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Background: Fulminant myocarditis presentation (FMP) is a rare and severe presentation of myocarditis. The natural history of FMP and its clinical features associated with poor outcomes are incompletely understood because there is a lack of generalizable evidence. Methods: This multicenter retrospective cohort study included patients hospitalized with histologically proven myocarditis who underwent catecholamine or mechanical support from 235 cardiovascular training hospitals across Japan between April 2012 and March 2017. Clinical features and the prognostic predictors of death or heart transplantation within 90 days on the basis of clinical and pathologic findings were determined using the Kaplan-Meier method, log-rank test, and Cox regression analysis. Results: This study included 344 patients with histologically proven FMP (median age, 54 years; 40% female). The median follow-up was 600 days (interquartile range, 36 to 1599 days) and the cumulative risk of death or heart transplantation at 90 days was 29% (n=98). Results from multivariable Cox regression analysis showed that older age, nonsinus rhythm, low left ventricular wall motion ( Conclusions: The results from analyses of data from this multicenter registry demonstrated that patients with FMP are at a higher risk of death or heart transplantation in real-world settings. These observations inform which clinical and pathologic findings may be useful for prognostication in FMP. Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000039763.

Background Although co‐occurrence of sleep disorder with heart failure is known, it is not clear whether that condition is a cause or consequence of heart failure. The present study was conducted as a longitudinal examination of the predictive value of sleep parameters on progression of left ventricular diastolic dysfunction. Methods and Results Four‐hundred fifty‐two subjects were followed for a mean of 34.7 months. An outcome of diastolic dysfunction was defined as increase in early inflow velocity/early diastolic tissue velocity >14. Sleep apnea‐hypopnea index, minimal oxygen saturation, sleep duration, and activity index (physical movement during sleep time, a potential parameter of poor sleep quality) were determined using apnomonitor and actigraphy findings, while heart rate variability was measured with a 24‐hour active tracer device. Sixty‐six of the patients developed diastolic dysfunction during the follow‐up period, with a median time of 25 months. Kaplan–Meier analysis results revealed that those with sleep apnea classified as moderate (apnea‐hypopnea index 15 to P P P P =0.27) had a significantly greater risk for a diastolic dysfunction event. Results of multivariable Cox proportional hazards regression analysis indicated that moderate to severe sleep apnea after a follow‐up period of 3 years (hazard ratio [HR], 9.26 [95% CI, 1.89–45.26], P P =0.04) were significantly and independently associated with future diastolic dysfunction. Moreover, significant association of high activity index with the outcome was not confounded by either minimal oxygen saturation or heart rate variability. Conclusions Sleep apnea and physical movement during sleep, but not sleep duration and autonomic nervous dysfunction, are independent important predictors for progression of left ventricular diastolic dysfunction.

Iron deficiency is linked to worse clinical status and outcomes in heart failure. Although metabolic syndrome contributes to the development of heart failure, the impact of iron deficiency in heart failure complicated with metabolic syndrome remains obscure. KKAy mice were used as a model of metabolic syndrome. Four-week-old male C57BL/6J and KKAy mice were fed either a normal diet or iron-restricted (IR) diet for 12 weeks. During the experiment, 40% of mice died due to pulmonary congestion in KKAy mice with IR diet (KKAy-IR), while no mice died in other groups. Necropsy showed the presence of multiple white lesions on the cardiac surface in those KKAy-IR mice. Echocardiography and histological analyses revealed that KKAy-IR mice exhibited cardiac hypertrophy and cardiac dysfunction with cardiac calcification. Cardiac mRNA of ectonucleotide pyrophosphatase/phosphodiesterase-1 (Enpp1), a key enzyme for bone mineralization, was highly abundant in KKAy-IR mice. Of note, iron restriction-induced cardiac calcification and dysfunction were attenuated by etidronate, an inhibitor of bone mineralization, with decreased cardiac Enpp1 mRNA abundance in KKAy-IR mice. In conclusion, iron deficiency leads to ectopic cardiac calcification and dysfunction with the increase of Enpp1 in metabolic syndrome model mice.

Introduction: As Chimeric Antigen Receptor T cell (CAR-T) therapy gains its clinical advantage in the management of diffuse large B cell lymphoma (DLBCL), accumulating evidence shows that it often accompanies cardiac dysfunction. Previous retrospective studies indicated the involvement of cytokine release syndrome (CRS) in cardiac dysfunction after CAR-T therapy, but their association is not fully investigated. Therefore, we designed a prospective study to clarify the association between the grade of CRS and cardiac dysfunction in the DLBCL patients after CAR-T therapy. Methods: In this prospective study, 14 DLBCL patients who underwent CAR-T therapy from July 2020 to May 2021 were enrolled. Before and after CAR-T therapy, we collected the levels of troponin T (TnT) as a marker for myocardial damage, left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) as markers for systolic function, and E/e’ and left atrial volume index (LAVI) as markers for diastolic function. We classified all patients into two groups according to the severity of CRS after CAR-T therapy, namely the low-CRS Group (CRS Results: Average age was 56.4 years and 7 patients (50%) were female. The number of patients in the low-CRS and high-CRS Group were 11 and 3, respectively. Before CAR-T therapy, there were no differences in cardiac function between the two groups. From the hyper-early phase of CAR-T therapy, the increase of TnT, E/e’ and LAVI from the baseline were significantly larger in the high-CRS Group compared to the low-CRS Group (P=0.023, 0.039, and 0.024, respectively). Subsequently, the decrease of GLS from the baseline became significantly larger in the high-CRS Group compared to the low-CRS Group (P=0.049). These results indicated that cardiac dysfunction after CAR-T therapy occurred in the order of myocardial damage, diastolic dysfunction, and systolic dysfunction. Conclusion: We for the first time demonstrated the association between high-grade CRS and cardiac dysfunction after CAR-T therapy through a prospective study.

Introduction: The slow conduction zone (SCZ) in the left atrium (LA) has attracted attention as an arrhythmia substrate of atrial fibrillation (AF). However, the occurrence mechanism of SCZ remains unclear. Hypothesis: The SCZ is related to the low voltage area (LVA) or the LA anatomical contact areas (CoAs) with other organs in patients with AF. Methods: We studied 100 patients (49 non-paroxysmal AF, 66 males, 67.9 ± 9.9 years) who received catheter ablation for AF. High-density LA mapping during right atrial appendage pacing at a rate of 100 bpm after pulmonary vein isolation were constructed. Isochronal activation maps were created at 5-ms interval setting, and the SCZ was identified on the activation map by finding a site with isochronal crowding of ≥3 isochrones, which are calculated as ≤27 cm/s (Figure). The LVA was defined as the following; mild ( Results: The SCZ was distributed linearly (Figure), and observed in 95 of 100 patients (95%). The SCZ was most frequently observed in the anterior wall region (77%). A longer SCZ was significantly associated with a larger LA size and a prevalence of non-PAF. The 51.2±36.2% of SCZ overlapped with mild LVA, 32.9±32.8% of SCZ with moderate LVA, and 14.6±22.0% of SCZ with severe LVA. In contrast, only 25.6±28.0 % of SCZ matched with the CoAs. Conclusion: The slow conduction zone reflects LA electrical remodeling and may be a precursor finding of the low voltage zone, not LA contact areas in patients with atrial fibrillation.

Background and aim: It has been known that bifurcation angles of common iliac artery (CIA) are not always bilateral symmetry. Previous study reported that mechanical stress initiate calcification in aortic valve. The aim of this study was to investigate the impact of CIA anatomical features on lesion characteristic of CIA. Methods and results: This study enrolled 72 patients with intermittent claudication who had undergone endovascular-therapy (EVT) for de novo CIA atherosclerotic lesions in our hospital during April 2012 to March 2017. Anatomical analysis of CIA bifurcation was assessed by frontal view of initial angiography at EVT. We calculated the bilateral CIA angles between axis of terminal aorta and axis of proximal CIA, and bilateral symmetry was expressed as absolute value of the difference between both CIA angles (Δangle). The patients were divided into 2 groups: symmetry group (Δangle≦10 degrees, n=40) and asymmetry group (Δangle>10 degrees, n=32), according to the mean of Δangle. Distribution characteristics were classified into 2 patterns: bilateral lesions pattern and unilateral lesion pattern, furthermore we assessed calcified nodule of CIA lesion using intravascular ultrasound. There was no difference between 2 groups about patient characteristics. Unilateral lesion was observed in asymmetry group much more than symmetry group (63% vs 22%, P Conclusions: These findings suggested that asymmetric bifurcation angle of CIA was associated with unilateral lesion and calcified nodule lesion. Asymmetry of CIA bifurcation might be predictor of unilateral calcified nodule lesion of CIA.

Background: Brain natriuretic peptide (BNP) is routinely measured for evaluating the severity of acute decompensated heart failure (ADHF). However, there are no other biomarkers for stratification of ADHF patients in clinical settings. Cardiac myosin I (CM-I) is one of a superfamily of motor proteins, which is mainly distributed in myocardium. Several papers reported that serum CM-I levels increased in patients with acute coronary syndrome (ACS). However, the role of CM-I in ADHF patients is not yet elucidated. Purpose: The aim of this study was to clarify the utility of CM-I in ADHF patients. Methods: We assessed 114 ADHF patients who visited our institution between December 2017 and May 2018 in a retrospective study. All patients were diagnosed ADHF using Framingham criteria. Eight ACS patients and 22 patients lacking in data of serum CM-I levels were excluded. Finally, we analyzed 84 patients. We calculated the difference in serum BNP levels between on admission and at discharge (delta BNP) as a prognostic surrogate marker. Results: Average age was 77.5 years old and 44 patients were male. Numbers of patients with NYHA III and IV were 30 and 36, respectively. Mean serum levels of BNP and Troponin T (TrT) on admission were 934.0 pg/ml and 0.092 ng/ml, respectively. Average left ventricular ejection fraction (LVEF) by echocardiography was 46.1%. Serum CM-I levels on admission and at discharge were 12.8 mg/ml and 7.30 mg/ml, respectively. Serum CM-I levels had a significant correlation with TrT levels (R=0.46, p Conclusion: We found CM-I was associated with the difference in BNP between on admission and at discharge in ADHF patients. CM-I may be a new potential prognostic biomarker in ADHF patients.

Background: Adverse cardiac remodeling (ACR) during pressure overload is a major concern in development of heart failure (HF). Cardiac reverse remodeling (CRR) normally occurs following induction of beta-receptor blockade and is linked to improved prognosis of HF. However, the detailed and regulatory mechanisms of both ACR and CRR remain to be fully elucidated. To solve these issues, a novel highly reproducible model that mimics these pathophysiological conditions is needed. Methods and results: We explored suitable experimental conditions for establishing a highly reproducible model that mimics adverse cardiac remodeling. To examine suitable durations of transverse aortic constriction (TAC) before one-week infusion of ISO (3mg/kg/day), mice were distributed into three groups according to TAC durations. Proportion of adverse cardiac remodeling was 44.4% (4 of 9) in one-week, 60.0% (6 of 10) in two-week, and 91.7% (11 of 12) in three-week TAC groups. Next we examined adequate dose of ISO infusion after three weeks of TAC. Proportion of adverse cardiac remodeling was 37.5% (3 of 8) in 1mg/kg/day, 83.3% (5 of 6) in 3mg/kg/day, and 100% (8 of 8) in 10mg/kg/day group. But infusion of 10mg/kg/day ISO caused an increase in systolic BP. Thus we identified 3-week TAC and subsequent one-week ISO (3mg/kg/day) infusion as a suitable model for ACR. To identify molecular signatures of failing hearts of our ACR model, we performed RNA-Seq analyses. We found the up-regulated genes were mainly related to fibrosis including Fbn1 , C1qtnf6 and Loxl2 and the down-regulated genes associated with mitochondrial functions including, Uqcrc1 , Ndufs3 , and Idh2 . Next, we followed the changes in cardiac function after ceasing ISO to investigate CRR. Decreased LVFS gradually recovered to baseline within 7 weeks after cessation of ISO and exhibited CRR. Gene expression signature of CRR hearts was almost identical to that of TAC hearts without ISO infusion. Conclusions: Our model exhibits a transition to adverse cardiac remodeling and subsequent reverse remodeling with high reproducibility. This novel mouse model might add new insights into these cardiac remodeling.

Objective: Angiogenesis can be triggered under conditions of ischemia and plays a protective role in peripheral artery disease. Iron is an essential trace mineral in the living body whose intracellular metabolism is regulated by transferrin receptor 1 (TfR1). Excess iron causes tissue damage and has been reported in patients with peripheral artery disease. Therefore, we hypothesized that TfR1 contributes to the pathophysiology of hind limb ischemia through iron overload. The aim of this study is to examine whether TfR1 deletion effects angiogenesis in hind limb ischemia. Methods and Results: Since homozygous TfR1 deletion is embryonically lethal, mice with heterozygous TfR1 deletion and their wild type littermates were used in this study. To induce hind limb ischemia, the left femoral artery in 8 - 9 week-old male mice was ligated and stripped. The non-ligated right hind limb was used as a control. Blood flow was measured by laser Doppler blood flowmetry at both a baseline of 1 hour and 28 days after the surgery. In wild type, the ratio of ischemc/non-ischemic hind limb blood flow was significantly decreased to 12% at baseline, and recovered to 62% at day 28. On the other hand, TfR1 deleted mice also showed similar reduction of blood flow at baseline, whereas blood flow recovery at day 28 was attenuated to 42%. Subsequently, both right and left adductor muscles were harvested for Western blot and immunohistochemistry. TfR1 expression in the adductor muscle was decreased in TfR1 deleted mice compared to wild type, regardless of the ligation. Ferritin, a marker for iron storage, was 10 times higher in ischemic muscles than in wild type non-ischemic muscles. In contrast, ferritin levels in TfR1 deleted mice were not altered by the surgery. Finally, immunohistochemistry for CD31 was performed to evaluate angiogenesis. The ischemic adductor muscle of TfR1 deleted mice had few CD31 positive vascular structures. Conclusions: Heterozygous deletion of TfR1 attenuated iron overload and angiogenesis in a mouse model of hind limb ischemia. TfR1 may be a novel therapeutic target for the treatment of peripheral artery disease.

AIM: How sildenafil acutely provides hemodynamic alterations in patients with decompensated congestive heart failure remains unknown. The aim of this study was to investigate whether myocardial and/or hemodynamic conditions affect hemodynamic response to sildenafil in patients with decompensated heart failure. METHODS AND RESULTS: Twenty-five consecutive patients with decompensated congestive heart failure were enrolled. The patients underwent echocardiography before and 1 hour after a single oral administration of sildenafil (20 mg). Sildenafil decreased pulmonary vascular resistance by 24% (P < 0.05), and increased left ventricular (LV) time-velocity integral by 17% (P < 0.05). Alteration of the ratio of peak velocity of early LV filling to early diastolic myocardial velocity (E/E'), an indicator of LV filling pressure, following administration of sildenafil, negatively associated with the deceleration time of early filling wave (DcT) at baseline. Patients with baseline DcT ≥ 200 milliseconds (n = 11) exhibited E/E' increase, whereas patients with baseline DcT

A 69-year-old woman and a 29-year-old man were admitted to our hospital after successful resuscitation of out-of hospital cardiac arrest. In the first case, electrocardiogram showed mild ST-segment elevation in leads V3-V5. Coronary angiography did not show any obstructive coronary artery disease, and left ventriculography showed apical ballooning of the left ventricular chamber. She was diagnosed as having the classic form of tako-tsubo cardiomyopathy. In the second case, electrocardiogram did not show ST-segment elevation in any lead. Coronary angiography showed no coronary artery disease and left ventriculography showed basal ballooning of the left ventricular chamber. He was diagnosed as having the variant form of tako-tsubo cardiomyopathy. In both cases, left ventricular function returned to normal, but they died of multiple organ failure. In conclusion, cardiologists should recognize that takotsubo cardiomyopathy can occur even after successful resuscitation of cardiac arrest. Early diagnosis and appropriate intensive care are essential in these critically ill patients.

Introduction: We have recently reported the cause of microcirculatory damage after percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) patients can be evaluated by analyzing the thermodilution-derived coronary blood flow pattern (CBFP), and only the capillary destruction pattern was associated with poor mid-term clinical outcomes. In this study, we extend our research on the contribution of acute hyperglycemia on microcirculatory damage and long-term clinical outcomes in STEMI patient. Methods: Ninety-seven consecutive STEMI patients undergoing primary PCI were prospectively enrolled. Using a pressure sensor/thermistor-tipped guidewire, CBFP was assessed from the thermodilution-curves immediately after successful PCI. All patients were classified into 3 groups according to the shape of thermodilution curve: no microvascular damaged group (n=47), arteriole microemboli group (n=33), or capillary destruction group (n=17). Blood glucose levels were measured on admission. Major adverse cardiac events (MACE) were defined as a composite of cardiac death, myocardial infarction, and heart failure rehospitalization within 3 years. Results: Mean admission glucose level was significantly higher in the capillary destruction group than in the microemboli and no microvascular damaged groups (259±134, 162±66, and 153±60 mg/dL, respectively, p Conclusions: Hyperglycemia on admission increases the risk of microvascular damage secondary to the capillary destruction and subsequent poor long-term clinical outcomes in STEMI patients.

Purpose: Several studies have reported gender difference in presentation, management and outcome in patients with acute myocardial infarction (AMI). In this study, we focused the impact of age on gender difference in mortality after AMI. Methods: Between July 2012 and March 2014, 3283 patients were admitted to the 28 hospitals participating to the J-MINUET group within 48 hours after the onset of AMI. AMI was diagnosed by universal definition (type 1 or type 2). Patients were divided into 5 strata according to their age: those with age Results: There were 813 women (24.8%). Women were significantly older than men (74.5±11.8 years vs 66.6±12.3 years, P Conclusions: Women had higher in-hospital mortality than men after AMI even in the contemporary troponin era. However, their high mortality was mostly explained by their advanced age.

Introduction: Ezetimibe (EZE) is a cholesterol absorption inhibitor and its clinical benefit, as combined with statin for pts with coronary artery disease (CAD), was shown by IMPROVE-IT trial. Campesterol (camp) is the cholesterol absorption marker and the benefit of EZE/statin combination therapy for pts with low camp (LC) value, in whom EZE appears to ineffective, is not clearly understood. The PRECISE-IVUS (Plaque REgression with Cholesterol absorption Inhibitor or Synthesis inhibitor Evaluated by IntraVascular UltraSound) trial was a prospective, randomized, controlled, multicenter study evaluating the effects of EZE addition to atorvastatin (atorva), compared with atorva monotherapy, on coronary atherosclerosis evaluated by IVUS and lipid profile. Hypothesis: In this study, we investigated the effect of EZE for pts with the LC value. Methods: 246 pts undergoing IVUS-guided percutaneous coronary intervention were randomized to EZE/atorva combination (EA) group or atorva alone (A) group. The dosage of atorva was uptitrated with a treatment goal of lowering low-density lipoprotein cholesterol (LDL-C) below 70mg/dL. Serial volumetric IVUS was performed at baseline and 9–12 months follow-up to quantify the coronary plaque response in 202 patients. Results: There were significantly positive correlation between baseline LDL-C level and baseline camp value (R=0.399, p Conclusions: Even in pts with CAD and LC value, statin-EZE combined therapy showed significantly decreased LDL-C and regressed coronary plaque burden. Even if the cholesterol absorption ability is declined, EZE-statin combined therapy might be the promising option for pts with CAD.

Background: Although recent guidelines recommend the use of fractional flow reserve (FFR) measurements to make decisions for patients with multi-vessel disease and borderline lesions, the presence of a concomitant chronic total coronary occlusion (CTO) may alter the FFR of the interrogated vessel due to collateral circulation. The purpose of this study was to investigate the change in donor artery FFR associated with PCI of a concomitant CTO. Methods: Nineteen consecutive patients who underwent PCI for CTO lesions were prospectively enrolled. All patients underwent myocardial stress perfusion scintigraphy before PCI. An intracoronary pressure/temperature sensor-tipped wire was advanced through a guiding catheter to a point 7cm distal from the ostium of both non-target arteries. At steady-state hyperemia, hemodynamics including FFR and the hyperemic mean transit time (Tmn), which are inversely proportional to coronary flow velocity, were calculated before and immediately after PCI. Coronary blood flow (CBF) was calculated as 1/Tmn х π х (diameter/2) 2 . Coronary wedge pressure was also measured after 30 s of balloon occlusion within the stented segment of the target arteries after PCI. Results: The average FFR values of the donor artery before PCI were 0.89±0.09. None of patients had signs of ischemia in the territory of the donor arteries, even though five patients had an FFR value of Conclusions: Revascularization of a CTO lesion provides moderate increase in the FFR value of the collateral donor artery as a result of the reduction of coronary blood flow. Therefore, the hemodynamic significance of intermediate stenosis in the donor artery by FFR should be carefully evaluated in the presence of CTO.

Backgrounds: Previous studies showed that worsening renal function (WRF) was associated with poor clinical outcome in acute decompensated heart failure (ADHF) patients. Hyperosmolarity is known to cause direct renal cell injury and decreases in renal blood flow and glomerular filtration rate. In ADHF setting, the plasma osmolality can be changed dramatically. However, the prognostic significance of plasma osmolality for the development of WRF in ADHF patients is unclear. Methods: We examined 320 consecutive ADHF patients who admitted to our institution between January 2013 and January 2014 from prospective registry. Patients who had acute coronary syndrome and without complete data-set at admission were excluded. Finally, 303 patients were divided into two groups according to lower plasma osmolality (below 297 mOsm/kg H2O, the cut-off value based on ROC analysis) or higher plasma osmolality (above 297 mOsm/kg H2O) at admission. WRF was defined as ≥ 0.3 mg/dl increase in serum creatinine from baseline to discharge. Results: During follow-up period (median 21 days, interquartile range 14-29), WRF was occurred in 58 patients (19.6 %). Patients with higher plasma osmolality had significantly higher incidence of WRF compared with those without (32.3% vs 13.6%, P Conclusions: In patients with ADHF, higher plasma osmolality on admission was an independent predictor of in-hospital WRF, suggesting the measurement of plasma osmolality might be useful for identifying patients at risk for WRF.

BACKGROUND: Elevation of serum erythropoietin (EPO) level is frequently observed in heart failure (HF) patients, and higher serum EPO level has been reported to be associated with worse clinical outcome in chronic HF. However, serum EPO level was highly influenced by the presence of anemia and its prognostic significance in acute HF (AHF) patients without anemia remains unknown. METHODS: We examined 320 consecutive AHF patients who admitted to our institution between January 2013 and January 2014 from prospective registry. Patients who had anemia defined as a hemoglobin concentration < 13g/dl (males) and RESULTS: Adverse events were occurred in 10 patients (11 %). Higher EPO group had significantly higher incidence of adverse events compared with lower EPO group (19.6% vs 10.9%, P CONCLUSIONS: Higher serum EPO level might be a predictor for worse short-term clinical outcome in AHF patients without anemia.

Background: Previous study showed that number of yellow plaque in a coronary artery was associated with future risk of acute coronary syndrome. However, impact of intrastent yellow plaque has not fully understood. Purpose: This study was investigated to assess the association of the grade of intrastent yellow plaque observed by coronary angioscopy at late phase after drug-eluting stents (DES) implantation and clinical outcome. Methods: This study consisted of 97 patients tread with DES implantation (39 patients with sirolimus-eluting stents ; 9 patients with paclitaxel-eluting stents; 24 patients with everolimus-eluting stents; 6 patients with zotalolimus-eluting stents; 19 patients with biolimus-eluting stents ). Coronary angioscopy was performed 8 months after DES implantation. The plaque color at stent segment was grade as 0 (white), 1 (light yellow), 2 (yellow), 3 (bright yellow). The maximum color grade of the plaques in stent segment was assessed. We divided these patients into 2 groups (53 patients with yellow plaque grade 2 or 3; 44 patients with yellow plaque grade 0 or 1). We evaluated the incidence of revascularization, such as percutaneous coronary intervention or coronary artery bypass graft. Results: Kaplan-Meier curves for 7-year Revascularization free rate are shown in Figure. Revascularization free rate was tend to be higher in patients with yellow grade 0/1 than those with yellow grade 2/3. Conclusion: The presence of intrastent yellow plaque at late phase after stent implantation might be associated with the future revascularization in coronary artery disease.

Backgrounds: Recent studies have elucidated the association between malnutrition and poor long-term prognosis in patients with chronic heart failure (HF), using controlling nutritional status (CONUT) score, a simple and useful index for evaluating malnutrition. In this study, we aim to investigate the prognostic significance of CONUT score in patients with acute decompensated HF. Methods: We examined 320 consecutive patients in our prospective acute decompensated HF registry database from January 2013 to January 2014. Patients with acute coronary syndrome, in-hospital death, and without complete data-set at discharge were excluded. Finally, we selected 206 patients as a study population and malnutrition was defined as CONUT score above 3 at discharge. Results: 112 (54%) patients showed malnutrition at discharge. Patients with malnutrition had higher age, serum creatinine and plasma brain natriuretic peptide levels, and lower serum sodium level at discharge than those without. There were no significant differences between the groups in terms of sex, blood pressure, heart rate, left ventricular ejection fraction, etiology of HF and cardiovascular medications at discharge. During the median follow-up of 192 days (interquartile range = 109-260 days), malnutrition was associated with higher short-term adverse events including death and HF admission (P = 0.008, Figure). Cox proportional-hazards model analysis demonstrated that malnutrition was independently associated with adverse events (HR 2.00, 95% CI 1.01-4.17, P = 0.047), even after adjustment among variables including age (HR 1.04, 95% CI 1.00-1.08, P = 0.03) and serum sodium level (HR 0.93, 95% CI 0.88-1.00, P = 0.04). Conclusions: In patients with acute decompensated HF, malnutrition at discharge was independently associated with worse short-term clinical outcomes. These findings suggest that earlier intensive nutrition management might need to be considered.

Backgrounds: Cardiac rehabilitation with exercise training (CR/ET) has been reported to be associated with reduction in C-reactive protein (CRP) levels in patients with coronary artery disease. However, determinants of reduction in CRP through CR/ET after acute myocardial infarction (AMI) are not fully understood. Methods: We studied 490 consecutive AMI patients (age 63±11 years, male 83%) who participated in our CR/ET program and underwent measurements for serum CRP and peak oxygen uptake (PVO2) by symptom-limited cardiopulmonary exercise test at the beginning and the end of the 3-month CR program. Patients with abnormally high CRP (>= 20mg/L at baseline, >=10mg/L at 3 months) or on hemodialysis were excluded. Results: After the 3-month CR/ET, body mass index (BMI, 23.3 to 23.1, P Conclusion: A greater increase in exercise capacity, in combination with obesity and statin use, significantly associated with a greater reduction in CRP in patients after AMI participating in CR/ET.

Backgrounds: Cardiac rehabilitation with exercise training (CR/ET) has been reported to be associated with reduction in C-Reactive Protein (CRP). In patients with acute coronary syndrome receiving statin therapy, achievement of CRP levels below 2mg/L is known to be important for long-term event-free survival. However, the determinants of achieving low CRP after CR/ET are not fully understood. Methods: To address this issue, we studied 490 consecutive acute myocardial infarction (AMI) patients who participated in our CR/ET program and underwent measurements for serum CRP at the beginning and the end of the 3-month CR program. Patients with abnormally high CRP (>= 20mg/L at baseline, >=10mg/L at 3 months) or on hemodialysis were excluded. Patients were divided into 2 groups according to CRP levels at the end of the 3-month CR/ET: Low-CRP group (CRP2.0mg/dl, n=76). Results: At baseline, there were no significant differences between the two groups in age (Low-CRP group 64years vs High-CRP group 63years, NS), body mass index (BMI, 23 vs 23, NS), prevalences of diabetes, smoking habit and statin use, left ventricular ejection fraction (LVEF, 46 vs 44%, NS), or brain natriuretic peptide (BNP) levels (169 vs 164pg/ml, NS). Although the prevalence of dyslipidemia was significantly higher (76% vs 63%, p Conclusion: Good attendance in CR/ET program is significantly associated with achievement of CRP levels below 2.0mg/L at 3 months, independent of baseline CRP levels, history of dyslipidemia, and statin use.

Introduction: Coronary embolism (CE) is recognized as an important non-atherosclerotic cause of acute myocardial infarction (AMI). Atrial fibrillation (AF) is associated with systemic thromboembolism, and the CHADS2 and CHA2DS2-VASc scores are known to be useful for risk stratification. Therefore, we investigated the clinical features and prognosis of CE, and assessed the potential usefulness of these scores for predicting CE. Methods: We studied a total of 2,115 consecutive patients with AMI (M/F 1,528/587, age 68±12 [SD] years) hospitalized between 2001 and 2013. CE was diagnosed according to the criteria shown in Figure 1 Results: The overall prevalence of CE in AMI was 2.4% (n=51, M/F 31/20, age 65±14 years). Compared with non-CE AMI patients, CE patients were characterized as lower prevalence of risk factors. Most common cause of CE was AF (73%). However, only 15 (41%) out of 37 AF patients were treated with vitamin K antagonists (VKAs) and their PT-INR was low, 1.42 (range, 0.95-1.80) at the onset of AMI. Importantly, among 28 CE patients with nonvalvular AF, 17 patients (59%) had a CHADS2 score of 0 or 1. When those particular patients were re-evaluated by CHA2DS2-VASc score, 10 out of 17 (59%) were categorized into a higher risk category (≥ 2) that would benefit from VKAs therapy. During a median follow-up of 4.1 years (interquartile range, 1.5-7.0 years), 8 patients (16%) had major adverse cardiovascular events and 5 patients (10%) recurred CE or systemic embolization (Figure 2). Conclusions: AF is the major underlying cause of CE, recurrence of which seems to be not rare. The CHA2DS2-VASc score may provide reliable risk stratification with a superior ability to predict CE.

Backgrounds: Malnutrition was reported to be associated with poor clinical outcome in acute heart failure (AHF) patients. Plasma omega-6 (n-6) polyunsaturated fatty acids (PUFA) were parts of the essential fatty acids absorbed with intestine, and its absorption impairment could occur in right side of heart failure (HF). Thus, we aim to investigate whether the n-6 PUFA level could be a marker for malnutrition and a determinant of prognosis in patients with AHF. Methods: We examined 320 consecutive AHF patients who admitted to our institution between January 2013 and January 2014 from prospective registry. Patients with acute coronary syndrome and without complete data-set at admission were excluded. Finally, 284 patients were divided into two groups according to the plasma n-6 PUFA level as follows; Group A [lower plasma n-6 PUFA (dihomo-gamma-linolenic acid plus arachidonic acid) (below 163 μg/ml, the median), Group B [higher plasma n-6 PUFA (above 163 μg/ml) level] at admission. Adverse events were defined as worsening HF and death. Results: During a mean period of 231 days, adverse events were occurred in 78 patients (27 %). Group A had higher incidence of adverse events compared with group B (35% vs 20%, P Conclusions: Lower plasma n-6 PUFA level was an independent determinant for adverse events in association with right HF sign and malnutrition, suggesting plasma n-6 PUFA could be a potential surrogate marker for clinical outcome in AHF patients.

This report describes a case of atrioventricular crosstalk during a stimulation threshold test. This phenomenon was likely due to the accidental connection between the atrial and ventricular stylets. Electrocardiologists should recognize atrioventricular crosstalk during a stimulation threshold test to avoid repositioning the atrial lead unnecessarily or inducing ventricular arrhythmia.

It has been well demonstrated that acute hyperglycemia is associated with high mortality after acute myocardial infarction (AMI). However, optimal plasma glucose (PG) level is not known. The relation between PG and mortality may be different between diabetic and non-diabetic patients. This study consisted of 3,750 patients who were admitted to the 35 hospitals participating to the Japanese Acute Coronary Syndrome Study (JACSS) group within 48 hours after the onset of AMI. PG was measured at the time of hospital admission. In non-diabetic patients, there was a linear relation between PG and in-hospital mortality. Non-diabetic patients with PG ). Diabetic patients with PG 9–10 mmol/L had the lowest mortality (1.9%); both diabetic patients with PG

Several studies have shown that both chronic kidney disease (CKD) and diabetes mellitus are risk factors for mortality in patients with acute myocardial infarction (AMI). This study was undertaken to investigate influence of CKD on the prognostic significance of diabetes in patients with AMI. Between January 1996 and December 2005, 888 patients with AMI underwent coronary angiography within 24 hours after the onset of chest pain. CKD was difined estimated glomerular filtration rate (eGFR) of less than 60.0 ml/minute/1.73 m 2 of body-surface area (stage3–5). Kaplan-Meier method was used to compare 5-year survival of diabetic and non-diabetic patients, in the presence (n=337) or absence (n=551). Kaplan-Meier curves for 5-year survival rate are shown in Figure . In the absence of CKD, there was no significant difference in 5-year survival rate between patients with diabetes and those without (93 % v.s. 94 %, p=0.82). In patients with CKD, however, diabetes was associated with lower 5-year survival rate (65 % v.s. 87 %, p

Background: Sirolimus-Eluting Stent (SES) is effective in reducing restenosis. Although several studies have reported the usefulness of SES in patients with acute myocardial infarction (AMI), the current major concerns of the use of SES in AMI are over-suppression of neointimal formation and late thrombosis. Coronary angioscopic examination provides an opportunity to assess neointimal coverage over stent and adherent thrombus in patients. Method: This study consisted of 18 patients who underwent primary angioplasty with SES for AMI. A mean average of 7.6 ± 2.5 months after SES implantation, coronary angioscopic examination was performed. Neointimal coverage of the SES was assessed by the grading as: grade 0 = complete exposure of the stent struts, grade 1 = dull light reflex from stent struts, grade 2 = no light reflex, but slightly visible stent struts, and grade 3 = complete coverage. Because the grade of neointimal coverage may vary from struts to struts, both maximum and minimum grade of neointimal coverage were assessed. The presence of thrombus was also evaluated. Results: All but one patient had at least 2 different grades of neointimal coverage; one patient had only grade 0. When the maximum grade of neointimal coverage was assessed, grade 0 was observed in 1 patient, grade 1 in 4 patients, grade 2 in 8 patients, and grade 3 in 5 patients. As to minimum grade, grade 0 was observed in 11 patients and grade 1 in 7 patients, however, grade 2 and 3 was not observed. Thrombus adherent to uncovered stent struts (grade 0 or 1) was observed in 8 patients (44%). Conclusion: The process of neointimal coverage over SES was heterogeneous. Even 7 months after SES implantation for AMI, most of the stent struts were not covered by neointimal with high incidence of adherent thrombus. Long-term aggressive anti-platelet therapy should be advocated for patients with AMI who were treated with SES.