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Our aim was to analyze the incidence of P-wave abnormalities in embolic and non-embolic strokes, and evaluate its clinical usefulness for predicting stroke etiology.We included 376 consecutive patients hospitalized for acute ischemic stroke from January 2015 to September 2021. Among the patients in sinus rhythm at admission, 31 had ischemic stroke due to atrial fibrillation (AF)-related embolism, 59 had embolic stroke of unknown source (ESUS), and 143 had non-embolic stroke. P-wave abnormalities were defined as 1. P-wave axis abnormality (PWAA); 2. P-wave terminal force in Vsub1/sub(PTFV1) ≤ -4000 μV*ms; 3. advanced inter-atrial block (A-IAB).The prevalence of each type of abnormality was consistently lower in patients with non-embolic stroke than in those with AF-related embolism (AF-related vs. ESUS vs. non-embolic; PWAA, 45% vs. 20% vs. 14%; PTFV1, 36% vs. 37% vs. 15%; and A-IAB, 55% vs. 31% vs. 13%, respectively). The identification of at least one type of P-wave abnormality improved the sensitivity compared to using a single abnormality parameter (sensitivity 72%, specificity 62%), while at least two types of abnormality had low sensitivity, but high specificity (sensitivity 29%, specificity 95%). Multivariate regression analysis revealed that identification of at least one type of P-wave abnormality was independently associated with embolic stroke (odds ratio 3.11, 95%CI 1.46-6.63).The incidence of each type of P-wave abnormality was significantly lower in patients with non-embolic stroke. A combination of PWAA, PTFV1, and A-IAB parameters could be useful for distinguishing embolic from non-embolic stroke.

Objective Early recurrence (ER) after pulmonary vein isolation (PVI) for atrial fibrillation (AF) is expected to resolve within the recommended 3-month blanking period, irrespective of the ablation device used. To compare the occurrence and relationship of AF within the blanking period and subsequent late recurrence (LR) with radiofrequency (RF) and cryoballoon (CB) ablation. Methods A retrospective analysis of 294 patients (mean age=62±9, 70.0% male) undergoing PVI for drug-refractory paroxysmal AF was done. After categorizing the patients into the RF group (n=152) and the CB group (n=142), a group-wise comparison was done to investigate the impact of ER on LR throughout a 2-year follow-up. Results The groups were similar regarding the occurrence of ER (RF=22.4%, CB=24.6%, p=0.62), while LR was significantly higher in the RF group (p=0.003). ER was associated with LR in the RF group (p0.01) but not in the CB group (p=0.08), while a significant independent association with an increased LR risk was observed [hazard ratio (HR) 6.12; 95% confidence interval (CI) 3.56-10.51, p0.01]. RF ablation also significantly increased the risk of LR (HR=2.93; 95% CI=1.64-5.23, p0.01). Conclusion A recurrence of atrial arrhythmia is more frequent with RF-PVI than with CB-PVI for patients with paroxysmal AF. ER and RF-ablation are strong predictors for LR after the 3-month blanking period.

Interventional radiology (IR) procedures tend to be complex, which delivers high radiation exposure to patient. In the present study, we measured the radiation exposure dose [Hp(3)] in the eye using a direct eye dosemeter placed next to the physician’s eye during procedures. Physicians wore a direct eye dosemeter just lateral to eyes and an additional direct eye dosemeter outside the radiation protective eyeglasses close to their eyes. Additionally, a neck glass badge was worn at the neck. Although we found a positive correlation between the left neck glass badge dose [Hp(0.07)] and the left eye lens dose [Hp(3)], the value of R2 of the regression equation were 0.62 and 0.71 (outside and inside). We thought that the exact eye lens dose might not be estimated from the neck glass badge. In conclusion, a correct evaluation of the lens dose [Hp(3)] using the direct eye dosemeter is recommended for tachyarrhythmia physicians.

Background Vascular inflammation plays a fundamental role in most vascular diseases including atherosclerosis and vasculitis syndrome, in which arterial wall vascularization (AWV) frequently develops. Visualization of AWV is informative in detecting the vascular inflammation but is challenging. A new ultrasound technique (superb micro-vascular imaging [SMI]) allows the detection of extremely low-velocity flows. We examined an availability of SMI for assessment of the instability of atherosclerotic plaques and the activity of Takayasu arteritis (TA). Methods and results The study consists of two independent and consecutive parts A and B, examined in carotid stenosis (A) and TA (B), respectively. In part A, 12 patients with symptomatic severe carotid stenosis (CS group) scheduled for carotid endarterectomy were enrolled. In six of 12 patients, preoperative ultrasonography with SMI showed intraplaque neovascularization at the plaque shoulder. Postoperatively, histopathology confirmed the neovessels at the corresponding sites of visualized AWV. SMI had a sensitivity of 67%, specificity of 90% for detection of AWV in CS group. In SMI analysis, false positive findings were caused by motion artifact and arterial wall calcification, and a false negative finding is attributed by intraplaque hemorrhage. In part B, 10 patients with TA were enrolled. All patients underwent 18F-FDG-PET/CT, and its vascular uptake were compared with AWV detected by SMI. Bilateral common carotid arteries (CCA), internal carotid arteries and common iliac arteries were examined by SMI. Active vascular 18F-FDG uptake (max SUV >2.1) were found at five sites in three patients, which were not significantly correlated with the prevalence of macaroni sign, increase in C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Of note, SMI revealed AWV at five sites corresponding to uptake of 18F-FDG, with a sensitivity/specificity of 100% and 98%, positive predictive value 71%, and a negative predictive value 100%. Conclusion SMI enables visualization of AWV at vulnerable plaque in CS patients and at 18F-FDG positive sites in TA patients. SMI has potential as a modality to detect the vascular inflammation. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Grant-in-Aid for Scientific Research, Japan

In a previous study, we reported on a novel (prototype) real-time patient dosimeter with non-toxic phosphor sensors. In this study, we developed new types of sensors that were smaller than in the previous prototype, and clarified the clinical feasibility of our newly proposed dosimeter. Patient dose measurements obtained with the newly proposed real-time dosimeter were compared with measurements obtained using a calibrated radiophotoluminescence glass reference dosimeter (RPLD). The reference dosimeters were set at almost the same positions as the new real-time dosimeter sensors. We found excellent correlations between the reference RPLD measurements and those obtained using our new real-time dosimeter (r2 = 0.967). However, the new type of dosimeter was found to underestimate radiation skin dose measurements when compared with an RPLD. The most probable reason for this was the size reduction in the phosphor sensor of the new type of dosimeter. We believe that, as a result of reducing the phosphor sensor size, the backscattered X-ray irradiation was underestimated. However, the new dosimeter can accurately determine the absorbed dose by correcting the measured value with calibration factors. The calibration factor for the new type dosimeter was determined (by linear regression) to be ~1.15. New real-time patient dosimeter design would be an effective tool for the real-time measurement of patient skin doses during interventional radiology treatments.

Recently, an increasing attention has been paid to foot microcirculation in critical limb ischemia (CLI). Although skin perfusion pressure (SPP) is the most frequently used marker of microcirculation, SPP is often unmeasurable at the most ischemic site in the foot. A new ultrasound technique (superb

The number of implanted cardiac devices has been growing steadily over the last several years. Systems to monitor device data remotely have been introduced with the goal of reducing follow-up burden for both patients and physicians. Since the introduction of telemedicine depends greatly on the situations that are unique to each country, the acceptance of cardiac device remote monitoring in Japan was analyzed.A total of 203 patients who had previously undergone cardiac device implantation were enrolled. The subjects were provided with a CareLink Monitor that performed interrogation and transmission of device data at home, and then the physicians reviewed the data via a website at one and 3 months after baseline visits. A total of 470 transmissions were made. Questionnaires were completed by subjects and physicians to evaluate acceptance, ease of use, and satisfaction with the system. More than 87% of the subjects felt the Monitor was easy to use and nearly all of the physicians were satisfied with the system. A majority of patients felt reassured by having their devices assessed from a remote location and preferred the decreased number of clinic visits that were possible when using the Monitor. The patients spent an average of 168.2 minutes per clinic visit, whereas follow-up time was reduced to 13.0 minutes by remote monitoring. Physician consultation time was reduced by 2.7 minutes.The CareLink Network was well accepted by both the patients and physicians. Underlying issues did emerge, but once they are overcome, the system appears to have great potential to improve the quality of care given by healthcare providers.

Thrombin (Thromb), activated as part of the clotting cascade, dilates conduit arteries through an endothelial pertussis toxin (PTX)-sensitive G-protein receptor and releases nitric oxide (NO). Thromb also acts on downstream microvessels. Therefore, we examined whether Thromb dilates human coronary arterioles (HCA). HCA from right atrial appendages were constricted by 30–50% with endothelin-1. Dilation to Thromb (10−4–1 U/ml) was assessed before and after inhibitors with videomicroscopy. There was no tachyphylaxis to Thromb dilation (maximum dilation = 87.0%, ED50 = 1.49 × 10−2). Dilation to Thromb was abolished with either hirudin or denudation but was not affected by PTX. Neither N ω-nitro-l-arginine methyl ester ( n = 7), indomethacin ( n = 9),1H-[1,2,4] oxadiazolo-[4,3-a]quinoxalin-1-one ( n = 6), tetraethylammonium chloride ( n = 5), nor iberiotoxin ( n = 4) reduced dilation to Thromb. However, KCl (maximum dilation = 89 ± 5 vs. 20 ± 10%; P < 0.05; n = 7), tetrabutylammonium chloride (maximum dilation = 79 ± 7 vs. 21 ± 4%; P < 0.05; n = 5), and charybdotoxin (maximum dilation = 89 ± 4 vs. 10 ± 2%; P < 0.05; n = 4) attenuated dilation to Thromb. In contrast to animal models, Thromb-induced dilation in human arterioles is independent of Gi-protein activation and NO release. However, Thromb dilation is endothelium dependent, is maintained on consecutive applications, and involves activation of K+ channels. We speculate that an endothelium-derived hyperpolarizing factor contributes to Thromb-induced dilation in HCA.

陳旧性心筋梗塞 (OMI) , 拡張型心筋症 (DCM) におけるQTc dispersion (QTcd) と心室性不整脈との関連性, QTcdとJTc dispersion (JTcd) および貫壁性のばらつきの指標とされるTransmural dispersion of repolarization (胸部誘導におけるT波頂点とT波終末点の差の最大値をTDRcmaxとして算出) との関連性, さらにQTcdと心機能との関連性について検討した, 対象はOMI: 61例, DCM: 20例 (男性59例, 女性22例, 平均年齢65.8±13.4歳) .12誘導心電図よりフクダ電子社製QT計測ソフトを用い, QTcdを自動計測し, JTcd, TDRcmaxを算出し, 心エコー図より左室駆出率, 左室拡張終期径を, OMIではasynergy scoreを算出した上OMI, DCMでは心室頻拍の有無に関するQTc dispersionのcut off値を70msecに設定することにより, 心室頻拍の有力な予知因子となる可能性が示唆された.OMlではQTcdはJTcd, TDRcmax, 心機能指標と有意な相関を示し, DCMではTDRcmaxを除く各指標と有意な相関を示した.OMI, DCMではQTcdは脱分極相より再分極相の不均一性を示し, また, 心機能指標としての有用性が示唆された.OMIでは貫壁性の再分極不均一性の存在が示唆された.

Hyperglycemia is associated with impaired endothelium-dependent dilation that is due to quenching of NO by superoxide (O 2 · − ). In small coronary arteries (CAs), dilation depends more on smooth muscle hyperpolarization, such as that mediated by voltage-gated K + (Kv) channels. We determined whether high glucose enhances O 2 ·− production and reduces microvascular Kv channel current and functional responses. CAs from Sprague-Dawley rats were incubated 24 hours in medium containing either normal glucose (NG, 5.5 mmol/L d -glucose), high glucose (HG, 23 mmol/L d -glucose), or l -glucose (LG, 5.5 mmol/L d -glucose and 17 mmol/L l -glucose). O 2 ·− production was increased in HG arteries. Whole-cell patch clamping showed a reduction of 4-aminopyridine (4-AP)–sensitive current (Kv current) from smooth muscle cells of HG CAs versus NG CAs or versus LG CAs (peak density was 9.95±5.3 pA/pF for HG versus 27.8±6.8 pA/pF for NG and 28.5±5.2 pA/pF for LG; P 2 ·− generation (xanthine+xanthine oxidase) decreased K + current density, with no further reduction by 4-AP. Partial restoration was observed with superoxide dismutase and catalase. Constriction to 3 mmol/L 4-AP was reduced in vessels exposed to HG (13±5%, P 2 ·− -induced impairment may reduce vasodilator responsiveness in the coronary circulation of subjects with coronary disease or its risk factors.

Adrenomedullin (ADM) is a vasodilator produced by vascular endothelium and smooth muscle cells. Although plasma ADM levels are increased in patients with hypertension, heart failure, and myocardial infarction, little information exists regarding the microvascular response to ADM in the human heart. In the present study we tested the hypothesis that ADM produces coronary arteriolar dilation in humans and examined the mechanism of this dilation. Human coronary arterioles were dissected and cannulated with micropipettes. Internal diameter was measured by video microscopy. In vessels constricted with ACh, the diameter response to cumulative doses of ADM (10−12–10−7 M) was measured in the presence and absence of human ADM-(22–52), calcitonin gene-related peptide-(8–37), N ω-nitro-l-arginine methyl ester (l-NAME), indomethacin (Indo),1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one, SQ-22536, or KCl (60 mM). ADM dilated human coronary arterioles through specific ADM receptors (maximum dilation = 69 ± 11%).l-NAME or N-monomethyl-l-arginine attenuated dilation to ADM (for l-NAME, maximum dilation = 66 ± 7 vs. 41 ± 13%, P < 0.05). Thus the mechanism of ADM-induced dilation involves generation of nitric oxide. However, neither1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one, SQ-22536, nor Indo alone altered dilation to ADM. High concentrations of KCl blocked dilation to ADM. The magnitude of ADM dilation was reduced in subjects with hypertension. We propose that, in human coronary arterioles, ADM elicits vasodilation in part through production of nitric oxide and in part through activation of K+ channels, with little contribution from adenylyl cyclase. The former dilator mechanism is independent of the more traditional pathway involving activation of soluble guanylate cyclase.

The number of implanted cardiac devices has been growing steadily over the last several years. Systems to monitor device data remotely have been introduced with the goal of reducing follow-up burden for both patients and physicians. Since the introduction of telemedicine depends greatly on the situations that are unique to each country, the acceptance of cardiac device remote monitoring in Japan was analyzed.A total of 203 patients who had previously undergone cardiac device implantation were enrolled. The subjects were provided with a CareLink Monitor that performed interrogation and transmission of device data at home, and then the physicians reviewed the data via a website at one and 3 months after baseline visits. A total of 470 transmissions were made. Questionnaires were completed by subjects and physicians to evaluate acceptance, ease of use, and satisfaction with the system. More than 87% of the subjects felt the Monitor was easy to use and nearly all of the physicians were satisfied with the system. A majority of patients felt reassured by having their devices assessed from a remote location and preferred the decreased number of clinic visits that were possible when using the Monitor. The patients spent an average of 168.2 minutes per clinic visit, whereas follow-up time was reduced to 13.0 minutes by remote monitoring. Physician consultation time was reduced by 2.7 minutes.The CareLink Network was well accepted by both the patients and physicians. Underlying issues did emerge, but once they are overcome, the system appears to have great potential to improve the quality of care given by healthcare providers.

Background Patients with certain CYP2C9 genetic variants have increased sensitivity to warfarin and are at increased risk of over-coagulation with standard warfarin dose. We report over-anticoagulation and hematuria manifest as a slow increase in the international normalized ratio (INR) due to warfarin treatment in a patient with the CYP2C9*3/*3 allele. Case A 58-y-old man with paroxysmal atrial fibrillation received a standard warfarin dose of 2.0 mg/day. Because INR was 2.00 one week after treatment initiation, he was discharged from the hospital. One month later, hematuria was present and INR had increased to 7.26. Although in normal cases (R)-warfarin plasma concentrations are higher than (S)-warfarin, this patient had the opposite warfarin enantiomer plasma concentration profile. Conclusions Increased anticoagulation was due to an increased concentration of (S)-warfarin, the more active warfarin enantiomer. INR response to warfarin in this CYP2C9*3/*3 patient was slow. The later INR response appears to be strongly affected by CYP2C9 variants. He also had the VKORC1 −1639G > A AA genotype, requiring a lower warfarin dose. In this case, increased risk of bleeding could have been identified by prospective genotyping of CYP2C9 and VKORC1 prior to initiating warfarin therapy.

Adenosine is a key myocardial metabolite that elicits coronary vasodilation in a variety of pathophysiological conditions. We examined the mechanism of adenosine-induced vasodilation in coronary arterioles from patients with heart disease. Human coronary arterioles (HCAs) were dissected from pieces of the atrial appendage obtained at the time of cardiac surgery and cannulated for the measurement of internal diameter with videomicroscopy. Adenosine-induced vasodilation was not inhibited by endothelial denudation, but A2receptor antagonism with 3,7-dimethyl-1-propargylxanthine and adenylate cyclase (AC) inhibition with SQ22536 significantly attenuated the dilation. In contrast, A1receptor antagonism with 8-cyclopentyl-1,3-dipropylxanthine significantly augmented the sensitivity to adenosine. Moreover, dilation to A2areceptor activation with 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxamido-adenosine hydrochloride was reduced by the A1receptor agonist (2 S)- N6-(2-endo-norbornyl)adenosine. The nonspecific calcium-activated potassium (KCa) channel blocker tetrabutylammonium attenuated adenosine-induced dilation, as did the intermediate-conductance KCablocker clotrimazole. Neither the large-conductance KCablocker iberiotoxin nor small-conductance KCablocker apamin altered the dilation. In conclusion, adenosine endothelium independently dilates HCAs from patients with heart disease through a receptor-mediated mechanism that involves the activation of intermediate-conductance KCachannels via an AC signaling pathway. The roles of A1and A2receptor subtypes are opposing, with the former being inhibitory to AC-mediated dilator actions of the latter. These observations identify unique fundamental physiological characteristics of the human coronary circulation and may help to target the use of novel adenosine analogs for vasodilation in perfusion imaging or suggest new strategies for myocardial preconditioning.

We examined the hypothesis that ONOO − , a product of the interaction between superoxide (O 2 ·− ) and nitric oxide (NO), inhibits calcium-activated K + (K Ca ) channel activity in vascular smooth muscle cells (VSMCs) of human coronary arterioles (HCAs), thereby reducing hyperpolarization-mediated vasodilation. HCAs were dissected from right atrial appendages. The interaction of ONOO − with microvessels was determined by immunohistochemistry using a nitrotyrosine antibody. Strong staining was observed in arteries exposed to authentic ONOO − or to sodium nitroprusside (SNP)+xanthine (XA)+xanthine oxidase (XO). Dilation to 10 −8 mol/L bradykinin (BK) was abolished in vessels exposed to ONOO − (−2.5±8%; P − (65±8%). Reduced dilation to BK was also observed after application of XO and SNP. Dilation to NS1619 (K Ca channel opener) was reduced in endothelial denuded arterioles treated with ONOO − . In isolated VSMCs, whole-cell peak K + current density was reduced by ONOO − (control 65±15 pA/pF; ONOO − 42±9 pA/pF; P + current. In inside-out patches, ONOO − but not DC-ONOO − decreased open state probability (NP o ) of K Ca channel by 50±12%. O 2 ·− generated by XA+XO had no effect on BK-induced dilation and NP o of K Ca channels. These results suggest that ONOO − , but not O 2 ·− , inhibits K Ca channel activity in VSMCs possibly by a direct effect. This mechanism may contribute to impaired EDHF-mediated dilation in conditions such as ischemia/reperfusion where increased activity of NO synthase occurs in the presence of excess of O 2 ·− .