therapeutic modality for PAH.

    View details for DOI 10.1536/ihj.17-683

    View details for PubMedID 30369578

  • A Translational Study of a New Therapeutic Approach for Acute Myocardial Infarction: Nanoparticle-Mediated Delivery of Pitavastatin into Reperfused Myocardium Reduces Ischemia-Reperfusion Injury in a Preclinical Porcine Model. PloS one Ichimura, K., Matoba, T., Nakano, K., Tokutome, M., Honda, K., Koga, J., Egashira, K. 2016; 11 (9): e0162425

    Abstract

    There is an unmet need to develop an innovative cardioprotective modality for acute myocardial infarction, for which interventional reperfusion therapy is hampered by ischemia-reperfusion (IR) injury. We recently reported that bioabsorbable poly(lactic acid/glycolic acid) (PLGA) nanoparticle-mediated treatment with pitavastatin (pitavastatin-NP) exerts a cardioprotective effect in a rat IR injury model by activating the PI3K-Akt pathway and inhibiting inflammation. To obtain preclinical proof-of-concept evidence, in this study, we examined the effect of pitavastatin-NP on myocardial IR injury in conscious and anesthetized pig models.Eighty-four Bama mini-pigs were surgically implanted with a pneumatic cuff occluder at the left circumflex coronary artery (LCx) and telemetry transmitters to continuously monitor electrocardiogram as well as to monitor arterial blood pressure and heart rate. The LCx was occluded for 60 minutes, followed by 24 hours of reperfusion under conscious conditions. Intravenous administration of pitavastatin-NP containing ≥ 8 mg/body of pitavastatin 5 minutes before reperfusion significantly reduced infarct size; by contrast, pitavastatin alone (8 mg/body) showed no therapeutic effects. Pitavastatin-NP produced anti-apoptotic effects on cultured cardiomyocytes in vitro. Cardiac magnetic resonance imaging performed 4 weeks after IR injury revealed that pitavastatin-NP reduced the extent of left ventricle remodeling. Importantly, pitavastatin-NP exerted no significant effects on blood pressure, heart rate, or serum biochemistry. Exploratory examinations in anesthetized pigs showed pharmacokinetic analysis and the effects of pitavastatin-NP on no-reflow phenomenon.NP-mediated delivery of pitavastatin to IR-injured myocardium exerts cardioprotective effects on IR injury without apparent adverse side effects in a preclinical conscious pig model. Thus, pitavastatin-NP represents a novel therapeutic modality for IR injury in acute myocardial infarction.

    View details for DOI 10.1371/journal.pone.0162425

    View details for PubMedID 27603665

    View details for PubMedCentralID PMC5014419