Functional mitral regurgitation (FMR) frequently coexists with left ventricular systolic dysfunction and advanced heart failure, and typically has poor clinical outcomes. Although various therapeutic options including cardiac resynchronization therapy and surgical mitral intervention, have been proposed, an optimal treatment strategy for functional mitral regurgitation has not yet been established. Over the last decade, transcatheter mitral valve repair using MitraClip has emerged as a novel alternative therapeutic option for functional mitral regurgitation. In 2018, the COAPT trial demonstrated that MitraClip treatment reduced rehospitalization due to heart failure and all-cause death in patients with functional mitral regurgitation and heart failure. As a consequence, the MitraClip has become a very promising potential treatment for functional mitral regurgitation. In this review, we discuss and summarize the current status and future perspectives of the treatment for functional mitral regurgitation and heart failure.

Cathepsin L (CatL) is a potent collagenase involved in atherosclerotic vascular remodeling and dysfunction in animals and humans. This study investigated the hypothesis that plasma CatL is associated with the prevalence of coronary artery disease (CAD). Between February May 2011 and January 2013, 206 consecutive subjects were enrolled from among patients who underwent coronary angiography and percutaneous coronary intervention treatment. Age-matched subjects (n = 215) served as controls. Plasma CatL and high-sensitive C-reactive protein (hs-CRP) and high-density lipoprotein cholesterol were measured. The patients with CAD had significantly higher plasma CatL levels compared to the controls (1.4 ± 0.4 versus 0.4 ± 0.2 ng/mL, P < 0.001), and the patients with acute coronary syndrome had significantly higher plasma CatL levels compared to those with stable angina pectoris (1.7 ± 0.7 versus 0.8 ± 0.4 ng/mL, P < 0.01). Linear regression analysis showed that overall, the plasma CatL levels were inversely correlated with the high-density lipoprotein levels (r = −0.32, P < 0.01) and positively with hs-CRP levels (r = 0.35, P < 0.01). Multiple logistic regression analyses shows that cathepsin L levels were independent predictors of CAD (add ratio, 1.8; 95% CI, 1.2 to 2.1; P < 0.01). These data demonstrated that increased levels of plasma CatL are closely associated with the presence of CAD and that circulating CatL serves as a useful biomarker for CAD.

The aim of this randomized prospective study was to evaluate the quality of life (QoL) using the "Seattle Angina Questionnaire" (SAQ) in patients with chronic total occlusion (CTO) in coronary arteries treated with either percutaneous coronary intervention (PCI) or optimal medical therapy (OMT), or only with OMT.

The potential benefits of recanalization of CTO by PCI have been controversial because of the scarcity of randomized controlled trials.

A total of 100 patients with CTO were randomized (1:1) prospectively into the PCI CTO or the OMT group (50 patients in each group). There were no baseline differences in the SAQ scores between the groups, except for physical limitation scores (P = 0.03). During the mean follow-up (FUP) of 275 ± 88 days, patients in the PCI group reported less physical activity limitations (72.7 ± 21.3 versus 60.5 ± 27, P = 0.014), less frequent angina episodes (89.8 ± 17.6 versus 76.8 ± 27.1, P = 0.006), better QoL (79.9 ± 22.7 versus 62.5 ± 25.5, P = 0.001), greater treatment satisfaction (91.2 ± 13.6 versus 81.4 ± 18.4, P = 0.003), and borderline differences in angina stability (61.2 ± 26.5 versus 51.0 ± 23.7, P = 0.046) compared to patients in the OMT group. There were no significant differences in SAQ scores in the OMT group at baseline and during the FUP. There was a statistically significant increase in all five domains in the PCI group.

Symptoms and QoL measured by the SAQ were significantly improved after CTO PCI compared to OMT alone.

The aim of this study was to explore potential predictive biomarkers and therapeutic targets of post-infarct heart failure (HF) using bioinformatics analyses.

CEL raw data of GSE59867 and GSE62646 were downloaded from the GEO database. Differentially expressed genes (DEGs) between patients with ST-segment elevation myocardial infarction (STEMI) and those with stable coronary artery disease (CAD) at admission and DEGs between admission and 6 months after myocardial infarction (MI) in patients with STEMI were analyzed. A gene ontology (GO) analysis and a gene set enrichment analysis (GSEA) were performed, and a protein-protein interaction network was constructed. Critical genes were further analyzed.

In total, 147 DEGs were screened between STEMI and CAD at admission, and 62 DEGs were identified in patients with STEMI between admission and 6 months after MI. The results of GO and GSEA indicate that neutrophils, neutrophil-related immunity responses, and monocytes/macrophages play important roles in MI pathogenesis. SLED1 expression was higher in patients with HF than in those without HF at admission and 1 month after MI. GSEA indicates that mTORC1 activation, E2F targets, G2M checkpoint, and MYC targets v1 inhibition may play key roles in the development of post-infarct HF. Furthermore, SLED1 may be involved in the development of post-infarct HF by activating mTORC1 and inhibiting E2F targets, G2M checkpoint, and MYC targets v1.

SLED1 may be a novel biomarker of post-infarct HF and may serve as a potential therapeutic target in this disease.

Although the incidence of acute myocardial infarction (AMI) has been decreasing in the elderly, it has been increasing in the young, especially in Japan. A social impact of AMI would be greater in the young, because loss of the young directly influences social activities such as business, child-raising, and tax payment. The aim of this study was to identify the specific characteristics of young AMI patients. We retrospectively included 408 consecutive AMI patients < 70 years of age, divided into a young group (< 55 years: n = 136) and an older group (55 to < 70 years: n = 272). The prevalence of overweight was greater in the young group (58.5%) than in the older group (40.7%) (P = 0.001). The frequency of current smokers was higher in the young group (67.6%) than in the older group (44.9%) (P < 0.001). Although the prevalence of hypertension was lower in the young group (66.7%) than in the older group (77.2%) (P = 0.017), that of untreated hypertension was greater in the young group (40.4%) than in the older group (27.2%) (P = 0.007). Furthermore, the prevalence of untreated dyslipidemia was greater in the young group (45.0%) than in the older group (26.6%) (P < 0.001). In conclusion, the young AMI patients had more modifiable risk factors such as obesity, smoking, untreated hypertension, and untreated dyslipidemia than the older patients. There is an unmet medical need for the prevention of AMI in the young generation.

Recent clinical studies suggest that newer-generation drug-eluting stents that combine ultrathin struts and nanocoating (biodegradable polymer sirolimus-eluting stents, BP-SES) could improve long-term clinical outcomes in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). However, the early vascular response to BP-SES in these patients has not been investigated so far.

We examined this response in 20 patients with STEMI caused by plaque rupture using frequency-domain optical coherence tomography (OCT) to understand the underlying mechanisms. Plaque rupture was diagnosed by OCT before PCI with BP-SES implantation was performed. OCT was again performed before the final angiography (post-PCI) and after 2 weeks (2W-OCT).

BP-SES placement caused protrusion of atherothrombotic material into the stent lumen and incomplete stent apposition in all patients. After 2 weeks, incomplete stent apposition was significantly reduced (% malapposed struts: post-PCI 4.7 ± 3.3%; 2W-OCT 0.9 ± 1.2%; P < 0.0001), and the percentage of uncovered struts also significantly decreased (% uncovered struts: post-PCI; 69.8 ± 18.3%: 2W-OCT; 29.6 ± 11.0%, P < 0.0001). The maximum protrusion area of the atherothrombotic burden was significantly reduced (post-PCI 1.36 ± 0.70 mm²; 2W-OCT 0.98 ± 0.55 mm²; P = 0.004).

This study on the early vascular responses following BP-SES implantation showed rapid resolution of atherothrombotic material and progression of strut apposition and coverage.

(UMIN000041324)

Diabetes mellitus (DM) is associated with an increased incidence of cardiovascular events and an elevated prevalence of sarcopenia. However, the relationship between cardiovascular events and sarcopenia in patients with DM remains unclear. This study examined this relationship and investigated the predictors of cardiovascular events in this population.

This study enrolled 161 patients with DM and no history of cardiovascular diseases who were admitted to our hospital for the treatment of DM between September 2012 and December 2015. Patients were divided into sarcopenia and non-sarcopenia groups, and were followed until March 2019. The primary endpoint was major adverse cardiovascular events (MACE).

The mean age was 65.9 ± 1.8 years old and the mean follow-up period was 4.1 ± 0.8 years. The log-rank test indicated that MACE differed significantly between the two groups (P < 0.0001). Multivariate Cox hazard analysis identified the cardio-ankle vascular index (CAVI) and handgrip strength as independent predictors of MACE (hazard ratio [HR] = 1.18, P = 0.039; and HR = 0.70, P = 0.016, respectively).

Handgrip strength is an indicator of sarcopenia in diabetic patients, and together with CAVI it was independently associated with the incidence of MACE. This suggests that the handgrip strength test might be useful in the management of patients with DM at high risk of cardiovascular outcomes.

Tricuspid valve (TV) surgery is associated with a high risk of postoperative pacemaker requirement. We set out to identify the incidence of atrioventricular block (AVB) after TV surgery and determine whether atrioventricular conduction recovers within time.

We investigated pre/intra- and postoperative predictors of AVB in patients who underwent tricuspid valve surgery (not only isolated TV surgery) at our institution between 2004 and 2017. Patients who had pacemakers prior to surgery were excluded.

One year after surgery, 5.8% of the surviving cohort had received a pacemaker due to AVB. In the complete follow-up time, 33 out of 505 patients required pacemaker implantation because of AVB. Of the 37 patients who presented to the intensive care unit postoperatively with AVB III, 14 (38%) underwent pacemaker implantation for AVB, and 20 (54%) did not require a pacemaker. AVB III at ICU admission was identified as a predictor of pacemaker implantation (OR: 9.7, CI: 3.8-24.5, P < 0.001). TV endocarditis was also identified as a predictor (OR: 12.4, CI: 3.3-46.3, P < 0.001). Eleven out of 32 patients (34%) with tricuspid endocarditis required a pacemaker for AVB. The mean ventricular pacing burden within the first 5 years after pacemaker implantation was 79%.

The issue of AVB after TV surgery is significant. Both the initial rhythm after surgery and etiology of the tricuspid disease can help predict pacemaker requirement. Within the first 5 years after surgery, the ventricular pacing burden remains high without relevant rhythm recovery.

Left atrial (LA) fibrosis is associated with a poor outcome after atrial fibrillation (AF) ablation. This study examined the extent of low-voltage areas in patients with recurrence of atrial tachyarrhythmia (ATA) after CB-based pulmonary vein isolation (PVI).

Sixty patients (mean age 67 ± 10 years, n = 32 female; n = 34 paroxysmal AF) who received radiofrequency redo-procedure due to recurrence of ATA within 6 months after CB-based PVI were included. A point-by point 3D-map was performed, and low-voltage sites were delineated based on bipolar voltage < 0.5 mV. The extent of fibrosis was categorized as stage A (0-10% of the LA wall), stage B (10-30%), stage C (30-50%), and stage D (> 50%).

The median area of LA low-voltage sites was 28.9 (9; 50.3) cm², corresponding to 17.4 (6; 30.6) % of the LA wall surface. 17/60 (28.3%) patients were categorized as fibrosis stage A, 21/60 (35%) as stage B, 18/60 (30%) as stage C, and 4/60 (6.7%) as stage D. Patient age and LA diameter were associated with more pronounced LA fibrosis; the extent of LA fibrosis was significantly higher in patients with LA tachycardia (LAT) during redo-procedures (P < 0.01), and ablation of linear lesions was more often performed (P < 0.01).

In patients after CB2-based PVI, expanded LA tissue fibrosis was associated with the occurrence of LAT and more extensive LA ablation during redo-procedures.

Atrioventricular nodal reentry tachycardia (AVNRT) is the most common regular supraventricular tachycardia (SVT). Slow pathway modification (SPM) is the accepted first line treatment with reported success rates around 95%. Information regarding possible predictors of AVNRT recurrence is scarce.

Out of 4170 consecutive patients with SPM in our department from 1993-2018, we identified 78 patients (1.9%) receiving > 1 SPM (69% female, median age 50 years) with a recurrence of AVNRT after a successful SPM. We matched these patients for age, gender and number of radiofrequency applications during first SPM with 78 patients who received one successful SPM in our center without AVNRT recurrence. Both groups were analyzed for possible predictors of a recurrence of AVNRT during long-term follow-up. The recurrence group contained a significantly lower proportion of patients with an occurrence of junctional beats during SPM (69% versus 89%, P = 0.006). Moreover, significantly more cases of previously diagnosed atrial fibrillation/tachycardia (AF/AT; 21% versus 5%, P = 0.007) and inducible AF/AT during electrophysiology study (23% versus 6%, P = 0.006) were present in the recurrence group. While more than half of patients had a recurrence within the first year, in 20% symptoms reappeared ≥ 4 years after ablation.

In a small percentage of patients, AVNRT recurs after an initially successful ablation. Interestingly, these patients had significantly fewer junctional beats during ablation and a higher rate of other (inducible) arrhythmias. AVNRT recurrence spanned a considerable timeframe and should remain a differential diagnosis, even years after ablation.

Left bundle branch pacing (LBBP) has been adopted as a new pacing therapy whether in routine pacing or patients with heart failure, but the criteria for a completely captured LBBP are too complicated and have a low success rate in routine clinical practice.

Consecutive patients with pacing therapy indications were enrolled. Left bundle branch area pacing (LBBAP) was conducted, and the presence of LBB potential, paced QRS duration, stimulus to left ventricular activation time (Stim-LVAT), and LBB potential to left ventricular activation time (LBB po-LVAT) were determined and utilized to characterize LBBAP modalities. Pacing parameters and safety were assessed at 6-month follow-up. LBBAP succeeded in 95.6% of patients (103/106) who completed the 6-month follow-up. Complete LBBP was achieved in 21 (20%) patients, characterized with a short Stim-LVAT equal to LBB po-LVAT. Incomplete LBBP was achieved in 58 (56%) patients with a short Stim-LVAT equal to LBB po-LVAT at a high pacing output and a relatively longer Stim-LVAT at a low pacing output. Deep septal pacing (DSP) characterized with no LBB potential and a longer Stim-LVAT (83.3 ± 7.7 ms) than that in LBBP (71.37 ± 7.1 ms, P < 0.01 versus DSP) was observed in 24 (23%) patients. Complete LBBP had a longer total procedure time and longer fluoroscopic time than the other two groups.

This study describes the similarities and differences in electrophysiological characteristics and the possible mechanisms of the different types of LBBAP, classified into 3 modalities in routine clinical practice, each with narrow paced QRS duration and stable parameters, indicating LBBAP can be a near-physiological pacing modality.

Intracardiac defibrillation (IDF) is performed to restore sinus rhythm (SR) during radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF). This study aimed to investigate the change in the IDF threshold before and after RFCA during the ablation procedure and determine whether the IDF threshold after RFCA was associated with the AF substrate and AF recurrence. A total of 141 consecutive patients with drug-refractory persistent AF (age 62.5 ± 10.3 years, 84.4% male) were enrolled in this study. Before RFCA, we initially performed IDF with an output of 1 J. When IDF failed to restore SR, the output was gradually increased to 30 J. After RFCA, we attempted pacing-induced AF to provoke other focuses of AF. When AF was induced, we performed IDF again to terminate AF with outputs of 1 to 30 J. The change in the IDF threshold to restore SR before and after RFCA was evaluated. After RFCA, the IDF threshold for restoring SR significantly decreased (from 11.5 ± 8.6 J to 4.0 ± 3.8 J, P < 0.001). During the follow-up (24.3 ± 12.2 months), SR was maintained in 107 patients (75.9%). The multivariate analysis using a Cox proportional-hazards model revealed that an IDF threshold of > 5 J after RFCA was significantly associated with the AF recurrence (HR, 3.99; 95% confidence interval 1.93-8.22; P = 0.0001). RFCA decreased the IDF threshold for restoring SR in patients with persistent AF. The IDF output of > 5 J after RFCA could be a predictor of AF recurrence independent of the AF substrate.

Enlargement of the mitral valve (MV) has gained attention as a compensatory mechanism for functional mitral regurgitation (FMR). We aimed to determine if MV leaflet area is associated with MV coaptation-zone area and identify the clinical factors associated with MV leaflet size and coaptation-zone area in patients with normal left ventricle (LV) systolic function and size using real-time 3D echocardiography (RT3DE).

We performed RT3DE in 135 patients with normal LV size and ejection fraction. MV leaflet and coaptation-zone areas were measured using custom 3D software. The clinical factors associated with MV leaflet and coaptation-zone areas were evaluated using univariate and multivariate linear regression analyses.

There was a significant relationship between MV leaflet and coaptation-zone areas (r = 0.499, P < 0.001). MV leaflet area was strongly associated with body surface area (BSA) (r = 0.905, P < 0.001) rather than LV size and age. MV leaflet area/BSA was independently associated with male gender (P = 0.002), lower diastolic blood pressure (P = 0.042), and LV end-diastolic volume (LVEDV) index (P = 0.048); MV coaptation-zone area/BSA was independently associated with lower LVEDV index (P = 0.01).

In patients with normal LV systolic function and size, MV leaflet size has a significant impact on competent MV coaptation. MV leaflet area might be intrinsically determined by body size rather than age and LV size, and the MV leaflet area/BSA is relatively constant. On the other hand, some clinical factors might also influence MV leaflet and coaptation-zone area.

There is scant information about the incidence, risk factors, and outcomes of coronary obstruction (CO) following valve-in-valve transcatheter aortic valve replacement (VIV-TAVR). A meta-analysis of the published studies from January 2000 to April 2020 was conducted, and the endpoint was CO. A total of 2858 patients were enrolled in this study. The mean age was 77.7 ± 9.8, and 39.9% of them were female. The Society of Thoracic Surgeons (STS) score, European System for Cardiac Operative Risk Evaluation (EuroSCORE), and Logistic EuroSCORE were 8.9 ± 7.8, 16.0 ± 10.9, and 26.3 ± 16.3, respectively. The overall incidence of CO was 2.58%. CO incidence between patients with prior stented and stentless valves were significantly different (1.67% versus 7.17%), with an odds ratio (OR) of 0.25 and a 95% confidence interval (CI) of 0.14-0.44 (P < 0.00001). The first-generation valves were significantly associated with higher CO incidence compared with the second-generation valves (7.09% versus 2.03%; OR, 2.44; 95%CI, 1.06-5.62; P = 0.04), while no statistical difference was found between self-expandable valves and balloon-expandable valves (2.45% versus 2.60%; OR, 0.99; 95%CI, 0.55-1.79; P = 0.98). Virtual transcatheter to coronary ostia (VTC) distance (3.3 ± 2.1 mm, n = 29 versus 5.8 ± 2.4 mm, n = 169; mean difference, −2.70; 95%CI, −3.46 to −1.95; P < 0.00001) and the sinus of Valsalva (SOV) diameter (27.5 ± 3.8 mm, n = 23 versus 32.3 ± 4.0 mm, n = 101; mean difference, −3.80; 95%CI, −6.55 to −1.05; P = 0.007) were enormously shorter in patients with CO. The 24-hour, in-hospital, and 30-day mortality of patients with CO were 10.5%, 30.8%, and 37.1%, respectively. In conclusion, device selections, VTC distances, and SOV diameters may be important factors in assessing the CO risk in VIV-TAVR.

Edge-to-edge repair using the MitraClip system is indicated in patients with severe mitral regurgitation (MR) who are at high risk for open-heart surgery due to comorbidity or reduced cardiac function. However, less is known about pre-procedural risk factors for mortality and morbidity following MitraClip implantation. Consecutive 25 patients with severe MR who underwent MitraClip therapy (mean age, 77 years old, 14 males) were included. Right heart catheterization and echocardiographic data before and after the procedure were collected and their prognostic impacts were investigated. Acute procedural success was 96%. At one week following MitraClip repair, left ventricular ejection fraction (LVEF) remained unchanged and left ventricular end-diastolic volume tended to be smaller. Cardiac index and mean pulmonary artery pressure (mPAP) were markedly improved following the procedure (P < 0.001 for both). In the multivariate analyses using baseline characteristics, both lower LVEF (hazard ratio 0.57, 95% confidence interval 0.30-0.89) and higher mPAP (hazard ratio 1.23, 95% confidence interval 1.06-1.56) were independently associated with post-procedural 1-year death or heart failure readmission (P < 0.05 for both). The lower LVEF and higher mPAP group had lower 1-year survival free from HF readmission compared with those without (16.7% versus 100%; P < 0.001). In conclusion, a combination of baseline mPAP and LVEF might be a useful tool in predicting post-MitraClip procedural clinical outcomes.

Tachycardia-induced cardiomyopathy (TIC) is a potentially reversible cardiomyopathy caused by tachyarrhythmia. For atrial flutter (AFL) -induced TIC, a rhythm control strategy, such as catheter ablation, has been recommended. However, the efficacy of rate control has remained unclear due to the difficulty of achieving control using arrhythmic medications.

We prospectively assessed 47 symptomatic heart failure (HF) patients with left ventricular ejection fraction (LVEF) < 50% and suspected persistent AFL-induced TIC. Patients were divided into the rhythm control strategy (n = 22; treatment with catheter ablation or electrical cardioversion) and rate control strategy (n = 25; treatment with bisoprolol) groups. The latter was further divided into the strict rate control strategy (average heart rate < 80 bpm) and lenient rate control strategy (average heart rate < 110 bpm) subgroups. The primary outcome was left ventricular (LV) function recovery, which was defined as an increase in LVEF ≥ 20% or to a value of ≥ 55% after 6 months.

In the rhythm control strategy group, more patients achieved LV function recovery after 6 months (95.2% versus 60.9%, P = 0.010). The cumulative incidence of worsening HF events was significantly higher in the rate control strategy group than in the rhythm control strategy group (hazard ratio, 4.66; 95% confidence interval, 1.01-21.57). The subgroup study revealed the advantage of the strict rate control strategy for achieving LV function recovery (83.3% versus 36.4%, P = 0.036).

The rate control strategy was significantly inferior to the rhythm control strategy for the LV function recovery in TIC patients with persistent AFL. Our findings suggest that the strict rate control strategy should be aimed if the rhythm control strategy cannot be performed.

Mutations in the sarcomeric protein filamin C (FLNC) gene have been linked to hypertrophic cardiomyopathy (HCM), as they have been determined to increase the risk of ventricular arrhythmia and sudden death. Thus, in this study, we identified a novel missense mutation of FLNC in a Chinese family with HCM, and, interestingly, a second novel truncating mutation of MYLK2 was discobered in one family member with different phenotype.

We performed whole-exome sequencing in a Chinese family with HCM of unknown cause. To determine and confirm the function of a novel mutation of FLNC, we introduced the mutant and wild-type gene into AC16 cells (human cardiomyocytes): we then used western blotting to analyze the expression of FLNC in subcellular fractions, and confocal microscope to observe the subcellular distribution of the protein.

As per our findings, we were able to identify a novel missense single nucleotide variant (FLNC c.G5935A [p.A1979T]) in the family, which segregates with the disease. FLNC expression levels were observed to be equivalent in both wild-type and p.A1979T cardiomyocytes. However, the expression of the mutant protein has resulted in cytoplasmic protein aggregations, in contrast to wild-type FLNC, which was distributed in the cytoplasm and did not form aggregates. Unexpectedly, a second truncating mutation, NM_033118:exon8:c.G1138T:p.E380X of the MYLK2 gene, was identified in the mother of the proband with dilated cardiomyopathy, which was not found in other subjects.

We then identified the FLNC A1979T mutation as a novel pathogenic variant associated with HCM in a Chinese family as well as a second causal mutation in a family member with a distinct phenotype. The possibility that there is more than one causal mutation in cardiomyopathy warrants clinical attention, especially for patients with atypical clinical features.

Although it is well known that patients with hypertrophic cardiomyopathy (HCM) have serious adverse events, such as life-threatening arrhythmia and heart failure, the prediction of such evens is still difficult. Recently, it has been reported that one of the causes of these serious adverse events is microvascular dysfunction, which can be noninvasively evaluated by employing cardiac magnetic resonance (CMR) imaging.

We analyzed 32 consecutive HCM patients via CMR imaging and myocardial scintigraphy and divided them into two groups: ventricular tachycardia (VT) group and non-VT group. Myocardial perfusion studies were conducted quantitatively using the QMass^® software, and each slice image was divided into six segments. The time-intensity curve derived from the perfusion image by CMR imaging was evaluated, and the time to 50% of the peak intensity (time 50% max) was automatically calculated for each segment.

Although no difference was observed in various parameters of myocardial scintigraphy between the two groups, the VT group exhibited a higher mean of time 50% max and wider standard deviation (SD) of time 50% max in each segment than the non-VT group. The cutoff values were obtained by the receiver operating characteristic curves derived from the mean of time 50% max and SD of time 50% max. The two groups divided by the cutoff values exhibited significant differences in the occurrence of serious adverse events.

CMR imaging may be useful for predicting serious adverse events of patients with HCM.

The aim of this study was to evaluate the clinical efficacy of N-acetylcysteine (NAC) in the treatment of ST segment elevation myocardial infarction (STEMI).

PubMed, EMBASE, Cochrane Library, and Web of Science were searched systematically from the establishment of the database to June 2020. Two researchers independently completed literature screening and data extraction and conducted a meta-analysis.

Nine articles including 1419 patients were enrolled. Meta-analysis showed that all-cause mortality [RR = 0.56, 95%CI (0.33, 0.93), P = 0.02], occurrence of major adverse cardiovascular events (MACE) [RR = 0.63, 95%CI (0.47, 0.85), P = 0.002], and myocardial enzyme hs-TnT level [SMD = -0.42, 95%CI (-0.71, -0.13), P = 0.005] were significantly lower in patients with STEMI treated with NAC than those in the control group. There was no significant difference between the NAC group and the control group in new congestive heart failure [RR = 0.94, 95%CI (0.48, 1.82), P = 0.84], ejection fraction [MD = 2.00, 95%CI (-0.59, 4.60), P = 0.13], and CK-MB [SMD = -0.18, 95%CI (-0.47, 0.11), P = 0.23]. There was no significant difference in the occurrence of adverse reactions between the NAC group and the control group [RR = 1.04, 95%CI (0.57-1.89), P = 0.90].

NAC can reduce the all-cause mortality and MACE cases of STEMI.

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is erupting and spreading globally. Cardiovascular complications secondary to the infection have caught notice. This study aims to delineate the relationship of cardiac biomarkers and outcomes in severe cases of corona virus disease 2019 (COVID-19). One hundred forty-eight critically ill adult patients with COVID-19 were enrolled. From these patients, the demographic data, symptoms, cardiac biomarkers, treatments, and clinical outcomes were collected. Data were compared between survivors and non-survivors. Four patients in the non-survivor group were selected, and their cardiac biomarkers were collected and analyzed. Among the 148 patients, the incidence of cardiovascular complications was 19 (12.8%). Five of them were survivors (5.2%), and 14 of them were non-survivors (26.9%). Compared with the survivors, the non-survivors had higher levels of high-sensitivity cardiac troponin I, creatine kinase isoenzyme-MB, myoglobin, and N-terminal pro-brain natriuretic peptide (P < 0.05). The occurrence of cardiovascular events began at 11-15 days after the onset of the disease and reached a peak at 14-20 days. COVID-19 not only is a respiratory disease but also causes damage to the cardiovascular system. Cardiac biomarkers have the potential for early warning and prognostic evaluation in patients with COVID-19. It is recommended that cardiac biomarker monitoring in patients with COVID-19 should be initiated at least from the 11th day of the disease course.

The aim of this study was to explore the pivotal genes or lncRNAs involved in the progression of atrial fibrillation (AF) -valvular heart disease (VHD). The mRNA profiling GSE113013 was obtained from the Gene Expression Omnibus database. The identification of differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs) was performed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were carried out for DEGs. Then, the construction of the protein-protein interaction (PPI) network was conducted. An lncRNA-miRNA-target ceRNA network was constructed after obtaining microRNAs (miRNA) related to DElncRNAs. Ultimately, key disease-related genes were screened. A total of 399 DEGs and 145 DElncRNAs were obtained. There were 283 nodes and 588 interaction pairs in the PPI network, and synaptosome-associated protein 25 (SNAP25) had higher degrees (degree = 22) in the PPI network. There were 65 interaction pairs in the ceRNA network. Here, Baculoviral IAP Repeat Containing 5 (BIRC5) was regulated by hsa-miR-1285-3p, which was regulated by lncRNA NPHP3-AS1. Gap Junction Protein Alpha 5 (GAJ5) was regulated by hsa-miR-4505, hsa-miR-1972, and hsa-miR-1199-5p. In particular, GAJ5 was enriched in the function of ion transmembrane transport regulation, whereas BIRC5 was enriched in the function of apoptosis-multiple species pathway. Similarly, Potassium Inwardly Rectifying Channel Subfamily J Member 6 (KCNJ6) was enriched in the function of an ion channel complex. VENN analysis identified BIRC5 and GJA5 as key AF-related genes. KCNJ6, SNAP25, GJA5, BIRC5, hsa-miR-1285-3p, and lncRNA NPHP3-AS1 were likely to be associated with AF-VHD development.

High-mobility group box 1 (HMGB1) is increased in the myocardium under pressure overload (PO) and is involved in PO-induced cardiac remodeling. The mechanisms of the upregulation of cardiac HMGB1 expression have not been fully elucidated. In the present study, a mouse transverse aortic constriction (TAC) model was used, and an angiotensin II (Ang II) type 1 (AT1) receptor inhibitor (losartan) or Ang II type 2 (AT2) receptor inhibitor (PD123319) was administrated to mice for 14 days. Cardiac myocytes were cultured and treated with Ang II for 5 minutes to 48 hours conditionally with the blockage of the AT1 or AT2 receptor. TAC-induced cardiac hypertrophy was observed at 14 days after the operation, which was partially reversed by losartan, but not by PD123319. Similarly, the upregulated HMGB1 expression levels observed in both the serum and myocardium induced by TAC were reduced by losartan. Elevated cardiac HMGB1 protein levels, but not mRNA or serum levels, were significantly decreased by PD123319. Furthermore, HMGB1 expression levels in culture media and cardiac myocytes were increased following Ang II treatment in vitro, positively associated with the duration of treatment. Similarly, Ang II-induced upregulation of HMGB1 in vitro was inhibited by both losartan and PD123319. These results suggest that upregulation of HMGB1 in serum and myocardium under PO, which are partially derived from cardiac myocytes, may be induced by Ang II via the AT1 and AT2 receptors. Additionally, amelioration of PO-induced cardiac hypertrophy following losartan treatment may be associated with the reduction of HMGB1 expression through the AT1 receptor.

A 41-year-old woman with chest pain for 6 hours was admitted to our chest pain center, presenting with acute myocardial infarction. Coronary angiography showed acute total occlusion in the proximal left anterior descending artery due to late stent thrombosis. After thrombus aspiration and intracoronary administration of 0.5 mg tirofiban, repeated angiography showed that no obvious residual stenosis remained. The patient underwent drug-coated balloon angioplasty 69 days ago and was then administered dual antiplatelet treatment (aspirin and clopidogrel) uninterruptedly. Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously. Thus, clopidogrel was replaced by ticagrelor and no more cardiovascular adverse events occurred during the 2-year follow-up.

Off-pump coronary artery bypass grafting (OPCABG) may be performed on patients with high surgical risk who are poor candidates for traditional mechanical circulatory support. Hemodynamic support with micro-axial mechanical circulatory devices has been performed with limited but promising results.

We report a case of a 66-year-old male with multiple comorbidities and low cardiac output undergoing OPCABG. Impella CP device was deployed for "in-pump" support during surgical coronary revascularization resulting in intraoperative stability and uncomplicated post-operative recovery.

Previous reports have described the use of the Impella Recover LP 5.0 device for use during OPCABG. We describe the successful and safe perioperative use of the Impella CP device. Despite lower flow rates, adequate support was achieved and the transfemoral cannulation and smaller outer diameter than the Impella 5.0 device may decrease the risk of complications and expedite recovery. Further research will be necessary to determine the optimal perioperative hemodynamic support strategy to offer hemodynamically unstable, high, and prohibitive risk patients.

Speech-induced atrial tachycardia (AT) is extremely rare. We presented a case of focal AT that could be triggered by speech and terminated with the cessation of conversation. An electrophysiological study showed that the outbreak was associated with left atrial pressure rose. Radiofrequency ablation at the left atrial posterior-superior wall (earliest activation site) resulted in the immediate termination of AT. These electrophysiological characteristics indicated that the cardiac autonomic nervous system and/or left atrial pressure might play essential roles in the occurrences of speech-induced AT.

Libman-Sacks endocarditis, characterized by verrucous vegetations formation, is a typical cardiac manifestation of autoimmune diseases such as systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Although typically mild and asymptomatic, Libman-Sacks endocarditis can lead to serious complications, including thromboembolic events, superimposed bacterial endocarditis, and severe valvular regurgitation and/or stenosis, and valve surgery may be required. Here, we report a case of mitral valve repair for a large Libman-Sacks vegetation in a 29-year-old woman with a history of APS with cerebral infarction. Transesophageal echocardiography (TEE) demonstrated an isolated large mobile vegetation on the atrial side of posterior mitral valve leaflet, with severe mitral regurgitation. Next, we organized a multidisciplinary team meeting to better evaluate the case before performing the surgery. To prevent further thromboembolic events, and due to the insufficiency of the mitral valve, the patient was accepted for mitral valve surgery, and she was discharged uneventfully 10 days after successful surgery. She was managed with long-term anticoagulation medicine after surgery and followed up for 2 years with no complications. The present case showed mitral repair is feasible and effective in young female patients of child-bearing age, and the lesion only localized mitral valve abnormalities caused by Libman-Sacks endocarditis.

Dysferlin is a sarcolemmal protein present in muscle cells. It is responsible for muscle membrane repair. Dysferlin gene (DYSF) mutation, resulting in deficiency in this protein, is termed dysferlinopathy. Clinically, it manifests as early adulthood onset of muscle weakness with markedly elevated creatine kinase levels. The main phenotypes are limb-girdle muscular dystrophy type 2B (LGMD2B), affecting proximal muscles, and Miyoshi myopathy (MM), affecting distal muscles. Dysferlin is also present in cardiomyocytes, and case reports have emerged of cardiac abnormalities in dysferlinopathy. While routine methods of cardiac screening, namely, electrocardiography or echocardiography, are convenient and noninvasive, they often exhibit insufficient diagnostic sensitivity for detecting subclinical cardiac remodeling during early stages of cardiomyopathy. Cardiac magnetic resonance imaging though can provide accurate assessment of cardiac chamber sizes and function. With gadolinium administration, it can also detect areas of myocardial scarring and fibrosis. Early diagnosis of neuromuscular disease-related cardiomyopathy is of clinical significance, as appropriate treatment can retard myocardial fibrosis, delaying cardiomyopathy progression. We present a case of a patient with MM incidentally diagnosed with concomitant cardiomyopathy.

Intravenous mineralocorticoid receptor antagonists (MRAs) have been used in some centers for decades to reduce the risk of hypokalemia and boost diuresis in acutely decompensated heart failure (ADHF). We report the well-tolerated use of intravenous MRAs as a rescue procedure in 3 patients admitted for ADHF with important diuretic resistance. Undertaking trials evaluating the effect of this therapeutic strategy in ADHF could represent a promising avenue.

A 52-year-old man with consciousness disorder following a 2-day history of general fatigue, diarrhea, vomiting and excessive thirst was admitted to our hospital. Severe hyperglycemia (1,739 mg/dL) with a slightly elevated HbA1c level (6.9%), ketonuria and low C-peptide level (0.07 ng/mL) confirmed the diagnosis of fulminant type 1 diabetes mellitus (FT1DM). Following sudden unexplained cardiogenic shock shortly after the initiation of insulin therapy with no evidence of myocardial ischemia assessed by coronary angiography, the patient was supported with percutaneous venoarterial extracorporeal membrane oxygenation. Electron microscopic analysis of the myocardium revealed massive lipid droplets without the infiltration of inflammatory cells. His left ventricular function began to recover during the following days and returned to a normal level on day 14. Currently, the impact of FT1DM on intramyocardial lipid deposition is poorly understood. However, this case suggests that even short-term exposure to high concentrations of glucose can be responsible for lipotoxicity followed by severe cardiac dysfunction.

The definite diagnosis of cardiac sarcoidosis (CS) can be difficult because it mimics other cardiomyopathies and morphological abnormalities during its time course. Distinguishing CS isolated cardiac sarcoidosis from other cardiomyopathies is very important for the introduction of immunosuppressive therapy.

In this study, we report a patient who had initially been diagnosed with hypertrophic obstructive cardiomyopathy (HOCM). The patient developed complete atrioventricular block (CAVB) and morphological abnormalities, which led to his primary diagnosis being re-conducted. Moreover, we made a definite diagnose of isolated CS (ICS) based on the guideline for the diagnosis and treatment using ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG-PET/CT)¹⁾ and performed tailor-made treatment including immunosuppressive therapy.

Mid-aortic syndrome (MAS) is a rare condition characterized by stenosis of the distal thoracic and/or abdominal aorta. Williams-Beuren syndrome (WBS) is a relatively rare cause of MAS. We report a case of incidentally diagnosed MAS caused by WBS without typical manifestations caused by an atypical small-sized deletion in chromosome 7q11.23, which was initially misdiagnosed as Takayasu arteritis.

Anticoagulation is recommended for the treatment of pulmonary embolism (PE) and deep vein thrombosis (DVT). In some cases, an inferior vena cava (IVC) filter is used to prevent PE. We report the case of a 70-year-old woman who developed non-massive PE and proximal DVT, which were treated using an IVC filter; two filters were placed owing to the fracture of the filters. Few previous reports have discussed IVC fractures and the difficulty in detecting such fractures on computed tomography before retrieval. Based on our experience, we suggest that a temporary IVC filter for DVT treatment should be considered carefully.

A 14 year-old boy developed infective endocarditis of the mitral valve caused by Methicillin-sensitive Staphylococcus aureus and became comatose. Isolated basilar artery dissection was initially observed on the 3rd day by magnetic resonance imaging (MRI), ie, it did not exist on day 1. He underwent successful urgent mitral valve repair on the 5th day because of highly mobile vegetations and a newly emerged brain infarction under optimal antibiotic administration. Postoperatively, he recovered well and the basilar artery dissection was found to have recovered on an MRI on the 25th day without any specific intervention. This clinical course indicated that intracranial artery dissection may occur as a complication of infective endocarditis and supports the importance of the careful evaluation of brain MRI in patients with infective endocarditis.

There were errors in the announcement of the UEDA Heart Awards for the Year 2020 in the November 2020 issue. We would therefore like to officially announce that the following 6 articles have been selected for the UEDA Heart Awards for 2020.