This single-center study aimed to evaluate the incidence of deep sternal wound infection (DSWI) following skeletonized bilateral internal mammary artery (BIMA) harvest in a Chinese cohort. Using propensity score matching, this study also provided a present-day assessment of the impacts of skeletonized BIMA grafting versus skeletonized single internal mammary artery (SIMA) grafting on early outcomes.

From January 2014 to December 2017, 2403 eligible patients were entered into either a BIMA group (n = 368) or a SIMA group (n = 2035). The incidence of DSWI was recorded. Analysis of early outcomes was further performed for propensity score-matched (1:1) cohorts.

The BIMA group received a similar incidence of DSWI as did the SIMA group (1.6% versus 0.9%, P = 0.247). No significant differences between subgroup diabetic-BIMA, subgroup nondiabetic-BIMA, subgroup diabetic-SIMA, and subgroup nondiabetic-SIMA were found regarding the incidence of DSWI (2.0%, 1.4%, 1.0%, and 0.7%, respectively; P > 0.05 between groups). After matching, treatment type (skeletonized BIMA grafting versus skeletonized SIMA grafting) was not an independent risk factor for postoperative DSWI (OR = 1.309, 95% CI 0.897-2.714, P = 0.704) or predictors of other early outcomes. Additionally, the two matched groups shared similar early outcomes (including postoperative DSWI), regardless of whether or not the merger with diabetes (all P > 0.05).

Skeletonized BIMA harvest as compared with skeletonized SIMA harvest was not associated with an increased risk of DSWI, regardless of whether or not the merger with diabetes. Patients with skeletonized BIMA grafting received similar surgical mortality and major postoperative morbidity as did matched patients with skeletonized SIMA grafting.

Recent guidelines do not recommend the routine use of intra-aortic balloon pumping (IABP) for patients with cardiogenic shock. However, IABP support is still selected for acute myocardial infarction (AMI) in clinical practice because an Impella device did not show superiority over IABP and the mortality of AMI with cardiogenic shock is still high. This study aimed to find factors associated with in-hospital mortality in patients with AMI who required IABP support. Overall, 104 patients with AMI who required IABP support were included as the study population. Of 104 patients, in-hospital death was observed in 19 (18.3%). Multivariate stepwise logistic regression analysis was performed to investigate the determinants of in-hospital death. Shock, resuscitation, estimated glomerular filtration rate (eGFR), pre-systolic blood pressure of IABP insertion, multi-vessel disease, fluoroscopy time, initial lactic acid dehydrogenase levels, and timing of IABP support were included as independent variables. Shock (OR 25.27, 95% CI 3.26-196.11, P = 0.002) was significantly associated with in-hospital death after controlling other covariates, whereas eGFR (every 10 mL/minute/1.73 m² increase: OR 0.65, 95% CI 0.51-0.82, P < 0.001) and pre-percutaneous coronary intervention (pre-PCI) insertion of IABP (versus on-PCI insertion of IABP: OR 0.06, 95% CI 0.008-0.485, P = 0.008) were inversely associated with in-hospital death. In conclusion, shock was significantly associated with in-hospital death, whereas eGFR and pre-PCI insertion of IABP were inversely associated with in-hospital death in patients with AMI who received IABP support. Pre-PCI insertion of an IABP catheter might be associated with better survival in AMI patients who potentially require IABP support.

Discordant results have been reported on outcomes of acute myocardial infarction (AMI) patients who present during off-hours.

We investigated 3283 consecutive patients with AMI who were selected from the prospective, nationwide, multicenter registry (J-MINUET) database comprising 28 institutions in Japan between July 2012 and March 2014 to determine the current impact of off-hours presentation (defined as weekends, holidays, and weekdays from 8:01 PM to 7:59 AM) at hospitals on long-term clinical outcomes. The primary endpoint was a composite of all-cause death, non-fatal MI, non-fatal stroke, cardiac failure, and urgent revascularization for unstable angina for up to 3 years from the index event.

During off-hours, 52% of patients presented. Primary percutaneous coronary intervention was performed in 85% of patients, and the door-to-balloon time was comparable between off-hours and regular hours (74, interquartile range [IQR] 52 to 113 versus 75, IQR 52 to 126 minutes, P = 0.34). Rate of overall primary endpoint overall did not overall significantly differ (25.3% versus 23.5%, log-rank P = 0.26), in patients with ST-elevation myocardial infarction (STEMI) (log-rank P = 0.93) and in patients with non-ST-elevation myocardial infarction (NSTEMI) (log-rank P = 0.14). Multivariate Cox regression analysis showed that off-hours presentation was not significantly associated with long-term clinical events in all cohorts.

The impact of presentation during off-hours or regular hours on the long-term clinical outcomes of Japanese patients with AMI is comparable in contemporary practice.

The predictors and prognostic implications of well-matured collaterals in those with a chronic total occlusion (CTO) are unknown. We sought to identify the determinants of collateral maturation and to determine its effects on procedural outcomes and prognosis.

Patients presenting for CTO percutaneous coronary intervention (PCI) between April 2010 and July 2019 were included. Patients with a previous coronary artery bypass (CABG) to the CTO and those with only bridging collaterals were excluded. The degree of collateral maturation was determined by the Rentrop grading classification. Demographic, biochemical, and anatomical factors and procedural and longer-term outcomes were identified.

A total of 212 patients were included in the study. Patients with well-matured collaterals were more likely to be females (29.7% versus 15.2% versus 0%, P < 0.005 for Rentrop grade 3, 2, and 0 or 1, respectively), less likely to have chronic kidney disease (CKD) (8.8% versus 4.5% versus 19.2%, P < 0.05) and less likely to have had a prior CABG (15.6% versus 18.7% versus 19.2%). Patients with well-matured collaterals had lower neutrophil-to-leukocyte ratio (NLR) (2.8 versus 4.0 versus 5.7, P < 0.0001). Patients with well-matured collaterals were more likely to have procedural success (90.5% versus 62.5% versus 34.6%, P < 0.0001). The degree of collateral maturation was not associated with longer-term mortality.

Improved collateral maturation was associated with female sex and lower rates of CKD and CABG and a lower NLR. Those with well-matured collaterals had a significantly higher rate of procedural success but not improved prognosis.

The efficacy and safety of non-vitamin K antagonist oral anticoagulants (NOACs) in atrial fibrillation (AF) with coronary or peripheral artery disease (CAD or PAD) remain largely unresolved. We, therefore, conducted a meta-analysis to explore the effect of NOACs compared with warfarin in these populations.

We systematically searched the Cochrane Library, PubMed, and Embase databases for randomized controlled trials (RCTs) involving NOACs versus warfarin in AF patients with CAD or PAD. A random-effect model was selected to pool the risk ratios (RRs) and 95% confidence intervals (CIs).

A total of 7 RCTs were included. In AF patients with CAD, compared with warfarin use, the use of NOACs was associated with reduced risks of stroke/systemic embolism (RR 0.82; 95% CI 0.70-0.96) and intracranial hemorrhage (RR 0.41; 95% CI 0.26-0.63), but NOACs versus warfarin showed similar risks of all-cause death (RR 0.95; 95% CI 0.86-1.05), cardiovascular death (RR 0.95; 95% CI 0.80-1.13), stroke (RR 0.80; 95% CI 0.64-1.00), myocardial infarction (RR 1.00; 95% CI 0.83-1.21), and major bleeding (RR 0.82; 95% CI 0.65-1.04). Among patients with AF and PAD, NOACs versus warfarin had similar risks for stroke (RR 0.93; 95% CI 0.61-1.42), myocardial infarction (RR 1.10; 95% CI 0.64-1.90), all-cause death (RR 0.91; 95% CI 0.70-1.19), major bleeding (RR 1.12; 95% CI 0.70-1.81), and intracranial hemorrhage (RR 0.54; 95% CI 0.16-1.85).

NOACs seem to be at least as effective and safe as warfarin in AF patients with CAD. whereas NOACs versus warfarin have similar efficacy and safety in patients with PAD.

Clinicians must consider renal function when administering anticoagulants for atrial fibrillation (AF). Determination of risk factors for renal function decline may enable identification of patients who require closer monitoring. We investigated the characteristics associated with renal function decline in patients with AF. The study cohort consisted of 631 AF patients who had at least one readmission during the follow-up period and stages 1-3 chronic kidney disease (CKD). The primary outcome measure was large renal function decline (≥30% decrease from baseline estimated glomerular filtration rate [eGFR]). The secondary outcome measure was a final eGFR < 60 mL/minute/1.73 m² for those with a baseline eGFR above this level. The mean eGFR was 74.4 ± 18.5 mL/minute/1.73 m², and the mean follow-up time was 30.2 ± 13.2 months. The primary outcome occurred in 155 patients (24.6%) and was associated with congestive heart failure (CHF), proteinuria, type of AF, and left atrial diameter (LAD) ≥ 45 mm. Among 478 patients with a baseline eGFR ≥ 60 mL/minute/1.73 m², 137 (28.7%) progressed to renal failure (eGFR < 60 mL/minute/1.73 m²). A decreasing eGFR was associated with age ≥ 75 years, CHF, lower baseline eGFR, and LAD ≥ 45 mm. CHF, proteinuria, type of AF, and LAD ≥ 45 mm were associated with eGFR decline ≥ 30% in AF patients with CKD stages 1-3. Advanced age, CHF, lower baseline eGFR, and LAD ≥ 45 mm were associated with progression to renal insufficiency. These results should be considered when identifying patients who require more frequent monitoring of eGFR.

Cryoballoon ablation is an established catheter-based approach to treat atrial fibrillation (AF). However, thromboembolic events cannot be avoided during cryoablation. There is little data regarding the blood coagulation status during freezing.

The thrombin antithrombin complex (TAT) and prothrombin fragment 1+2 (F 1+2) of patient blood were measured during cryoballoon application when the cryoballoon temperature reached the nadir in 63 AF patients. TAT was also measured from porcine blood during cryoballoon freezing in 5 pigs.

The TAT and F 1+2 increased from 6.60 ± 5.65 to 9.16 ± 7.28 ng/mL (P = 0.004) and from 279.6 ± 146.4 to 323.6 ± 169.1 pmol/L (P = 0.003) between the control and during freezing, respectively. The TAT increased from 0.46 to 0.87 ng/mL during freezing compared to that of pre-freezing (P < 0.05), and it returned to 0.39 ng/mL in 30 minutes after an intravenous edoxaban administration (N.S.).

Dabigatran failed to exert sufficient anticoagulant effects during cryofreezing. In contrast, intravenous edoxaban seemed to provoke anticoagulation effects under extreme low temperature circumstances.

The effect of post-cardiac arrest care in children with out-of-hospital cardiac arrest (OHCA) has not been adequately established, and the long-term outcome after pediatric OHCA has not been sufficiently investigated. We describe here detailed in-hospital characteristics, actual management, and survival, including neurological status, 90 days after OHCA occurrence in children with OHCA transported to critical care medical centers (CCMCs).

We analyzed the database of the Comprehensive Registry of Intensive Care for OHCA Survival (CRITICAL) study, which is a multicenter, prospective observational data registry designed to accumulate both pre- and in-hospital data on OHCA treatments. We enrolled all consecutive pediatric patients aged <18 years who had an OHCA and for whom resuscitation was attempted and who were transported to CCMCs between 2012 and 2016.

A total of 263 pediatric patients with OHCA were enrolled. The average age of the patients was 6.3 years, 38.0% were aged < 1 year, and 60.8% were male. After hospital arrival, 4.9% of these pediatric patients received defibrillation; 1.9%, extracorporeal life support; 6.5%, target temperature management; and 88.2% adrenaline administration. The proportions of patients with 90-day survival and a pediatric cerebral performance category (PCPC) score of 1 or 2 were 6.1% and 1.9%, respectively. The proportion of patients with a PCPC score of 1 or 2 at 90 days after OHCA occurrence did not significantly improve during the study period.

The proportion of pediatric patients with a 90-day PCPC score of 1 or 2 transported to CCMCs was extremely low, and no significant improvements were observed during the study period.

This study aims to evaluate the effect of dexmedetomidine (DEX) sedation for relieving anxiety and the incidence of atrial fibrillation (AF) after off-pump coronary artery bypass graft (OPCABG).

This randomized, double-blind, controlled trial was conducted on 196 patients who underwent OPCABG in Shandong Provincial Hospital from July 2017 to June 2018. The patients were randomly assigned to two groups, intervention of DEX group and Propofol (PROP) group. Episodes of postoperative AF (POAF) were identified within 5 days after OPCABG. Perioperative anxiety status was assessed using Zung's Self-Rating Anxiety Scale (SAS). The baseline demographic and surgical characteristics of the population and other outcome variables were evaluated.

We analyzed 62 patients in the DEX group and 61 patients in the PROP group. There was no significant difference in SAS anxiety scores between two groups before surgery (P = 0.104), while SAS had significantly after surgery (P = 0.018). The incidence of POAF in the DEX group was lower than that of the PROP group (16.1% versus 32.8%, P = 0.037), and a total of 30 patients (30/123, 24.4%) manifested POAF after OPCABG. Some univariable predictors of POAF were detected. The conceptual model of mediator analyses showed DEX was not only directly related to POAF but was also indirectly related through the independent effect of anxiety level.

The findings indicated that patients receiving DEX were more likely to have less incidence of POAF, also uniquely showed DEX administration and POAF processes as a function of anxiety status.

For its high occurrence and elevated risks for aortic valve dysfunction and vascular complications, bicuspid aortic valve (BAV) represents a great health challenge. However, the prevalence and clinical features of BAV in the Chinese population are inadequately illustrated.

From January 2011 to December 2015, 3,673 BAV patients with 69.1% male predominance were identified among 325,910 recipients of transthoracic echocardiography in our institution, demonstrating 58.4% overt aortic valve dysfunction, 52.5% ascending aortic dilatation, and 19.2% aortic root dilatation. The prevalence of pure aortic stenosis and mixed aortic valve dysfunction rose strikingly with age (both P < 0.0001), while pure aortic regurgitation showed significant decrease with age (P < 0.0001). Males showed elevated prevalence of pure aortic regurgitation (OR 3.16, 95% CI 2.55-3.91, P < 0.0001) and mixed aortic valve dysfunction than females (OR 1.63, 95% CI 1.23-2.17, P = 0.0008), but lower prevalence of pure aortic stenosis (OR 0.51, 95% CI 0.43-0.60, P < 0.0001). Aortic root dilatation was associated with male gender (OR 5.02, 95% CI 3.74-6.74, P < 0.0001), pure aortic regurgitation (OR 2.61, 95% CI 2.15-3.17, P < 0.0001), and right-left (RL) cusp fusion type (OR 1.98, 95% CI 1.64-2.40, P < 0.0001). Ascending aortic dilatation was associated with an elder age (OR 1.04, 95% CI 1.04-1.05, P < 0.0001), pure aortic stenosis (OR 1.37, 95% CI 1.16-1.61 P = 0.0002), and mixed aortic valve dysfunction (OR 2.51, 95% CI 1.89-3.33, P < 0.0001).

Bicuspid aortic stenosis and ascending aortic dilatation demonstrate a similar pattern of age escalation, while aortic regurgitation is more prevalent in younger BAV patients. Aortic root dilatation intervenes closely with a unique phenotypic subgroup of male BAV patients with pure aortic regurgitation and RL fusion type.

It has been recently recognized that recovery of left ventricular ejection fraction (EF), termed "recovered EF", occurs in a proportion of heart failure patients with reduced EF (HFrEF), and is associated with better prognosis. However, the clinical characteristics of "recovered EF" have not been fully examined.

Consecutive 567 patients hospitalized due to HFrEF (EF < 40% at 1st assessment at hospital discharge) were enrolled, and EF was re-assessed within half a year in an outpatient setting (2nd assessment). Among these HFrEF patients, 235 remained EF < 40% (reduced, rEF group), 82 changed to EF 40-49% (midrange, mrEF group), and 250 recovered to EF > 50% (preserved, pEF group "recovered EF" ) at the 2nd examination. Age was lower and body mass index and systolic blood pressure were higher in pEF than in rEF. The prevalence of atrial fibrillation (AF) and usage of an implantable cardiac defibrillator and cardiac resynchronization therapy were highest in pEF. Left ventricular end diastolic dimension (LVDd) was the smallest in the pEF group. Multivariable logistic regression analysis revealed that younger age, presence of AF, and lower levels of LVDd were predictors of "recovered EF". Kaplan-Meier analysis found that pEF presented the lowest cardiac event rate (P = 0.003) and all-cause mortality (P = 0.001). In multivariable Cox proportional hazard analyses, pEF (versus rEF) was an independent predictor of both cardiac event rate (HR = 0.668, 95%CI 0.450-0.994, P = 0.046) and all-cause mortality (HR = 0.655, 95%CI 0.459-0.934, P = 0.019).

Hospitalized HFrEF patients with recovered EF are associated with younger age, higher presence of AF, and better prognosis.

High heart rate (HR) is associated with increased risks of adverse outcomes in patients with heart failure. This study aimed to evaluate which measures of HR were associated with all-cause mortality in patients with heart failure and reduced ejection fraction (HFrEF). This study involved 741 HFrEF patients (age 65.1 ± 14.7 years, 71% male) who underwent 24 hour Holter electrocardiogram and resting electrocardiogram within 7 days between 2011 and 2015. We examined the associations of resting, 24 hour, and nighttime HRs with all-cause mortality. Nighttime and 24 hour HRs were determined as the mean HRs between 11:00 p.m. and 7:00 a.m. and over 24 hours, respectively. Nighty patients (12.1%) died during the 2-year follow-up. Resting, nighttime, and 24 hour HRs were significantly associated with all-cause mortality, also after adjusting for conventional risk factors. Resting HR did not remain as an independent factor when 24 hour HR (hazard ratio 1.10, 95% confidence interval 1.04-1.18) was included in the model. Including nighttime HR (hazard ratio 1.11, 95% confidence interval 1.05-1.17) in the model also eliminated 24 hour HR as an independent variable. Compared with the lowest quartile of nighttime HR (< 65 beats/minute), the highest quartile of nighttime HR (> 87 beats/minute) was significantly associated with a higher risk of all-cause mortality (hazard ratio 2.89, 95% CI 1.49-5.60). In conclusion, 24 hour HR and nighttime HR were significantly associated with an increased risk of mortality in patients with HFrEF. Nighttime HR appeared to be more strongly associated with all-cause mortality compared with 24 hour HR.

Many patients are transferred to hospital due to out-of-hospital cardiac arrest (OHCA), and, unfortunately, most suffer from cerebral damage. Currently, it is difficult to predict the recovery of neurological function after return of spontaneous circulation (ROSC) in the acute phase. Increased intracellular Ca²⁺ induces cell death in the acute phase. Accordingly, we predicted that serum adjusted Ca²⁺ will decrease following Ca²⁺ influx into cells. Consequently, serum adjusted Ca²⁺ in the acute phase may be able to predict recovery of neurological function in patients with ROSC from OHCA. This is a retrospective and observational study from 2 centers. A total of 190 consecutive patients with ROSC from OHCA were recruited, with 33 patients meeting the inclusion criteria. The relationship between serum adjusted Ca²⁺ within 48 hours after ROSC and neurological function at discharge (as evaluated by the Glasgow-Pittsburgh cerebral performance category) was examined. Serum adjusted Ca²⁺ was measured every 4 hours within a 48-hour period after ROSC. There were no significant differences in hemodynamical state and laboratory data between the 2 groups. However, lowest serum adjusted Ca²⁺ within 48 hours after ROSC was significantly lower in the poor neurological outcome group (0.96 ± 0.06 versus 1.02 ± 0.06 mmol/L, P = 0.011). Thus, lowest serum adjusted Ca²⁺ within 48 hours after ROSC may be a predictive factor for recovery of neurological function at discharge in patients with ROSC from OHCA.

Pulmonary hypertension (PH) caused by left-sided heart disease (LHD-PH) is classified into 2 types: isolated post-capillary PH (Ipc-PH) and combined pre- and post-capillary PH (Cpc-PH). However, the impact of pulmonary vascular resistance (PVR) or diastolic pressure gradient (DPG) on the prognosis of LHD-PH has varied among previous studies. Thus, we verified the significance of PVR or DPG on the prognosis of LHD-PH in our series.

We analyzed 243 consecutive LHD-PH patients. The patients were divided into 3 groups: Group A, patients with PVR ≤ 3 Wood unit (WU) and DPG < 7 mmHg; Group B, patients with either PVR > 3 WU or DPG ≥ 7 mmHg; and Group C, patients with PVR > 3 WU and DPG ≥ 7 mmHg.

The Kaplan-Meier curve demonstrated that Group B had lower cardiac death-free survival compared with Group A, whereas no significant differences were observed when compared with Group C. In the Cox hazard model, DPG was not associated with cardiac death in the LHD-PH patients. However, only in the ischemic heart disease group, patients with DPG ≥ 7 mmHg had worse prognosis compared with those with normal DPG.

The cardiac death-free rate of patients with either increased PVR or DPG was close to that of patients with both increased PVR and DPG. It seems reasonable to define Cpc-PH only by PVR in the new criteria. However, the significance of DPG in LHD-PH might be dependent on the underlying cause of LHD-PH.

Despite its clinical relevance, a subclass of acute decompensated heart failure (ADHF) with elevated blood pressure, known as hypertensive ADHF (HT-ADHF), has been less intensively evaluated. This study aimed to characterize the prognostic nature and pathophysiology of HT-ADHF. A total of 509 consecutive patients with first-time ADHF hospitalization were subjects of the study. Participants were divided into two groups: an HT-ADHF group (systolic blood pressure, SBP > 140 mmHg at presentation) and a non-HT-ADHF group (SBP ≤ 140 mmHg). Median follow-up duration measured 253 days. Unadjusted Kaplan-Meier analysis demonstrated both a lower cardiovascular mortality rate in the HT-ADHF group and similar incidences of heart failure rehospitalization in both groups. Adjusted Cox hazard analysis showed an association of elevated SBP at presentation with significantly lower cardiovascular mortality, though no such association was observed with heart failure rehospitalization. Moreover, elevated heart rate in combination with elevated SBP at presentation predicted a significantly lower risk of cardiovascular mortality (Hazard Ratio: 0.32, 95% CI: 0.14-0.77, P = 0.01). Also, significantly lower cardiovascular mortality was observed in this subtype, compared with other types of ADHF.

The mechanisms of urgently presenting acute heart failure (AHF) are not clear. We evaluated the serum catecholamine values of AHF patients immediately after admission. A total of 1,475 AHF patients were screened, and 484 who were admitted from their homes and in whom serum catecholamine could be evaluated immediately after admission were analyzed. The patients were divided into three groups according to the time interval from the onset of symptoms to admission (OA): < 3 hours (early-OA group; n = 283), 3-24 hours (middle-OA group; n = 142), and ≥24 hours (late-OA group; n = 59). In the early-OA group, the systolic blood pressure (SBP) was significantly higher, orthopnea was more frequent, the pH value was significantly decreased, and the use of noninvasive positive-pressure ventilation was required significantly more often than in the other groups. The serum noradrenaline level was significantly increased in the early-OA group (1.96 [1.02-3.60] ng/mL) than in the middle-OA (1.49 [0.73-3.41] ng/mL) and late-OA (1.40 [0.91-2.42] ng/mL) groups, and the adrenaline level was significantly increased in the early-OA group (0.36 [0.13-1.17] ng/mL) than in the late-OA (0.22 [0.09-0.52] ng/mL) group. A multivariate logistic regression model indicated the early-OA group was independently associated with the SBP > 140 mmHg (odds ratio [OR]: 2.219, 95% CI: 1.375-3.581), midnight/early morning admission (OR: 3.158, 95% CI: 2.048-4.868), and high serum catecholamine value (adrenaline > 0.96 ng/mL, noradrenaline > 3.39 ng/mL, and dopamine > 0.21 ng/mL) (OR 2.091, 95% CI: 1.161-3.767). In conclusion, urgently presented AHF might be induced by an endogenous catecholamine surge, which causes an excessive rise in blood pressure leading to increased after-overload and volume-shift lung congestion.

Prediction of short-term mortality in elderly patients with heart failure (HF) would be useful for clinicians when discussing HF management or palliative care.

A prospective multicenter cohort study was conducted between July 2014 and July 2018. A total of 504 consecutive elderly patients (age ≥ 75 years) with HF (mean age 85 years, 50% women) were enrolled. We used a multiple logistic regression analysis with stepwise variable selection to select predictive variables and to determine weighted point scores. After analysis, the following variables predicted short-term mortality and comprised the risk score: previous HF admission (3 points), New York Heart Association III or IV (2 points), body mass index < 17.7 kg/m² (4 points), serum albumin < 3.5 g/dL (9 points), and left ventricular ejection fraction < 50% (2 points). The c-statistic was 0.820. We compared mortality in low-risk (0-6 points, n = 188), intermediate-risk (7-13 points, n = 241), and high-risk (14-20 points, n = 75) groups. A total of 43 (8.5%) patients died within 6 months after discharge. Mortality was significantly higher in groups with higher scores (low-risk group, 0.5%; intermediate-risk group, 9.1%; high-risk group, 26.7%; P < 0.001).

We developed a predictive model for 6-month mortality in elderly patients with HF. This risk score could be useful when discussing advanced HF therapies, palliative care, or hospice referral with patients.

Increased arterial stiffness is strongly associated with cardiovascular morbidity and mortality in dialysis patients. Ischemia-modified albumin (IMA) is a useful biomarker of cardiac ischemia. This study was aimed to explore the association between IMA and arterial stiffness in hemodialysis patients. An observational study was conducted with 120 hemodialysis patients. Clinical data and laboratory characteristics were collected. Arterial stiffness was evaluated by brachial-ankle pulse wave velocity (baPWV). Hemodialysis patients had extensive arterial stiffness and high levels of IMA. Comparing to hemodialysis patients with normal baPWV, those with high baPWV had significantly higher levels of IMA (93.7 ± 8.6 versus 73.1 ± 10.7 Ku/L, P = 0.027). The multiple linear regression analysis showed that IMA was significantly associated with arterial stiffness in hemodialysis patients (β = 0.43, P < 0.001). Moreover, IMA, with a threshold value of 90.4 Ku/L, provided 77.4% sensitivity and 86.6% specificity for predicting arterial stiffness. Hemodialysis patients with arterial stiffness had high levels of IMA. IMA was a good predictive marker of arterial stiffness for hemodialysis patients.

Sympathetic nerve activity has arrhythmogenic potential for ventricular arrhythmias associated with structural heart diseases. However, a sufficient amount of beta-blockers occasionally cannot be prescribed in some patients.

An experimental study was performed to clarify the therapeutic effects of bepridil, a multiple ionic current inhibitor that does not affect beta-adrenergic receptors, for premature beats occurring during enhanced sympathetic nerve activity. Cardio-sympathetic nerve activity was augmented via stellate-ganglion (SG) stimulation in a canine model (n = 8), and the arrhythmogenic potential and anti-arrhythmic effects of bepridil (2 and 4 mg/kg intravenously) were assessed. For safe use, vagal-stimulation-induced slow HR and programmed electrical stimulation were applied to evaluate possible pro-arrhythmic effects of the drug. Heart rate variability (HRV) indexes were used to estimate cardio-autonomic nerve activity.

Either side of the SG-stimulation increased BP and HR. Premature beats were induced in 10/16 SG-stimulations and it was more frequent in left (8/8) rather than right stimulation (2/8). Following 2 mg/kg drug administration, premature beats were still inducible in 8/16 stimulations (7/8 in left and 1/8 in right), but burden of the premature beats decreased from 87.1 ± 46.8 to 62.1 ± 42.6 beats. After 4 mg/kg administration, premature beats were inducible in one SG-stimulation. Proarrhythmic effects were not observed in all experiments. Steady-state HRV indexes and percent increases in SG-stimulation-induced BP-elevation and HR-acceleration were similar among the 3 periods (before, 2 and 4 mg/kg of the drug).

Bepridil may be an option for ventricular arrhythmias developed during enhanced cardio-sympathetic nerve activity with minimal effect on autonomic nerve responses.

Myocardial infarction (MI) is one of the major causes of death worldwide, and the therapeutic strategies of MI are still limited. In this study, we investigated the function of miR-665 in MI. In the present study, an ischemia/reperfusion (I/R) rat model and a hypoxia/reoxygenation (H/R)-induced H9c2 cell model were successfully established to mimic the MI for in vivo and in vitro studies. The concentrations of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), tumor necrosis factor alpha (TNF-α), IL-6, and reactive oxygen species (ROS) were then measured. Moreover, cell viability and apoptosis were detected by MTT assay, TdT-mediated dUTP nick end labeling (TUNEL), and PI/FITC-annexin V assay. The binding of miR-665 and Pak1 was determined by luciferase assay. miR-665 was upregulated in I/R rats, and the overexpression of miR-665 significantly increased LDH, CK-MB, TNF-α, IL-6, and ROS concentrations and induced cell apoptosis, while knockdown of miR-665 had opposite results. Consistent with in vivo results, miR-665 induced cell apoptosis and ROS generation in H/R-treated H9c2 cells. More importantly, Pak1 was the target gene of miR-665, and knockdown of miR-665 depressed the accumulation of ROS and cell apoptosis by targeting Pak1 and promoting the phosphorylation of Akt, whereas knockdown of Pak1 could attenuate the protection of miR-665 inhibitor in H/R-treated H9c2 cells. Therefore, knockdown of miR-665 protects against cardiomyocyte ischemia/reperfusion injury-induced ROS accumulation and apoptosis through activating Pak1/Akt signaling in MI. In general, understanding the biology and modulation of miR-665 may have the potential to counteract the development of MI.

Heart failure (HF) is a disease with high morbidity and mortality. In patients with HF, decreased cardiac output and blood redistribution results in decreased intestinal perfusion and destruction of intestinal barrier. Microorganisms and endotoxins can migrate into the blood circulation, aggravating systemic inflammation and HF. Trimethylamine N-oxide (TMAO) is highly closed to the occurrence of HF. However, the exact mechanism between TMAO and HF remains unclear.

To investigate the role of TMAO in transverse-tubule (T-tubule) in the cultured cardiomyocytes.

T-tubule imaging and analysis detected T-tubule network in cardiomyocytes. Ca²⁺ handling dysfunction was identified by confocal Ca²⁺ imaging. Tubulin densification and polymerization were assessed by western blot and immunofluorescent staining of cardiomyocytes.

TMAO induced T-tubule network damage in cardiomyocytes and Ca²⁺ handling dysfunction in cardiomyocytes under the TMAO stress via promoting tubulin densification and polymerization and therefore Junctophilin-2 (JPH2) redistribution. Mice treated with TMAO represented cardiac dysfunction and T-tubule network disorganization.

TMAO impairs cardiac function via the promotion of tubulin polymerization, subsequent translocation of JPH2, and T-tubule remodeling, which provides a novel mechanism for the relationship between HF and elevated TMAO.

Atherosclerosis is a chronic inflammatory disease with multiple characteristic facets, including vascular inflammation, endothelial dysfunction, plaque development, impaired blood flow, and cholesterol deposition through dyslipidemia. Toll-like receptors (TLRs) of the innate immune system have been closely linked to the development of atherosclerotic lesions. TLR7 recognizes viral or endogenous single-stranded RNA, which is released during vascular apoptosis and necrosis. The role of TLR7 in vascular disease remains controversial, and therefore, we sought to investigate the effects of TLR7 stimulation in mice.

Intravenous injection of a ligand for TLR7 (R848) induced a significant pro-inflammatory cytokine response in mice. This was associated with impaired reendothelialization upon acute denudation of the carotid artery, as measured by Evan's blue staining, and increased numbers of circulating endothelial microparticles (EMPs) and circulating Sca1/Flk1 positive cells as a marker for increased endothelial damage. Chronic subcutaneous stimulation of TLR7 in apolipoprotein E-deficient (ApoE^−/−) mice increased aortic production of reactive oxygen species (ROS), the number of circulating EMPs, and most importantly, augmented the formation of atherosclerotic plaque when compared with vehicle-treated animals.

Systemic stimulation of TLR7 leads to impaired reendothelialization upon acute vascular injury and is associated with the production of pro-inflammatory cytokines and increased levels of circulating EMPs and Sca1/Flk1 positive cells. Importantly, ApoE^−/− mice chronically treated with R848 displayed increased atherosclerotic plaque development and elevated levels of ROS in the aortic tissue. In addition, TLR7-activation-induced apoptosis and impaired migration in human coronary artery endothelial cells and showed significant upregulation of the signaling cascade of IL-1 receptor-associated kinase (IRAK) 2 and IRAK4. Our data highlight the importance of fully understanding the pathomechanisms involved in atherogenesis, and further studies are necessary to identify the ligand-specific effects of TLR7 for possible therapeutic targeting.

We aimed to investigate the relationship between neutrophil-to-lymphocyte ratio (NLR), C-reactive protein (CRP), brain natriuretic peptide (BNP), and left ventricular hypertrophy (LVH) in hypertension. Methods: This study included 386 patients with hypertension. Mann-Whitney U test and multivariate binary logistic regression analysis were used to investigate the relationship between NLR, CRP, BNP, and LVH in patients with hypertension, as well as compare the levels of NLR, CRP, and BNP in the four configurations. Receiver operator characteristic (ROC) curve was used to compare the diagnostic efficacy of NLR, CRP, and BNP on LVH. Results: The NLR and CRP and BNP levels of the LVH group were significantly higher than those of the non-LVH group. In the multivariate logistic regression analysis, NLR as well as age, BMI, and SBP were associated with LVH. In addition, in patients with eccentric and concentric hypertrophy, the NLR and CRP and BNP levels were higher than those of the normal left ventricular geometry and concentric remodeling groups. The cutoff values of NLR, CRP, and BNP obtained by ROC curve were 2.185, 2.205, and 283.45, respectively, for the prediction of LVH. Conclusions: NLR is independently associated with LVH in patients with hypertension, and this is consistent with the diagnostic efficacy of CRP and BNP, which may be a simple and convenient indicator for judging LVH.

We report a case of atypical slow-slow atrioventricular nodal reentrant tachycardia (AVNRT) utilizing a superior slow pathway as a retrograde limb. The standard electrophysiological criteria confirm the diagnosis of this AVNRT by successfully excluding a diagnosis of atrial tachycardia and atrioventricular reentrant tachycardia. The earliest atrial activation during tachycardia was found at the interatrial septum 17.5 mm superior to the site identified during retrograde conduction with the fast pathway. The tachycardia was not inducible after ablation at the right posterior septum, consistent with successful ablation of the typical slow pathway.

Tachycardia and supraventricular tachyarrhythmias often impair cardiovascular capacity in patients with decompensated heart failure (dHF) treated with inotropes. Normalization of heart rhythm or rate typically improves diastolic filling and stroke volume (SV). Thus, isochronal administration of an ultra-short-acting and highly selective β₁-blockers, such as landiolol, along with inotropic calcium-sensitizer medications, such as levosimendan, could benefit patients with dHF.

We present a case series of three patients with severe dHF and low ejection fraction who were successfully treated with a combination of landiolol and levosimendan. The co-administration of landiolol and levosimendan was well tolerated, improved cardiac function, normalized SV, and enabled the reduction of norepinephrine dosing in all patients. Additionally, the combination improved the vectorcardiographic spatial QRS-T angle and decreased the corrected QT interval. All patients were successfully discharged from the intensive care unit (ICU).

A combination of levosimendan and landiolol was safe and well-tolerated. This combination may be a new option for successful treatment of patients with acute dHF complicated by sinus or supraventricular tachycardias.

A 77-year-old woman with extremely high risk of mortality due to severe aortic stenosis (AS) and multiple organ failure was admitted to the affiliated hospital of Jiangsu University. She did not receive regular treatment since being diagnosed with AS 17 months previously. Frequent breakout of acute left heart failure after admission, with a low ostium of the left coronary artery showed by computed tomography, the patient underwent transcatheter aortic valve replacement (TAVR). Though cardiac conduction system abnormalities and a short-term elevation of pulmonary arterial pressure occurred in this patient after TAVR, she eventually recovered and her quality of life improved significantly. As the population adapted to TAVR keeps expanding, we believe this operation will play a more important role in the treatment of AS patients.

A 50-year-old man who suffered from dyspnea on effort with hearing loss was referred to our hospital. Computed tomography angiography revealed a giant 90-mm diameter ascending aortic aneurysm with severe calcification and neck vessel occlusion. Transthoracic echocardiography revealed moderate-to-severe aortic regurgitation. His condition was diagnosed as Takayasu arteritis and he underwent aortic valve reimplantation with total arch replacement. Postoperative computed tomography angiography showed complete aneurysm resection and the patient was discharged without any complications and his hearing loss improved. He is currently being followed up as an outpatient.

Takotsubo cardiomyopathy (TC) is a temporal dysfunction of the left ventricle (LV) due to psychological or physiological stress; however, it rarely causes LV thrombus. We report a case of a 49-year-old woman who developed LV thrombi due to TC despite anticoagulation therapy. The thrombi caused acute systemic infarction, with the most severe occlusion being in the right renal artery. The patient underwent percutaneous catheter aspiration thrombectomy of the right renal artery and her renal function recovered shortly after. The results of this case suggest that catheter aspiration thrombectomy is effective in the treatment of thromboembolism in TC.

A man in his 40s with a history of congenitally corrected transposition of the great arteries (CCTGA) and closure of ventricular septal defect was referred to our hospital with purpura and hematuria. Presence of purpura, renal damage, and pathological findings on skin biopsy led to the diagnosis of IgA vasculitis (IgAV). Oral prednisolone (PSL) was initiated. However, Streptococcus pseudoporcinus was isolated from blood cultures, and transthoracic echocardiogram revealed vegetation on the pulmonary valve. From these findings, the diagnosis of infective endocarditis (IE) was made. Although the patient's condition improved after PSL interruption and antibiotic administration, his purpura relapsed. PSL readministration improved symptoms, with no further relapse even after gradual PSL dose reduction. The present case raises awareness of the importance of recognizing the occurrence of IE in IgAV patients, especially in those with congenital heart disease. CCTGA should be acknowledged as a risk factor for IE in the right-sided heart.

We report here a 70-year-old female patient with a history of breast cancer who presented with dyspnea that had lasted for 2 weeks following a long-distance trip by bus. She was at first suspected of having a pulmonary embolism given the typical presentation, elevated D-dimer level, and enlargement of the right-side heart. However, her systemic condition deteriorated despite the initiation of anti-coagulation therapy. Given the absence of a major thrombus in the pulmonary major arteries but multiple low perfusion lesions in the periphery of the lungs, refractoriness to conventional therapy, an increase in tumor markers, and anaplastic cells demonstrated by aspiration cytology from the pulmonary artery, we diagnosed her as pulmonary tumor thrombotic microangiopathy (PTTM). She died on day 23 due to respiratory failure despite administration of inotropes and prostaglandin I2. The patient had an obvious history of malignancy, but we should emphasize that PTTM can develop even in patients with early-stage or completely cured malignancies. Although an early and definite diagnosis of PTTM is currently challenging, an optimal diagnostic and therapeutic strategy is warranted.

Anticentriole autoantibodies-positive systemic sclerosis (SSc) has been reported to develop pulmonary arterial hypertension (PAH) at a high rate. In this report, we describe two patients with anticentriole antibodies-positive SSc-PAH who were treated with pulmonary vasodilators. Both cases were elderly women with poor physical conditions and clinical findings of SSc. Case 1 was resistant to combination therapy with pulmonary vasodilators; in Case 2, hemodynamic improvement was obtained by upfront combination therapy at an early stage. Because anticentriole antibodies-positive SSc-PAH rapidly deteriorates, careful hemodynamic observation and timely aggressive use of pulmonary vasodilators should be considered.