Hidenori Komiyama

Calcified nodules (CNs) are challenging lesions in percutaneous coronary intervention (PCI), often requiring repeated interventions after balloon angioplasty. The biomechanical behavior of CNs remains poorly characterized, limiting the development of optimized strategies. This study aimed to evaluate the time-dependent mechanical response of CNs using a viscoelastic finite element model. A coronary artery segment with a protruding CN was modeled, with distinct material properties for the vessel wall and nodule. A Voigt-type viscoelastic model was applied, and internal pressure was simulated on both the luminal and nodule surfaces. Simulations were performed for short (15 s) and prolonged (120 s) inflation durations. The results demonstrated that the calcified region exhibited viscoelastic creep, with displacement accumulating over time under constant pressure. Notably, prolonged inflation led to a greater increase in luminal area compared to short inflation. These findings suggest that CNs deform gradually due to time-dependent mechanical behavior, and that prolonged balloon inflation may facilitate improved luminal expansion. This study provides a mechanics-informed rationale for incorporating inflation duration into PCI strategy for CNs.

Peripheral artery disease (PAD) compromises walking and physical activity, which results in further loss of skeletal muscle. The cross-sectional area of the thigh muscle has been shown to be correlated with systemic skeletal muscle volume. In our previous pilot study, we observed an increase in thigh muscle mass following endovascular treatment (EVT) in patients with proximal vascular lesions affecting the aortoiliac and femoropopliteal arteries. Considering the potential interactions between skeletal muscle, lipid profile, and glucose metabolism, we aimed to investigate the relationship between thigh muscle mass and apolipoproteins as well as glucose metabolism in PAD patients undergoing EVT. This study is a prespecified sub-study conducted as part of a pilot study. We prospectively enrolled 22 symptomatic patients with peripheral artery disease (PAD) and above-the-knee lesions, specifically involving the blood vessels supplying the thigh muscle. The mid-thigh muscle area was measured with computed tomography before and 6 months after undergoing EVT. Concurrently, we measured levels of apolipoproteins A1 (Apo A1) and B (Apo B), fasting blood glucose, 2 h post-load blood glucose (using a 75 g oral glucose tolerance test), and glycated hemoglobin A1c (HbA1c). Changes in thigh muscle area (delta muscle area: 2.5 ± 8.1 cm²) did not show significant correlations with changes in Apo A1, Apo B, fasting glucose, 2 h post-oral glucose tolerance test blood glucose, HbA1c, or Rutherford classification. However, among patients who experienced an increase in thigh muscle area following EVT (delta muscle area: 8.41 ± 5.93 cm²), there was a significant increase in Apo A1 (pre: 121.8 ± 15.1 mg/dL, 6 months: 136.5 ± 19.5 mg/dL, p < 0.001), while Apo B remained unchanged (pre: 76.4 ± 19.2 mg/dL, 6 months: 80.5 ± 4.9 mg/dL). Additionally, post-oral glucose tolerance test 2 h blood glucose levels showed a decrease (pre: 189.7 ± 67.5 mg/dL, 6 months: 170.6 ± 69.7 mg/dL, p = 0.075). Patients who exhibited an increase in thigh muscle area demonstrated more favorable metabolic changes compared to those with a decrease in thigh muscle area (delta muscle area: −4.67 ± 2.41 cm²). This pilot sub-study provides insights into the effects of EVT on thigh muscle, apolipoproteins, and glucose metabolism in patients with PAD and above-the-knee lesions. Further studies are warranted to validate these findings and establish their clinical significance. The trial was registered on the University Hospital Medical Information Network Clinical Trials Registry (UMIN000047534).

Background and Aims: As the population of aging societies continues to grow, the prevalence of complex coronary artery diseases, including calcification, is expected to increase. Rotational atherectomy (RA) is an essential technique for treating calcified lesions. This study aimed to assess the usefulness of the drilling noise produced during rotablation as a parameter for evaluating the safety and effectiveness of the procedure.Methods: A human body model mimicking calcified stenotic coronary lesions was constructed using plastic resin, and burrs of sizes 1.25 and 1.5 mm were utilized. To identify the noise source during rotablation, we activated the ROTAPRO™ rotablator at a rotational speed of 180,000 rpm, recording the noise near the burr (inside the mock model) and advancer (outside). In addition to regular operation, we simulated two major complications: burr entrapment and guidewire transection. The drilling noise recorded in Waveform Audio File Format files was converted into spectrograms for analysis and an autoencoder analyzed the image data for anomalies.Results: The drilling noise from both inside and outside the mock model was predominantly within the 3000 Hz frequency domain. During standard operation, intermittent noise within this range was observed. However, during simulated complications, there were noticeable changes: a drop to 2000 Hz during burr entrapment and a distinct squealing noise during guidewire transection. The autoencoder effectively reduced the spectrogram data into a two‐dimensional representation suitable for anomaly detection in potential clinical applications.Conclusion: By analyzing drilling noise, the evaluation of procedural safety and efficacy during RA can be enhanced.

Peripheral artery disease impairs walking and physical activity, resulting in further loss of skeletal muscle. However, peripheral artery disease can be treated with endovascular treatment. The thigh muscle has been shown to correlate with systemic skeletal muscle volume. We assessed the changes in the metabolism of apolipoproteins A1 and B, blood glucose, and thigh muscle mass after endovascular treatment in above-the-knee peripheral artery disease where vessels supply the thigh muscle. Mid-thigh muscle volume was measured with computed tomography before and at 6 months after endovascular treatment. Apolipoproteins A1 and B, fasting blood glucose, post-load (75 g oral glucose tolerance test) 2 h-blood glucose, and glycated hemoglobin A1c (HbA1c) levels were measured concomitantly. The relationships between changes in apolipoproteins A1, apolipoproteins B, blood glucose, post-oral glucose tolerance test 2 h-blood glucose, Rutherford classification, and gain or loss of thigh muscle were investigated. Thigh muscle mass did not correlate with changes in apolipoproteins A1, B, fasting glucose, post-oral glucose tolerance test 2 h-blood glucose, HbA1c, and Rutherford classification. Among patients with muscle gain post-endovascular treatment, apolipoproteins A1 increased significantly, while apolipoproteins B levels were similar. Post-oral glucose tolerance test 2 h-blood glucose levels decreased. Preferable metabolic changes were observed in patients with skeletal muscle gain contrasted with muscle loss.

Background: Peripheral artery disease (PAD), intermittent claudication, and impaired mobility lower patients’ quality of life, contributing to the loss of skeletal muscle. This study sought to investigate the impact of endovascular treatment (EVT) by measuring the mid-thigh level of muscle volume in above the knee PAD patients before and after EVT.Methods: In this prospective, observational study, symptomatic PAD patients with above the knee lesions who had intermittent claudication and were undergoing optimal medical treatment were enrolled. The mid-thigh level of muscle area was measured by computed tomography initially, and then 3 and 6 months after EVT. Patients were categorized into ipsilateral or bilateral based on clinical symptoms and initial ABI value. The muscle area in ischemic and non-ischemic legs were compared in ipsilateral PAD patients. The correlations between alterations in the total thigh muscle area and clinical characteristics were analyzed in univariable and multivariable analysis to investigate the factor contributing skeletal muscle loss.Results: A total of 22 patients were analyzed. The muscle area of the thighs increased after EVT. Fourteen patients had ipsilateral lesions and 8 had bilateral stenosis. In patients with ipsilateral lesions, the mid-thigh muscle area of ischemic lower limbs was significantly lesser than that of non-ischemic lower limbs (118.2±16.5 cm² vs 124.0±17.3 cm², p=0.0002). The thigh muscle area of ischemic lower limbs increased after EVT (before: 118.2±16.5 cm² vs 3 months: 124.0±18.7 cm², p=0.0166; before vs 6 months: 123.0±17.7 cm², p= 0.0566), but this was not the case for non-ischemic lower limbs. Multivariate regression analysis revealed that baseline glycated hemoglobin was the only factor that negatively correlated with the change in the muscle area after 3 (β= -3.74, 95% confidence interval [CI] = -7.3 to -0.2, p=0.0417) and 6 months (β= -5.24, 95%CI = -10.1 to -0.4, p=0.03567). Muscle area significantly increased in normoglycemic HbA1c < 6.5 patients (before: 246.1±33.5 cm², before vs 3 months: 249.6±34.6 cm², p = 0.032, before vs 6 months: 250.6±35.7 cm², p = 0.0455) while there was no significant alternation in hyperglycemic (HbA1c ≥ 6.5) patients (before: 225.2±43.4 cm², 3 months: 224.6±44.8 cm², 6 months: 222.2±45.5 cm²).Conclusions: Ischemia induces muscle atrophy in PAD patients. However, ischemic muscle atrophy was ameliorated after EVT in normoglycemic patients. There is a need for large scale trial to investigate the impact of EVT if it would protect or even delay skeletal muscle loss in all-comer population.

We investigated the influence of geographical predisposition on the spatial distribution and composition of coronary plaques. Thirty coronary arteries were evaluated. A total of 1441 cross-sections were collected from intravascular ultrasound (IVUS) and radio-frequency signal-based virtual histology (VH-IVUS) imaging. To exclude complex geographical effects of side branches and to localise the plaque distribution, we analysed only eccentric plaques in non-branching regions. The spatial distribution of eccentric plaques in the coronary artery was classified into myocardial, lateral, and epicardial regions. The composition of eccentric plaques was analysed using VH-IVUS. The plaque was concentric in 723 sections (50.2%) and eccentric in 718 (49.9%). Eccentric plaques were more frequently distributed towards the myocardial side than towards the epicardial side (46.7 ± 7.5% vs. 12.5 ± 4.2%, p = 0.003). No significant difference was observed between the myocardial and lateral sides (46.7 ± 7.5% vs. 20.8 ± 5.0%) or between the lateral and epicardial sides. Eccentric thin-capped fibroatheromas were more frequently distributed towards the myocardial side than towards the lateral side (p = 0.024) or epicardial side (p = 0.005). Geographical predisposition is associated with distribution, tissue characterisation, and vulnerability of plaques in non-branching coronary arteries.

The Official Journal of EuroPCR and the European Association of Percutaneous Cardiovascular Interventions (EAPCI)

Mast cells are widely distributed in the body and affect their surrounding environment through degranulation and secretion of cytokines. Conversely, mast cells are influenced by environmental stimuli such as cyclical mechanical stretch (CMS), such as that induced by heartbeat and respiration. Peripherally distributed mast cells are surrounded by extracellular matrix, where they bind IgE on their surface by expressing the high‐affinity Fc receptor for IgE (FcεRI), and they release mediators after cross‐linking of surface‐bound IgE by allergen. To analyse how CMS affects mast cell responses, we examined the effect of applying CMS on the behaviour of IgE‐bound mast cells (RBL‐2H3 cell line) adhering to fibronectin as a substitute for extracellular matrix. We found that CMS enhanced FcεRI‐mediated secretion in the presence of antigen (2,4‐dinitrophenol–bovine serum albumin). CMS increased expression of IL‐4 mRNA and secretion of IL‐4 protein. Western blot analysis showed that CMS changes the signal transduction in mitogen‐activated protein kinases and AKT, which in turn alters the regulation of IL‐4 and increases the secretion of IL‐4. These results suggest that CMS modulates the effect of mast cells on inflammation and resultant tissue remodelling. Understanding how CMS affects mast cell responses is crucial for developing therapies to treat mast cell‐related diseases. Copyright © 2013 John Wiley & Sons, Ltd.