Hiroyuki Fujinaga
University of Tokushima
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Featured researches published by Hiroyuki Fujinaga.
Heart and Vessels | 2003
Kohzou Uehara; Masahiro Nomura; Yuji Ozaki; Hiroyuki Fujinaga; Hiroyuki Ikefuji; Masaru Kimura; Kazumasa Chikamori; Yutaka Nakaya; Susumu Ito
Abstract Inflammatory cytokines are suspected to play an important role in the pathophysiology of left ventricular (LV) remodeling. We investigated whether high-sensitivity C-reactive protein (CRP) (hs-CRP) is a predictor for LV remodeling in patients with acute myocardial infarction (AMI) with successful reperfusion, and also whether such a situation can be avoided by the administration of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB). The subjects were 139 patients with an initial attack of anterior myocardial infarction successfully treated by reperfusion therapy. They were randomly divided into the following two groups: an angiotensin (AG) group (91 patients treated with ACEI/ARB) and a NON-AG group (48 patients not treated with ACEI/ARB). Levels of hs-CRP, creatine kinase, human atrial natriuretic polypeptide, brain natriuretic peptide (BNP), fasting blood glucose, serum lipids, fibrinogen, fibrin degradation product, prothromloin time, and activated partial thromboplastin time were measured immediately after 1, 2, 3, and 7 days, and 1 months after the onset of AMI. ACEI or ARB administration lowered hs-CRP levels and prevented the development of LV remodeling. Peak CRP levels significantly correlated with BNP levels during the acute stage (r = +0.54, P < 0.0001), end-diastolic volume index (r = +0.78, P < 0.0001), end-systolic volume index (r = +0.36, P = 0.0405), ejection fraction (r = −0.45, P = 0.0052), left ventricular end-diastolic diameter (r = +0.61, P < 0.0001), cardiac output (r = −0.52, P = 0.0005), cardiac index (r = −0.41, P = 0.0099), and systolic pulmonary arterial pressure (r = +0.48, P = 0.0017) 1 month after the onset of AMI in the NON-AG group but not in the AG group. Logistic multivariate analysis revealed that peak CRP alone was an independent risk factor for the development of LV remodeling in the NON-AG group (odds ratio = 1.79, P = 0.002). These results suggest that hs-CRP is a useful factor for predicting LV remodeling. Furthermore, ACEI or ARB administration to AMI patients showing increased hs-CRP levels during the early stage of the disease could prevent LV remodeling.
Angiology | 2005
Tomonori Watanabe; Hiroyuki Fujinaga; Yasumasa Ikeda; Teruo Higashi; Masaru Murakami; Keiji Kawahara; Ikuro Hayashi; Toshiharu Niki; Toshio Shigekiyo; Tetsuzo Wakatsuki
Essential thrombocythemia (ET) can cause systemic vascular thrombosis, but involvement of coronary arteries in the setting of ET is rare. This report describes a case of acute myocardial infarction (MI) in a patient with ET. A 67-year-old man with ET complained of severe acute chest pain. Emergent coronary angiography revealed subtotal thrombotic occlusion of the left main trunk (LMT) coronary artery. Coronary angioplasty and stenting were performed successfully. Coronary angiography 4 weeks later revealed no significant restenosis. The patient has done well after primary coronary stenting with the use of only an antiplatelet agent to treat the thrombocythemia.
Acta Cardiologica | 2005
Yasumasa Ikeda; Hiroyuki Fujinaga; Toshiharu Niki
Percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is a common therapeutic method. Although two or more culprit lesions are rarely observed simultaneously in AMI patients, we present two cases of AMI caused by simultaneous occlusion of two major coronary arteries, the left anterior descending and right coronary arteries. In both cases, emergency PCI for the two major vessels was successful. Both patients had type 2 diabetes mellitus, which might have contributed to simultaneous occlusion of the two coronary arteries.
Coronary Artery Disease | 1998
Koichi Sakabe; Tetsuzo Wakatsuki; Hisanori Shinohara; Jiro Ikata; Hiroyuki Fujinaga; Yoshifumi Oishi; Toshihiro Toyoshima; Akiyoshi Nishikado; Takashi Oki; Susumu Ito
BackgroundIt is difficult to evaluate the extent of myocardial injury after successful reperfusion following acute myocardial infarction (AMI). We investigated the relationship between the coronary flow velocity pattern immediately after reperfusion and pathologic characteristics after myocardial reperfusion injury in dogs. MethodsWe measured distal coronary flow velocity variables in the left circumflex coronary artery in a canine model of AMI (n = 12) 10 min after the release of a clamp (3–10 h clamp procedure) using a 0.35 mm Doppler guide-wire. Dogs were divided into two groups according to presence or absence of early systolic retrograde coronary flow. Hearts were excised 2 h after reperfusion and examined histopathologically. ResultsThe clamping time tended to be longer in dogs with early systolic retrograde coronary flow. Neutrophil infiltration was observed in the myocardium of dogs without systolic retrograde flow (n = 9); hemorrhage was rarely detectable and the myocardium maintained a bundle form. However, the bundle form of the myocardium became rough, and the severity of the incidence of hemorrhage tended to increase as the ratio of the diastolic coronary flow velocity to systolic velocity (DSVR) decreased. Vacuolar degeneration of the myocardium was also observed in hearts with a relatively low DSVR. In the group with systolic retrograde flow (n = 3), hearts were characterized by coagulation necrosis, marked vacuolar degeneration of the myocardium and diffusely distributed red cells in the intermyocytes. Systolic antegrade flow velocity was much reduced in this group, resulting in a markedly increased DSVR. These findings appeared to be related to severe myocardial damage. ConclusionsCoronary flow velocity patterns immediately after successful reperfusion appear to reflect the pathologic characteristics of the reperfused myocardium in dogs with AMI. Coronary Artery Dis 9:21–27
European heart journal. Acute cardiovascular care | 2017
Kenji Harada; Takashi Yamamoto; Takanobu Okumura; Masahito Shigekiyo; Naho Terada; Ayumi Okada; Atsushi Kawata; Tsutomu Iima; Takafumi Harada; Kazutoshi Fujisawa; Norihito Kageyama; Akihiro Saito; Hirofumi Yamamoto; Hiroyuki Fujinaga
Background: Vasodilators, such as nitroglycerin, have long been first-line treatments for acute heart failure syndromes (AHFS). Nicorandil is a vasodilator with dual potassium channel opening and nitrate properties. However, there are no randomized controlled studies of intravenous nicorandil safety and efficacy in the urgent phase AHFS. We examined the symptomatic, hemodynamic, and echocardiographic effects and safety, and 60-day clinical outcomes of intravenous nicorandil, in addition to standard therapy, in patients with AHFS in the urgent phase. Methods: In this prospective, randomized controlled trial, 106 AHFS patients were randomized within one hour of arrival to receive either standard therapy (control group, n=56) or standard therapy plus simultaneous intravenous nicorandil (0.2 mg/kg bolus followed by 0.2 mg/kg/h for 24 h; nicorandil group, n=50). Outcomes were assessed at 60 days. Results: Patients in the nicorandil group exhibited greater improvement of dyspnea as measured by change in a five-point Likert scale compared to those in the control group (after 1 h infusion: p=0.006, 6 h; p<0.001). The nicorandil group also showed significantly improved E/e′, an estimate of left ventricular filling pressure, at 1 and 24 h (p=0.001 and p=0.004, respectively). In addition, intravenous nicorandil therapy was safe and did not cause side effects such as excessive hypotension or reflex tachycardia. However, it did not reduce all-cause mortality and readmission rates at 60 days. Conclusions: Addition of intravenous nicorandil to standard therapy for urgent phase AHFS improved dyspnea and left ventricular diastolic function but not 60-day outcome.
Platelets | 2015
Toshio Shigekiyo; Etsuko Sekimoto; Hironobu Shibata; Shuji Ozaki; Hiroyuki Fujinaga; Takanori Hirose
A standard treatment for acquired amegakaryocytic thrombocytopenic purpura (AATP) has not yet been established. Once AATP is diagnosed, a therapeutic trial of cyclosporine, with or without antithymocyte globulin (ATG), is indicated [1]. Allogeneic bone marrow transplantation (BMT) is considered to be an appropriate treatment for patients with refractory or progressive AATP, who are relatively young and have matched siblings [2]. Recently, successful treatment of AATP with a thrombopoietin (TPO) receptor agonist, eltrombopag, has been reported [3]. We herein describe a patient with AATP refractory to other therapies, including eltrombopag, who was successfully managed with another TPO receptor agonist, romiplostim. This publication was approved by the ethics committee of Tokushima Prefectural Central Hospital. A 55-year-old male was referred to us for thrombocytopenia in December 2004. He had a past history of myocardial infarction at 51 years of age, and had therefore been taking numerous drugs, such as aspirin, nicorandil, quinapril hydrochloride, carvedilol, candesartan cilexetil, azosemide, spironolactone, and allopurinol. He was not a heavy drinker. A physical examination revealed many petechiae and ecchymoses on the extremities and the abdominal wall. The peripheral blood results were as follows: Hb, 13.2 g/dl; RBC, 4.19 10/ml; WBC, 7.6 10/ml (seg., 63.5%; eos., 7.0%; baso., 1.5%; mono., 7.5%; lym., 23.0%) and PLT, 4 10/ml. His blood chemistry values, including total bilirubin, AST, ALT, ALP, LDH, BUN and creatinine, were all within the normal limits. The prothrombin time, activated partial thromboplastin time, plasma fibrinogen level, and plasma FDP concentration were all normal. The platelet-associated IgG level was 57.6 ng/10 cells (reference range, 5–25 ng/10 cells). Tests for rheumatoid factor and antinuclear antibody were negative. Screening assays for the human immunodeficiency virus, human T-cell leukemia virus type-1, hepatitis B virus, hepatitis C virus and human parvovirus B19 (IgM) were negative. Bone marrow aspiration showed normal cellularity and the absence of megakaryocytes, with a normal appearance of erythroid and myeloid elements (Figure 1A and B). A bone marrow cytogenetic study showed normal karyotypes. The patient was therefore diagnosed with AATP. Unfortunately, a bone marrow biopsy was not carried out. Of the drugs that the patient had received, both aspirin and allopurinol had previously been given to patients with AATP [1, 3, 4]. However, since it was impossible to show that none of the other drugs were associated with AATP, all medications were discontinued [5]. Pulse therapy with methylprednisolone (1 g/day 3), followed by prednisolone (1 mg/kg/day), was conducted at the same time, but his platelet count remained low for one month. Cyclosporine (5 mg/kg/day) was initiated in January 2005, but his thrombocytopenia had not improved after two months. Horse ATG (1 g/day 5) was administered in March 2005. His platelet count oscillated between 15 10/ml and 470 10/ml in 35–39-day intervals, but became consistently low in December 2005. Bone marrow aspiration in March 2006 gave the same results as in December in 2004 (data not shown). Rabbit ATG (0.5 g/day 5) was administered in March 2006. The change in his platelet count was similar to that after the administration of horse ATG. Danazol (300 mg/day) treatment was initiated in October 2006, but his thrombocytopenia had not improved after three months. Although he was referred to a hospital for allogeneic BMT in May 2007, he was refused a transplant because of his age, complications and the absence of related donors. Cyclophosphamide hydrate (1 and 2 g) was intravenously administered in June and August 2007, respectively, with no improvement of his thrombocytopenia. Since successful treatment of AATP with rituximab (375 mg/m intravenously, weekly, for two consecutive weeks) in a patient with systemic lupus erythematosus was reported, he was given rituximab (375 mg/m) twice in November 2008 [6]. However, his platelet count did not increase at all. When a test dose of horse ATG was given in March 2009, he developed hypotension and a skin rash. We therefore abandoned a second course of both horse and rabbit ATG. Intravenous immunoglobulin was not tested due to its potential risk of thrombosis [7]. Eltrombopag was initiated at 12.5 mg/day in September 2011, and was increased by 12.5 mg/day every two weeks. After one month of treatment Keywords
Coronary Artery Disease | 1998
Hiroyuki Fujinaga; Tetsuzo Wakatsuki; Akiyoshi Nishikado; Takashi Oki; Susumu Ito
BACKGROUND There have been few studies concerning the electrophysiologic changes associated with the use of angiotensin-converting enzyme inhibitors in patients with acute myocardial infarction. We examined the electrophysiologic effects of quinaprilat in dogs during acute myocardial ischemia and following reperfusion. METHODS The left anterior descending coronary artery was occluded for 10 min and reperfused for 10 min. Animals received intravenous quinaprilat (3 micrograms/kg per min, quinaprilat group) or saline (control group). We measured the ventricular effective refractory period and intra-myocardial conduction time within the left anterior descending coronary artery region (ischemic region) during myocardial ischemia and following reperfusion, and determined the frequency of ventricular fibrillation. RESULTS The effective refractory period in the ischemic region decreased during myocardial ischemia and decreased further immediately after reperfusion in the control group. The intra-myocardial conduction time in the ischemic region increased during myocardial ischemia but rapidly shortened after reperfusion in the control group. In the quinaprilat group, however, no significant differences were evident between the ischemic and non-ischemic regions in either the effective refractory period or the intra-myocardial conduction time during myocardial ischemia or following reperfusion. The percentage shortening of the effective refractory period and the percentage prolongation of the intra-myocardial conduction time in the ischemic region were significantly lower in the quinaprilat group than in the control group during myocardial ischemia and following reperfusion. The frequency of ventricular fibrillation during myocardial ischemia and following reperfusion was significantly lower in the quinaprilat group (21%) than in the control group (74%; P < 0.01). CONCLUSIONS Quinaprilat protects against electrophysiologic abnormalities, and may decrease arrhythmias during acute myocardial ischemia and following reperfusion.
Echocardiography-a Journal of Cardiovascular Ultrasound and Allied Techniques | 2017
Kenji Harada; Kazuhiro Mori; Chiyo Ichimiya; Naho Terada; Tsutomu Iima; Takafumi Harada; Kazutoshi Fujisawa; Atsushi Kawata; Ayumi Okada; Hirofumi Yamamoto; Hiroyuki Fujinaga
Double‐chambered left ventricle (DCLV) is a particularly rare congenital entity characterized by the presence of two ventricular cavities separated by an abnormal muscle band. An asymptomatic 15‐year‐old boy was referred to our hospital because of electrocardiographic (ECG) abnormalities. His initial transthoracic echocardiography (TTE) demonstrated a DCLV with mild left ventricular systolic dysfunction. During a 5‐year follow‐up period, he remained symptom free with no changes in ECG and conventional TTE findings. However, two‐dimensional speckle tracking echocardiography revealed a subtle progressive deterioration of left ventricular systolic function during the 5‐year follow‐up.
Echocardiography-a Journal of Cardiovascular Ultrasound and Allied Techniques | 2017
Kenji Harada; Ushio Tamura; Chiyo Ichimiya; Naho Terada; Yasuhiro Yokoyama; Norihito Kageyama; Akira Hirono; Yuya Hiroshima; Takeshi Omura; Hirofumi Yamamoto; Hiroyuki Fujinaga
A 76‐year‐old man was admitted to our emergency department owing to chest pain, which started immediately after lunch. Although electrocardiogram revealed ST‐segment elevation with hyperacute T‐wave changes in the anterior lead tracings, emergency coronary angiography revealed normal coronary arteries. Echocardiography revealed left ventricular (LV) compression with left ventricular obstruction (LVO) caused by an echogenic mass. Computed tomography clearly revealed compression of both left atrial (LA) and LV by a large hiatal hernia. A large hiatal hernia can induce cardiac symptoms resulting from cardiac compression. This case highlights a possible association between chest pain and LVO caused by a hiatal hernia.
Journal of the American College of Cardiology | 2015
Kenji Harada; Hiroyuki Fujinaga; Takanobu Okumura
Controlling Nutritional Status (CONUT), an easy-to-use nutrition assessment system which scores laboratory data including serum albumin, total cholesterol level and peripheral blood lymphocyte count, has been considered to be efficient for early detection of hospital undernutrition. Prior studies