Severe ventricular arrhythmias such as high-grade atrioventricular block and ventricular tachycardia may cause lethal conditions or sudden death in patients with cardiac sarcoidosis (CS). Physicians should examine patients carefully for these conditions and treat them appropriately. As arrhythmias are being better diagnosed and treated, physicians are increasingly aware of atrial arrhythmias, which have not been focused upon as CS-related conditions, in patients with CS. This article reports a case of atrial flutter in sarcoidosis, and discusses literature findings on atrial arrhythmias and atrial involvement of CS. It is highly likely that atrial arrhythmia and supraventricular conduction disorder associated with or caused by CS are more common than previously thought. Physicians should pay careful attention for these conditions in the diagnosis and treatment of CS.

The benefits of concomitant mitral valve procedure (MVP) for treating moderate chronic ischemic mitral regurgitation (IMR) during coronary artery bypass grafting (CABG) have not been clearly established. This study aimed to determine the incidence of moderate or more residual mitral regurgitation (MR) following CABG plus MVP for moderate chronic IMR, and to evaluate the impacts of concomitant MVP vs. CABG alone on clinical outcomes based on propensity-matched data.

All eligible patients were entered into either the MVP group (CABG plus MVP, n = 184) or CABG group (CABG alone, n = 162). Moderate or more residual MR rate was investigated, and in-hospital and follow-up outcomes between the groups were compared after matching.

Moderate or more residual MR rate was 11.4% at 1 year and 22.9% at 2 years after CABG plus MVP, respectively. Patients in the MVP group as compared with the CABG group had significantly lower moderate or more residual MR rates at various postoperative time points (all P < 0.001). Grouping was not an independent risk factor for in-hospital adverse events in multivariate logistic regression analysis. Also, grouping was a significant variable related to moderate or more residual MR rate and NYHA class III-IV at the latest follow-up in Cox regression analysis (HR = 0.391, 95% CI 0.114-0.628; HR = 0.419, 95% CI 0.233-0.819, respectively).

Concomitant MVP as compared with CABG alone for treating moderate chronic IMR was associated with a reduction in moderate or more residual MR rate and an improvement in NYHA functional status, with no increase in in-hospital adverse events or follow-up death.

In a previous meta-analysis, it was demonstrated that the resting heart rate (RHR) is a potential risk factor for atrial fibrillation (AF). However, the results of that meta-analysis were conflicting, and the relationship between the RHR and AF is still not well established. In the current meta-analysis, our aim is to update evidence with a better statistical model. We searched the Cochrane Library, PubMed, and Embase databases for relevant studies and used a "one-stage approach" with a restricted cubic spline model to summarize the dose-specific relationships between the RHR and AF. Relative risk (RR) was used to measure the effects. In total, 10 studies were included, with a total of 18,630 cases of AF among 431,432 participants. In the dose-response analysis, there was evidence of a nonlinear association between the RHR and the risk of AF (nonlinearity, P < 0.0001), which exhibited a significant J-shaped association between the two factors. An RHR between 68 and 80 bpm had the lowest risk of AF. Among people who had RHR < 70 bpm, the summary RR was 1.09 per 10-RHR decrease (95% confidence interval [CI] = 1.06-1.12; P < 0.001). The results were similar for participants with RHR > 70 bpm (per 10 bpm increase) (RR = 1.06, 95% CI = 1.03-1.08; P < 0.001). Our dose-response meta-analysis revealed a significant J-shaped association between the RHR and AF. Both low RHR and high RHR were associated with an increased risk of AF compared with a modest RHR of 68-80 bpm.

Pulmonary vein isolation (PVI) of atrial fibrillation (AF) can reduce the AF burden and, potentially, reduce the long-term risk of strokes and death. However, it remains unclear whether anticoagulants can be stopped after PVI because of post-ablation AF recurrence in some patients. This study aimed to investigate the discontinuation rate of anticoagulants and long-term incidence of strokes after PVI.

We enrolled 512 consecutive Japanese patients with AF (mean age, 63.4 ± 10.4 years; 123 women; 234 with non-paroxysmal AF; CHADS2 score/CHA2DS2-VASC score, 1.32 ± 1.12/2.21 ± 1.54) who underwent PVI between 2012 and 2015. During a 28.0 ± 17.1 -month follow-up, anticoagulants were terminated in 230 (44.9%) of the 512 patients, AF recurred in 200 (39.1%), and 10 (1.95%) suffered from a stroke. Death occurred in 5 (0.98%) patients. Although the incidence of strokes, by a Kaplan-Meier analysis, was similar, the incidence of death was lower (Hazard ratio 0.37, 95% confidence interval 0.12-0.93, P = 0.041) in the AF ablation group than the control group without ablation after 1:1 propensity score matching (the control data was derived from 2,986 patients in the SAKURA AF Registry, a large-cohort AF registry).

Anticoagulants were discontinued in nearly half the patients who underwent AF ablation; of these, 39.1% experienced AF recurrences, 1.95% suffered from strokes, and 0.98% died, but the risk of death after AF ablation appeared to be lower than that in a propensity score-matched control group without ablation during long-term follow-up.

Atrial fibrillation (AF) is an independent risk factor for intracranial hemorrhage in patients receiving recombinant-tissue-type plasminogen activator (rt-PA) thrombolytic therapy. Research showed that patients with acute ischemic stroke (AIS) could benefit from multimode computed-tomography- (CT-) guided intravenous thrombolysis over 4.5 hours. The medical data of patients with AIS in our center were retrospectively reviewed, and the data of the multimode CT-guided thrombolytic therapy or nonthrombolytic therapy within different time windows (3-9 hours) were evaluated. 134 AIS cases were selected successfully and divided into three groups: patients with AF treated by rt-PA (AF rt-PA), patients with AF not treated by rt-PA (AF non-rt-PA), and patients without AF treated by rt-PA (non-AF rt-PA). After correcting for the baseline NIH Stroke Scale (NIHSS), sex, age, and hypertension data, the comparison results showed that the NIHSS improved significantly at hospital discharge for rt-PA-treated patients (n = 47) compared to non-rt-PA-treated patients with AIS (n = 31) with AF (P = 0.0156). The NIHSS evaluation at 90 days of follow-up also improved in rt-PA-treated patients (P = 0.0157). The NIHSS at hospital discharge was higher in AF rt-PA-treated patients compared to non-AF rt-PA-treated patients (P = 0.0167) after correction; the difference was not statistically significant at 90 days of follow-up (P = 0.091). Our research showed that the neural function improved after 3-9 hours of thrombolytic therapy with rt-PA in patients with AIS and AF. If there is no thrombolytic taboo, the patients could benefit from the thrombolytic therapy, although the onset time window has been extended to 9 hours.

Uric acid is associated with cardiovascular disease (CVD) and its risk factors. Here, we examined the association between the serum uric acid level and incident metabolic syndrome in a Japanese general population. This retrospective, observational study was based on data obtained from an annual health checkup program in Gunma Prefecture, Japan. We evaluated 14,793 participants who did not use antihypertensive or antidiabetic medications and did not present with CVD or metabolic syndrome at the study baseline in 2009. Metabolic syndrome was defined as per the Japanese diagnostic criteria. A discrete proportional hazards regression model was used to evaluate the association between the serum uric acid level at baseline and the incident metabolic syndrome through 2012 and was adjusted for age, gender, waist circumference, systolic and diastolic blood pressure, fasting blood glucose, high-density lipoprotein cholesterol, and triglyceride. At baseline, the average age of the participants was 48.9 years, who were comprised of 40% women. The mean serum uric acid level at baseline was 5.3 ± 1.4 mg/dL. During the three-year follow-up, 7% of the cohort (n = 1,031) developed metabolic syndrome. The uric acid level was strongly associated with incident metabolic syndrome in the multivariable model (adjusted hazard ratio: 1.10; 95% confidence interval, 1.04-1.17; P < 0.01 per 1 mg/dL increase for uric acid). Higher uric acid levels were independently associated with a greater risk of incident metabolic syndrome in a Japanese general population.

Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure (PAP) ≥ 25 mmHg at rest as assessed by right heart catheterization (RHC), and Doppler-derived systolic PAP (sPAP_ECHO) or tricuspid regurgitation pressure gradient (TRPG) is widely used to screen for PH. However, the cutoff value of sPAP_ECHO or TRPG for detecting a mean PAP ≥ 25 mmHg that was determined invasively has not been well defined.

We studied 189 patients who underwent RHC. Echocardiography was performed within 24 hours of invasive evaluation, and sPAP_ECHO was defined as the TRPG with right atrial pressure estimated on the basis of the current guideline.

From the receiver operating characteristic (ROC) curve analysis, the optimal sPAP_ECHO, and TRPG cutoffs for detecting PH were 41 mmHg (sensitivity, 92%; specificity, 91%; area under the curve = 0.95) and 36 mmHg (sensitivity, 90%; specificity, 93%; area under the curve = 0.95), respectively. The area under the TRPG ROC curve was similar to the area under the sPAP_ECHO ROC curve.

Given that Doppler echocardiography is required to accurately detect PH rather than to accurately estimate systolic PAP, our results provide useful information with regard to screening patients for PH and recommending further investigations on PH.

The aim of this study was to summarize the clinical experience of postoperative extracorporeal membrane oxygenation (ECMO) support in Stanford type A aortic dissection (STAAD) patients.

We retrospectively reviewed 246 consecutive acute STAAD patients undergoing operations at our institution from January 2012 to December 2016. Postoperative ECMO was used in 7 patients. There were 5 males and 2 females with a mean age of 43.1 ± 9.3 years. All 7 patients with acute STAAD underwent ascending aorta replacement and total arch repair with a self-designed stent graft (Micropart Corp, Shanghai, China). Concomitant procedures were aortic root replacement in 1 patient and coronary artery bypass grafting (CABG) in 2 patients. All patients received veno-arterial ECMO through the femoral artery and vein. Five patients were extubated before being removed from ECMO. The mean ECMO supporting time was 244.5 ± 57.8 hours. All 7 patients were successfully weaned from ECMO support, and 6 (85.7%) patients survived to discharge. The average hospital time was 26.3 ± 8.8 days. One patient died of cardiac arrest after being weaned from ECMO. Two patients underwent reoperation for bleeding and 1 patient showed transient delirium. The remaining patients all survived during a median follow-up of 19 months.

ECMO provides a good temporary cardiopulmonary support in STAAD patients with refractory cardiogenic shock after surgery for aortic dissection. The early use of ECMO and preventing its complications actively can improve the patient survival rate.

The diagnostic performance of 320-detector cardiac computed tomography (CCT) for the detection of thrombi in the left atrial appendage (LAA), relative to transesophageal echocardiography (TEE) as the gold standard, has not yet been evaluated. A total of 91 consecutive patients who were scheduled to undergo pulmonary vein isolation and underwent TEE and CCT were enrolled in this study. Delayed scanning on CCT was performed following early scanning, at 60 seconds after the start of the contrast injection. The radiation dose was estimated for both scans. The early scans showed a contrast medium filling defect (FD) in the LAA in 27 patients, whereas the delayed scans showed an FD in the LAA in six patients. Of these, five patients were confirmed to have a thrombus in the LAA by TEE. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were 100, 74.4, 18.5, 100, and 75.8% for early scanning and 100, 98.8, 83.3, 100, and 98.9% for delayed scanning, respectively. The area under the curve for the detection of a thrombus in the LAA on the delayed scans was significantly larger than that for the detection on the early scans (0.99 versus 0.87, P < 0.001). The estimated median radiation doses for the early and delayed scans were 2.86 and 0.42 mSv, respectively. Addition of delayed scanning to early scanning improved the diagnostic performance for the detection of a thrombus in the LAA and may obviate unnecessary TEE, with minimal additional radiation exposure.

The aim of this single-arm pilot study was to determine the effects of whole-body vibration training (WBVT) on endothelial function in elderly patients with cardiovascular diseases, as well as its safety. A total of 20 elderly patients with stable cardiovascular diseases underwent WBVT, which consisted of five static resistance training exercises (squats, wide stance squats, toe-stands, squats + band, and front lunges). The parameters of WBVT included vertical vibrations, 30 Hz frequency, and a 3-mm peak-to-peak amplitude. Each vibration session lasted 30 seconds, with 120 seconds of rest between sessions. Before and after WBVT, the reactive hyperemia peripheral arterial tonometry index (RH-PAT index) and transcutaneous oxygen pressure (tcPO₂) were recorded as a measure of endothelial function and peripheral blood circulation. Systolic blood pressure, diastolic blood pressure, heart rate, and arterial oxygen saturation of pulse oximetry (SpO₂) were measured at each rest interval as well as before and after WBVT. All patients completed our WBVT protocol without adverse events. The RH-PAT index significantly increased following WBVT (1.42 to 2.06, P < 0.001). There were no significant changes in heart rate (P = 0.777), systolic blood pressure (P = 0.183), diastolic blood pressure (P = 0.925), or SpO₂ (P = 0.248) during WBVT. In conclusion, we demonstrated the acute effects of WBVT on endothelial function, with no reports of adverse events. These findings support the need for further randomized controlled studies to investigate the long-term effects of WBVT.

According to recent guidelines, a new category of patients with heart failure (HF) with mid-range left ventricular ejection fraction (LVEF) (HFmrEF) (LVEF = 40%-49%) has been defined. The purpose of this study was to investigate the clinical characteristics and long-term outcomes of patients with HFmrEF. This was a single-center, retrospective, observational study in which we examined the clinical characteristics and outcomes of 494 consecutive patients with acute decompensated heart failure who were admitted to our institution between January 2014 and December 2016. Of this population, 282 (57.1%), 75 (15.2%), and 137 (48.6%) patients had heart failure with reduced ejection fraction (HFrEF), HFmrEF, and heart failure with preserved ejection fraction (HFpEF), respectively. Ischemic heart disease was the primary etiology in HFmrEF and HFrEF. At the time of discharge, β-blockers and renin-angiotensin system inhibitors were more frequently prescribed in HFmrEF than in HFpEF. The composite outcome of cardiovascular mortality and HF readmission was significantly lower in HFmrEF than in HFrEF. Further studies are needed to determine the effectiveness of the management of coronary artery disease and cardioprotective medications for HFmrEF.

So far, there remains a controversy regarding the efficacy of epinephrine (Ep) in patients with cardiopulmonary arrest (CPA). In this study, we evaluated the importance of the plasma levels of catecholamines prior to the administration of Ep in patients with CPA. Patients with out-of-hospital cardiac arrest (OHCA) who were transferred to Gunma University Hospital were enrolled prospectively between July 2014 and July 2017. The levels of catecholamines [Ep, norepinephrine (NEp), and dopamine] and vasopressin (antidiuretic hormone) in the plasma were measured using blood samples of cardiogenic patients with OHCA not treated with Ep. Patients were divided into two groups: the return of spontaneous circulation [ROSC (+) ] group and the no return of spontaneous circulation [ROSC (−) ] group. The plasma levels of these agents and the conditions of resuscitation were compared between these two groups. 48 patients with cardiogenic CPA had not been treated with Ep prior to obtaining the blood samples. The ROSC (+) and ROSC (−) groups included 14 and 34 patients, respectively. The frequency of prehospital defibrillation was significantly higher in the ROSC (+) group. However, the prehospital resuscitation time was significantly shorter in the ROSC (+) group. Moreover, the levels of Ep and NEp in the plasma were significantly lower in the ROSC (+) group. The increased levels of Ep in the plasma may not be associated with the acquisition of ROSC in patients with cardiogenic CPA.

The clinical scenario, which is based on systolic blood pressure (SBP) upon admission, is useful for classifying and determining initial treatment for acute heart failure (HF). However, the prognostic significance of SBP following the initial treatment is unclear.

The Japanese Heart Failure Syndrome with Preserved Ejection Fraction (JASPER) registry is a nationwide, observational, and prospective registration of consecutive Japanese patients hospitalized with HF with preserved ejection fraction (HFpEF) and left ventricular ejection fraction ≥ 50%. We divided 525 patients into three groups based on their SBP on the day following hospitalization: high (SBP > 140 mmHg, n = 72, 13.7%); normal (100 ≤ SBP ≤ 140 mmHg, n = 379, 72.2%); and low (SBP < 100 mmHg, n = 74, 14.1%) groups. This analysis had two primary endpoints: (1) all-cause death and (2) all-cause death or rehospitalization for HF. In the Kaplan-Meier analysis, both of the endpoints were the highest in the low group (Log-Rank < 0.05, respectively). Compared to the normal and high groups, the low group demonstrated a higher prevalence of atrial fibrillation (67.1%, 63.9%, and 47.8%, P = 0.026) and the lowest left ventricular outflow tract velocity time integral determined by echocardiography (16.4 cm, 19.4 cm, and 23.3 cm, P = 0.001). In the multivariable Cox proportional hazard analysis, low SBP on the day following hospitalization was an independent predictor of all-cause death (hazard ratio 1.868, 95% confidence interval 1.024-3.407, P = 0.042) and the composite endpoint (hazard ratio 1.660, 95% confidence interval 1.103-2.500, P = 0.015).

Classification based on SBP on the day following initial treatment predicts post-discharge prognosis in hospitalized patients with HFpEF.

Current studies demonstrating the effects of nicorandil in the prognosis of coronary artery disease (CAD) patients who received percutaneous coronary intervention (PCI) are inconclusive due to the small sample size and small events rate.

PubMed, OVID, CBM and CNKI databases were searched using a pre-specified search string to collect randomized controlled trials (RCTs) studying the effects of nicorandil on CAD patients receiving PCI. Data on all-cause mortality and cardiovascular events were collected. RevMan 5.3 software was used for meta-analysis. Subgroup analysis was conducted in patients receiving primary PCI (PPCI) and elective PCI (EPCI).

A total of 18 RCTs were included in our final analysis. Nicorandil treatment significantly reduced total mortality in PPCI (Peto OR = 0.44, 95%CI 0.25-0.79, P = 0.006) and EPCI (Peto OR = 0.41, 95%CI 0.25-0.67, P = 0.0004), cardiovascular death in both PPCI (Peto OR = 0.41, 95%CI 0.20-0.84, P = 0.01) and EPCI (Peto OR = 0.40, 95%CI 0.20-0.80, P = 0.009), and heart failure in PPCI (RR = 0.36, 95%CI 0.22-0.59, P < 0.0001). When compared with placebo plus standard treatment or standard treatment alone, nicorandil plus standard treatment was associated with reduced total mortality in both PPCI and EPCI, CV death in EPCI, and heart failure in PPCI. Nicorandil is associated with lower risks of total mortality and CV death in PPCI and EPCI in those who received nicorandil > 28 days.

Nicorandil as an adjunct therapy along with PCI is associated with reduced total mortality and cardiovascular death in PPCI and EPCI patients, and reduced heart failure in PPCI patients.

To systematically review and conduct a meta-analysis of the ivabradine-induced improvement in cardiopulmonary function, exercise capacity, and primary composite endpoints in patients with chronic heart failure (CHF).

This study was a systematic review and meta-analysis.

Databases, including PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and Clinical Trials and European Union Clinical Trials, were searched for randomized placebo-controlled trials. The efficacy and safety of ivabradine treatment in patients with CHF were assessed and compared to those of the standard anti-heart failure treatment. Review Manager 5.3 software was used to analyze the relative risk (RR) for dichotomous data and the mean difference (MD) for continuous data.

In total, 22 studies with 24,562 patients were included. Cardiopulmonary function analysis showed that treatment with added ivabradine reduced the heart rate (MD = −17.30, 95% confidence interval (CI): 19.52-−15.08, P < 0.00001), significantly increased the left ventricular ejection fraction (LVEF) (MD = 3.90, 95% CI: 0.40-7.40, P < 0.0001), and led to a better New York Heart Association (NYHA) classification. Ivabradine significantly reduced the minute ventilation/carbon dioxide production (VE/VCO₂) (MD = −2.68, 95% CI: −4.81-−0.55, P = 0.01) and improved the peak VO₂ (MD = 2.80, 95% CI: 1.05-4.55, P = 0.002) and the exercise capacity, including the exercise duration with a submaximal load (MD = 7.82, 95% CI: −2.57-−18.21, P < 0.00001) and the 6-minute walk distance. The RR of cardiovascular death or worsening heart failure was significantly decreased (RR = 0.93, 95% CI: 0.87-−0.98, P = 0.01) in the patients treated with ivabradine. Additionally, the RRs of heart failure and hospitalization also decreased (RR = 0.91, 95% CI: 0.85-−0.97, P = 0.006; RR = 0.86, 95% CI: 0.79-−0.93, P = 0.0002). Safety analysis showed no significant difference in the RR of severe adverse events between the ivabradine group and the standard anti-heart failure treatment group (P = 0.40). However, ivabradine significantly increased the RR of visual symptoms in CHF patients (RR = 3.82, 95% CI: 1.80-−8.13, P = 0.0005).

Existing evidence showed that adding ivabradine treatment significantly improved the cardiopulmonary function and increased the exercise capacity of patients with CHF. Adding ivabradine to the standard anti-heart failure treatment reduced the mortality and hospitalization risk and improved the quality of life. Finally, ivabradine significantly increased the RR of visual symptoms in CHF patients.

This is the first systematic review and meta-analysis to focus on the efficacy of ivabradine, which improved the cardiac function and increased the exercise capacity in patients with chronic heart failure (CHF). Therefore, this study will help evaluate the quality of life after adding ivabradine to the treatment of patients with CHF, even though there are differences in the standard for resting heart rate, left ventricular ejection fraction (LVEF), and New York Heart Association (NYHA) class in the included studies. This hybrid effect might be smaller when analyzed separately but might have a higher heterogeneity when analyzed in multiple studies.

Previous studies have provided established evidence on adverse outcomes of the coadministration of proton pump inhibitors (PPIs) and clopidogrel, whereas cerebro-cardiovascular outcomes of PPI use in the absence of clopidogrel therapy remain controversial.

In this study, we aimed to assess the association between PPIs and cerebro-cardiovascular outcomes independent of clopidogrel.

Systematic searches were conducted in the Cochrane Library, PubMed, and Embase databases for all relevant studies up to August 2018. Odds ratios (ORs) with its 95% confidence intervals (CIs) were abstracted and pooled using the random-effects model.

A total of 14 observational studies (13 cohort studies and 1 case-control study) were identified. Compared with non-PPI users, PPI users experienced higher risks of stroke (OR: 1.22, 95% CI: 1.08-1.36), myocardial infarction (MI; OR: 1.23, 95% CI: 1.14-1.32), cardiovascular death (OR: 1.83, 95% CI: 1.69-1.98), and major adverse cardiovascular events (MACEs; OR: 1.22, 95% CI: 1.05-1.40) independent of clopidogrel use, but not all-cause death (OR: 1.50, 95% CI: 0.99-2.25). In the subgroup analysis, PPI alone was associated with significant risks of new-onset MI (OR: 1.23, 95% CI: 1.13-1.35) and stroke (OR: 1.17, 95% CI: 1.05-1.30) in patients without previous MI or stoke and recurrent MI (OR: 1.24, 95% CI: 1.02-1.51) and stroke (OR: 1.36, 95% CI: 1.19-1.55) risks in patients with a previous MI.

Based on current publications, PPI use seems to be associated with increased risks of stroke, MI, cardiovascular death, and MACEs independent of clopidogrel. Greater caution should be therefore exercised while considering its clinical benefits and further investigate any causal relationships.

Tenascin-C (TNC) is involved in aortic disease pathophysiology. This study aims to evaluate TNC's value for predicting in-hospital death in acute aortic dissection (AD).

We prospectively enrolled consecutive patients with suspected acute AD within 48 hours from symptom onset. Serum TNC and C-reactive protein (CRP) levels were examined on admission. Their baseline clinical characteristics and serum D-Dimer (DD) were collected. The endpoint was in-hospital death from AD.

In the study cohort,78 survivors and 31 non-survivors with acute AD were enrolled. Compared to survivors, elevated median levels of serum TNC (141.10 pg/mL versus 75.30 pg/mL, P < 0.001), DD (8.74 μg/mL versus 4.58 μg/mL, P < 0.001), and CRP (19.20 mg/L versus 13.40 mg/L, P < 0.001) were found in non-survivors. Multiple logistic regressions revealed TNC, DD, and CRP were independent predictors of in-hospital death from acute AD. The OR and 95% CI were 1.038, 1.017-1.055; 1.084, 1.009-1.165 and 1.386, 1.107-1.643, respectively. Furthermore, TNC's sensitivity and specificity in predicting in-hospital death in acute AD were 83.87% and 83.33%. The combination of TNC and DD can improve the sensitivity and specificity to 90.30% and 88.46%.

TNC is a valuable biomarker for predicting in-hospital death from acute AD. The combination of TNC and DD can improve predictions of in-hospital death from acute AD.

Our previous studies have revealed that long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and genes were abnormally expressed in the pulmonary artery tissues of the chronic thromboembolic pulmonary hypertension (CTEPH) patients. We aim to establish the CTEPH-related miRNA-gene-lncRNA network for finding the core genes and associated miRNA and lncRNA in CTEPH patients.

Firstly, the target genes of differential miRNAs were predicted by searching TargetScan databases, and the predicted target genes were intersected with the mRNAs from the gene chip. Secondly, the intersective genes were analyzed by the Gene Ontology function and Kyoto Encyclopedia of Genes and Genomes pathway software for obtaining differential intersective genes and then establish the miRNA-gene networks. Thirdly, the possible genes regulated by the differential lncRNAs from the gene chip were intersected with the above-screened mRNA to build the lncRNA-mRNA networks. Subsequently, the miRNA-gene-lncRNA networks were constructed according to the two networks above (miRNA-gene networks and lncRNA-mRNA networks). Finally, the core genes of the networks in the experimental group were screened according to Diffk > 0.6 and used to construct the miRNA-core gene-lncRNA networks of CTEPH.

The pathway network, miRNA-mRNA network, lncRNA-mRNA networks, and miRNA-gene-lncRNA networks were successfully constructed. The core genes of the miRNA-gene-lncRNA networks (Diffk > 0.6) were the human Beta-type platelet-derived growth factor receptor (PDGFRB) and hypoxia-inducible factor-1a (HIF-1A), the miRNAs-PDGFRB-lncRNAs and miRNAs-HIF1A-lncRNAs networks were constructed. Finally, miRNA-149-5p-PDGFRB-TCONS_l2_00020587-XLOC_l2_010723 and miRNA-338-5p/miRNA-199b-5p-HIF1A- TCONS_l2_00020587-XLOC_l2_010723 were found in the analysis of the network.

miRNA-149-5p-PDGFRB-lncRNA CTEPH-associated 1 (CTEPHA1) (TCONS_l2_00020587-XLOC_l2_010723) and miRNA-338-5p/miRNA-199b-5p-HIF1A-lncRNA CTEPHA1 are related to the development of CTEPH.

The literature on malignant cardiac tumors is relatively limited because they are rare, especially among the Chinese population. We analyzed 14 patients diagnosed with malignant cardiac tumors in Fuwai Hospital and present the results of surgical treatments on the tumors. The mean age at tumor diagnosis was 47 years in a male-dominated cohort. There was a high frequency of pericardial effusion and coronary artery involvement in our group. We compared the survival times of patients who received different treatments and found that surgery improved prognosis of tumors, especially for patients who underwent orthotopic heart transplantation.

Cardiac fibrosis plays an important role in cardiac remodeling after myocardial infarction (MI). The molecular mechanisms that promote cardiac fibrosis after MI are well studied; however, the mechanisms by which the progression of cardiac fibrosis becomes attenuated after MI remain poorly understood. Recent reports show the role of cellular senescence in limiting tissue fibrosis. In the present study, we tested whether cellular senescence of cardiac fibroblasts (CFs) plays a role in attenuating the progression of cardiac fibrosis after MI. We found that the number of γH2AX-positive CFs increased up to day 7, whereas the number of proliferating CFs peaked at day 4 after MI. Senescent CFs were also observed at day 7, suggesting that attenuation of CF proliferation occurred simultaneously with the activation of the DNA damage response (DDR) system and the appearance of senescent CFs. We next cultured senescent CFs with non-senescent CFs and showed that senescent CFs suppressed proliferation of the surrounding non-senescent CFs in a juxtacrine manner. We also found that the blockade of DDR by Atm gene deletion sustained the proliferation of CFs and exacerbated the cardiac fibrosis at the early stage after MI. Our results indicate the role of DDR activation and cellular senescence in limiting cardiac fibrosis after MI. Regulation of cellular senescence in CFs may become one of the therapeutic strategies for preventing cardiac remodeling after MI.

Myocardial infarction (MI) occurs when the heart muscle is severely damaged due to a decrease in blood flow from the coronary arteries. During recovery from an MI, cardiac fibroblasts become activated and produce extracellular matrices, contributing to the wound healing process in the damaged heart. Inappropriate activation of the fibroblasts leads to excessive fibrosis in the heart. However, the molecular pathways by which cardiac fibroblasts are activated have not yet been fully elucidated.

Here we show that serum deprivation, which recapitulates the cellular microenvironment of the MI area, strikingly induces collagen production in C3H/10T1/2 cells. Based on transcriptomic and pharmacological studies, we found that cell cycle perturbation is directly linked to collagen production in fibroblasts. Importantly, collagen synthesis is increased independently of the transcriptional levels of type I collagen genes. These results reveal a novel mode of fibroblast activation in the ischemic area, which will allow us to gain insights into the molecular mechanisms underlying cardiac fibrosis and establish a basis for anti-fibrotic therapy.

Acute myocardial infarction (AMI) is a serious heart disease and the main reason for heart failure and sudden death worldwide. This study investigated the effects of polysaccharides from Enteromorpha prolifera (PEP) on AMI in vitro and in vivo, as well as the underlying mechanisms.

Human cardiac microvascular endothelial cells (HCMVEC) were cultured in vitro in an oxygen-glucose deprivation (OGD) environment to induce injury. The viability and apoptosis of HCMVEC were then detected using CCK-8 assay and Annexin V-FITC/PI staining, respectively. ELISA was performed to measure the concentrations of inflammatory cytokines. Cell transfection was conducted to reduce the expression of HIF-1α. Expression of key factors involving in cell proliferation, apoptosis, autophagy, MEK/ERK, and the NF-κB and mTOR pathways were evaluated using Western blotting. In vivo, Wistar rats were pre-treated by PEP and AMI was induced. The infarct size and cardiac functions (LVEDD, LVEF and LVFS) were measured.

In vitro, PEP treatment significantly protected HCMVEC from OGD-induced viability loss, proliferation inhibition, apoptosis, inflammatory cytokine expression, and autophagy. Moreover, PEP enhanced the expression of HIF-1α in HCMVEC via the MEK/ERK pathway. HIF-1α participated in the protective effects of PEP on OGD-treated HCMVEC. Furthermore, PEP attenuated OGD-induced NF-κB pathway activation and promoted the mTOR pathway in HCMVEC. In vivo, PEP pre-treatment reduced the infarct size and enhanced the LVEDD, LVEF and LVFS of rats via up-regulation of HIF-1α.

PEP ameliorated AMI in vitro and in vivo through up-regulation of HIF-1α. In vitro, PEP could activate the MEK/ERK and mTOR pathways, but inactivate the NF-κB pathway in OGD-treated HCMVEC.

A 72-year-old woman with hypertension, dyslipidemia, and diabetes mellitus presented to our hospital because of the sudden onset of chest pain. Emergency coronary angiography showed acute occlusion of the distal left anterior descending artery and coronary intervention with a drug-eluting stent was performed. Sudden cardiopulmonary arrest occurred on the sixth day of hospitalization, but coronary angiography showed no remarkable progression of the coronary artery diseases, including the site of stent implantation. An autopsy revealed that the cause of the sudden death was apical free wall rupture. In addition, the different timing of acute and sub-acute infarct findings were observed in the apical wall by histology, which indicated cardiac rupture was due to reinfarction at early phase of apical acute myocardial infarction. Although the rate of mechanical complications, including cardiac rupture, is decreasing in the era of primary coronary intervention, in addition to the well-known risk factors of cardiac rupture, the reinfarction of the culprit myocardial site in the early phase of acute myocardial infarction was considered as a possible risk factor of cardiac rupture.

Congenital long QT syndrome (LQTS) is a cardiac channelopathy that leads to the prolongation of the QT interval. This prolongation can lead to ventricular tachyarrhythmia, syncope, and sudden cardiac death. There are various types of LQTS. Treatment of LQT1 and LQT2 is mainly based on antiadrenergic therapy. LQT3, on the other hand, is a result of a mutation of the SCN5A gene, which encodes the sodium channels. In this type, patients are sensitive to vagal stimuli and episodes tend to occur at rest. Sodium channel blocking compounds, such as ranolazine, mexiletine, and flecainide, have been found to be effective in selective mutations.

In this case report, we report the case of a child with congenital LQT3 (V411M) who presented first with sudden cardiac death and three weeks later with an implantable cardioverter defibrillator storm. Knowing the specific mutation and understanding the mechanism at the molecular level through an in vitro study yielded a clinically meaningful result. The patient's arrhythmia burden was totally eliminated following successful treatment with flecainide.

Infective endocarditis (IE) is a lethal complication inpatients with congenital heart disease. We report a case of percutaneous implanted pulmonary valve IE in a 49-year-old female. She underwent a previous surgery for tetralogy of Fallot with transannular patching of the right ventricular outflow tractat the age of 18 years. Echocardiography showed chronic moderate to severe pulmonary regurgitation with right heart enlargement. She underwent transcatheter pulmonary valve implantation with a 26 mm Venus-P valve (Venus Medtech, Shanghai, China) in order to release pulmonary insufficiency. Two months after implantation, she presented with recurrent chills and febrile for one week, and percutaneous implanted pulmonary valve IE was diagnosed. According to the antibiotic susceptibility test, she was given penicillin and gentamycin. At 12 months follow-up, TTE showed vegetation completely disappeared and the valve functioned normally. The patient recovered uneventfully without any complications like recurrent IE.

So far, there is still controversy regarding the optimal prosthetic valve for patients with active infective valve endocarditis with annular abscess. Here, we report the case of a 65-year-old woman who was diagnosed with infective endocarditis associated with extensive annular abscess. The patient underwent debridement of the abscess cavity followed by aortic valve replacement using a Solo Smart (SS) stentless bioprosthesis. Postoperative recovery was uneventful, with no signs of recurrent infection. Since the SS valve is designed for supra-annular and subcoronary implantation, it is considered to be an alternative to conventional prosthetic valves in patients with infective endocarditis with aortic annular abscess.

A 92-year-old man with acute heart failure due to severe aortic stenosis underwent transcatheter aortic valve implantation (TAVI). Computed tomography demonstrated severe stenosis of the right common iliac artery, occlusion of the left external iliac artery, and stenosis of the left subclavian artery. Severe calcification was observed in the sinotubular junction, which was considered a risk factor for aortic dissection with transapical TAVI using a balloon-expanding bioprosthetic valve. Therefore, transaortic (TAo) access was the only option for this high-risk surgical patient. As the maximum distance from the aortic valve annulus to the sheath insertion point was less than 60 mm, TAVI was performed transaortically using a vascular graft that extended this distance, in order to avoid sheath dislocation. Our experience demonstrates that vascular graft application is a viable option in patients with an inadequate distance between the aortic valve annulus and the puncture site in TAo-TAVI.

Pump thrombosis (PT) is a serious complication after continuous-flow left ventricular assist device (LVAD) implantation. To detect PT, echocardiographic ramp test using left ventricular end-diastolic diameter (LVEDD) is known to be useful. However, this method has several limitations. In this study, we propose an alternative novel ramp test using the flow velocity of outflow graft (OG). A 46-year-old man underwent continuous-flow LVAD (HeartMate II, Abbott Laboratories, Lake Forest, IL, USA) implantation for advanced heart failure due to idiopathic dilated cardiomyopathy. About 2 years after implantation, he suffered from hemolysis and symptoms of heart failure, and PT was strongly suspected. The change in LVEDD was minimal with increase in pump speed (−0.06 cm/400 rotations per minute (rpm)), suggesting PT. The systolic to diastolic velocity (S/D) ratio of OG flow, which we proposed as a new indicator of PT, also showed minimal change (−0.07/400 rpm). His clinical symptoms improved with anticoagulation therapy, and the changing slope of the S/D ratio dramatically improved to −0.92/400 rpm. Although its consistency should be verified in many other cases, this novel method can be useful for detecting PT and evaluating its clinical course.

Ventricular pseudoaneurysm (PSA) is a rare, yet life-threatening complication of myocardial infarction, cardiac surgery, and transcatheter valve replacement. Although conventional surgery is the preferred treatment strategy, transcatheter closure has emerged as an effective alternative in selected candidates. In this report, we describe successful transcatheter closure of two unique cases of ventricular pseudoaneurysm (PSA): first, a complex post-myocardial infarction left ventricular PSA (LVPSA) with multi-communications, and second, a case of post-traumatic right ventricular PSA (RVPSA) following blunt chest injury caused by domestic violence.

A 14-year-old boy collapsed suddenly after a basketball game and was transported to our hospital after recovering from ventricular fibrillation by an automated external defibrillator. He had experienced loss of consciousness twice and has been examined for suspected long-QT syndrome at another hospital. The 12-lead electrocardiogram on admission revealed a prolonged QTc interval of 480 milliseconds. After the patient recovered without any sequelae, computed tomography revealed an anomalous left coronary artery arising from the opposite sinus of Valsalva and coursing between the aorta and the pulmonary artery. Furthermore, genetic testing identified a KCNE1-D85N abnormality. An anomalous coronary artery is one of the major causes of sudden death in young people; therefore, surgical revascularization is recommended for left coronary arteries arising from the contralateral sinus and coursing between the aorta and the pulmonary artery, regardless of myocardial ischemia. Transient myocardial ischemia may have exaggerated the instability from the arrhythmic substrate, even though KCNE1-D85N abnormalities alone are not thought to cause fatal arrhythmias. Besides routine electrocardiography, further examinations, including imaging and genetic testing, can characterize the pathophysiology of fatal cardiac disease.

Incomplete Kawasaki disease (iKD), which does not satisfy the standard KD diagnostic criteria because the required number of principal symptoms is not met, sometimes causes coronary aneurysms. Here we report the case of a patient with iKD who presented with only one principal symptom that resulted in the development of coronary aneurysm, as evidenced by angiography.

Spontaneous coronary artery rupture (SCAR) is an extremely rare, life-threatening entity without any previous underlying diseases. The clinical presentation may differ according to the site of the rupture and some patients may deteriorate early into sudden death due to the abrupt evolution of the associated cardiac tamponade and cardiogenic shock.¹⁾ The correct diagnosis of SCAR deserves a high level of suspicion. It may be confirmed as a differential diagnosis in patients with cardiac tamponade using transthoracic echocardiography (TTE) and computed tomography angiography (CTA) following emergency pericardiocentesis, and a definite diagnosis can be achieved by selective angiography. Although SCAR is associated with a dismal prognosis, some patients have recovered through emergency surgical operations or catheter interventions.²⁾ We report the case of a patient presenting cardiac tamponade and cardiogenic shock due to spontaneous rupture of the circumflex branch of the left coronary artery, which was successfully isolated by bilateral ligation.

Errors appeared in the article entitled "Increased Plasma Soluble Fractalkine in Patients with Chronic Heart Failure and Its Clinical Significance" by Cui-Ling Ji, Adnan Nomi, Bin Li, Cheng Shen, Bing-Chun Song, and Jin-Guo Zhang (Vol. 60, No. 3, 701-707, 2019). The affiliations of the authors and the address for correspondence on the bottom of page 701 should be replaced by the following.

From the ¹Department of Cardiology II, Affiliated Hospital of Jining Medical University, Jining, China, ²Teaching and Research Section of International Students, Jining Medical University, Jining, China, and ³Department of Cardiology IV, Affiliated Hospital of Jining Medical University, Jining, China.

Address for correspondence: Jin-Guo Zhang, MD, Department of Cardiology II, Affiliated Hospital of Jining Medical University, No. 89 Guhuai Road, Jining, Shandong 272100, China.