Marfan syndrome (MFS) is an autosomal dominant heritable disorder of connective tissue that affects the cardiovascular, skeletal, ocular, pulmonary, and nervous systems and is usually caused by mutations in the FBN1 gene, which encodes fibrillin-1. MFS is traditionally considered to result from the structural weakness of connective tissue. However, recent investigations on molecular mechanisms indicate that increased transforming growth factor-β (TGF-β) activity plays a crucial role in the pathogenesis of MFS and related disorders, such as Loeys–Dietz syndrome (LDS), which is caused by mutation in TGF-β signaling-related genes. In addition, recent studies show that angiotensin II type 1 receptor (AT1R) signaling enhances cardiovascular pathologies in MFS, and the angiotensin II receptor blocker losartan has the potential to inhibit aortic aneurysm formation. However, the relationship between TGF-β and AT1R signaling pathways remains poorly characterized. In this review, we discuss the recent studies on the molecular mechanisms underlying cardiovascular manifestations of MFS and LDS and the ensuing strategies for management.
Individuals with intermediate to high cardiac risk for major noncardiac surgery suffer from perioperative myocardial ischemic injury. The purpose of this study was to evaluate the long-term impact of postoperative cardiac troponin elevation on clinical outcome after major noncardiac surgery. Patients (n = 750) aged ≥ 50 years who underwent major noncardiac surgery were eligible for the study. Postoperative cardiac troponin-I data were collected retrospectively and consecutively. The primary outcome measure was allcause mortality. The median follow-up period was 1727 days in all patients. Among 750 patients, 92 (12.2%) showed elevated postoperative troponin-I above 0.10 ng/mL. Operative mortality was 4.1% (31 subjects), and patients with troponin-I elevation showed a higher operative mortality rate (RR: 4.23, 95% CI: 2.67–11.31, P < 0.001). In multivariate Cox regression analysis, a troponin-I concentration above 0.10 ng/mL was associated with all-cause mortality (RR: 1.73, 95% CI: 1.27–2.36, P < 0.001). It should be noted that there was a significant difference between patients with elevated and non-elevated troponin-I in the rate of mortality until 6 months. However, these differences disappeared after 6 months. An elevated troponin-I level conferred an increase in mortality during the 7 year follow-up period after major noncardiac surgery. This difference in mortality was mainly derived from the result within the first 6 months.
It has been reported that coronary vasa vasorum is associated with plaque vulnerability, and low-echoic structures in grayscale intravascular ultrasound (IVUS) are consistent pathologically with vasa vasorum. However, the association of low-echoic structures with plaque composition and no-reflow phenomenon during percutaneous coronary intervention (PCI) is unclear. We investigated plaque composition in virtual histology IVUS (VH-IVUS) and no-reflow phenomenon during PCI of low-echoic structures. A total of 106 lesions being treated by VH-IVUS before PCI were included in this study. Low-echoic structure was defined as a small tubular structure exterior to media without a connection to the vessel lumen in ≥ 3 consecutive crosssectional IVUS images. Lesions with low-echoic structures were found in 42% (45/106). Lesions with low-echoic structures were more prevalent in acute coronary syndrome (ACS) patients (53% [24/45] versus 20% [12/61], P < 0.001), had more positive remodeling (49% [22/45] versus 21% [13/61], P = 0.003), a larger number of VH-IVUS derived thin-cap fibroatheromas (VH-TCFAs) (0.64 ± 0.53 versus 0.05 ± 0.22, P < 0.001), more VH-TCFAs with a baseline plaque burden of 70% or more and minimal luminal area of 4.0 mm2 or less (29% [13/45] versus 2% [1/61], P < 0.001), and more frequent no-reflow phenomenon after stent implantation and more final TIMI flow grade 0/1/2 (38% [17/45] versus 5% [3/61], P < 0.001; 9% [4/45] versus 0% [0/61], P = 0.03) than lesions without low-echo structures. Lesions with low-echoic structures in grayscale IVUS had high plaque vulnerability and were more prevalent in ACS patients, positive remolding, and VH-TCFAs, and they had more frequent no-reflow phenomenon during PCI than lesions without low-echoic structures.
We explored the relationships between heart rate variability (HRV) and levels of N-terminal Pro-B-type natriuretic peptide (NT-proBNP) in patients with unstable angina pectoris (UA). A total of 90 consecutive patients admitted < 48 hours for UA were included. Serum levels of NT-proBNP were measured from blood samples. The cohort was divided into tertiles according to NT-proBNP levels. HRV parameters including SDNN, RMSSD, LF, HF, TP, and VLF were assessed by 24-hour Holter ECG monitoring. The median (IQR) NT-proBNP level was 177.02 (64.76, 740.70) pg/mL. Patients with SDNN < 100 ms had higher levels of NT-proBNP than those with SDNN > 100 ms (P = 0.003). With increasing levels of NT-proBNP, both the 24hour monitoring HRV and night-monitoring HRV showed that SDNN and VLF gradually decreased (P < 0.01), and patients in the NT-proBNP lowest tertile group had higher LF values than the other two groups (P < 0.05); however, no difference was found in RMSSD, HF, and TP. During the daytime, the LF, VLF, and TP values were lower in the NTproBNP highest group compared with the lowest tertile group (P < 0.05). NT-proBNP levels correlated negatively with SDNN (r = -0.314, P = 0.003) and VLF (r = -0.397, P < 0.001) but not with other HRV parameters. Multiple regression analysis showed that serum levels of NT-proBNP remained predictive of SDNN (β = -0.060, P = 0.001) and VLF (β = -0.145, P < 0.001), even after adjustment for confounders. Our study showed that the elevated serum levels of NT-proBNP predict reduced HRV parameters, and the increased NT-proBNP levels combined with decreased HRV represent the degree of neurohormonal dysfunction and may be better prognostic predictors for risk stratification in UA patients.
Pulmonary vein isolation (PVI) is a cornerstone therapy in patients with atrial fibrillation (AF). With increasing numbers of PVI procedures, demand arises to reduce the cumulative fluoroscopic radiation exposure for both the physician and the patient. New technologies are emerging to address this issue. Here, we report our first experiences with a new fluoroscopy integrating technology in addition to a current 3D-mapping system. The new fluoroscopy integrating system (FIS) with 3D-mapping was used prospectively in 15 patients with AF. Control PVI cases (n = 37) were collected retrospectively as a complete series. Total procedure time (skin to skin), fluoroscopic time, and dose-area-product (DAP) data were analyzed. All PVI procedures were performed by one experienced physician using a commercially available circular multipolar irrigated ablation catheter. All PVI procedures were successfully undertaken without major complications. Baseline characteristics of the two groups showed no significant differences. In the group using the FIS, the fluoroscopic time and DAP were significantly reduced from 571 ± 187 seconds versus 1011 ± 527 seconds (P = 0.0029) and 4342 ± 2073 cGycm2 versus 6208 ± 3314 cGycm2 (P = 0.049), respectively. Mean procedure time was not significantly affected and was 114 ± 31 minutes versus 104 ± 24 minutes (P = 0.23) by the FIS. The use of the new FIS with the current 3D-mapping system enables a significant reduction of the total fluoroscopy time and DAP compared to the previous combination of 3D-mapping system plus normal fluoroscopy during PVI utilizing a circular multipolar irrigated ablation catheter. However, the concomitant total procedure time is not affected. Thus, the new system reduces the radiation exposure for both the physicians and patients.
The avoidance of inappropriate shock therapy is an important clinical issue in implantable cardioverter-defibrillator (ICD) patients. We retrospectively analyzed therapeutic events in ICD patients, and the effect of tachycardia detection interval (TDI) and tachycardia cycle length (TCL) guided reprograming on the reduction of inappropriate ICD therapy. The clinical determinants of after reprogramming were also evaluated. A total of 254 consecutive ICD patients were included in the study, and the incidence of antitachycardia therapy was evaluated during the follow-up period of 27.3 ± 18.7 months. When inappropriate antitachycardia therapy appeared, TDI was reprogrammed not to exceed the detected TCL and the patients continued to be followed-up. Various clinical parameters were compared between patients with and without inappropriate ICD therapy. During the initial follow-up period of 18.6 ± 15.6 months, ICD therapy occurred in 127/254 patients (50%) including inappropriate antitachycardia pacing (ATP) (12.9%) and shock (44.35%). Determinants of initial inappropriate therapy were dilated cardiomyopathy (DCM), history of therapeutic hypothermia, and QRS duration. Of the 61 patients with inappropriate therapy, 24 received TCL guided reprogramming. During the additional observation period of 17.0 ± 16.8 months, inappropriate therapy recurred in 5/24 patients (2 ATP, 3 shocks). The determinant of these inappropriate therapy events after reprogramming was the presence of supraventricular tachycardia. By applying simple TCL and TDI guided reprogramming, inappropriate therapy was reduced by 79%. The determinant of inappropriate therapy after reprogramming was the presence of supraventricular tachycardia.
Emergency care for patients with chest pain can be a challenge in remote areas. Digital communication technology has the potential to improve outcomes by allowing early diagnosis and faster treatment. The aim of the present study was to investigate whether implementation of a coordinated digital-assisted program (CDAP) for Chinese hospitals can reduce the door-to-balloon (D2B) time for percutaneous coronary intervention (PCI) in acute chest pain patients in China. From March to December 2011, 609 patients (CDAP group) requiring an emergency response for acute chest pain were evaluated using this CDAP. The results were compared in terms of time interval reduction (including D2B) and economic indices with those of 528 patients (non-CDAP group) previously treated by conventional protocols after admission. We screened 154 and 127 eligible patients under PCI in the CDAP and non-CDAP groups, respectively. PCI patients achieved a D2B time < 90 minutes using CDAP (82.5 versus 26.0%, P < 0.001). CDAP reduced D2B time under PCI and reduced hospitalization lengths and costs (all P < 0.001).
The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner. In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated. Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001). Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR.
Endoscope-assisted surgery and robot-assisted surgery are not common in cardiac surgery, particularly coronary artery bypass grafting, because of the complex nature of the procedures. We developed a new suturing device that allows for easy performance of such cardiac surgeries in comparison with conventional suturing methods. A total of 63 rabbits were used in this study. The right carotid artery was bypassed using the same side of the jugular vein under endoscopic guidance. Of these, 48 rabbits were operated on using the new devices and 15 rabbits were operated on using conventional polypropylene sutures. The proximal suturing time was 16.6 ± 5.3 minutes in the group that underwent surgery using the new device (group D) and 22.8 ± 7.6 minutes in the control group (group C; P < 0.05). The distal suture time was 16.3 ± 4.2 minutes in group D and 22.8 ± 6.0 minutes in group C (P < 0.05). The operation time was 113.0 ± 15.8 minutes in group D and 136.7 ± 20.6 minutes in group C (P < 0.05). Graft flow was 19.9 ± 12.8 mL/minute in group D and 12.1 ± 11.3 mL/minute in group C (P < 0.05). Thus, the operation time and the suture time differed significantly between the groups. This device provides advantages in endoscopic surgery compared to the conventional suture method.
The factors responsible for the ST-T wave alternans (STTA) and associated arrhythmias during acute ischemia have not been clarified. In acutely ischemic porcine myocardium, we recorded transmural unipolar and bipolar electrocardiograms and mid-myocardial extracellular K+ ([K+]e) from the center of the ischemic zone during 8-minute episodes of ischemia. Two different STTAs occurred. The initial STTA, which occurred at 4 minutes 15 seconds ± 12 seconds of ischemia during sinus rhythm, was most prominent in the subendocardium, independent of [K+]e and activation block, and heart rate dependent. It occurred in 13/19 (68%) occlusions at heart rates ≤ 100 bpm and in 22/23 (96%) at > 100 bpm. The second STTA was more obvious and greatest in the subepicardium. It began in the later phase of ischemia and was also heart rate dependent (5/19 [26%] occlusions at heart rates ≤ 100 bpm and 10/23 [44%] at > 100 bpm). This STTA was consistently associated with 2:1 change in the bipolar electrogram morphology, possibly due to 2:1 conduction block. Ventricular fibrillation (VF) occurred only at > 100 bpm. The initial STTA may be independent of conduction abnormalities and represent primary repolarization alternans. The second STTA may be secondary to and indicative of 2:1 activation block or marked alternans of the action potential amplitude/duration. The associated VF most likely reflects the underlying conduction abnormality.
Chronic inflammation is known to occur in diabetes mellitus (DM) and contributes to atrial fibrosis, possible substrates for atrial fibrillation. We tested the hypothesis that dipeptidyl peptidase (DPP)-4 inhibitors prevent the formation of atrial fibrosis through their anti-inflammatory activity, beyond the effects of controlling blood glucose. DM models obtained by administration of streptozotocin (STZ) were divided into 3 groups: with PKF275-055, a DPP-4 inhibitor in group D, glibenclamide in group SU, and no additional drug in group P. At 8 weeks after STZ administration, the heart was subjected to Masson trichrome staining and immunohistochemistry with anti-ED2, ED3, and smooth muscle actin antibody. The % area of fibrosis in atria of group P accounted for 14.7% ± 4.1%, showing a significant increase in fibrosis when compared with the control group. In group SU, the % area accounted for 7.9% ± 2.9%, indicating significant deceased fibrosis by sulfonylurea. Meanwhile, we could not find significant differences in group D when compared to group P or group SU. While ED3-positive cells increased in group P (1.12% ± 0.24%), they were significantly decreased in groups D and SU (0.41% ± 0.22% and 0.55% ± 0.29%, respectively). Between group D and SU, however, there were no significant differences in the amount of cells positive to ED2, ED3, and smooth muscle actin antibodies. In STZ-induced DM rats, administration of sulfonylurea and DPP-4 inhibitors inhibited inflammation and fibrosis of the atria. However, no significant differences were observed between the 2 antidiabetic drugs.
Genome-wide association study has identified that the genetic variations at NOS1AP (neuronal nitric oxide synthase-1 adaptor protein) were associated with QT interval and sudden cardiac death (SCD). However, the mechanism linking a genetic variant of NOS1AP and SCD is poorly understood. We used Nos1ap knockout mice (Nos1ap-/-) to determine the involvement of Nos1ap in SCD, paying special attention to oxidative stress. At baseline, a surface electrocardiogram (ECG) and ultrasound echocardiography (UCG) showed no difference between Nos1ap-/- and wild-type (WT) mice. Oxidative stress was induced by a single injection of doxorubicin (Dox, 25 mg/kg). After Dox injection, Nos1ap-/- showed significantly higher mortality than WT (93.3 versus 16.0% at day 14, P < 0.01). ECG showed significantly longer QTc in Nos1ap-/- than WT, and UCG revealed significant reduction of fractional shortening (%FS) only in Nos1ap-/- after Dox injection. Spontaneous ventricular tachyarrhythmias were documented by telemetry recording after Dox injection only in Nos1ap-/-. Ex vivo optical mapping revealed that the action potential duration (APD)90 was prolonged at baseline in Nos1ap-/-, and administration of Dox lengthened APD90 more in Nos1ap-/- than in WT. The expression of Bnp and the H2O2 level were higher in Nos1ap-/- after Dox injection. Nos1ap-/- showed a reduced amplitude of calcium transient in isolated cardiomyocytes after Dox injection. Administration of the antioxidant N-acetyl-L-cysteine significantly reduced mortality of Nos1ap-/- by Dox injection, accompanied by prevention of QT prolongation and a reduction in %FS. Although Nos1ap-/- mice have apparently normal hearts, oxidative stress evokes ventricular tachyarrhythmia and heart failure, which may cause sudden cardiac death.
Vagus nerve stimulation (VNS), targeting the imbalanced autonomic nervous system, is a promising therapeutic approach for chronic heart failure (HF). Moreover, calcium cycling is an important part of cardiac excitation-contraction coupling (ECC), which also participates in the antiarrhythmic effects of VNS. We hypothesized that low-level VNS (LL-VNS) could improve cardiac function by regulation of intracellular calcium handling properties. The experimental HF model was established by ligation of the left anterior descending coronary artery (LAD). Thirty-two male Sprague-Dawley rats were divided into 3 groups as follows; control group (sham operated without coronary ligation, n = 10), HF-VNS group (HF rats with VNS, n = 12), and HF-SS group (HF rats with sham nerve stimulation, n = 10). After 8 weeks of treatment, LL-VNS significantly improved left ventricular ejection fraction (LVEF) and attenuated myocardial interstitial fibrosis in the HF-VNS group compared with the HF-SS group. Elevated plasma norepinephrine and dopamine, but not epinephrine, were partially reduced by LL-VNS. Additionally, LL-VNS restored the protein and mRNA levels of sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), Na+–Ca2+ exchanger 1 (NCX1), and phospholamban (PLB) whereas the expression of ryanodine receptor 2 (RyR2) as well as mRNA level was unaffected. Thus, our study results suggest that the improvement of cardiac performance by LL-VNS is accompanied by the reversal of dysfunctional calcium handling properties including SERCA2a, NCX1, and PLB which may be a potential molecular mechanism of VNS for HF.
The clinical goal of cell-based treatment for chronic heart failure is to coordinately reconstitute the cardiomyocytes and associated circulation environment including coronary resistance arteries, arterioles, and capillary profiles.1) This goal can be possibly achieved by implementing multipotent adult stem cells. However, it remains a challenge to modify the capillary network in the decompensated heart. A mechanical stress model was used in this study to mimic the hemodynamic and hormonal states of the decompensated heart in vitro. The angiogenesis role of endothelial progenitor cells (EPCs) under stress has been well-recognized in vascular repair. We investigated the molecular mechanisms of EPCs in this model. We found that expression of vascular endothelial growth factor (VEGF) in EPCs was significantly decreased by mechanical stress, and this effect was accompanied by a decrease in angiogenesis in vitro. Interestingly, the defective angiogenesis can be reversed by upregulating the membrane VEGF receptor (VEGFR) endocytosis. An atypical protein kinase C (aPKC) inhibitor can promote the VEGFR internalization in EPCs and enhance the formation of vascular networks. Thus, the upregulation of VEGFR endocytosis in EPCs could be a potential therapy for the cell–based treatment of chronic heart failure by enhancing the cardiomyocytes.
A 73-year-old man was admitted to our hospital because of chest pain at rest. Electrocardiography (ECG) showed an ST-segment depression, a negative U-wave in the precordial leads, and a right axis deviation (RAD) tendency. Coronary angiography revealed occlusion of the right coronary artery. Collateral flow from the jeopardized left anterior descending artery to the posterior descending artery (PDA) was fair. After successful revascularization, improvement in the ECG findings was noted. Since blood supply to the left posterior fascicle is dependent on the PDA, the RAD tendency could be explained by the presence of a transient ischemic left posterior hemiblock.
Rotational atherectomy with/without low-pressure balloon dilation has been a mainstay of interventional treatment for stenosis due to the coronary sequelae of Kawasaki disease (KD). Here, we report a restenosis case of probable coronary sequelae of KD treated with rotational atherectomy with low-pressure 2.5-mm balloon dilation 6 months previously. Under the guidance of optical frequency domain imaging, we performed rotational atherectomy followed by 2.5-mm drug-coated balloon (DCB) dilation for an atherosclerotic restenosis at the inlet of a calcified aneurysm in the proximal left anterior descending coronary artery. Coronary angiography 6 months later showed no apparent progression of vessel narrowing, and we could defer repeat intervention. The present case suggests that rotational atherectomy followed by DCB dilation could be an alternative revascularization therapy of choice in coronary KD sequelae complicated with atherosclerosis.
We describe a patient who underwent coronary artery bypass grafting (CABG) surgery with the presentation of acute coronary syndrome (ACS). The diagnostic coronary angiogram showed acute thrombotic and occluded saphenous vein graft (SVG) and proximal right coronary artery (RCA) drug eluting stent (DES) instent restenosis (ISR) with chronic total occlusion (CTO). Our strategy was to recanalize the native left circumflex coronary artery (LCx) CTO instead of SVG or RCA instent CTO. After heparinization for 5 days, the LCx antegrade approach and the retrograde approach from left anterior descending coronary artery (LAD) septal branches were first attempted but failed, and the LCx CTO was successfully revascularized retrogradely via the acute thrombotic SVG without an embolic protection device (EPD).
Rotational atherectomy to an angulated calcified lesion is always challenging. The risk of catastrophic complications such as a burr becoming stuck or vessel perforation is greater when the calcified lesion is angulated. We describe the case of an 83-year-old female suffering from unstable angina. Diagnostic coronary angiography revealed an angulated calcified lesion in the proximal segment of the right coronary artery. We performed rotational atherectomy to the lesion, but intentionally did not advance the rotational atherectomy burr beyond the top of the angulation. We controlled the rotational atherectomy burr and stopped it just before the top of the angulation to avoid complications. Following rotational atherectomy, balloon dilatation with a non-compliant balloon was performed, and drug-eluting stents were successfully deployed. In this manuscript, we provide a review of the literature on this topic, and discuss how rotational atherectomy to an angulated calcified lesion should be performed.
A 79-year-old Asian man was hospitalized because of progressive exertional dyspnea with decreasing left ventricular ejection fraction and frequent non-sustained ventricular tachycardia. Pre-procedure venography for implantable cardioverter defibrillator (ICD) implantation showed occlusion of the bilateral subclavian veins. In consideration of subcutaneous humps in the sterno-clavicular area and palmoplantar pustulosis, we diagnosed him as having synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome and speculated that it induced peri-osteal chronic inflammation in the sterno-clavicular area, resulting in occlusion of the adjacent bilateral subclavian veins. An automatic external defibrillator (AED) was installed in the patient’s house and total subcutaneous ICD was considered. Venous thrombosis in SAPHO syndrome is not frequent but has been reported. To the best of our knowledge, this is the first case of bilateral subclavian vein occlusion in a SAPHO syndrome patient who needs ICD implantation.
For 6 years after heart transplantation, a 23-year old female recipient had been treated with immunosuppressants including tacrolimus and mycophenolate mofetil (MMF), without any major rejection or graft dysfunction. She unexpectedly became pregnant for the first time, and we converted MMF to azathioprine (AZA), but she soon experienced a spontaneous abortion. After careful counseling under the continuation of AZA, she became pregnant again 3 months after the abortion. We closely monitored the concentration of immunosuppressive agents, cardiac function, fetal condition, and serological assay including human leukocyte antigen (HLA) sensitization, and she eventually delivered a normal male infant at 38 weeks gestation without any complications. AZA was converted to MMF soon after the delivery. There have been no complications in either the patient or infant after the delivery. Because pregnancy itself involves a risk of cardiac graft rejection in the recipient as well as fetal complications, it is important to educate HTx recipients about planned pregnancy and to conduct careful follow-up after pregnancy.
Emerging concerns regarding heart failure, arrhythmia, and sudden death in patients with muscular dystrophy are of significant clinical importance. On the other hand, little attention has been paid to renal dysfunction because these patients have low serum creatinine levels. Serum cystatin C, unaffected by muscle quantity, is a potentially superior marker for estimating renal function. Here, we present cases with muscular dystrophy in which estimated glomerular filtration rate (GFR) by cystatin C (eGFRcys) provided good agreement with simultaneously measured GFR by inulin renal clearance (differences less than 20%). Sudden death with acute heart failure occurred in a patient with underlying renal dysfunction and elevated BNP. Neurologists and cardiologists should evaluate renal function using GFR with cystatin C in patients with muscular dystrophy.
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