Daigo Hiraya's research while affiliated with University of Tsukuba and other places

Background: Women with acute myocardial infarction (AMI) often present a worse risk profile and experience a higher rate of in-hospital mortality than men. However, sex differences in post-discharge prognoses remain inadequately investigated. We examined the impact of sex on 1-year post-discharge outcomes in patients with AMI undergoing percutaneous coronary intervention. Methods and Results: We extracted patient-level data for the period January 2017–December 2018 from the J-PCI OUTCOME Registry, endorsed by the Japanese Association of Cardiovascular Intervention and Therapeutics. One-year all-cause and cardiovascular mortality and major adverse cardiovascular events were compared between men and women. In all, 29,856 AMI patients were studied, with 6,996 (23.4%) being women. Women were significantly older and had a higher prevalence of comorbidities than men. Crude all-cause mortality was significantly higher among women than men (7.5% vs. 5.4% [P<0.001] for ST-elevation myocardial infarction [STEMI]; 7.0% vs. 5.2% [P=0.006] for non-STEMI). These sex-related differences in post-discharge outcomes were attenuated after stratification by age. Multivariate analysis demonstrated an increase in all-cause mortality in both sexes with increasing age and advanced-stage chronic kidney disease (CKD). Conclusions: Within this nationwide cohort, women had worse clinical outcomes following AMI than men. However, these sex-related differences in outcomes diminished after adjusting for age. In addition, CKD was significantly associated with all-cause mortality in both sexes.

The establishment of a strategy for rapid heart recovery in patients with cardiogenic shock is required. Impella is a percutaneous left ventricular (LV) assist device that maintains hemodynamic stability and also causes LV mechanical unloading. However, the timing at which Impella should be started and a systematic strategy after the start of Impella have not been established. We report a representative case of dilated cardiomyopathy requiring catecholamines and intra-aortic balloon pumping (IABP). The hemodynamics were unstable under IABP support, and withdrawal from IABP or catecholamines was considered impossible. However, the exchange of the IABP with Impella CP made it possible to suppress the heart rate with ivabradine, introduce intensive heart failure medication, and discontinue catecholamines. The patient was weaned from Impella 24 days after the start of the first Impella CP. Rapid heart recovery was achieved with favorable outcomes. We present a comprehensive strategy for rapid heart recovery using Impella in a patient with cardiogenic shock.

A 74-year-old male who had undergone percutaneous coronary intervention over 20 years ago presented with chest pain and was diagnosed with ST elevation acute myocardial infarction. Emergency coronary angiography revealed occlusion of the middle left anterior descending artery (LAD) (panel A, blue arrow), a growing vascular network above the LAD (panel A, white arrows, Supplementary data online, Video S1), and coronary aneurysms (panel B, yellow arrows). Balloon dilatation was performed for the LAD, resulting in thrombolysis in myocardial infarction flow Grade 3. Contrast-enhanced computed tomography (CT) showed a large mass lesion above the LAD (panel C, white arrows, Supplementary data online, Video S2), pericoronary arteritis (panel D, yellow arrows), and abdominal aortic aneurysm (AAA) (panel E, yellow arrow). Fluorodeoxyglucose positron emission tomography-CT demonstrated high uptake in the mass lesion, and the maximum standardized uptake value was 10.19 (panel F, white arrows). On the other hand, no uptake was observed in the AAA (panel G, yellow arrow). The patient had a markedly elevated immunoglobulin G4 (IgG4) level of 687 mg/dL. The patient underwent endovascular aortic repair for the AAA. However, the patient did not receive corticosteroid therapy for IgG4-related disease, because corticosteroids are ineffective in already well-developed aneurysms, and might even thin the aneurysm walls and increase the risk of rupture.1,2 The patient had no cardiovascular events for 1 year. IgG4-related disease can present with a variety of clinical manifestations, including coronary aneurysms, pericoronary arteritis, and mass formation.³ Optimal treatment for patients with IgG4-related disease and aneurysms remains controversial.

A 63-year-old man with a hobby of full marathon and triathlon fainted while commuting on a 25-km one-way bicycle trip and was admitted to the hospital after return of spontaneous circulation. The patient was diagnosed with acute coronary syndrome, and contrast-enhanced computed tomography for trauma diagnosis indicated suspicion of liver injury. Although coronary angiography revealed a severe stenotic lesion in the left anterior descending artery, percutaneous coronary intervention (PCI) was deferred because of thrombolysis in myocardial infarction grade 3 flow. Following neurological recovery, the patient was started on dual antiplatelet therapy (aspirin and clopidogrel). On day 11, a 3.0/34-mm Resolute Onyx stent (Medtronic, Dublin, Ireland) was deployed following rotablation. As a pre-discharge evaluation, a maximum-load cardiopulmonary exercise test was performed 8 days after PCI. However, the patient developed stent thrombosis after 2 h. Subsequently, the patient was diagnosed as a clopidogrel poor metabolizer using a blood test. Learning objective Existing guidelines recommend a cardiopulmonary exercise test (CPET) before or immediately after the discharge of patients with acute coronary syndrome (ACS). However, the safety of the maximum-load CPET has not been established, especially in clopidogrel poor metabolizers with ACS. Acute maximal exercise induces platelet aggregation; therefore, further discussion is needed regarding the timing of CPET, exercise load level, and patient observation post-CPET in ACS patients after stent placement.

The posterior circumflex humeral artery, a branch of the axillary artery, is compressed by the humeral head during repeated abduction and external rotation of the shoulder joint owing to its anatomical structure. This damages the vascular endothelium, resulting in thrombi, arterial dissection, and aneurysms, a condition known as posterior, circumflex humeral artery pathological lesions. A thrombus may form at the site and becomes a peripheral embolus, resulting in peripheral arterial occlusion.A 21-year-old right-handed elite man college volleyball player noticed coldness and pain in his right hand during a game. Cyanosis was present except in the middle finger, and the beating radial artery was palpable; however, the ulnar artery was not. Doppler ultrasound examination revealed thrombus occlusion of the ulnar artery and common palmar artery of the index finger. Peripheral arterial occlusion was diagnosed due to embolization of a thrombus from this site. The patient stopped practicing volleyball immediately after the onset of symptoms and was started on cilostazol 200 mg and rivaroxaban 15 mg. Subjective coldness of the fingers improved one week after the start of treatment. The patient resumed practice four weeks after the start of treatment and participated in a game by the seventh week.Posterior circumflex humeral artery pathological lesions are caused by overhead motions such as pitching. They are most commonly reported in athletes playing volleyball, although rare, and many cases of aneurysm formation have been reported.Observing a cold sensation in the periphery after practice is necessary for screening.

Objectives To investigate the relationship between periprocedural myocardial injury (PMI) and plaque characteristics detected by multidetector computed tomography (MDCT) and cardiac magnetic resonance imaging (CMR).Materials and methodsThis observational retrospective study, between July 2012 and October 2019, included chronic coronary syndrome patients undergoing elective percutaneous coronary intervention (PCI) after MDCT and CMR. High-intensity plaque (HIP) on non-contrast T1-weighted imaging was defined as a coronary plaque-to-myocardium signal intensity ratio of ≥ 1.4. High-risk plaque (HRP) in MDCT displayed ≥ 2 features: positive remodeling, low-attenuation plaque, spotty calcification, and napkin-ring sign. PMI was defined as an increase in cardiac troponin T levels > 5 times the upper normal limit at 24 h after PCI.ResultsNinety-five target lesions in 76 patients (mean age ± standard deviation, 67 years ± 9; 62 males [82%]) were included. Twenty-one patients (24 lesions) were assigned to the PMI group, while 55 patients (71 lesions) to the non-PMI group. Presence of HRP characteristics on MDCT and HIP on CMR was significantly higher in the PMI group. Multivariate logistic regression analysis showed that HRP in MDCT and HIP in CMR were significant independent predictors of PMI. Target lesions with HRP on MDCT and HIP on CMR were significantly more likely to develop PMI. In 141 plaques with ≥ 50% stenosis (76 patients), patients with PMI had significantly more frequent HRP in MDCT and HIP in CMR in target and non-target lesions.ConclusionsMDCT and CMR can play an important role in the detection of high-risk lesions for PMI following elective PCI.Key Points • Multivariate logistic regression analysis showed that high-risk plaque on MDCT and high-intensity plaque on MRI were significant independent predictors of periprocedural myocardial injury (PMI). • Target lesions with high-risk plaque on MDCT and high-intensity plaque on CMR were significantly more likely to develop PMI. • In 141 plaques with ≥ 50% stenosis, patients with PMI were significantly more likely to have high-risk plaques on MDCT and high-intensity plaque on CMR in target and non-target lesions.

An 82-year-old man was referred to our department for angina with an abnormal perfusion scan. Coronary computed tomography angiography showed severe stenosis with napkin-ring sign, positive remodelling, and low-attenuation plaques in the proximal right coronary artery (RCA; Panel A). Non-contrast T1-weighted magnetic resonance imaging (T1WI MRI) revealed high-intensity plaque (HIP) in the same lesion (see Supplementary data online, Video A, Panel B). Coronary angiogram showed severe stenosis in the proximal and distal RCA (Panel C). Hence, an elective percutaneous coronary intervention (PCI) was performed with a distal protection device. After stent deployment, a slow-flow phenomenon was observed. However, the defect disappeared after the device was retrieved. Non-obstructive general angioscopy (NOGA) after stenting showed plaque prolapse through the stent struts (Panel D). After PCI, a large amount of debris was collected on the device filter (Panel E), and cholesterol...

Electrocardiogram (ECG) findings showing ST-segment depression in a wide range of leads and ST-segment elevation in aVR are found in patients with acute coronary syndrome with multivessel coronary lesions and left main trunk lesions. A 64-year-old man with a history of eosinophilic granulomatosis presented with chest pain and dyspnea. Although an ECG showed the above findings, he was diagnosed with acute severe aortic regurgitation (AR) complicating aortic root dissection and successfully underwent urgent Bentall operation. These ECG findings indicated that acute severe AR caused subendocardial ischemia.

Background Nilotinib, a second-generation BCR-ABL tyrosine kinase inhibitor (TKI), is highly effective in the treatment of patients with chronic myeloid leukemia (CML), despite being more vasculotoxic than older TKIs such as imatinib. Herein, we present a case of nilotinib-associated vasospastic angina confirmed by an acetylcholine spasm provocation test. Case presentation A 62-year-old CML patient treated with 300 mg nilotinib twice daily complained of several episodes of rest angina and was hospitalized at our institution. Coronary angiography revealed no severe organic stenosis, and the acetylcholine spasm provocation test confirmed the diagnosis of vasospastic angina. Although treatment with a calcium channel blocker and nicorandil reduced the frequency of chest pain, angina symptoms continued to occur. At 10 months post discharge, the patient complained of increased frequency of angina; therefore, the nilotinib dosage was reduced to 150 mg twice daily. Consequently, the patient reported a significant improvement in chest symptoms. Conclusions This case report highlights the potential vasculotoxic effects of nilotinib. Cardiologists and hematologists should be vigilant for coronary artery spasm as a possible vascular adverse event caused by nilotinib.