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Transcatheter mitral valve repair with the MitraClip system has been established in selected high-risk patients. The MitraClip procedure results in a relatively large iatrogenic atrial septal defect (iASD). This study aimed to investigate the prevalence and clinical course of iASD requiring transcatheter closure following the MitraClip procedure.Methods and Results: This study was conducted at all 59 institutions that perform transcatheter mitral valve repair with the MitraClip system in Japan. The data of patients on whom transcatheter iASD closure was performed were collected. Of the 2,722 patients who underwent the MitraClip procedure, 30 (1%) required transcatheter iASD closure. The maximum iASD size was 9±4 mm (range, 3-18 mm). The common clinical course of transcatheter iASD closure was hypoxemia with right-to-left shunt or right-sided heart failure with left-to-right shunt. Of the 30 patients, 22 (73%) required transcatheter closure within 24 h following the MitraClip procedure, including 12 with hypoxemia and 5 with right-sided heart failure complicated with cardiogenic shock. Of the 5 patients, 2 required mechanical circulatory support devices. Twenty-one patients immediately underwent transcatheter iASD closure, and hemodynamic deteriorations were resolved; however, 1 patient died without having undergone transcatheter closure.Transcatheter iASD closure was required in 1% of patients who underwent the MitraClip procedure. Many of these patients immediately underwent transcatheter iASD closure because of hypoxemia with right-to-left shunt or right-sided heart failure with left-to-right shunt.

A 68-year old man underwent bare metal stent (BMS; Palmaz-Shatz stent) implantation in the distal right coronary artery (RCA; #4PL) and balloon angioplasity (BA) in the proximal left circumflex coronary artery (LCX; #11) for stable angina. After 5 years after initial stent implantation, de novo lesion located in mid RCA was treated by BMS (NIR stent) implantation additionally. After 16 years from first BMS implantation, the patient died from heart failure due to cardiac amyloidosis, and pathologic examination was performed for the specimen of stented RCA segment and LCX BA segment. An autopsy demonstrated that the lesions of stented site at RCA and BA site LCX were histopathologically different. In the stented segment, severe luminal stenosis is observed due to marked proliferation of the neointima in all stented sites. In addition, neovascularization and spotty calcification with mild lymphocyte infiltration were observed especially around the struts. In contrast, at the BA site of the proximal LCX lesion, in the neointima, the smooth muscle cells were rather atrophic and abundant collagen fibers were evident in the intercellular spaces, which showed very stable findings. Compared with these BMS implanted portions, the site of BA was associated with a trend for smaller late lumen loss. These findings suggested that in the stented site, chronic inflammatory reaction to the stent struts could evoke continuous proliferation of neointima resulting in severe late lumen loss.

ObjectiveTherapeutic strategies for atrial septal defect (ASD) with severe pulmonary arterial hypertension (PAH) are controversial. This study aimed to evaluate the efficacy of PAH-specific medications and subsequent transcatheter closure (ie, treat-and-repair strategy) on clinical outcomes.MethodsWe enrolled 42 patients who were referred to 13 institutions for consideration of ASD closure with concomitant PAH and underwent the treat-and-repair strategy. The endpoint was cardiovascular death or hospitalisation due to heart failure or exacerbated PAH.ResultsAt baseline prior to PAH-specific medications, pulmonary to systemic blood flow ratio (Qp:Qs), pulmonary vascular resistance (PVR), and mean pulmonary artery pressure (PAP) were 1.9±0.8, 6.9±3.2 Wood units and 45±15 mm Hg. Qp:Qs was increased to 2.4±1.2, and PVR and mean PAP were decreased to 4.0±1.5 Wood units and 35±9 mm Hg at the time of transcatheter ASD closure after PAH-specific medications. Transcatheter ASD closure was performed without any complications. During a median follow-up period of 33 months (1–126 months) after transcatheter ASD closure, one older patient died and one patient was hospitalised due to heart failure, but the other patients survived with an improvement in WHO functional class. PAP was further decreased after transcatheter ASD closure.ConclusionsThe treat-and-repair strategy results in low complication and mortality rates with a reduction in PAP in selected patients with ASD complicated with PAH who have a favourable response of medical therapy.

Background Biomarkers for detection of transient myocardial ischemia in patients with unstable angina (UA) or for very early diagnosis of acute myocardial infarction (AMI) are not currently available. Methods and results We performed two sequential screenings of autoantibodies elevated shortly after the onset of acute coronary syndrome (ACS), and focused on metalloendopeptidase nardilysin (NRDC) among 19 identified candidate antigens. In a retrospective analysis among 93 ACS and 117 non-ACS patients, the serum level of NRDC was significantly increased in patients with ACS compared with that in patients with non-ACS (2073.5±189.8pg/ml versus 775.7±63.4pg/ml, P N =35 and UA: N =8), serum concentration of NRDC was significantly increased even in UA patients with a peak serum NRDC levels reached at admission both in AMI and UA patients. In a mouse model of AMI, we found an acute increase in serum NRDC and reduced NRDC expression in ischemic regions shortly after coronary artery ligation. NRDC expression was also reduced in infarcted regions in human autopsy samples from AMI patients. Moreover, the short treatment of primary culture of rat cardiomyocytes with H 2 O 2 or A23187 induced NRDC secretion without cell toxicity. Conclusion NRDC is a promising biomarker for the early detection of ACS, even in UA patients without elevation of necrosis markers.

Background Data are scarce on the role of aortic valve area (AVA) to identify those patients with asymptomatic severe aortic stenosis (AS) who are at high risk of adverse events. We sought to explore the prognostic impact of AVA in asymptomatic patients with severe AS in a large observational database. Methods and Results Among 3815 consecutive patients with severe AS enrolled in the CURRENT AS (Contemporary Outcomes After Surgery and Medical Treatment in Patients With Severe Aortic Stenosis) registry, the present study included 1309 conservatively managed asymptomatic patients with left ventricular ejection fraction ≥50%. The study patients were subdivided into 3 groups based on AVA (group 1: AVA >0.80 cm2, N=645; group 2: 0.8 cm2 ≥AVA >0.6 cm2, N=465; and group 3: AVA ≤0.6 cm2, N=199). The prevalence of very severe AS patients (peak aortic jet velocity ≥5 m/s or mean aortic pressure gradient ≥60 mm Hg) was 2.0%, 5.8%, and 26.1% in groups 1, 2, and 3, respectively. The cumulative 5‐year incidence of AVR was not different across the 3 groups (39.7%, 43.7%, and 39.9%; P=0.43). The cumulative 5‐year incidence of the primary outcome measure (a composite of aortic valve–related death or heart failure hospitalization) was incrementally higher with decreasing AVA (24.1%, 29.1%, and 48.1%; P, See Editorial by Tribouilloy et al

Copeptin, a surrogate marker of pro-arginine vasopressin, is expected to be a marker in cardiovascular diseases. Its utility for predicting long-term clinical outcomes in heart failure (HF), however, has not been adequately evaluated in daily clinical practice in Japan.To assess the relationship of serum copeptin at admission with long-term clinical outcomes, we evaluated serum copeptin at admission in consecutive 107 patients hospitalized for HF between April 2011 and July 2012. The primary outcome measure was defined as a composite of all-cause death and re-admission for HF (all-cause death/HF).In this study population, median serum copeptin at admission was 15.5 (6.7-32.0)pmol/L. As compared with the low-copeptin group (18pmol/L, N=60), the high-copeptin group (≥18pmol/L, N=47) included more male patients and those with prior myocardial infarction, prior HF, low left ventricular ejection fraction, and chronic kidney disease. During median 4.5 (1.0-5.5) years of clinical follow-up, the cumulative incidence of all-cause death/HF was significantly higher in the high-copeptin than in the low-copeptin group (63.4% versus 33.0% at 1 year, and 85.2% versus 77.2% at 5 years, log-rank p=0.03). After adjusting for confounders, high-copeptin was still an independent predictor for all-cause death/HF [hazard ratio (95% confidence interval): 1.77 (1.04-3.01), p=0.03].Copeptin was suggested as a useful marker for predicting long-term clinical outcomes in patients with HF.

Balloon aortic valvuloplasty (BAV) has played a limited role in the management of patients with severe aortic stenosis. However, BAV is being performed more frequently these days with the emergence of transcatheter aortic valve implantation (TAVI). We previously described a technique named "looped Inoue balloon technique" to simplify the antegrade transvenous BAV by making a loop in the left atrium using two stylets. We present a case in which the looped Inoue balloon technique was successfully applied. The patient was an 83-year-old woman with progressive dyspnea due to severe aortic stenosis. The aortic valve area was 0.39 cm(2) with a mean transvalvular gradient of 46 mmHg. The patient was deemed high risk for surgical aortic valve replacement or TAVI in view of the multiple comorbidities and frailty. Antegrade BAV using the looped Inoue balloon technique was performed. The procedure was successful without any complications. The post procedural aortic valve area increased to 1.15 cm(2) with a mean pressure gradient of 23 mmHg. This is the first report of clinical use of the looped Inoue balloon technique for antegrade BAV.

In Japan, transcatheter aortic valve implantation (TAVI) with Edwards-SAPIEN XT valve (Edwards Lifesciences Inc., Irvine, CA, USA) started in October 2013. All institutions should undergo a training period to perform TAVI independently. Balloon aortic valvuloplasty (BAV) as a bridge to TAVI during the training period should be performed with caution to avoid severe aortic regurgitation (AR) because bailout TAVI is not possible. We present a case in which BAV was successfully performed as a bridge to TAVI during the training period. The patient was an 85-year-old man with medically uncontrollable congestive heart failure due to severe aortic valve stenosis. The aortic valve area was 0.60cm2 with a left ventricular ejection fraction of 20%. TAVI was considered a safe but high-risk strategy owing to the unstable hemodynamic condition. We chose BAV as a bridge therapy to TAVI. The aortic annulus diameter was 25.3mm on computed tomography scans. We chose a 20-mm balloon catheter to avoid BAV-induced AR. Transfemoral TAVI was performed successfully 16 days after BAV using a 26-mm SAPIEN XT valve. The postoperative course was uneventful. The case demonstrated BAV as a bridge therapy to TAVI can be safely and effectively performed during the training period.

A 68-year-old female underwent bare-metal stent (BMS) implantation in the right coronary artery (RCA) for ST-segment elevation myocardial infarction. Recurrent refractory restenosis with peri-stent contrast staining (PSS) formation was observed in the stented lesion at follow-up angiography at 7, 11, and 14 months after the index stent implantation. After 2 repeated interventions, this patient was referred to coronary artery bypass grafting due to occlusion of RCA and progression of proximal left anterior descending coronary artery lesion at 15 months after stent implantation. Pathologic examination of the surgically resected specimen of stented RCA segment revealed total occlusion with dense fibrous collagenous tissue and significant inflammatory cell infiltration including scattered eosinophils. Extensive loss of medial smooth muscle layer was observed in the vessel wall, which was likely to be the cause of PSS. In the course of treatment, this patient was found to have chromium allergy with positive patch test. Allergic reactions to chromium released from the stent might be one of the triggering mechanisms for in-stent restenosis and PSS after BMS implantation.

Background Multifunction cardiogram (MCG) is a computer-enhanced, resting electrocardiogram analysis developed to detect hemodynamically relevant coronary artery disease (CAD). Based on data from previous studies suggesting excellent diagnostic accuracy in detecting CAD, MCG (approved by the Food and Drugs Administration) received a Current Procedure Terminology (CPT) code in 2010 in United States. However, there is no previous study validating MCG by using fractional flow reserve (FFR) as the reference standard. Methods Multifunction cardiogram Evaluation in Diagnosis of Functional coronary Ischemia sTudy (MED-FIT) was designed as a single-center, prospective study enrolling 100 stable patients with suspected CAD scheduled for coronary angiography. The primary and secondary analyses evaluated the diagnostic performance of the MCG severity score to detect functional myocardial ischemia by FFR ≤0.80, and angiographically significant coronary stenosis (percent diameter stenosis ≥50%) by quantitative coronary angiography. Results The current analysis set consisted of 91 patients in whom MCG data with adequate quality was obtained. The prevalence of positive functional myocardial ischemia and angiographically significant stenosis in the current study was 42.7% and 41.8%, respectively. Area under the receiver operating characteristics curve (AUC) of the MCG severity score for functional myocardial ischemia and angiographically significant stenosis was low (AUC 0.51, 95% confidence interval [CI] 0.38–0.63, and AUC 0.58, 95%CI 0.46–0.70, respectively). Sensitivity, and specificity of the MCG severity score for functional myocardial ischemia and angiographically significant stenosis was also low (32%/67%, and 37%/72%) using a cutoff value of 4.0. Conclusions Diagnostic performance of the MCG severity score was poor for both functional myocardial ischemia, and angiographically significant stenosis.

Background A hyperdynamic state of the basal left ventricle sometimes results in obstruction of the left ventricular outflow tract (LVOT). However, the prevalence, clinical presentation, and prognostic effect of LVOT obstruction in takotsubo cardiomyopathy (TC) have not been fully evaluated. Methods and results Among 933 consecutive patients who underwent emergency coronary angiography for suspected acute coronary syndrome, 35 patients (3.8%) were diagnosed as TC. The cumulative 3-year incidence of all-cause death, cardiac death, hospitalization for congestive heart failure (CHF), and recurrent TC was 24.2%, 0.0%, 6.5%, and 12.2%, respectively. Among 27 patients with information of a LVOT pressure gradient, LVOT obstruction was present in 9 (33%). The prevalence of moderate to severe mitral regurgitation (67% vs. 11%, P=0.003), CHF (78% vs. 28%, P=0.02), and hypotension (56% vs. 5.6%, P=0.008) was significantly higher in patients with LVOT obstruction than in those without. Nevertheless, the cumulative 3-year incidence of all-cause death was not significantly different between the 2 groups (49.2% vs. 23.0%, P=0.22) with no cardiac deaths in either group. Hospitalization for CHF and recurrent TC were significantly more frequent in patients with LVOT obstruction (25.0% vs. 0.0%, P=0.04, and 25.0% vs. 6.7%, P=0.02). Conclusions In 35 consecutive patients with TC, those with significant LVOT obstruction (33%) had a more serious clinical presentation such as CHF and hypotension, but had similar 3-year mortality rate as compared with those without.

An 86-year-old woman with severe aortic stenosis was referred for transcatheter aortic valve replacement (TAVR). The transfemoral TAVR procedure was conducted under general anesthesia. Aortography during pre-dilatation with a 20-mm balloon demonstrated reduced blood flow through the left main

The aim of this study was to evaluate the prognostic impact of left ventricular ejection fraction (LVEF) in patients with severe aortic stenosis (AS).The prognostic impact of LVEF in severe AS remains controversial.Among 3,815 consecutive patients with severe AS enrolled in the CURRENT AS (Contemporary Outcomes After Surgery and Medical Treatment in Patients With Severe Aortic Stenosis) registry, the present study population consisted of 3,794 patients after excluding 21 patients without LVEF data. Patients were divided into 4 groups according to LVEF at index echocardiography (50%, 50% to 59%, 60% to 69%, and ≥70%; conservative strategy: n = 388, n = 390, n = 1,025, and n = 800; initial aortic valve replacement strategy: n = 206, n = 170, n = 375, and n = 440). Echocardiographic data were site reported, and there was no echocardiography core laboratory.In the conservative group, the cumulative 5-year incidence of the primary outcome measure (a composite of aortic valve-related death or heart failure hospitalization) was significantly higher in patients with LVEFs 50% and 50% to 59% than in those with LVEFs 60% to 69% and ≥70% (72.3%, 58.4%, 38.7%, and 35.0%, respectively, p 0.001), whereas in the initial aortic valve replacement group, the negative effect of low LVEF was markedly attenuated (20.2%, 20.3%, 17.7%, and 12.4%, respectively, p = 0.03). After adjusting for confounders, LVEF 50% (hazard ratio: 1.82; 95% confidence interval: 1.44 to 2.28; p 0.001) and 50% to 59% (hazard ratio: 1.77; 95% confidence interval: 1.42 to 2.20; p 0.001) but not 60% to 69% (hazard ratio: 1.14; 95% confidence interval: 0.94 to 1.39; p = 0.17) were independently associated with poorer outcomes compared with LVEF ≥70% (reference) in the conservative group. In the initial aortic valve replacement group, the adjusted risk for the primary outcome measure was not significantly different across the 4 LVEF groups.This study demonstrates that survival in patients with severe AS is impaired when LVEF is 60%, and these findings have implications for decision making with regard to the timing of surgical intervention.

Background There are limited data regarding the risk stratification based on peak aortic jet velocity (Vmax) in patients with severe aortic stenosis ( AS ). Methods and Results Among 3815 consecutive patients with severe AS enrolled in the CURRENT AS (Contemporary Outcomes After Surgery and Medical Treatment in Patients With Severe Aortic Stenosis) registry, the study population consisted of 1075 conservatively managed patients with Vmax ≥4.0 m/s and left ventricular ejection fraction ≥50%. The study patients were subdivided into 3 groups based on Vmax (group 1, 4.0 ≤ Vmax AS ‐related events (aortic valve–related death or heart failure hospitalization) was incrementally higher with increasing Vmax (entire population; 38.0%, 49.4%, and 62.8%, P P =0.008; and asymptomatic patients; 29.4%, 38.9%, and 47.7%, P =0.005). After adjusting for confounders, the excess risk of group 2 and group 3 relative to group 1 for AS ‐related events remained significant (hazard ratio, 1.39; 95% CI , 1.07–1.81; P =0.02, and hazard ratio, 1.53; 95% CI , 1.17–2.00; P =0.002, respectively). The effect size of group 3 relative to group 1 for AS ‐related events in asymptomatic patients (N=479) was similar to that in symptomatic patients (N=596; hazard ratio, 1.59; 95% CI , 1.01–2.52; P =0.047, and hazard ratio, 1.67; 95% CI , 1.16–2.40, P =0.008, respectively), and there was no significant overall interaction between the symptomatic status and the effect of the Vmax categories on AS ‐related events (interaction, P =0.88). Conclusions In conservatively managed severe AS patients with preserved left ventricular ejection fraction, increasing Vmax was associated with incrementally higher risk for AS ‐related events. However, the cumulative 5‐year incidence of the AS ‐related events remained very high even in asymptomatic patients with less greater Vmax.

A 31-year-old male patient with a history of situs inversus, dextrocardia, and interrupted inferior vena cava (IVC) with azygous continuation referred to our hospital ([Figure 1A][1]). Transesophageal echocardiography revealed a 9 mm × 16 mm atrial septal defect (ASD) with continuous left-to

An 80-year-old male underwent a transcatheter aortic valve implantation (TAVI) for severe senile aortic stenosis. Six weeks after the surgery, he was readmitted to our institution because of a high-grade fever. Transesophageal echocardiography revealed thickening of all three leaflets of the aortic prosthesis and mobile mass on the leaflet, and Streptococcus sanguis was identified from his blood culture. Therefore, he was diagnosed with prosthetic valve endocarditis (PVE) and received intensive intravenous antibiotic therapy. Because he did not respond to the pharmacological therapy, surgical aortic valve replacement (AVR) was indicated although it was considered a relatively high-risk procedure. Herein, we report on the successful surgical AVR in this patient using a pericardial valve after removal of the infected prosthetic valve, and discuss some issues related to this rare complication after TAVI.

Purpose To assess the efficacy of the Inoue stent-graft placement for thoracoabdominal aortic aneurysm (TAAA). Methods Patients with TAAA underwent Inoue stent-graft placement with single branched stent-graft in 4 patients, straight graft in 3 patients and double branched stent-graft in 1 patient. Half the patients required additional open surgical revascularizations of involved visceral arteries (Hybrid procedures). Results Stent-grafts were deployed successfully in all patients. One patient with Hybrid procedure developed major complications, required haemodialysis and died in hospital. In another patient the post-operative CT scan demonstrated a type I endoleak, but this had resolved by 3 months. Conclusion Inoue stent-grafting for TAAA with or without adjunctive open surgical revascularization is feasible.

Aim Severe gastrointestinal bleeding sometimes occurs in patients with aortic stenosis (AS), known as Heyde's syndrome. This syndrome is thought to be caused by acquired von Willebrand syndrome and is characterized by reduced large von Willebrand factor (vWF) multimers. However, the relationship between the severity of AS and loss of large vWF multimers is unclear. Methods We examined 31 consecutive patients with severe AS. Quantitative evaluation for loss of large vWF multimers was performed using the conventional large vWF ratio and novel large vWF multimer index. This novel index was defined as the ratio of large multimers of patients to those of controls. Results Loss of large vWF multimers, defined as the large vWF multimer index ＜80%, was detected in 21 patients (67.7%). The large vWF multimer ratio and the large vWF multimer index were inversely correlated with the peak aortic gradient (R = -0.58, p=0.0007, and R=-0.64, p＜0.0001, respectively). Anemia defined as hemoglobin ＜9.0 g/dl was observed in 12 patients (38.7%), who were regarded as Heyde's syndrome. Aortic valve replacement was performed in 7 of these patients, resulting in the improvement of anemia in all patients from a hemoglobin concentration of 7.5±1.0 g/dl preoperatively to 12.4±1.3 g/dl postoperatively (p＜0.0001). Conclusions Acquired von Willebrand syndrome may be a differential diagnosis in patients with AS with anemia. The prevalence of AS-associated acquired von Willebrand syndrome is higher than anticipated.

Percutaneous coronary intervention (PCI) for anomalous coronary arteries is often difficult because the support provided by the guide catheter is insufficient. We encountered a patient with severe three-vessel coronary disease including a totally occluded anomalous right coronary artery (RCA) originating from the left sinus of Valsalva. Initial PCI for the anomalous RCA via the transradial approach failed. Therefore, we constructed a three-dimensional (3D) aortocoronary model and conducted an in vitro simulation to plan the second PCI and found that a Judkins left (JL) 3.5 guide catheter in the power position yielded maximum backup support for the anomalous RCA. Thus, the second PCI was conducted using an 8 Fr JL 3.5 guide catheter in the power position via the transfemoral approach. The procedure was smooth and successful, without any adverse events. Our experience suggests that case-specific 3D models are useful for strategic planning of complex PCIs.

A 73-year-old man underwent sirolimus-eluting stent (SES) implantation for chest pain on exertion with left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX). The patient died due to non-obstructive mesenteric ischemia after 57 months of SES implantation. An autopsy demonstrated that the lesions of stented site at LAD and LCX were histopathologicaly similar images. In short, only mild neointimal formation with enough patent lumen was observed in all stented sites with no evidence of restenosis. In addition, complete coverage of endothelial cells in the surface of neointima was visible. Furthermore, necrotic core formation with a lot of circumferential cholesterol clefts was evident around the struts. In spite of these findings, observations of neointimal rupture and stent thrombosis were not found in this very late period autopsy study. In this histopathological examination, although neointimal coverage with enough lumen was observed, accumulation of extracellular lipid and cholesterol crystal was shaping necrotizing core, in short neoatherosclerosis. In the future, biocompatible drug-eluting stents which do not induce inflammation to the arterial wall post stenting should be appropriately addressed by the future development of improved coronary stents. Learning objective: This manuscript contains original materials from pathological analysis of very long-term SES implantation. The current case report is the first one with very long-term course after SES implantation over 4 years and 9 months. In this pathological examination, although neointimal coverage with enough lumen was observed, neoatherosclerotic change around stent struts was evident. We should observe close clinical follow up after SES implantation.>

Background: Recent randomized clinical trials have reported favorable clinical outcomes after the use of drug-eluting stents (DES) in patients with acute coronary syndrome (ACS). However, the long-term efficacy and safety outcomes, bleeding outcome in particular, after DES implantation in ACS patients have not been thoroughly evaluated in a real-world population. Methods and Results: We evaluated long-term clinical outcomes in 565 consecutive ACS patients who underwent DES implantation in an emergency setting between 2004 and 2011 (ST-segment elevation acute myocardial infarction [STEMI]: n=269, non-STEMI/unstable angina pectoris: n=296). Mean clinical follow-up period in this study was 4.6±2.0 years. The cumulative incidence of all-cause death, cardiac death, myocardial infarction, stent thrombosis and target-lesion revascularization was 6.9%, 4.0%, 2.2%, 1.3% and 8.4% at 1 year, and 19.6%, 6.7%, 5.6%, 3.0% and 13.9% at 5 years, respectively. The cumulative 5-year incidence of major bleeding events was 8.4% (n=42). Fatal bleeding events, however, occurred in only 4 patients, even including 2 patients who required resuscitation upon arrival at the hospital. Of the 42 patients with major bleeding events, 39 were taking dual antiplatelet therapy (DAPT) at the time of bleeding. Conclusions: DES implantation provided favorable long-term clinical outcomes with an acceptably low incidence of fatal bleeding in a real-world population of ACS patients. However, prolonged DAPT seems to be associated with major bleeding after DES implantation. (Circ J 2014; 78: 1628–1635)

Contrast-induced nephropathy (CIN) is the major cause of hospital-acquired renal failure. Although the efficacy of sodium bicarbonate to prevent CIN was reported, long-term cardiovascular and renal outcome is unclear. Between May 2006 and March 2010, 161 patients of multicenter with CKD (Scr ≥1.2

Background— We have sometimes noted abnormal angiographic coronary dilatation, Methods and Results— Between May 2008 and March 2010, we performed optical coherence tomography for 90 in-stent restenosis lesions after sirolimus-eluting stent implantation. We found PSS in 20 of the 90 lesions by coronary angiography. The differences in optical coherence tomography findings, including incomplete stent apposition, multiple interstrut hollows (MIH), strut coverage, and thrombus, were compared between lesions with PSS and those without PSS. PSS is defined as contrast staining outside the stent contour extending to >20% of the stent diameter measured by quantitative coronary angiography. MIH is defined as multiple hollows (the maximum depth >0.5 mm) existing between and outside well-apposed stent struts. Both incomplete stent apposition (60.0% versus 10%; P P P =0.001), malapposed struts (2.0% versus 0.0%; P P =0.012) were frequently observed in lesions with PSS than in lesions without PSS. Conclusions— PSS might be closely associated with 2 different optical coherence tomography findings, MIH and incomplete stent apposition, in lesions after sirolimus-eluting stent implantation.

In a 77-year-old man with apical hypertrophic cardiomyopathy and nonsustained ventricular tachycardia, a pulmonary nodule in the right middle lobe was incidentally detected on a chest computed tomography (CT), which was performed for screening purposes of the interstitial pneumonia as a side effect of amiodarone. To establish the diagnosis of lung cancer, the patient was admitted to undergo a CT-guided transthoratic needle biopsy of the lung. The procedure was performed by an experienced pulmonologist using the 18-gauge outer coaxial needle of a disposable core biopsy instrument under CT guidance. The patient was placed in a supine position for the procedure. The biopsy needle was advanced into the lesion, and a specimen was successfully obtained (Figure 1A). Immediately after removing the biopsy needle followed by a postprocedure CT, the patient coughed, discharged a small amount of bloody phlegm, and developed chest pain. Then, he lost consciousness and developed shock with severe hypotension and decreased oxygen saturation. After he was administered 100% oxygen through a mask and received a large quantity of hydration, a chest CT was obtained again for suspected pulmonary hemorrhage …

Percutaneous transcatheter mitral valvuloplasty is the indicated treatment of choice for symptomatic native mitral valve stenosis, but there have been limited reports of successful procedures of balloon valvuloplasty for bioprosthetic mitral valve stenosis. We present the case of a 62-year-old woman suffering from progressive dyspnea due to bioprosthetic mitral valve stenosis. The measured mean pressure gradient across the mitral valve was 30 mmHg and the mitral valve area was 0.73 cm(2). Redoing mitral replacement was considered high risk and was refused by the patient. Percutaneous balloon valvuloplasty was performed with an Inoue balloon catheter inflated to 20 mm. The patient's symptoms immediately improved after the procedure, with no procedure-related complications. The mean pressure gradient across the valve decreased to 19 mmHg, and the mitral valve area increased to 1.21 cm(2) in postprocedural echocardiography. We conducted a literature search and identified 26 cases of balloon valvuloplasty for degenerated bioprosthetic valves. Of these, 14 cases were bioprosthetic mitral valves, and the results were favorable. However, more case reports are required to establish an evidence base for future expert recommendation of balloon valvuloplasty of prosthetic mitral valve. Meanwhile, balloon valvuloplasty will serve a niche role in highly selected patients with prosthetic mitral valve stenosis.

Aim Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel is essential after percutaneous coronary intervention (PCI). Clopidogrel is a prodrug and changed into active metabolite by cytochrome p450 enzymes (CYPs), especially CYP2C19. Proton pump inhibitors (PPIs) are used for the prevention of aspirin-induced gastrointestinal bleeding. PPIs are also metabolized by CYP2C19, although the degree of its contribution is dependent on the kind of PPI. Omeprazole, a PPI, has been reported to weaken the antiplatelet effects of clopidogrel. Famotidine, a histamine receptor type 2 (H2) blocker, could also be an alternative to PPIs. The aim of this study was to evaluate the effects of PPIs and an H2 blocker on the antiplatelet function of clopidogrel. Methods Patients receiving DAPT due to prior PCI, who took either omeprazole or rabeprazole, were enrolled (n=25). The initial PPI was changed to the other PPI as a crossover study. In another study, patients undergoing DAPT without taking PPIs or H2 blockers were enrolled (n=30) and famotidine was added. Results Platelet aggregability when taking omeprazole was higher than when taking rabeprazole, evaluated by an optical aggregometer using collagen as a stimulus (p=0.0051) and by the VerifyNow P2Y12 assay (p=0.0060). Platelet aggregability when taking rabeprazole was comparable to that in control patients (n=15). Concomitant use of famotidine had no effect. Conclusion Omeprazole significantly reduced the antiplatelet effect of clopidogrel and this effect on clopidogrel was stronger than that of rabeprazole. Concomitant use of famotidine had no effect on the antiplatelet effect of clopidogrel.

Background— Recently, elevation of circulating muscle-specific microRNA (miRNA) levels has been reported in patients with acute myocardial infarction. However, it is still unclear from which part of the myocardium or under what conditions miRNAs are released into circulating blood. The purpose of this study was to identify the source of elevated levels of circulating miRNAs and their function in cardiovascular diseases. Methods and Results— Serum levels of miRNA (miR)-1 and miR-133a were increased significantly in patients not only with acute myocardial infarction but also with unstable angina pectoris and Takotsubo cardiomyopathy without elevation of serum creatine phosphokinase or cardiac troponin. MicroRNA microarray analysis of the heart from a mouse model of myocardial infarction indicated that the levels of miR-1, miR-133a, miR-208a, and miR-499 were significantly reduced in the infarcted myocardium. In situ hybridization of miR-133a also showed that miR-133a levels were very low in the infarcted and peri-infarcted myocardium. It has been shown that circulating miRNAs are localized inside exosomes, which are released after Ca 2+ stimulation. We stimulated H9c2 cardiomyoblasts with A23187 and measured miR-133a levels in the exosome fraction of the culture medium. A23187 induced a dose-dependent release of miR-133a, and significant elevation was observed only at concentrations where dead cells were detected. We also found that miR-133a–containing exosomes reduced the luciferase activity of 293FT cells transfected with an miR-133a sensor vector. Conclusions— These results suggest that elevated levels of circulating miR-133a in patients with cardiovascular diseases originate mainly from the injured myocardium. Circulating miR-133a can be used as a marker for cardiomyocyte death, and it may have functions in cardiovascular diseases.

Background— Optimal treatment strategies for restenosis of sirolimus-eluting stents (SES) have not been adequately addressed yet. Methods and Results— During the 3-year follow-up of 12 824 patients enrolled in the j-Cypher registry, 1456 lesions in 1298 patients underwent target-lesion revascularization (TLR). Excluding 362 lesions undergoing TLR for stent thrombosis or TLR using treatment modalities other than SES or balloon angioplasty (BA), 1094 lesions with SES-associated restenosis in 990 patients treated with either SES (537 lesions) or BA (557 lesions) constituted the study population for the analysis of recurrent TLR and stent thrombosis after the first TLR. Excluding 24 patients with both SES- and BA-treated lesions, 966 patients constituted the analysis set for the mortality outcome. Cumulative incidence of recurrent TLR in the SES-treated restenosis lesions was significantly lower than that in the BA-treated restenosis lesions (23.8% versus 37.7% at 2 years after the first TLR; P P P =0.4) and 0.6% versus 0.6%, respectively. Conclusions— Repeated implantation of SES for SES-associated restenosis is more effective in preventing recurrent TLR than treatment with BA, without evidence of safety concerns.

The distribution of mouse mammary tumor virus (MMTV) antigens was studied by the immunoper‐oxidase method in the II‐TES and I‐TES mouse strains as well as their progenitors, CS and DBA/2 strains. In the II‐TES, I‐TES and CS strains, and BALB/c mice foster‐nursed with these strains, MMTV antigens were found not only in epithelial cells of the mammary glands but also in those of other tissues including the seminal vesicle, vas deferens, epididymis, prostate, parotid, submandibular, lacrimal, sebaceous, and urethral glands. In DBA/2 and BALB/cfDBA/2 mice, however, the MMTV antigens were found only in the mammary glands. Electron microscopic examination showed MMTV particles in these organs. When we examined the presence of Mtv‐1 and 2 proviruses, which are known to be responsible for MMTV expression, in the genomes of the II‐TES, I‐TES, CS and DBA/2 strains by Southern blotting, Mtv‐2 was not found in any of the mice and Mtv‐1 was found in the II‐TES and DBA/2 mice but not in the I‐TES and CS mice. Instead, four new endogenous MMTV loci, which have never previously been reported in laboratory mouse strains, were detected in the genomes of the II‐TES, I‐TES and CS strains. One (designated Mtv‐42) was common in the three strains and the other three (designated Mtv‐43, 44 and 45) were common in the II‐TES and I‐TES strains or the II‐TES and CS strains. These results thus suggest that new endogenous MMTV loci may be responsible for MMTV expression in a variety of tissues of these three strains.

Background: The clinical guideline for unprotected left main (LM) disease has been updated and percutaneous coronary intervention (PCI) for LM disease has become a common procedure in daily clinical practice. Long-term clinical outcome, however, has not been adequately addressed yet, especially late adverse events beyond 1 year after stent implantation for LM disease. Methods and results: We evaluated long-term clinical outcome including late adverse events beyond 1-year after LM-PCI in consecutive 134 patients who received unprotected LM stenting with sirolimus eluting stents (SES) at Kyoto university hospital between September, 2004 and December, 2009. The mean clinical follow-up period of this study was 4.0±1.8 years. Late Adverse events were defined as sudden cardiac death, target-vessel myocardial infarction (MI), emergent revascularization for LM disease, and acute congestive heart failure (ACHF), which occurred beyond 1 year after stent implantation. The cumulative incidence of all-cause death, cardiac death, and target-lesion revascularization (TLR) for LM disease was 26.5%, 8.1%, and 12.9%, at 5 years after LM-PCI, respectively. The cumulative incidence of cardiac death was significantly higher in patients with 2 stenting technique compared to those with single stenting. Late adverse events were occurred in 6 patients. There are no late adverse events in patients with non-bifurcation LM disease at initial procedure. View this table: Table 1. Late adverse events Conclusions: Five-year clinical outcome of SES implantation for unprotected LM disease was relatively favorable and the risk of late adverse events seemed to be an acceptable range. However, the high risk patient for late adverse events, such as those with true bifurcation lesion and receiving complex stenting, seems to require close observation.

Backgrounds: We previously reported that Peri-Stent contrast Staining (PSS) after Sirolimus-Eluting Stent (SES) was associated with subsequent Very Late Stent Thrombosis (VLST) in a cohort with larger number of patients and longer follow-up duration. However, real clinical characteristics of PSS on VLST remain unknown due to the small numbers of patients with PSS. Methods and results: The j-Cypher PSS substudy included 5712 patients (7838 lesions) with angiographic follow-up within 12 months after SES implantation in 19 participating centers. Late acquired PSS without TLR within 12 months was observed in 174 patients (3.3%) or 183 lesions (2.5%). We found association between VLST and morphologic classification of PSS, 6 out of 8 cases of VLST was segmental types of PSS. Progressive increase in the severity of PSS over time before the onset of VLST was observed in 4 lesions out of 8 lesions with VLST and PSS. Among patients with PSS, those patients who had subsequent VLST were less often had hypertension than those patients without subsequent VLST. Among lesions with PSS, lesion length was significantly longer in lesions with VLST than in lesions without VLST. In patients with PSS finding within the first year, cumulative incidence of VLST through 4 years after the index follow-up angiography was not significantly different between the 2 groups of patients either on or off thienopyridine at 1 year after initial SES implantation. ![Figure][1] Conclusions: Progressive increase in the severity of PSS over time and segmental types of PSS was associated with higher risks for subsequent VLST. Either on or off thienopyridine at 1 year after initial SES implantation was not associated with VLST in the patients with PSS. [1]: pending:yes

The possibility that virus multiplication may be inhibited by interaction of infected cells with uninfected cells was tested by experiments, using human adenovirus type 12 (Ad 12). Permissive human cells (human embryonic kidney = HEK, KB or HeLa) were infected and seeded on uninfected or infected “nonpermissive” cell (human embryonic lung = HEL) monolayers, and virus yields or proportions of viral antigen-synthesizing cells were compared with each other. Both the virus yields and the proportions of viral antigen-positive cells were not reduced significantly when seeded on infected HEL cells, while when seeded on uninfected HEL cells both of them were reduced remarkably, compared with the yield and the proportion of controls seeded on glass. Similar results were obtained regardless of the type of permissive cells, HEK, KB, or HeLa. Similar reduction of the yield was observed when seeded on HEL cells infected with Ad 12 inactivated by heat or by antiserum, and partial reduction was observed when seeded on HEL cells infected with UV-inactivated Ad 12, depending on the extent of UV dosis. These experiments showed that intracellular virus multiplication may be inhibited by interaction of infected cells with uninfected cells, and this may be due to the difference in the cell surface structure.