The importance of atrial fibrillation (AF) as a cause of mortality and morbidity has prompted research on its pathogenesis and treatment. Recognition of AF risk factors is essential to prevent it and reduce the risk of death. Hyperuricemia has been widely accepted to be associated with the incidence of paroxysmal or persistent AF, as well as to the risk of AF in post cardiovascular surgery patients. The possible explanations for this association have been based on their relation with either oxidative stress or inflammation. To investigate the link between hyperuricemia and AF, it is necessary to refer to hyperuricemia-induced atrial remodeling. So far, both ionic channel and structural remodeling caused by hyperuricemia might be plausible explanations for the occurrence of AF. Inhibition of xanthine oxidase and nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, or the use of antioxidants, along with serum uric acid (SUA) level reduction to prevent inflammation, might be useful. Uric acid transporters (UATs) play a key role in the regulation of intracellular uric acid concentration. Intracellular rather than serum uric acid level is considered more important for the pathogenesis of AF. Identification of UATs expressed in cells is thus important, and targeting UATs might become a potential strategy to reduce the risk of hyperuricemia-induced atrial fibrillation.

T1 or longitudinal relaxation time is one of the very fundamental magnetic resonance imaging (MRI) time constants and a tissue characterizing parameter. Only during the last decade did it become possible to quantify T1 values of the myocardium through T1 mapping. Evolving from only region of interest analysis and long acquisition times to the pixel-based parametric mapping and short breath-hold sequences, T1 mapping is reaching maturity among cardiac magnetic resonance (CMR) techniques. Both inversion recovery methods such as MOdified Look-Locker Inversion (MOL-LI) and Shortened MOLLI (ShMOLLI) and saturation recovery methods such as Saturation recovery Single-Shot Acquisition (SASHA) are available for T1 quantification with variable degrees of accuracy, precision, and reproducibility. Native (non-contrast) T1 values increase with edema, amyloid deposition, and fibrosis, while they decrease in fat or iron deposition in the myocardium. These features enabled significant expansion of the clinical applications of native T1 mapping where it provides high sensitivity and specificity and even acts as a disease biomarker or a predictor of prognosis. It is of particular usefulness in diffuse myocardial diseases where conventional CMR techniques might be deceiving. A brighter future for the technique is expected if certain challenges are to be faced, examples of which are the need for standardization of normal values, acquisition techniques, and improving analysis tools.

We published a cardiac event risk score (CERS) predicting the risk of major cardiac events (MCEs) within 3 years. The purpose of this study was to verify the prognostic value of the CERS before and after treatment in Japanese patients with coronary artery disease.
We retrospectively investigated 612 patients who underwent rest ²⁰¹Tl and stress ^99mTc-tetrofosmin myocardial perfusion single photon emission computed tomography (SPECT) between October 2004 and March 2013 and who had a significant stenosis with ≥ 75% narrowing of the arterial diameter detected by coronary angiography performed after confirmation of ≥ 5% ischemia with the SPECT. The patients underwent treatment including revascularization and medication, and thereafter, were re-evaluated with SPECT during a chronic phase and followed-up to confirm prognosis for ≥ 1 year. The endpoint was the onset of MCEs during the follow-up.
During the follow-up (36.7 ± 14.5 months), 50 patients (8.7%) experienced MCEs comprising cardiac death (n = 16), non-fatal myocardial infarction (n = 4), and unstable angina pectoris (n = 30). The multivariate Cox proportional hazards regression model analysis for the actual occurrence of MCEs showed the summed difference score % and MCE risks estimated with the CERS after treatment to be significant independent variables. Ischemic reduction after treatment contributed significantly to a decrease in the MCE risks. The MCE risks estimated with the CERS after treatment were generally consistent with the incidence of the MCEs actually observed.
The CERS after treatment is a valuable formula for predicting prognosis in Japanese patients with coronary artery disease.

The optimal timing of a staged percutaneous coronary intervention (PCI) for non-culprit lesions in patients with STsegment elevation myocardial infarction (STEMI) patients with multi-vessel disease (MVD) remains controversial. We focused on patients with anterior wall STEMI with MVD and determined the clinical effects for timing of staged PCI.
From November 2005 to December 2014, 258 patients were diagnosed with anterior wall STEMI with MVD in our hospital. Among them, 37 patients received staged PCI within 3 weeks, 50 patients received staged PCI during 3 weeks to one year, and 167 patients received only primary PCI for culprit lesions. Clinical outcomes such as admission for angina or heart failure, target vessel revascularization, myocardial infarction, stroke, cardiovascular mortality, and allcause mortality were compared among the 3 groups.
Acute kidney injury (AKI) after PCI occurred in 18.9% of the 3-week group, 0% of the one-year group, and 7.6% of the control group (P = 0.005). Of the one-year and 3-year clinical outcomes, the one-year group had better results, such as fewer major adverse cardiac cerebral events (P = 0.028, P = 0.023), and lower recurrent MI (P = 0.065; P = 0.018), cardiovascular mortality (P = 0.043; P = 0.020), and all-cause mortality (P = 0.047; P = 0.005).
In patients with anterior wall STEMI with MVD, staged PCI for a non-culprit lesion over 3 weeks to one year had a better clinical outcome. Staged PCI for a non-culprit lesion within 3 weeks may be related to the occurrence of AKI, may lead to worse clinical outcomes, and did not decrease the occurrence of angina or post-MI heart failure.

Radiofrequency catheter ablation (RFCA) is a useful therapeutic option for atrial fibrillation (AF), although outcomes are less effective for persistent AF. The aim of this study was to elucidate the echocardiographic parameters associated with successful RFCA in patients with persistent AF.
A total of 159 patients (mean age, 60.8 ± 9.6 years, 125 males [78.6%]) who underwent RFCA for persistent AF from April 2009 to May 2014 were included, retrospectively. Transthoracic echocardiography was performed at baseline, 3 months, 6 months, and 1 year following RFCA. The subjects were divided into 2 groups, a recurrence group and a non-recurrence group. One hundred eleven of the 159 patients (69.8%) remained free from recurrent atrial tachyarrhythmia during follow-up (mean, 20.6 ± 17.4 months). Peak A wave velocity (38.1 ± 14.1 in the recurrence group; 48.0 ± 20.7 in the non-recurrence group, P = 0.01), peak E wave velocity (76.4 ± 19.1 versus 68.8 ± 19.5, P = 0.03), deceleration time (196.3 ± 54.4 versus 219.9 ± 64.1, P = 0.04), and left atrial (LA) diameter (44.5 ± 7.3 versus 41.0 ± 5.6, P = 0.01) at 3 months after ablation were significantly different between the two groups. Among echocardiographic parameters, peak A wave velocity (OR 0.96, 95% confidence interval [CI] 0.92-0.99) and LA diameter (OR 1.13, 95% CI 1.011.25) were associated with AF recurrence.
After RFCA for persistent AF, LA anatomical and functional changes occurred during a 3-month blanking period. Restoration of peak A wave velocity and LA size are associated with successful ablation.

Chronic intravascular hemolysis has been identified in patients with cardiac valve prostheses, but only a few case reports have evaluated intravascular hemolysis in patients with native valvular heart disease. To detect intravascular hemolysis in patients with aortic stenosis, erythrocyte creatine was evaluated with hemodynamic indices obtained by echocardiography.
Erythrocyte creatine, a marker of erythrocyte age, was assayed in 30 patients with aortic stenosis and 10 aged matched healthy volunteers. Peak flow velocity of the aortic valve was determined by continuous-wave Doppler echocardiography. Twenty of 30 patients with aortic stenosis had high erythrocyte creatine levels (> 1.8 µmol/g Hb) and erythrocyte creatine was significantly higher as compared with control subjects (1.98 ± 0.49 versus 1.52 ± 0.19 µmol/g Hb, P = 0.007). Peak transvalvular pressure gradient ranged from 46 to 142 mmHg and peak flow velocity ranged from 3.40 to 5.95 m/second. Patients with aortic stenosis had a significantly lower erythrocyte count (387 ± 40 versus 436 ± 42 × 10⁴ µL, P = 0.002) and hemoglobin (119 ± 11 versus 135 ± 11 g/L, P < 0.001) as compared with control subjects. Erythrocyte creatine had a fair correlation with peak flow velocity (r = 0.55, P = 0.002).
In conclusion, intravascular hemolysis due to destruction of erythrocytes was detected in patients with moderate to severe aortic stenosis and the severity of intravascular hemolysis was related to valvular flow velocity of the aortic valve.

The aim of this study was to determine how older age and co-morbidities affect the treatment decision-making and long-term survival in elderly patients with symptomatic severe valvular heart diseases.
A total of 181 elderly patients (mean age, 78.4 ± 3.4 years) hospitalized between January 2003 and June 2012 with symptomatic severe valvular heart diseases were enrolled. Cardiac and geriatric factors associated with treatment decision-making were analyzed. Survival outcomes were investigated.
Surgical treatment was performed in 116 (64%) patients (surgical group) and 65 patients (36%) were treated conservatively (conservative group). The most common [62% (40/65)] reason for refusing surgical treatment was high operative risk as assessed by the physicians who initially cared for the patients. Multivariate logistic regression analysis identified female gender, chronic renal insufficiency, older age, pneumonia, and emergent status as independent predictors of the conservative treatment. Patients with isolated aortic valve disease tended to undergo an operation. Overall 5-year survival in the surgical group was 76.8% versus 42.9% in the conservative group (P < 0.0001). After matching using the propensity score, the surgical group still had a better long-term survival than the conservative group (P = 0.001). Cox regression analysis revealed conservative treatment as the single risk factor associated with poor long-term survival in all series.
Approximately 40% of the elderly patients with symptomatic severe heart valve disease were treated conservatively despite a definite indication for surgical intervention. Cardiac and geriatric co-morbidities profoundly affect the treatment decision-making. Interdisciplinary discussion should be encouraged to optimize therapeutic options for elderly patients with valvular heart disease.

This study sought to examine the relationships between right ventricular (RV) function and geometry, morbid obesity with and without the metabolic syndrome, and the effect of long-term weight loss. Obese (n = 153, BMI 41.2 ± 8.7 kg/m²) and healthy non-obese control subjects (n = 38, BMI 25.5 ± 3.3 kg/m²) of similar age and gender distribution were prospectively studied during the course of a 1-year weight reduction program with echocardiography at baseline and after one year of follow up. Function and geometry of the right heart were evaluated by tricuspid annular plane systolic excursion (TAPSE), tricuspid annular systolic velocity (TDI S’), RV myocardial performance index (TEI), RV end-diastolic (RVEDD) and end-systolic diameter (RVESD), area of the right atrium (RAA), and systolic pulmonary artery pressure (PAP). Whereas parameters of systolic and diastolic LV function were significantly worse in the obese subjects than those in the non-obese subjects (EF 66 ± 6 versus 69 ± 6%, P = 0.004; E/E’ 7.4 ± 2.5 versus 6.3 ± 2.6, P = 0.010), parameters of RV function (TAPSE 25.6 ± 4.5 versus 25.1 ± 3.5 mm, P = 0.528; TDI S’ 13.5 ± 2.9 versus 13.8 ± 2.9 mm/second, P = 0.553; TEI 0.25 ± 0.13 versus 0.28 ± 0.09, P = 0.283) as well as geometry measurements were comparable between the obese and non-obese participants and also in obese subjects with full blown metabolic syndrome. Additionally, successful weight reduction did not alter the RV parameters. Nevertheless, in the few obese subjects with RV dysfunction (n = 7), metabolic syndrome parameters were more pronounced than in obese with normal RV function.
Morbid obesity with and without the metabolic syndrome is accompanied by an impaired LV systolic and diastolic function. In contrast, RV function appears to be less affected by obesity independent of the presence of the metabolic syndrome.

The use of measured data as boundary conditions renders hemodynamic simulations more patient-specific. However, synchronized acquisition of data at multiple locations is often difficult in clinical practice. This study proposes a method for resynchronizing measured data for use as boundary conditions for flow simulations using frequency analyses, and discusses the optimal cut-off frequency for differentiating cardiac and respiratory variation in hemodynamic data during resynchronization. To demonstrate the utility of the method, a Fontan circulation, which is the final palliative result with single-ventricle physiology, was used. The results suggest that it is optimal to set a cut-off frequency that gives a local minimum in the power spectrum that is slightly lower than the peak frequency of the heartbeat. Additionally, the total energy loss depended on the cut-off frequency, although the overall flow patterns appeared to be similar. The method is applicable to cardiovascular systems other than the Fontan circulation, where hemodynamic data with multifactorial fluctuations are required at various locations but simultaneous measurements are not possible.

Marfan syndrome (MFS) is a systemic connective tissue disorder that is caused by mutations of fibrillin-1. While MFS patients are at a high risk of periodontitis and aortic diseases, little causal information has been provided to date. To clarify the relationship, their oral condition and sinus of Valsalva (SoV) were evaluated.
The subjects were patients with MFS (n = 33) who attended the University of Tokyo Hospital. We divided them into two groups; MFS patients with highly dilated (the diameters were equal to or more than 39 mm) SoV (high group, n = 18) and MFS patients with mildly dilated (less than 39 mm) SoV (mild group, n = 15). Blood examinations, echocardiograms, and full-mouth clinical measurements, including number of teeth, probing pocket depth (PPD), bleeding on probing (BOP), and community periodontal index (CPI) were performed.
We found that the high group patients had greater rates of BOP compared to that of the mild group. Furthermore, the high group tended to have higher serum levels of C-reactive protein, matrix metalloproteinase-9, and transforming growth factor-β compared to the mild group.
Periodontitis may deteriorate SoV dilatation in MFS patients.

The renin-angiotensin-aldosterone system (RAAS) and arginine vasopressin (AVP) regulate body fluids. Although conventional diuretics have been used for treating heart failure, they activate RAAS and exacerbate renal function. Tolvaptan, a newly developed vasopressin-2 receptor antagonist, elicits aquaresis and improves volume overload in heart failure patients, however, the predictors of tolvaptan effectiveness and the influence on the RAAS and renal function according to tolvaptan therapy are not established. We evaluated 26 chronic heart failure patients receiving therapy with 15 mg/day tolvaptan and examined their laboratory and urinary data before and after tolvaptan therapy. A response to tolvaptan was defined as a body weight decrease by more than 2 kg in a week and a urine volume increase by 500 mL/ day compared with that before tolvaptan administration. Body weight, urine volume, and brain natriuretic peptide levels significantly improved (P < 0.05), without any worsening of renal function represented by serum creatinine, sodium, and potassium. Moreover, no significant changes were observed in the plasma renin activity and plasma aldosterone concentration (PAC). In the responder group, urine osmolality before tolvaptan administration was significantly higher (P < 0.05) but declined significantly after tolvaptan administration (P < 0.05). The AVP/PAC ratio before administration was positively correlated with the efficacy of tolvaptan. Tolvaptan treatment could prevent RAAS activation in chronic heart failure patients. Moreover, monitoring the AVP/PAC ratio may be useful in predicting the tolvaptan response.

Pulmonary arterial hypertension (PAH) is a disease that imposes a significant burden on patients. Although multiple treatment options for PAH are available, head-to-head comparisons are difficult to conduct. Network meta-analysis (NMA) can be a useful alternative for direct comparison to estimate the relative effectiveness of multiple treatments. The objective of the present study was to conduct a systematic review and NMA to evaluate the relative effectiveness among oral PAH medications.
Data collection was performed by searching the Cochrane Central Register of Controlled Trials (CENTRAL) and Ichushi-Web. Randomized controlled trials (RCTs) assessing at least 1 of the following 3 outcome measurements; 6-minute walk distance test (6MWD), WHO functional class (WHOFC), and mean pulmonary artery pressure (mPAP) were included (PROSPERO registration number: CRD42015016557). Outcomes were evaluated by estimating the differences in the mean change from baseline or by estimating the odds ratios. Analyses were performed using WinBUGS 1.4.3.
Seven double-blind RCTs were eligible. NMA results showed similar improvements in 6MWD for all medications assessed. Bosentan and sildenafil caused a statistically significant improvement in WHOFC compared to other medications.
The relative effectiveness of oral PAH medications could be compared using NMA, which suggested the superiority of bosentan and sildenafil in the improvement of WHOFC.

To summarize the therapeutic effects of modified double root translocation (MDRT) in the management of congenital heart disease-transposition of great arteries (TGA) with ventricular septum defect (VSD) and left ventricular outflow tract obstruction (LVOTO). From May 2013 to March 2015, we treated 6 patients (4 males, 2 females, aged from 1 year and 8 months old to 5 years old) with complete transposition of great arteries with left ventricular outflow tract obstruction, SaO₂ 54 ± 7.3%; the outflow velocity of the left ventricular or pulmonary valve measured by Doppler was 4.46 ± 0.15 m/s, and the Nakata index was 217 ± 32 cm²/m². We carried out a double root translocation operation on these 6 patients.
One patient developed low cardiac output syndrome 4 hours after the operation. Extracorporeal membrane oxygenation (ECMO) was performed, but the patient died of multiple organ failure. The other 5 patients all recovered and were discharged from the hospital. During the 3-month to 2-year follow-up period, these 5 patients all demonstrated NYHA Class I or NYHA Class II LVEF (65 ± 2.7) %; 4 had mild pulmonary regurgitation, 1 moderate pulmonary regurgitation; 3 no aortic regurgitation, and 2 micro aortic regurgitation, SaO₂ 99 ± 0.4%.
Modified double root translocation is an effective treatment method in the management of complete transposition of great arteries with left ventricular outflow tract obstruction.

Sirt1 is a highly conserved nicotinamide adenine dinucleotide (NAD⁺) dependent histone deacetylase which plays an important role in heart diseases. Studies performed with Sirt1 activators indicated that it protects cells from ischemia/ reperfusion (I/R) injury. The protective effects of H₂S against I/R injury also have been recognized. Hence, the present study was designed to explore whether Sirt1/PGC-1α participates in the protection of exogenous H₂S postconditioning against I/R injury in isolated rat hearts. Isolated rat hearts were subjected to 30 minutes of global ischemia followed by 60 minutes of reperfusion after 20 minutes of equilibrium. During this procedure, the hearts were exposed to NaHS (10 μmol/L) treatment in the absence or presence of the selective Sirt1 inhibitor EX-527 (10 μmol/L). NaHS exerted a protective effect on isolated rat hearts subjected to I/R, as shown by the improved expression of Sirt1/PGC-1α associated with restoration of Sirt1 nuclear localization, cardiac function, decreased myocardial infarct size, decreased myocardial enzyme release, and several biochemical parameters, including up-regulation of the ATP and SOD levels, and down-regulation of the MDA level. However, treatment with EX-527 could partially prevent the above effects of NaHS postconditioning. These results indicate that H₂S confers protective effects against I/R injury through the activation of Sirt1/PGC1α.

This study aimed to investigate the effects and molecular mechanism of cyclosporin A (CsA) on cobalt chloride (CoCl₂)-induced injury in H9c2 embryonic rat cardiac cells. The results showed that CsA could protect H9c2 cells against CoCl₂-induced hypoxic injury. CsA effectively improved cell viability, and decreased LDH leakage, cell apoptosis, MDA concentration, and ROS generation, and increased SOD activity, GSH production, and CAT activity in a dosedependent manner. In addition, CsA treatment blocked the CoCl₂-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways. The results also suggested that CsA protected H9c2 cells against CoCl₂-induced hypoxic injury, possibly by suppressing the MAPK signaling pathway. Thus, CsA is a potential therapeutic agent for cardiac hypoxic injury.

Down syndrome (DS) is a common chromosome 21 abnormality disease, leading to various health problems, especially atrioventricular septal defect (AVSD). Genes and microRNAs (miRNAs) associated with AVSD in DS patients still need in-depth study.
Gene expression data (GSE34457) of 22 DS patients without congenital heart disease and 7 DS patients with AVSD were downloaded from Gene Expression Omnibus. After screening differentially expressed genes (DEGs) based on limma package in R (criteria: P < 0.05 and |log2 fold change (FC)| > 0.5), pathway and functional enrichment analyses were performed using the online software DAVID (criterion: P < 0.05). The protein-protein interaction (PPI) networks of DEGs were constructed based on the online server STRING (criterion: combined score > 0.4). Next, miRNAs that targeted DEGs were predicted based on Webgestalt (criteria: P < 0.05 and target DEGs ≥ 2), and miRNA-DEG regulatory networks were visualized through Cytoscape.
A total of 179 DEGs were identified. Next, 5 functions and 1 pathway were enriched by up-regulated DEGs, while 4 functions were enriched by down-regulated DEGs. Furthermore, miRNA-DEG regulatory networks were constructed. IL1B was the hub-gene of PPI networks, and AUTS2 and KIAA2022 were predicted to be targeted by miR-518a, miR518e, miR-518f, miR-528a, and miR-96.
IL1B, IL12RB2, AUTS2, and KIAA2022 might participate in AVSD in DS patients, and AUTS2 and KIAA2022 might be targeted by miR-518a, miR-518e, miR-518f, miR-528a, and miR-96. The identified genes and miRNAs might provide a theoretical basis for understanding AVSD in DS patients.

This study was conducted to evaluate the safety and efficacy of tolvaptan following open heart surgery.
We retrospectively reviewed 109 patients who were administered tolvaptan following open heart surgery between August 2011 and July 2014. We divided the patients according to their urine output index (amount of urine output/body surface area) into tertiles as follows: T1 (low responders; n = 36), T2 (intermediate responders; n = 36), and T3 (high responders; n = 37). No fatal adverse events were observed following tolvaptan administration. The factors that showed a significant difference among the 3 groups were body surface area (BSA) and preoperative body weight. Body weight rapidly decreased and a greater increase in the serum sodium level was observed on day 1 in the T3 group than in the other 2 groups. No decrease in blood pressure and no significant differences in the occurrence of atrial fibrillation were observed among the 3 groups during tolvaptan administration.
Tolvaptan can be safely and effectively administered to increase the urine output without adversely affecting the cardiovascular system or renal function following open heart surgery. However, careful attention is required regarding the possibility of a rapid increase in the serum sodium level so it is important to monitor changes in serum Na levels.

In recent years, the use of a retrograde approach has become a common practice in the treatment of chronic total occlusion (CTO) of the coronary ostium and artery with an anomalous origin. Use of this approach has increased the chances of a successful percutaneous coronary intervention (PCI). However, the approach requires capturing the retrograde guidewire within the aorta, which can often pose a problem. Therefore, we developed a technique in which the retrograde guidewire is passed through the CTO and inserted directly into the antegrade guiding catheter in the ascending aorta. This technique enabled the successful treatment of the ostial CTO of the right coronary artery using retrograde PCI.

We report the case of a 66 year-old woman with chronic atrial fibrillation, hypertrophic cardiomyopathy (HCM), and spinocerebellar atrophy (SCA). Her mother and first-born son had died of heart disease at the ages of 65 and 16 years, respectively. Four of her 8 siblings had died suddenly of unknown cause or of heart disease, and 2 others of cerebral infarction by the 7th decade. Genetic testing revealed that she had a novel mutation (c. 482C > A, p. Ala161Asp) in the troponin I gene (TNNI3), and no abnormality of the GAA repeat in the frataxin gene. Her older brother with SCA but without HCM was also analyzed, with no abnormality noted in either gene. The Ala161Asp mutation in TNNI3 was implicated in the pathogenesis of her HCM, though an association between HCM and SCA was not revealed.

Adaptive servo-ventilation support and Waon therapy are recently developed non-pharmacological and noninvasive therapies for patients with heart failure refractory to guideline-directed medical therapy. These therapies decrease both preload and afterload, increase cardiac output, and appear to ameliorate autonomic nerve activity. However, the time course of autonomic nerve activity during these therapies remains unclear. We performed heart rate variability analysis using the MemCalc power spectral density method (MemCalc system; Suwa Trust Co, Tokyo) to assess autonomic nerve activity during adaptive servo-ventilation support and Waon therapy in two different cases and determined the time course of autonomic nerve activity during these therapies. During both therapies, we found a drastic increase in parasympathetic nerve activity and continuous suppression of sympathetic nerve activity. Heart rate variability analysis using the MemCalc method may be promising for the assessment of the efficacy of various treatments, including adaptive servo-ventilation support and Waon therapy, from the viewpoint of autonomic nerve activity.

We experienced a patient who had received an implantable continuous-flow left ventricular assist device (LVAD) (HeartMate II, Thoratec Corp, Pleasanton, CA, USA) and was admitted to our hospital because of repeated ventricular tachyarrhythmias refractory to electrical defibrillation as well as intensive pharmacological therapy. We decided to discontinue defibrillating, but under ventricular fibrillation his hemodynamics were maintained without end-organ dysfunction during LVAD support (mean right atrial pressure 18 mmHg; pulmonary vascular resistance 1.6 WU; pulmonary capillary wedge pressure 11 mmHg; cardiac index 2.04 L/minute/m²) due to optimization of the rotation speed (from 8800 to 9200 rpm). Such “Fontan-like circulation” could be accomplished by adequate volume control, lowering pulmonary vascular resistance, and potent LV blood removal by optimal rotation speed of the LVAD, although the precise conditions to maintain the Fontan-like circulation during LVAD therapy remained uncertain. Considering the severe donor heart shortage and high degree of difficulty of the catheter ablation procedure to manage ventricular tachyarrhythmias, constructing a Fontan-like circulation in the presence of ventricular tachyarrhythmias may be one unique strategy. Longterm prognosis in patients with sustained ventricular tachyarrhythmias during LVAD support would be a future concern.

Traumatic ventricular septal defect (VSD) resulting from chest trauma, either penetrating or blunt, is a relatively rare occurrence. Herein, we describe the case of a previously healthy 26-year-old man who presented with congestive heart failure, which was secondary to a large traumatic VSD following violent blunt chest trauma. The traumatic VSD was initially closed percutaneously using an Amplatzer atrial septal defect occluder. Post-device closure, however, the patient developed severe intravascular hemolysis refractory to medical treatment. The patient subsequently underwent surgical removal of the Amplatzer device, with concomitant VSD patch closure.

Postoperative junctional ectopic tachycardia (JET) is a narrow complex tachycardia and most frequently occurs during and after surgical repair of certain types of congenital heart defects. Postoperative junctional ectopic tachycardia may produce unfavorable hemodynamics that prolongs stays in the cardiac intensive care unit and hospital, prolongs time on a ventilator, and occasionally requires the use of extracorporeal membrane oxygenation (ECMO) as rescue therapy. The present report describes a rare case of late-onset postoperative junctional ectopic tachycardia, which occurred 13 days after the deployment of a perimembranous ventricular septal defect (PmVSD) occluder in a 17-year-old female teenager. To the best of our knowledge, late-onset postoperative junctional ectopic tachycardia has not previously been reported as a complication in nonsurgical procedures. In this case, the junctional ectopic tachycardia remained resistant to medicines and the haemodynamic imbalance caused a serious life-threatening situation in the patient. The occluder was removed by an emergent thoracotomy; then, the patient was successfully cured by being supported with extracorporeal membrane oxygenation. The findings suggest that during follow-up management, the physician should pay attention postoperatively to junctional ectopic tachycardia even after discharge from the hospital.