Both cardiogenic shock (CS) and critical culprit lesion locations (CCLLs), defined as the left main trunk and proximal left anterior descending coronary artery, are associated with worse outcomes in ST-elevation myocardial infarctions (STEMIs). We aimed to examine how the combination of CS and/or CCLLs affected the prognosis in Japanese STEMI patients in the primary percutaneous coronary intervention era (PPCI-era). The subjects included 624 STEMI patients admitted to our hospital between January 2013 and April 2020. They were divided into four groups according to the combination of CS and CCLLs: CS (−) CCLL (−) group [n = 405], CS (−) CCLL (+) group [n = 150], CS (+) CCLL (−) group [n = 25], and CS (+) CCLL (+) group [n = 44]. The cumulative incidences of all-cause death at 30 days and 1 year were 3.5% and 6.4% in the CS (−) CCLL (−), 3.3% and 5.6% in the CS (−) CCLL (+), 32.0% and 32.0% in the CS (+) CCLL (−), and 50.0% and 65.9% in the CS (+) CCLL (+) group, respectively. After a multivariate adjustment, the CS (+) CCLL (+) group was independently associated with all-cause death (hazard ratio: 17.00, 95% confidence interval: 7.12-40.59 versus the CS (−) CCLL (−) group). In the CS (+) CCLL (+) group, compared to years 2013-2017, the IMPELLA begun to be used (44.4% versus 0%), and intra-aortic balloon pumps significantly decreased (44.4% versus 92.3%) during years 2018-2020, while the medications upon discharge did not significantly differ. The 30-day mortality was numerically lower during years 2018-2020 than years 2013-2017 (Log-rank test, P = 0.092). In conclusion, the prognosis of STEMIs varies greatly depending on the combination of CS and CCLLs, and in particular, patients with both CS and CCLLs had the poorest prognosis during the modern PPCI-era.

¹³N-ammonia positron emission tomography (NH₃-PET) can evaluate myocardial blood flow (MBF) at rest, stress, and myocardial flow reserve (MFR) as well as the ratio of MBF at stress to that at rest. MFR is useful in predicting the prognoses of patients with various heart diseases. Cadmium-zinc-telluride single photon emission computed tomography (CZT-SPECT) enables us to acquire dynamic images of radiotracer kinetics and measure original MBF and MFR using ^99mTc-sestamibi. This study aimed to investigate the utility of CZT-SPECT for quantitative assessment of MBF compared to NH₃-PET. We validated the correlation of MBF and MFR between CZT-SPECT and NH₃-PET. Fourteen patients using one-day rest/stress CZT-SPECT, D-SPECT followed by NH₃-PET within 1 month were enrolled and analyzed prospectively. The reproducibility of the MBF and MFR obtained with these two methods was examined using Spearman's correlation coefficient and Bland-Altman plot analysis. The diagnostic value of D-SPECT for abnormal MFR defined using NH₃-PET results as MFR < 2.0 was assessed using receiver-operating characteristic (ROC) analysis. The median duration between D-SPECT and NH₃-PET was 20 days. Although MBF was overestimated by D-SPECT compared to NH₃-PET at high value (mean difference, 0.43 [0.34-0.53]), MBF and MFR were correlated with the two modalities (MBF: r = 0.71, P < 0.0001, MFR: r = 0.60, P < 0.0001). The ROC curve analysis demonstrated a cutoff of 1.6 for detecting abnormal MFR with D-SPECT (sensitivity, 68%; specificity, 91%; AUC, 0.75). MBF and MFR obtained using D-SPECT and NH₃-PET had a good correlation, suggesting that the quantitative MFR evaluation by CZT-SPECT may help understand the trend of NH₃-PET MFR.

This study aimed to investigate clinical and preintervention optical coherence tomography (OCT) findings to predict irregular protrusion (IRP) immediately after stent implantation.

We evaluated 84 lesions treated with cobalt-chromium everolimus-eluting stent (CoCr-EES) from the MECHANISM Elective study. Patients were divided into two groups according to the presence of IRP [IRP: n = 16, non-IRP: n = 68]. Optical coherence tomography images before intervention and immediately after stenting were evaluated with standard qualitative and quantitative OCT analyses.

Total cholesterol and the prevalence of ruptured plaque before intervention were significantly higher in the IRP group than in the non-IRP group [199 ± 37 mg/dL versus 176 ± 41 mg/dL; P = 0.022, 31% versus 7%; P = 0.008]. Total lipid length tended to be longer in the IRP group than in the non-IRP group [19.6 ± 9.2 mm versus 15.5 ± 9.3 mm; P = 0.090]. The prevalence of ruptured plaque, and total cholesterol levels were independent predictors of IRP immediately after stenting by multivariate logistic regression analysis [OR: 4.6, 95% confidence interval: 1.01-21.23, P = 0.048, OR: 1.02, 95% confidence interval: 1.00-1.03, P = 0.046]. IRP post-CoCr-EES implantation was completely resolved at follow-up OCT.

The prevalence of ruptured plaque before intervention and total cholesterol levels were independent predictors of IRP after CoCr-EES implantation in patients with stable coronary artery disease.

We conducted a single-center, retrospective, lesion-based study to examine the safety and efficacy of drug-coated balloons (DCBs) for de novo coronary stenosis in patients with acute coronary syndrome (ACS) by comparing them with those of drug-eluting stents (DESs).

A total of 309 consecutive lesions in patients with ACS who were successfully treated by emergent procedures using either a DCB (n = 107) or a DES between January 2016 and December 2019 were included in the study. The primary endpoint was the incidence of target lesion failure (TLF), defined as cardiac death without mortality due to ACS, non-fatal myocardial infarction, and any target lesion revascularization, including acute occlusion, after DCB use and definite stent thrombosis after DES placement. A propensity score-matched analysis was used to adjust the 36 baseline variables. Retrospective investigations were conducted in January 2021.

Baseline adjustment yielded 91 lesions in each group, with a mean balloon size of 3.02 ± 0.22 mm and a mean length of 20.9 ± 6.2 mm in the DCB group. The frequency of TLF in the DCB group (9.9% during the mean observational interval of 671 ± 508 days) was not significantly different from that in the DES group (13.2% during a period of 626 ± 543 days, P = 0.467). The cumulative TLF-free ratio in the DCB group was not significantly different from that in the DES group (P = 0.475, log-rank test).

The present propensity score-matched comparison showed statistically equivalent midterm clinical outcomes after DCB use to those of DES placement for de novo lesions in patients with ACS treated by emergent procedures.

The coronavirus disease 2019 pandemic occurred in several countries, making the conventional medical system difficult to maintain. Recent recommendations aim to prevent nosocomial infections and infections among health care workers. Therefore, establishing a cardiovascular medical system under an emergency for patients with ST-segment elevation myocardial infarction (STEMI) is desired. This study aimed to determine the relationship between prognosis and door-to-balloon time (DBT) shortening based on the severity on arrival.

This retrospective, multi-center, observational study included 1,127 consecutive patients with STEMI. These patients were transported by emergency medical services and underwent primary percutaneous coronary intervention. Patients were stratified according to the Killip classification: Killip 1 (n = 738) and Killip ≥ 2 (n = 389) groups.

Patients in the Killip ≥ 2 group were older, with more females, and more severity on arrival than those in the Killip 1 group. The 30-day mortality rate in the Killip 1 and Killip ≥ 2 groups was 2.2% and 18.0%, respectively. The Killip ≥ 2 group had a significant difference in the 30-day mortality between patients with DBT ≤ 90 minutes and those with DBT > 90 minutes; however, this did not occur in the Killip 1 group. Furthermore, multivariate analysis revealed that DBT ≤ 90 minutes was not a significant predictive factor in the Killip 1 group; however, it was an independent predictive factor in the Killip ≥ 2 group.

DBT shortening affected the 30-day mortality in STEMI patients with Killip ≥ 2, although not those with Killip 1.

Sustained ventricular tachycardia (sVT), leading to sudden cardiac death, is one of the common manifestations in cardiac sarcoidosis (CS). Although late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) has been reported to be associated with sVT, the relationships of its localization to sVT have not been fully evaluated.

To evaluate the localization of LGE and its relationships to sVT in patients with CS, we reviewed medical record of consecutive 31 patients with CS who underwent CMR. The localization of LGE was divided into four categories: Left ventricular (LV) septum, LV free wall, right ventricular (RV) septum, and RV free wall. We investigated the association of sVT with localization of LGE and other parameters including serum biomarkers LV ejection fraction on echocardiography and Fluorine-18-fluorodeoxyglucose (FDG) accumulation on positron emission tomography (PET) -CT.

Of the studied population, 8 patients (25.8%) were known to present with sVT among 31 CS patients. LGE was observed in the RV free wall in 6 patients with sVT, whereas it was in 5 patients without sVT (75.0% versus 21.7%, P = 0.022). Univariate analysis showed that only LGE in the RV free wall was associated with sVT (odds ratio [OR]: 10.80; 95% confidence interval [CI]: 1.64-70.93, P = 0.013).

LGE in the RV free wall was associated with sVT in patients with CS.

There are no studies examining interventricular (VV) delay optimization by an electrical cardiometry method in relation to subsequent cardiac function in cardiac resynchronization therapy (CRT) -implanted patients. This study aimed to compare the VV delay in CRT-implanted patients by the dp/dt and electrical cardiometry and to examine the optimization of VV delay and improvement of cardiac function. We examined 19 consecutive CRT-implanted patients. The protocol included biventricular stimulation with either simultaneous or sequential pacing, and we evaluated systolic volume (SV) using an electrical cardiometry and the dp/dt of the left ventricle. The optimal VV delay was determined by the maximum SV using the electrical cardiometry. Two groups were defined, those whose increase in SV was at or above the median and those whose SV increase was below the median; changes in left ventricular ejection fraction (LVEF). The correlation between the VV delay optimized by the electrical cardiometry and dp/dt methods was high (R = 0.61, P = 0.006). Compared to the baseline SV (43.4 mL), the SV increased to 47.8 mL with simultaneous biventricular pacing (versus baseline P = 0.008) and further increased to 49.8 mL with optimized VV delay (versus simultaneous biventricular pacing P = 0.020). LVEF after 6 months significantly improved in the above-median SV increase group (37.6 versus 28.2%, P = 0.041), but not in the below-median SV increase group (26.5 versus 26.5%, P = 0.985). In conclusion, the optimal VV delay by electrical cardiometry method was almost concordant with that by the dp/dt method. Cardiac function significantly improved in the group with the above-median SV increase.

The recommended starting dose of Tolvaptan for heart failure (HF) is 7.5 mg/day in Japan; the recommended dose is 3.75 mg/day for older patients to avoid excessive diuresis and hypernatremia. However, low-dose Tolvaptan may delay the release of congestion in some patients. We aimed to develop a score to predict treatment responders to 3.75 mg tolvaptan.

We retrospectively analyzed 106 patients with HF who initially received 3.75 mg/day of Tolvaptan in the derivation cohort (April 2013-December 2017) and 63 patients receiving 3.75 mg/day of Tolvaptan in the validation cohort (January 2018-April 2021). Treatment responders to 3.75 mg tolvaptan did not require dose escalation of Tolvaptan for congestion relief. In multivariate analysis, blood urea nitrogen (BUN) < 39 mg/dL and hematocrit > 35% were selected as variables to predict treatment responders. These were assigned 1 point each, and patients were stratified into groups with 2 points (n = 32), 1 point (n = 39), and 0 points (n = 35). The frequency of treatment responders was 82.9% in the 2-point group, 61.5% in the 1-point group, and 34.4% in the 0-point group (P < 0.05). The predictive ability of the score was acceptable with an area under the receiving operator characteristic curve (AUC) 0.726 (P < 0.05); its performance was maintained in the validation cohort (AUC 0.733, P < 0.05).

A simple score using BUN and hematocrit could identify treatment responders to 3.75 mg tolvaptan, which may help determine the appropriate starting dose of Tolvaptan, balancing efficiency with safety for older patients with HF.

The role of the right to left ventricular (RV/LV) diameter ratio in predicating long-term outcomes in patients with pulmonary thromboembolisms (PTEs) treated with direct oral anticoagulants is unclear.

We investigated the association between the RV/LV diameter ratio and clinical outcomes in PTE patients under rivaroxaban from the data of a multicenter, prospective, observational study (J'xactly Study) in Japanese patients with acute venous thromboembolisms (VTEs) including deep vein thromboses, PTEs, or both. Of a total of 1,039 patients with an acute VTE (from December 2016 to April 2018), 429 were diagnosed with PTEs, however, the population in this study consists of 216 patients in whom the RV/LV diameter ratio measured on the axial CT or transthoracic echocardiogram was available.

The RV/LV diameter ratio increased significantly with the severity of the PTE classification (nonmassive 0.79 [0.67-0.93], submassive 1.10 [0.83-1.31], massive 1.13 [0.94-1.19], arrest or collapse 1.38 [0.66-2.38], P < 0.001). During a median follow-up of 624 (550-690) days, a sum of the composite adverse events including recurrent VTEs, acute coronary syndrome, ischemic strokes, death from any cause, or major bleeding events occurred in 26 patients (12.0%, 7.58 events per 100 patient-years). Multivariate analysis revealed that an RV/LV diameter ratio ≥ 1.0 had no association with the incidence of composite adverse events (HR 1.34, 95% confidence interval 0.59-2.91, P = 0.48).

In summary, in Japanese PTE patients under rivaroxaban, the RV/LV diameter ratio measured on the CT or transthoracic echocardiogram was associated with the PTE severity, but not with the clinical outcomes.

The cost and/or cost-effectiveness for inpatient management according to the gender of attending physicians remain to be elucidated.

Hospitalization costs were extracted from the Diagnosis Procedure Combination (DPC) -based payment system. Using a dataset of 7,457 hospitalized patients with cardiovascular diseases in our hospital from 2012 to 2018, we compared the actual cost of inpatient management by female cardiologists with that by male cardiologists. Next, we estimated the cost-effectiveness of inpatient management according to the gender of the attending cardiologist. The cost of initial hospitalization per patient was similar between the patients treated by a female or male middle-grade cardiologist ($17,527 ± 14,158, versus $17,358 ± 15,183, P = 0.69). As an analysis on cost-effectiveness, the incremental cost of hospitalization managed by male middle-grade cardiologists was $67 per patient as compared with female middle-grade cardiologists. Concordantly, evaluation of the incremental cost-effectiveness ratio per quality-adjusted life year gained showed that the inpatient management by female cardiologists was dominant over that by male cardiologists.

Inpatient management by female cardiologists was more cost-effective as compared with that by male cardiologists. Physician gender might have a considerable effect on medical economics.

Heart failure (HF) can cause liver congestion and stiffness. Elastography is used to noninvasively measure organ stiffness. Liver fibrosis (LF) is monitored by shear wave and strain elastography. However, shear wave velocity (Vs) on shear wave elastography varies under the influence of fibrosis and congestion, and the LF index by strain elastography reflects only LF progression. Little is known about the usefulness of these methods in HF patients. This prospective study evaluated combined shear wave and strain elastography (i.e., combinational elastography) for assessing liver congestion. A total of 51 patients with HF (33 outpatients and 18 inpatients) and 10 healthy participants were included. Further, the relationships between combinational elastography and clinical characteristics in 51 patients with HF and the effects of medical treatment on these relationships in 18 inpatients with HF were investigated. Vs was significantly higher in the HF group than in the control group (1.68 ± 0.47 versus 1.21 ± 0.16, P = 0.002). The LF index did not significantly differ (1.39 ± 0.40 versus 1.33 ± 0.15, P = 0.680). Vs decreased after treatment (from 2.01 ± 0.61 to 1.62 ± 0.49 m/seconds; P = 0.026), while the LF index did not change (from 1.21 ± 0.29 to 1.26 ± 0.27; P = 0.664). Brain natriuretic peptide level (r = 0.343; P = 0.003) and composite congestion scores (r = 0.455; P < 0.001) were correlated with Vs. Combinational elastography is useful for assessing liver congestion, differentiating between liver congestion and fibrosis, and assessing therapeutic effects in HF patients.

This study examined quality indicators (QIs) for heart failure (HF) in patients' referral documents (PRDs).

We conducted a nationwide questionnaire survey to identify information that general practitioners (GPs) would like hospital cardiologists (HCs) to include in PRDs and that HCs actually include in PRDs. The percentage of GPs that desired each item included in PRDs was converted into a deviation score, and items with a deviation score of ≥ 50 were defined as QIs. We rated the quality of PRDs provided by HCs based on QI assessment.

We received 281 responses from HCs and 145 responses from GPs. The following were identified as QIs: 1) HF cause; 2) B-type natriuretic peptide (BNP) or N-terminal pro-BNP concentration; 3) left ventricular ejection fraction or echocardiography; 4) body weight; 5) education of patients and their families on HF; 6) physical function, and 7) functions of daily living. Based on QI assessment, only 21.7% of HCs included all seven items in their PRDs. HCs specializing in HF and institutions with many full-time HCs were independently associated with including the seven items in PRDs.

The quality of PRDs for HF varies among physicians and hospitals, and standardization is needed based on QI assessment.

Data are scarce regarding retrograde type A dissection (RTAD) after thoracic endovascular aortic repair (TEVAR). This study aimed to investigate the clinical characteristics and surgical treatment outcomes of patients who developed RTAD after TEVAR.

From January 2015 to January 2020, 25 consecutive patients (aged 52 ± 11.69 years) of RTAD after TEVAR received open surgery. All patients received total arch replacement (TAR) with the frozen elephant trunk (FET). The proximal part of the TEVAR stent was removed using a wire scissor. The distal part of the TEVAR stent in the descending aorta was preserved. Data of 50 random patients of type A aortic dissection without prior TEVAR were collected during the same period. We compared the perioperative and midterm follow-up outcomes between patients with prior TEVAR and patients without prior TEVAR.

The mean cardiopulmonary bypass time, aortic cross-clamp time, and deep hypothermic circulatory arrest time were 173.7 ± 44.1, 109.5 ± 31.4, and 21.6 ± 6.8 minutes in the RTAD group, respectively. These times are similar to those of the no-RTAD group. The median interval between the initial TEVAR procedure and RTAD was 8.5 months (range, 0-72 months). New entry tears that were induced by the proximal end of the TEVAR stent were found in 23 (92%) patients of the RTAD group. There were no significant differences in major adverse events and overall survival between the two groups.

TAR with the FET technique was feasible for the treatment of RTAD after TEVAR, with acceptable early and midterm results.

Immune checkpoint inhibitors (ICIs) are widely used in various types of cancers and patients. Recently, it has been reported that ICIs aggravate atherosclerosis. This study aimed to identify characteristics that are related to the progression of atherosclerosis.

This study was conducted in a single medical center and included 32 patients who were grouped based on the presence of an immune-related adverse event (IRAE). There were 16 IRAE patients and 16 non-IRAE patients. Atherosclerosis was measured as the volume of calcified plaque at the aortic arch on a computed tomography (CT) scan. We measured the volume on CT at 3 time points as follows: before treatment, at ICI initiation, and after 180 days or more.

After the first ICI administration, the IRAE group showed significant exacerbation of atherosclerosis compared to the non-IRAE group (P = 0.002). A high volume of plaque was observed in IRAE patients after ICI treatment as compared to before ICI administration (P = 0.058).

ICIs tend to hasten atherosclerosis progression in IRAE patients, indicating that high-risk cardiovascular patients should be concerned about cardiovascular events. Moreover, this study suggests the possibility of predicting IRAEs based on the volume of calcified plaques.

P-wave terminal force in lead V1 (PTFV1) is a marker of increased left atrial (LA) overload. Whether PTFV1 is associated with left ventricular (LV) diastolic function remains undetermined. We tested the hypothesis that PTFV1 is associated with LV diastolic parameters derived from gated myocardial perfusion single-photon emission computed tomography (SPECT) in patients with no significant perfusion abnormalities.

The study population included 158 patients with preserved ejection fraction and no significant perfusion abnormalities. The amplitude and duration of the P-wave negative phase in lead V1 were measured using an electrocardiogram, and PTFV1 was calculated. The peak filling rate (PFR) and one-third mean filling rate (1/3 MFR) were obtained as LV diastolic parameters using gated SPECT.

PTFV1 showed a weak correlation with the LA volume index (r = 0.31; P < 0.001). Significant associations were observed between PTFV1 and PFR (r = −0.27; P < 0.001) and 1/3 MFR (r = −0.26; P = 0.001). A multivariate linear regression analysis showed that age (β = −0.26; P < 0.001), LV end-diastolic volume index (β = −0.27; P = 0.001), and PTFV1 (β = −0.15; P = 0.036) were significant factors associated with PFR. Moreover, male gender (β = −0.16; P = 0.041), LV mass index (β = −0.17; P = 0.046), and PTFV1 (β = −0.17; P = 0.022) were significant factors associated with the 1/3 MFR.

PTFV1 is associated with LV diastolic function, as derived from gated SPECT in patients with no significant perfusion abnormalities.

Since permanent inferior vena cava (IVC) filters increase deep vein thrombosis (DVT), filter retrieval should be performed as possible. Despite the guideline recommendation, IVC filters are not always retrieved in clinical practice. To date, many patients with not-retrieval IVC filters have been prescribed anticoagulant therapy, but the long-term prognosis, including venous thromboembolism (VTE) and bleeding events, remains unknown. In this study, 195 patients who underwent IVC filter implantation between 2006 and 2017 at 3 institutions in Niigata City have been investigated about their deaths, VTE recurrence, and bleeding events. After peaking 2009, the number of IVC filter implantation gradually decreased. During observational period, there were 158 patients with not-retrieval IVC filters (the overall retrieval rate of 19.0%). The not-retrieval group included significantly older and more patients with cancer compared to the retrieval group. Anticoagulation therapy was continued in 88% of the not-retrieval group. During a mean follow-up of 5.0 years, 6 symptomatic DVT events associated with inadequate control of anticoagulation and 13 bleeding events were observed. A total of 52 patients died and only the presence of cancer was prognostic risk factor. Although long-term anticoagulation therapy may be associated with bleeding events, there were few recurrent VTE under optimal anticoagulation. It is anticipated that even if the IVC filter cannot be retrieved, appropriate anticoagulation is useful for prevention of DVT recurrence despite the risk of bleeding.

This paper aims to observe the effect of recombinant human brain natriuretic peptide (rhBNP) on treatment of acute carbon monoxide poisoning (ACMP) complicated with heart failure with reduced ejection fraction (HFREF).

A total of 103 patients with ACMP complicated with HFREF admitted to our department from October 2016 to March 2020 were observed. Patients were divided into control group (50 cases) and experimental group (53 cases). The control group was given diuretic, vasodilator, and digitalis treatment, and the experimental group was supplemented with rhBNP treatment based on the control group. Patients' general information was collected. The levels of myocardial injury-associated indicators of patients were detected at and after admission.

No significant differences were observed in the general data of patients compared with control group. The acute physiology and chronic health enquiry II score of patients was positively correlated with left ventricular ejection fraction (LVEF). At admission, the levels of myocardial injury indicators, N-terminal B-type brain natriuretic peptide, and cardiac ultrasound indexes had no significant difference between the control group and experimental group. However, after admission, the LVEF and stroke output levels were elevated, while the other indicators were all decreased compared with the control group.

The rhBNP exerts a protective effect on ACMP-induced cardiomyocyte injury to improve cardiac function, shorten the length of hospital stay, and reduce the incidence and mortality of delayed encephalopathy after carbon monoxide poisoning.

Bicuspid aortic valve (BAV) patients with aortic stenosis (AS) are known to develop dilatation of the ascending aorta at a younger age, but the morphology of the aorta in these patients is yet to be investigated. Thus, in this study, we aim to evaluate the aortic morphology of BAV patients with severe AS using thin-slice electrocardiogram (ECG) -gated computed tomography (CT) and identify the possible contributing effect of age.

In this retrospective study, 122 BAV and 154 tricuspid aortic valve (TAV) patients who received aortic valve replacement for severe AS were assessed by thin-slice ECG-gated CT and three-dimensional reconstruction. The morphology of the ascending aorta was also evaluated among BAV patients aged < 70 (n = 72) and ≥ 70 (n = 50) years old. As per our findings, BAV patients with severe AS had significantly greater diameter (P < 0.01), elongation (P < 0.01), and tortuosity (P = 0.03) of the ascending aorta; minimum aortic arch angle (P < 0.01); and significantly lower calcified plaque (P < 0.01) compared with those of TAV patients even after adjusting for background. Multiple regression analysis showed that standardized partial regression coefficients (β) of dilatation (0.5) and elongation (0.35) were higher among other measurements of aortic morphology for BAV patients. BAV patients with severe AS aged ≥ 70 years had significantly greater diameter (42.0 [37.2-46.1] mm versus 40.4 [35.2-44.2] mm, P = 0.049) and elongation (133.8 [123.5-147.3] mm versus 127.0 [111.0-140.0] mm, P = 0.01) of the ascending aorta than those aged < 70 years.

BAV patients with severe AS were determined to have greater dilatation and elongation of the ascending aorta. Moreover, BAV patients older than 70 years had greater diameter and elongation of the ascending aorta.

Emerging literature suggests that pyroptosis plays a critical role in ischemia/hypoxia (I/R) -induced myocardial injury. Melatonin has been implicated in attenuating I/R-induced injury of cardiomyocytes. Nevertheless, whether melatonin inhibits I/R-induced pyroptosis of cardiomyocytes and the underlying molecular mechanisms remain unexploited.

H9c2 cardiomyocytes were cultured under oxygen-glucose deprivation/reperfusion (OGD/R) condition to establish a myocardial pyroptosis model in vitro. OGD/R-induced pyroptosis was evaluated by CCK-8 assay, IL-1β and IL-18 release, and western blotting. Luciferase reporter assay was utilized to validate the association between miR-155 and Forkhead box O3a (FOXO3a).

Melatonin could inhibit OGD/R-induced pyroptosis of H9c2 cells and upregulation of FOXO3a contributed to the antipyroptotic effect of melatonin. Melatonin reduced miR-155 expression, which led to FOXO3a upregulation and inhibition of pyroptosis in OGD/R-exposed H9c2 cells. miR-155 inhibitor enhanced the antipyroptotic effect of melatonin in OGD/R-exposed H9c2 cells. Melatonin-induced downregulation of miR-155 and upregulation of FOXO3a were reversed by melatonin receptor 2 (MT2) siRNA. Melatonin treatment also led to an increased level of apoptosis repressor with caspase recruitment domain (ARC), which was inhibited by FOXO3a siRNA. Moreover, silencing ARC by siRNA significantly blocked the antipyroptotic actions of melatonin, whereas ARC overexpression enhanced the antipyroptotic actions of melatonin in OGD/R-exposed H9c2 cells.

Our findings demonstrated that melatonin prevented OGD/R-induced pyroptosis via regulating the MT2/miR-155/FOXO3a/ARC axis in cardiomyocytes.

Dilated cardiomyopathy (DCM) is caused by various gene variants and characterized by systolic dysfunction. Lamin variants have been reported to have a poor prognosis. Medical and device therapies are not sufficient to improve the prognosis of DCM with the lamin variants. Recently, induced pluripotent stem (iPS) cells have been used for research on genetic disorders. However, few studies have evaluated the contractile function of cardiac tissue with lamin variants. The aim of this study was to elucidate the function of cardiac cell sheet tissue derived from patients with lamin variant DCM. iPS cells were generated from a patient with lamin A/C (LMNA) -mutant DCM (LMNA p.R225X mutation). After cardiac differentiation and purification, cardiac cell sheets that were fabricated through cultivation on a temperature-responsive culture dish were transferred to the surface of the fibrin gel, and the contractile force was measured. The contractile force and maximum contraction velocity, but not the maximum relaxation velocity, were significantly decreased in cardiac cell sheet tissue with the lamin variant. A qRT-PCR analysis revealed that mRNA expression of some contractile proteins, cardiac transcription factors, Ca²⁺-handling genes, and ion channels were downregulated in cardiac tissue with the lamin variant.

Human iPS-derived bioengineered cardiac tissue with the LMNA p.R225X mutation has the functional properties of systolic dysfunction and may be a promising tissue model for understanding the underlying mechanisms of DCM.

Atrial inflammation and fibrosis have long been considered culprits in the development of atrial fibrillation (AF). Prior clinical studies showed that corticosteroid therapy is beneficial in patients with AF. Here we sought to determine whether prednisone treatment prevents atrial tachypacing (ATP) induced atrial fibrosis.

Dogs were randomized into the sham, ATP, ATP + low-dose prednisone (ALP), and ATP + high-dose prednisone (AHP) groups. After 6 days of recovery from surgery, dogs were subjected to ATP at 400 beats per minute for 4 weeks while being treated with prednisone (15 or 40 mg/day) or a placebo. Pacemakers were not activated in the sham group.

Compared with the ATP group, the expression of collagen I, collagen III, α-smooth muscle actin, transforming growth factor-β1 and connective tissue growth factor were significantly reduced in the ALP and AHP groups. Fluorescence assays showed that reactive oxygen species formation in the right atrium was suppressed in the ALP and AHP groups compared with the ATP group. The protein level of NADPH oxidase 2 was reduced in the ALP and AHP groups' versus ATP group, while NOX4 and NOX5 were unchanged. ATP-induced downregulation of BH4 and eNOS uncoupling in the atria was partially restored in the prednisone-treated groups.

Our study demonstrated that atrial fibrosis induced by ATP were suppressed by prednisone. Low-dose prednisone was also effective in suppressing the development of atrial fibrosis.

Recent studies demonstrated that circular RNAs play important roles in exosome-mediated cardio-protective effects after acute myocardial infarction (AMI). A previous study reported that circ_0001747 level is down-regulated in mouse hypoxia/reoxygenation (H/R) injury model. However, its biological role and working mechanism in AMI remain largely unknown.

Exosomes were isolated from the culture supernatant of adipose-derived stem cells (ADSCs) using an ExoQuick precipitation kit. We treated mouse myocardial cells HL-1 with H/R to explore the role of exosomal circ_0001747 in AMI pathology. Cell viability, proliferation, apoptosis, and inflammation were analyzed by Cell Counting Kit-8 assay, 5-ethynyl-2'-deoxyuridine assay, flow cytometry, and enzyme-linked immunosorbent assay. Dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to confirm the interaction between microRNA-199b-3p (miR-199b-3p) and circ_0001747 or MCL1 apoptosis regulator, BCL2 family member (MCL1).

H/R-induced HL-1 dysfunction was attenuated by the incubation of exosomes derived from ADSCs, especially the exosomes with high amounts of circ_0001747. Circ_0001747 directly targeted miR-199b-3p in HL-1 cells. miR-199b-3p overexpression partly overturned exosomal circ_0001747-mediated protective effects in H/R-induced HL-1 cells. MCL1 was a direct target of miR-199b-3p in HL-1 cells. miR-199b-3p silencing alleviated H/R-induced damage in HL-1 cells partly by up-regulating MCL1. Circ_0001747 can elevate the messenger RNA and protein levels of MCL1 by sequestering miR-199b-3p.

Overall, these results indicated that ADSCs-derived exosomes with high amounts of circ_0001747 attenuated H/R-induced HL-1 dysfunction partly by targeting miR-199b-3p/MCL1 signaling.

Excessive mechanical stress causes fibrosis-related atrial arrhythmia. Herein, we tried to investigate the mechanism of atrial fibrogenesis in response to mechanical stress by ex vivo approach. We collected atrial tissues from mice and then cultured them as "explants" under atmospheric pressure (AP group) or 50 mmHg hydrostatic pressure loading (HP group) conditions. Pathway-specific PCR array analysis on the expression of fibrosis-related genes indicated that the loading of atrial tissues to 50 mmHg for 24 hours extensively upregulated a series of profibrotic genes. qRT-PCR data also showed that loading atrial tissues to 50 mmHg enhanced Rhoa, Rock2, and Thbs1 expression at different time points. Interestingly, the enhanced expression of Thbs1 at 1 hour declined at 6-24 hours and then increased again at 72 hours. In contrast, an enhanced expression of Tgfb1 was observed at 72 hours. In contrast, daily loading to 50 mmHg for 3 hours significantly accelerated the outgrowth of mesenchymal stem-like stromal cells from atrial tissues; however, we did not observe significant phenotypic changes in these outgrowing cells. Our ex vivo experimental data clearly show the induction of profibrotic transcription of atrial tissues by HP loading, which confirms the common pathological feature of atrial fibrosis following pressure overload.

Excess psychological stress is one of the precipitating factors for paroxysmal atrial fibrillation (AF), although the involved mechanisms are still uncertain. To test a hypothesis that one of the stress-induced hormones, glucocorticoid, is involved in the pathogenesis of stress-induced AF, we investigated whether the glucocorticoid could alter the temporal profile of cardiac ion channels gene expression, thereby leading to atrial arrhythmogenesis.

Dexamethasone (DEX, 1.0 mg/kg) was injected subcutaneously in Sprague-Dawley rats. At predetermined times after DEX injection (0, 1, 3, 6, 12, and 24 hours), the mRNA levels of cardiac ion channel genes (erg, KvLQT1, Kv4.3, Kv4.2, Kv2.1, Kv1.5, Kv1.4, Kv1.2, SUR2A, Kir6.2, Kir3.4, Kir3.1 Kir2.2, Kir2.1, SCN5A, and α1C) were determined using RNase protection assay. DEX induced immediate and transient increase in the mRNA level of Kv1.5 and Kir2.2 with peaks at 6 (5.0 fold) and 3 hours (3.3 fold) after DEX injection, respectively. Patch-clamp studies revealed a significantly increased current density of the corresponding current, I_Kur and I_K1 at 6 hours after DEX injection. Simultaneously, electrophysiological study in isolated perfused hearts showed significantly increased number of repetitive atrial responses induced by single atrial extrastimulus (3.2 ± 2.4 to 26.7 ± 16.4, P = 0.004) with shorting of the refractory period (36.4 ± 4.6 to 27.4 ± 5.5 ms, P = 0.049) after DEX injection.

Glucocorticoid immediately modified Kv1.5 and Kir2.2 gene expression at pretranslational levels, thus leading to effective refractory period shortening that could be arrhythmogenic. These results implied that transient glucocorticoid-induced biochemical modification of cardiac ion channels might be one of the mechanisms underlying the stress-induced paroxysmal AF.

Coronary ostial stenosis, treated by either percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), is a rare but potentially life-threatening complication following surgical aortic valve replacement. However, in cases of complete occlusion of the coronary ostium (COCO), CABG is the typical treatment because guiding catheter engagement is extremely challenging. Herein, we presented a case of a patient with COCO who underwent successful PCI through a retrograde approach, and this case first demonstrates the feasibility of PCI for the treatment of COCO, which could help avoid the high risk of redo surgery.

CoronaVac is an inactivated coronavirus disease (COVID-19) vaccine that was granted an emergency authorization by the World Health Organization in June 2021. We present the two cases of patients presenting with chest pain, abnormal electrocardiography, and elevated troponin consistent with non-ST-elevation myocardial infarction within 24 hours after receiving the CoronaVac COVID-19 vaccine.

Sleep apnea syndrome (SAS) is a condition in which apnea and hypoventilation at night cause hypoxemia and impaired wakefulness during the day, resulting in a general malaise and dozing. Sleep apnea has been implicated in the development of hypertension, ischemic heart disease, arrhythmia, heart failure, and cerebrovascular disease.¹⁾ Approximately 50% of patients with sleep-disordered breathing have an arrhythmia. In severe cases with an apnea-hypopnea index (AHI) of 30 or more, the frequency of arrhythmias during sleep is two to four times that of individuals without SAS. Bradyarrhythmias such as sinus bradycardia, sinus arrest, and atrioventricular block occurs at night in about 5%-10% of patients with sleep-disordered breathing.²⁾

During nocturnal sleep, vagal excitation causes excessive muscle relaxation of the upper airway, leading to periodic airway diameter reduction, which increases snoring and obstructive apnea. As a result, hypoxemia is likely, further increasing vagal tone and leading to bradycardia. An increase in ventilation rate and volume quickly compensates for the decrease in arterial partial pressure of oxygen during apnea, which leads to new bradycardia due to a decrease in the partial pressure of oxygen in arterial blood, which suppresses vagal tone and respiration.³⁾

We experienced a case of a 44-year-old patient with bradyarrhythmia that might be associated with SAS. After continuous positive airway pressure treatment, AHI decreased, and very long cardiac arrests resolved.

Mutant cardiac ryanodine receptor channels (RyR2) are "leaky," and spontaneous Ca²⁺ release through these channels causes delayed afterdepolarizations that can deteriorate into ventricular fibrillation. Some patients carrying RYR2 mutations in type 1 catecholaminergic polymorphic ventricular tachycardia exhibit QT prolongation and are initially diagnosed with long QT syndrome. However, none have been reported to cause drug-induced ventricular fibrillation in patients with RYR2 variants. We describe the first case of an elderly woman with drug-induced QT prolongation and ventricular fibrillation who carried a novel RYR2 variant but no other mutations related to long QT syndrome. Oral adrenergic agents might induce QT prolongation and subsequent ventricular fibrillation in patients carrying an RYR2 variant. Screening for RYR2 could be valuable in patients with suspected drug-induced long QT syndrome.

An aortic valve with a coronary cusp adherent to the aortic wall is a rare anomaly. Furthermore, an adherent coronary cusp with fenestration is even rarer. Here, we report a case of aortic valve regurgitation with an adherent and fenestrated left coronary cusp. A 45-year-old man with complaints of dyspnea on exertion was hospitalized. Clinical examination revealed severe aortic valve regurgitation associated with poor cardiac function. He had a history of cardiac murmur present since childhood; however, the details of his cardiac history are unknown. During surgery, a fenestrated left coronary cusp adherent to the aortic wall was observed. Following resection of all aortic cusps, we performed an aortic valve replacement with a mechanical valve. The postoperative recovery was uneventful. In this case, the left coronary artery was perfused by a small fenestration in the adherent coronary cusp. In such cases, the adherent coronary cusp should be released to alleviate the possibility of sudden death and ischemic myocarditis.

We sometimes encounter patients with systolic heart failure and cardiac amyloidosis. Neurohormonal blockers are guideline-directed medical therapy for those with systolic heart failure. However, its implication among the above cohort remains controversial. Of 3 patients with systolic heart failure and cardiac amyloidosis who we encountered, cardiac reverse remodeling was achieved in 2 patients who received neurohormonal blockers, whereas cardiac function remained unchanged in a patient not receiving neurohormonal blockers. Neurohormonal blockers might be keys to achieve cardiac reverse remodeling and favorable clinical outcomes even in patients with systolic heart failure and cardiac amyloidosis, although further larger-scale studies are required to validate our hypothesis.

Cardiac double-hit and triple-hit lymphomas (DHLs, THLs) are rare; in fact, studies examining both DHL and THL remain scarce. THL with cardiac involvement constitutes a rare disease with few cases reported so far. Thus, in this study, we report the case of a 67-year-old woman who presented with initial symptoms of pulmonary embolism. Upon further evaluation, a right atrial mass was detected incidentally, and this was surgically removed under the assumption of a cardiac myxoma. Later, immunohistochemistry analysis of the mass revealed a THL. Aggressive treatment with chemotherapy was necessary; however, the patient refused treatment and had a poor prognosis.

We report a child with an unusual coronary bridge crossing over the left anterior descending (LAD), circumflex (CX), and right coronary artery (RCA). The bridges range from 0.8-1.2 mm depth. The patient presented with exercise-induced syncope and myocardial infarction (MI). She exhibited no syncope after medicine and exercise control.