Kazuma Ohyama

Increased Coronary Perivascular Adipose Tissue Volume in Patients With Vasospastic Angina

BACKGROUND Recent studies have suggested that coronary perivascular adipose tissue (PVAT) impairs coronary vasomotion, so we examined whether PVAT is increased at the spastic coronary segment in patients with vasospastic angina (VSA). METHODSANDRESULTS PVAT volume in the left anterior descending (LAD) coronary arteries on CT coronary angiography was significantly increased in 48 VSA patients with LAD spasm compared with 18 controls (30.7±2.0 vs. 21.0±3.2 cm(3), P=0.01), whereas that of total epicardial adipose tissue was comparable between the 2 groups. CONCLUSIONS The results suggested an important role of PVAT in the pathogenesis of coronary spasm. (Circ J 2016; 80: 1653-1656).

Enhanced Adventitial Vasa Vasorum Formation in Patients With Vasospastic Angina: Assessment With OFDI.

Coronary artery spasm plays important roles in the pathogenesis of a wide range of ischemic heart disease. Recent studies have demonstrated that coronary spasm is frequently noted in Caucasians as in Asians [(1)][1]. We previously demonstrated that vascular smooth muscle cell hypercontraction

Association of Coronary Perivascular Adipose Tissue Inflammation and Drug-Eluting Stent–Induced Coronary Hyperconstricting Responses in Pigs: 18 F-Fluorodeoxyglucose Positron Emission Tomography Imaging Study

Objective— Although coronary perivascular adipose tissue (PVAT) may play important roles as a source of inflammation, the association of coronary PVAT inflammation and coronary hyperconstricting responses remains to be examined. We addressed this important issue in a porcine model of coronary hyperconstricting responses after drug-eluting stent implantation with 18F-fluorodeoxyglucose (18F-FDG) positron emission tomographic imaging. Approach and Results— An everolimus-eluting stent (EES) was randomly implanted in pigs into the left anterior descending or the left circumflex coronary artery while nonstented coronary artery was used as a control. After 1 month, coronary vasoconstricting responses to intracoronary serotonin (10 and 100 &mgr;g/kg) were examined by coronary angiography in vivo, followed by in vivo and ex vivo 18F-FDG positron emission tomographic/computed tomographic imaging. Coronary vasoconstricting responses to serotonin were significantly enhanced at the EES edges compared with the control site (P<0.01; n=40). Notably, in vivo and ex vivo 18F-FDG positron emission tomographic/computed tomographic imaging and autoradiography showed enhanced 18F-FDG uptake and its accumulation in PVAT at the EES edges compared with the control site, respectively (both P<0.05). Furthermore, histological and reverse transcription polymerase chain reaction analysis showed that inflammatory changes of coronary PVAT were significantly enhanced at the EES edges compared with the control site (all P<0.01). Importantly, Rho-kinase expressions (ROCK1/ROCK2) and Rho-kinase activity (phosphorylated myosin phosphatase target subunit-1) at the EES edges were significantly enhanced compared with the control site. Conclusions— These results indicate for the first time that inflammatory changes of coronary PVAT are associated with drug-eluting stent–induced coronary hyperconstricting responses in pigs in vivo and that 18F-FDG positron emission tomographic imaging is useful for assessment of coronary PVAT inflammation.

Focal Vasa Vasorum Formation in Patients With Focal Coronary Vasospasm – An Optical Frequency Domain Imaging Study –

Coronary adventitia has attracted much attention as a source of inflammation because it harbors nutrient blood vessels, oronary artery spasm plays important roles in the pathogenesis of a wide range of ischemic heart disease, not only in vasospastic angina (VSA) but also in other forms of ischemic heart disease.1 Although VSA is believed to be more prevalent in Asian compared with Caucasian subjects,2 it has been recently suggested that the prevalence of VSA could be similar in both populations.3 Thus, coronary spasm is an emerging issue in the world. Furthermore, given C

Reply: New Aspects of Vasospastic Angina: Coronary Adventitial and Perivascular Adipose Tissue Inflammation

We greatly appreciate Dr. Ciliberti and colleagues and Drs. Antonopoulos and Antoniades for their interests and comments on our recent study “Coronary adventitial and perivascular adipose tissue inflammation in patients with vasospastic angina” [(1)][1]. First, in response to the comments by Dr

Absence of adventitial vasa vasorum formation at the coronary segment with myocardial bridge - An optical coherence tomography study

BACKGROUND Myocardial bridge (MB) is a myocardial bundle through which coronary segment tunnels and could compress coronary arteries causing myocardial ischemia. However, the characteristic structural findings of MB remain to be fully elucidated. Recently, we demonstrated that optical coherence tomography (OCT) enables us to visualize adventitial vasa vasorum (VV) formation in humans. In this study, we examined adventitial VV formation at the coronary segment with MB in humans using OCT. METHODS We examined 15 consecutive patients with suspected angina pectoris and MB in the left anterior descending (LAD) coronary arteries but no angiographic coronary stenosis. MB was detected on coronary angiography as a segment with milking effect. We performed intracoronary OCT imaging along the entire LAD. Morphometric analysis was performed at MB and proximal/distal segments at every 1mm. RESULTS OCT examination showed the absence of adventitial VV formation at MB in the LAD, while VV was clearly noted at both the proximal and distal reference segments. Adventitial VV area was significantly less at MB compared with the proximal or distal references. CONCLUSIONS These results with OCT imaging indicate that coronary segments with MB lack adventitial VV formation in humans, suggesting that MB could influence morphological and functional changes of the coronary artery.

Impact of epicardial adipose tissue volume quantified by non-contrast electrocardiogram-gated computed tomography on ergonovine-induced epicardial coronary artery spasm.

Article history: Received 27 September 2016 Accepted 11 October 2016 Available online xxxx [3–5]. These our findings indicated that not systemic but local adventitial inflammation including PVAT plays important roles in the pathogenesis of coronary spasm, and thus, it could be speculated that increased PVATV of the spastic coronary segment might result in enhanced overall EATV in the study by Ito and colleagues [1]. Although volumetric enlargement of the PVAT in the VSA patients

Development of a novel shock wave catheter ablation system—A validation study in pigs in vivo

Aims Although the radiofrequency catheter ablation (RFCA) is widely used for the treatment of tachyarrhythmias, it has three fundamental weaknesses as a thermal ablation system, including a limited lesion depth, myoendocardial injury linking to thromboembolism, and prolonged inflammation followed by subsequent recurrences. In order to overcome these limitations, we have been developing a shock wave (SW) catheter ablation (SWCA) system as a novel non-thermal therapy. In the present study, we validated our new SWCA system with increased SW intensity. Methods and results In a total of 36 pigs, we applied our new SWCA to ventricular muscle in vivo for the following protocols. (i) Epicardial approach (n = 17): The lesion depth achieved by the SWCA from the epicardium was examined. High intensity SW achieved 5.2 ± 0.9 mm lesions (35 applications), where there was a strong correlation between SW intensity and lesion depth (R = 0.80, P < 0.001, 54 applications). (ii) Endocardial approach (n = 6): The extent of endocardial injury with the two energy sources was examined by electron microscopy (8 applications each). Shock wave catheter ablation markedly reduced myoendothelial injury compared with RFCA (4.3 ± 1.2 vs. 79.6 ± 4.8%, P < 0.01). The electrophysiological effects on the SW lesions were also confirmed using three-dimensional mapping system. (iii) Time-course study (n = 6 each): The healing process after ablation therapy was examined. We found transient inflammatory responses and accelerated reparative process with preserved blood flow in the SWCA group. Conclusion These results indicate that our SWCA system is characterized, as compared with RFCA, by deeper lesion depth, markedly less myoendocardial injury and accelerated tissue repair process.

European Society of Cardiology (ESC) Annual Congress Report From Barcelona 2017

From August 26th to 30th, the 2017 Annual Congress of the European Society of Cardiology (ESC 2017) was held in Barcelona, Spain. Despite the terrorism tradegy just before the ESC congress, the congress attracted many medical professionals from all over the world to discuss the recent topics in cardiovascular medicine in more than 500 sessions, including COMPASS (Cardiovascular OutcoMes for People using Anticoagulation StrategieS Trial), CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study), and ORION (which assessed the effect of a novel siRNA inhibitor to PCSK9 on reductions in low-density lipoprotein cholesterol). Japanese cardiologists and the Japanese Circulation Society greatly contributed to the congress. This report briefly introduces some late-breaking registry results, late-breaking clinical trials, and ESC Guidelines from the ESC 2017 Congress.

Renal Denervation Suppresses Coronary Hyperconstricting Responses After Drug-Eluting Stent Implantation in Pigs In Vivo Through the Kidney–Brain–Heart Axis

Objective— Drug-eluting stent–induced coronary hyperconstricting responses remain an important issue. The adventitia harbors a variety of components that potently modulate vascular tone, including sympathetic nerve fibers (SNF) and vasa vasorum. Catheter-based renal denervation (RDN) inhibits sympathetic nerve activity. We, thus, examined whether RDN suppresses drug-eluting stent–induced coronary hyperconstricting responses, and if so, what mechanisms are involved. Approach and Results— Protocol 1: pigs implanted with everolimus-eluting stents into the left coronary arteries underwent coronary angiography at 1 month after implantation for assessment of coronary vasomotion and adventitial SNF formation. Drug-eluting stent–induced coronary hyperconstricting responses were significantly enhanced associated with enhanced coronary adventitial SNF and vasa vasorum formation. Protocol 2: pigs implanted with everolimus-eluting stents were randomly assigned to the RDN or sham group. The RDN group underwent renal ablation. At 1 month, RDN significantly caused marked damage of the SNF at the renal arteries without any stenosis, thrombus, or dissections. Notably, RDN significantly upregulated the expression of &agr;2-adrenergic receptor–binding sites in the nucleus tractus solitarius, attenuated muscle sympathetic nerve activity, and decreased systolic blood pressure and plasma renin activity. In addition, RDN attenuated coronary hyperconstricting responses to intracoronary serotonin at the proximal and distal stent edges associated with decreases in SNF and vasa vasorum formation, inflammatory cell infiltration, and Rho-kinase expression/activation. Furthermore, there were significant positive correlations between SNF and vasa vasorum and between SNF and coronary vasoconstricting responses. Conclusions— These results provide the first evidence that RDN ameliorates drug-eluting stent–induced coronary hyperconstricting responses in pigs in vivo through the kidney–brain–heart axis.