Platelets play an important role in the pathophysiology of coronary artery disease. However, the clinical value of platelet indices in premature coronary heart disease remains largely unknown.

Consecutive patients referred for coronary angiography were evaluated (n = 1675). Patients were stratified into premature coronary heart disease (n = 679, age < 55 for male and age < 65 for female), late-onset coronary heart disease (n = 772, age ≥ 55 for male and age ≥ 65 for female), and control (n = 224, age < 55 for male and age < 65 for female). Their clinical and laboratory parameters were collected. The relationship between platelet indices and premature coronary artery disease was analyzed.

In univariate analysis, platelet indices showed no significant association with the presence of premature coronary heart disease (P > 0.05). After adjustment for traditional risk factors, mean platelet volume (0.823 [0.683-0.993], P = 0.042) and platelet-large cell ratio (0.976 [0.954-0.999], P = 0.040) were negatively correlated with the presence of premature coronary heart disease. The platelet-to-lymphocyte ratio was statistically significant among different numbers of coronary lesions (P = 0.035). In subgroup analysis, platelet-large cell ratio (1.190 [1.010-1.403], P = 0.038) was an independent risk factor of coronary restenosis after percutaneous coronary intervention.

Platelet indices were associated with the prevalence, severity, and coronary restenosis after percutaneous coronary intervention suggesting their possible clinical application in premature coronary heart disease.

Although there is no sign of reinfection, individuals who have a history of coronavirus disease 2019 (COVID-19) may experience prolonged chest discomfort and shortness of breath on exertion. This study aimed to examine the relationship between atherosclerotic coronary plaque structure and COVID-19. This retrospective cohort comprised 1269 consecutive patients who had coronary computed tomographic angiography (CCTA) for suspected coronary artery disease (CAD) between July 2020 and April 2021. The type of atherosclerotic plaque was the primary outcome. Secondary outcomes included the severity of coronary stenosis as determined via the Coronary Artery Disease-Reporting and Data System (CAD-RADS) classification and the coronary artery calcium (CAC) score. To reveal the relationship between the history of COVID-19 and the extent and severity of CAD, propensity score analysis and further multivariate logistic regression analysis were performed. The median age of the study population was 52 years, with 53.5% being male. COVID-19 was present in 337 individuals. The median duration from COVID-19 diagnosis to CCTA extraction was 245 days. The presence of atherosclerotic soft plaque (OR: 2.05, 95% confidence interval [CI]: 1.32-3.11, P = 0.001), mixed plaque (OR: 2.48, 95% CI: 1.39-4.43, P = 0.001), and high-risk plaque (OR: 2.75, 95% CI: 1.98-3.84, P < 0.001) was shown to be linked with the history of COVID-19 on the conditional multivariate regression analysis of the propensity-matched population. However, no statistically significant association was found between the history of COVID-19 and the severity of coronary stenosis based on CAD-RADS and CAC score. We found that the history of COVID-19 might be associated with coronary atherosclerosis assessed via CCTA.

Although the primary percutaneous coronary intervention (PCI) is an established treatment for acute ST-elevation myocardial infarction (STEMI), relevant guidelines do not recommend it for recent-STEMI cases with a totally occluded infarcted related artery (IRA). However, PCI is allowed in Japan for recent-STEMI cases, but little is known regarding its outcomes. We aimed to examine the details and outcomes of PCI procedures in recent-STEMI cases with a totally occluded IRA and compared the findings with those in acute-STEMI cases.

Among the 903 consecutive patients admitted with acute coronary syndrome, 250 were treated with PCI for type I STEMI with a totally occluded IRA. According to the time between symptom onset and diagnosis, patients were divided into the recent-STEMI (n = 32) and acute-STEMI (n = 218) groups. The background, procedure details, and short-term outcomes were analyzed. No significant differences between the groups were noted regarding patient demographics, acute myocardial infarction severity, or IRA distribution. Although the stent number and type were similar, significant differences were observed among PCI procedures, including the number of guidewires used, rate of microcatheter or double-lumen catheter use, and application rate of thrombus aspiration. The thrombolysis rate in the myocardial infarction flow 3-grade post-PCI did not differ significantly between the groups. Both groups had a low frequency of procedure-related complications. The in-hospital mortality rates were 0% and 4.6% in the recent-STEMI and acute-STEMI groups, respectively (P > 0.05).

Although recent-STEMI cases required complicated PCI techniques, their safety, success rate, and in-hospital mortality were comparable to those of acute-STEMI cases.

One benefit of an implantable cardioverter-defibrillator is the prevention of sudden cardiac death (SCD). It is recommended for patients with a low left ventricular ejection fraction (LVEF). However, the choice of cardiac resynchronization therapy (CRT) with or without a defibrillator (CRT-D and CRT-P) in elderly patients is controversial. To understand the current situation for proper device selection, we investigated the impact of defibrillators on mortality in elderly patients with heart failure.

Consecutive patients who underwent CRT implantation were retrospectively recruited. Baseline characteristics, all-cause mortality, cardiac death, and defibrillator implantation rates were investigated in patients aged > 75 or ≤ 75 years.

A total of 285 patients (79 patients aged > 75 years) were analyzed. Elderly patients had more comorbidities, but a lower proportion had ventricular arrhythmia. During the mean follow-up of 47 months, 109 patients died (67 due to cardiac death). Kaplan-Meier analysis showed higher mortality in elderly patients (P = 0.0428) but no significant difference in cardiac death by age group (P = 0.7472). There were no significant differences in mortality between patients with CRT-D versus CRT-P (P = 0.3386).

SCD was rare. A defibrillator had no significant impact on mortality. In elderly patients, comorbidities are common and related to mortality. The selection of CRT-D versus CRT-P should take those factors into account.

Gefitinib (GEF) may increase the risk of corrected QT prolongation (QTc). We aimed to evaluate whether gefitinib increases the risk of corrected QT interval (QTc) prolongation and analyze the associated risk factors.

A total of 122 cases of advanced EGFR-mutated non-small cell lung cancer (NSCLC) who received gefitinib therapy from January 2015 to December 2020 were evaluated. The results of at least two resting 12-lead electrocardiogram before and after gefitinib treatment were obtained. The Bazett and Fridericia formulas were used to calculate the QTc interval, and the changes of QTc interval values before and after treatment were evaluated. The correlation between gefitinib and QTc interval prolongation and related risk factors were analyzed.

After gefitinib-targeted therapy, 23 patients (18.9%) had a prolonged QTc interval, which increased from a mean of 446 ± 25 ms at baseline to 478 ± 18 ms (P < 0.001). Three of the patients met criteria for Grade 3 QTc prolongation in the common term V5.0 for clinical adverse events. Univariate analysis showed that age (ORR, 1.054; 95% confidence interval [CI], 1.003-1.107; P = 0.038), history of hypertension (ORR, 3.409; 95% CI, 1.334-8.713; P = 0.01), CCB medication history (ORR, 0.259; 95% CI, 0.094-0.712; P = 0.009), history of lung cancer surgery (ORR, 0.231; 95% CI, 0.064-0.829; P = 0.025), and baseline QT interval (ORR, 0.978; 95% CI, 0.964-0.993; P = 0.004) were important predictors of QTc interval prolongation in patients treated with gefitinib. The results of multivariate analysis showed that the history of lung cancer surgery and the baseline QT interval were important factors affecting QTc interval prolongation in patients treated with gefitinib.

Gefitinib increases the risk of QTc prolongation in NSCLC patients, which may be more pronounced in patients with advanced age, hypertension, CCB therapy, lung cancer surgery, and a long QT interval at baseline.

Acute viral myocarditis is a serious complication of viral infectious diseases, including coronavirus disease 2019 (COVID-19). To better understand the pathogenesis of acute viral myocarditis, we retrospectively analyzed the incidence and prognostic significance of hypocalcemia among patients with acute myocarditis, most of whom were considered to have acute viral myocarditis. We retrospectively reviewed the demographic and clinical data of patients with clinically confirmed acute myocarditis treated in our hospital over a 13-year period from 2006 to 2019, including laboratory results, cardiac imaging findings, and clinical outcomes. These data were compared between lower, middle, and higher calcium groups depending on the minimum calcium level measured during hospitalization. Among the 288 patients with acute myocarditis included, the hypocalcemia group (lower calcium group) had poorer clinical and laboratory results, received more medications and device support, and experienced poorer outcomes, including heart failure, arrhythmias, and death. Specifically, the left ventricular ejection fraction was significantly lower, and the length of hospital stay was significantly longer in the hypocalcemia group than in the other two groups. Furthermore, the incidence rates of atrioventricular block, ventricular tachycardia/ventricular fibrillation, cardiogenic shock, and mortality were significantly higher in the hypocalcemia group. Multivariate Cox regression analysis identified hypocalcemia as an independent risk factor for 30-day mortality in patients with acute myocarditis. In conclusion, the clinical evidence provided by the present study indicates that hypocalcemia is a risk factor for poorer outcomes in patients with acute myocarditis that should be considered carefully in the diagnosis and treatment of these patients.

Arrhythmia-induced cardiomyopathy (AIC) occurring in patients with atrial fibrillation (AF) is a reversible form of cardiomyopathy characterized by LV systolic dysfunction. However, it is difficult to predict the reversibility before rhythm control therapy. We performed this study to develop a parameter for the identification of AIC in routine transthoracic echocardiography (TTE) in patients with presumptive AIC due to AF.

We retrospectively studied 72 patients treated with catheter ablation therapy for persistent AF, and LV ejection fraction (LVEF) ≤ 45%. The patients were divided into 2 groups by follow-up TTE performed within 12 ± 6 months postoperatively. Patients with ≥ 15% improvement in LVEF or ≥ 10% improvement and ≥ 50% in LVEF were classified as the AIC group, and the others were classified as the non-AIC group.

A total of 57 (79%) patients were classified as the AIC group. In the stepwise multivariate logistic regression model, LV end-diastolic dimension (LVDd) and e' (septal) were independent predictors of AIC. The sensitivities of LVDd ≤ 53 mm and e' (septal) ≥ 6.3 cm/second were 60% and 75%, respectively. Their specificities were 80% and 67%, respectively. The presence of either LVDd ≤ 53 mm or e' (septal) ≥ 6.3 cm/second had a higher sensitivity (90%); their co-occurrence had a higher specificity (93%) in predicting AIC.

The functional recovery in patients with AIC can occur in LV systolic dysfunction without remodeling and impairment of relaxation. The combination of LVDd and e' (septal) is useful in predicting AIC due to AF with routine TTE.

The association between polypharmacy/multiple drug use (MDU) and prognosis in patients hospitalized with heart failure (HF) is unclear. It is also unknown whether the prognostic values of MDU vary depending on the presence/absence of a previous history of HF and preserved/reduced left ventricular ejection fraction (LVEF). We analyzed consecutive 1,034 patients hospitalized with HF (age, 74.9 ± 11.5 years; 58.7% male). MDU was defined as ≥5 drugs at discharge. The primary endpoint was a composite of all-cause death and HF readmission. MDU was observed in 695 patients (67.2%). Patients with MDU use had higher prevalences of a previous history of HF, reduced LVEF, and comorbidities than those without MDU. Cox proportional hazard analysis showed that MDU was significantly associated with the primary endpoint after adjustment for possible confounders (hazard ratio [HR], 1.36; 95% confidence interval [CI], 1.03-1.79; P = 0.030). There was significant interaction between the presence/absence of a history of HF and the prognostic impact of MDU (HF history [-]: HR, 0.86; 95% CI, 0.54-1.40; P = 0.553; HF history [+]: HR, 1.72; 95% CI, 1.16-2.55; P = 0.007; P for interaction = 0.005). However, there was no significant interaction between preserved/reduced LVEF and the prognostic impact of MDU (P for interaction = 0.274). In conclusion, MDU at discharge is an independent risk factor for the composite of death or HF readmission in patients hospitalized with HF. We observed a significant interaction between the presence of de novo versus recurrent HF and the prognostic value of MDU.

Outcome-based evidence shows that women have a higher risk of heart failure than men at a similar level of blood pressure. Left ventricular wall stress (Ó) or afterload is an important determinant of myocardial performance. Thus, it might play a key role in determining the sex differences in heart failure.

The Ó at the beginning of aortic valve opening (Ó-AVO), the systolic peak value of the Ó (Ó-peak), and the Ó at the end systole (Ó-ES) were determined using transthoracic echocardiography combined with cuff-measured brachial blood pressure in 990 age- and heart rate- and cuff-measured blood pressure-matched apparently healthy adults (495 men). The sex differences in the aortic pressure, the ratio of left ventricular wall volume to cavity volume (V_W/V_C), and Ó were analyzed.

Compared with men, women demonstrated higher aortic systolic blood pressure (106.7 versus 101.7 mmHg), smaller V_W/V_C (1.12 versus 1.25 for the end-diastole V_W/V_C, 3.49 versus 3.82 for the end-systole V_W/V_C), and greater Ó (340.0 versus 315.6 for Ó-AVO, 471.9 versus 412.5 for Ó-peak, and 256.2 versus 230.3 kdynes/cm² for Ó-ES) (all P < 0.001).

At the same level of cuff-measured blood pressure, women have a greater Ó or afterload than men in consequence of the sex differences in left ventricular geometry and pulse pressure amplification. The evidence indicates that non-sex-specific categories of blood pressure factitiously impose a relatively higher afterload on the left ventricle in women and may therefore increase potential risk of heart failure in women.

Chronic heart failure (CHF) is a complicated syndrome caused by structural and functional abnormalities. Long noncoding RNA (LncRNA) lung cancer-associated transcript 1 (LUCAT1) downregulation inhibits cardiomyocyte apoptosis. This study aimed to measure LUCAT1 expression in patients with CHF and to explore its clinical value on CHF diagnosis and prognosis. A total of 94 patients with CHF and 90 participants without CHF were registered, followed by recording of their clinical characteristics and grading of their cardiac function. LUCAT1 expression in sera of patients with CHF and participants without CHF was detected. The correlation of LUCAT1 with brain natriuretic peptide (BNP) and left ventricular ejection fraction (LVEF) in patients with CHF and the diagnostic efficiency of LUCAT1, BNP, and LUCAT1 combined with BNP on patients with CHF were analyzed. Patients with CHF were treated with conventional drugs and followed up. The LUCAT1 expression in patients with CHF was lower than that in participants without CHF and was downregulated with the increase of New York Heart Association stage. LUCAT1 expression was negatively associated with BNP but positively associated with LVEF in the sera of patients with CHF. The receiver operating characteristic curve of LUCAT1 combined with BNP had better result than that of LUCAT1 and BNP alone. Low LUCAT1 expression indicated poor prognosis of patients with CHF and was an independent prognostic factor for the survival of patients with CHF. To summarize, low lncRNA LUCAT1 expression might help diagnose and predict the poor prognosis of CHF.

Nutritional risk is closely related to the poor prognosis of hospitalized patients. However, the association of pre-procedural nutritional risk with periprocedural myocardial infarction (PMI) after percutaneous coronary intervention (PCI) remains unclear.

A total of 22,267 patients who underwent elective PCI were enrolled in this retrospective cross-sectional study. Nutritional risk was evaluated by three nutritional risk assessment tools, namely, controlling nutritional status (CONUT), prognostic nutritional index (PNI), and geriatric nutritional risk index (GNRI). PMI after PCI was defined as elevation of cardiac troponin I (cTnI) values > 5 × 99th percentile upper reference limit. Linear regression analysis was performed to explore the association of nutritional risk assessment tools with cTnI fold elevation. Log-binomial regression analysis was conducted to determine the association of nutritional risk assessment tools with PMI.

The average age of the enrolled patients was 66.4 years old, and 2,647 of them (11.9%) suffered PMI after PCI. Multivariable linear regression analysis determined a linear association between nutritional risk assessment tools and cTnI fold elevation (CONUT: β = 0.220, 95% CI [0.088-0.352], P = 0.001; PNI: β = −0.105, 95% CI [−0.146 to −0.065], P < 0.001; GNRI: β = −0.090, 95% CI [−0.122 to −0.057], P < 0.001). Log-binomial regression analysis showed that nutritional risk assessment tools were strongly associated with PMI after PCI (CONUT [4-12 versus 0-1]: RR = 1.168, 95% CI [1.054-1.295], P = 0.003; PNI [< 44 versus ≥ 52]: RR = 1.168, 95% CI [1.038-1.315], P = 0.010; GNRI [< 98 versus ≥ 108]: RR = 1.128, 95% CI [1.006-1.264], P = 0.039).

Pre-procedural nutritional status, assessed by CONUT, PNI, and GNRI, was significantly and strongly associated with PMI in patients undergoing elective PCI.

Surgical treatment is the most effective method to improve the prognosis of type A acute aortic dissection (TAAAD) patients. Thus, this investigation aimed to evaluate the value of postoperative platelet to mean platelet volume ratio (PMR) in predicting in-hospital mortality in postoperative TAAAD patients and to compare it with preoperative PMR.

A retrospective study (171 postoperative patients) was conducted in the hospital from January 2017 to December 2019. Clinical (age, gender, and outcome of the patients' in-hospital mortality), preoperative PMR, and postoperative laboratory results were gathered. The area under the receiver operating characteristic curve (AUC) and logistic regression were employed.

Preoperative and postoperative PMR levels were higher in the survivors than in the nonsurvivors (13.44 ± 7.15 versus 9.15 ± 4.05, P = 0.002; 12.02 ± 6.79 versus 6.85 ± 2.42, P < 0.001; respectively). Multivariate logistic regression indicated that postoperative PMR was an independent factor even adjusted with different variables. Moreover, postoperative PMR had the highest area under the receiver operating characteristic curve (AUC) (AUC: 0.778, 95% CI: 0.708-0.838, P < 0.001), with the best prognostic accuracy, followed by preoperative PMR (AUC: 0.721, 95% CI: 0.648-0.787, P < 0.001). The best cutoff value for postoperative PMR was 9.9206, with a high sensitivity (90.3%) and specificity (55.7%).

Postoperative PMR should serve as an independent index to predict in-hospital mortality in TAAAD patients. In addition, postoperative PMR are superior to preoperative PMR to recognize high-risk patients.

This study aimed to compare the clinical burden and healthcare utilization outcomes of hematologic versus solid malignancies in patients hospitalized with acute pulmonary embolism (PE). This population-based, retrospective study extracted and analyzed the discharge data from the 2016-2018 US National Inpatient Sample (NIS) of hospitalized patients with a primary diagnosis of acute PE and a subsequent diagnosis of hematologic malignancies or solid tumors. Prolonged length-of-stay (LOS) was defined as ≥75th percentile LOS of the study cohort. Unfavorable discharge was defined as discharged to nursing home or long-term facility. Univariate and multivariate regression analyses were conducted to determine associations between cancer type, presence of unstable PE, and in-hospital outcomes in acute PE patients. Patients with acute PE with solid tumors had higher rates of in-hospital deaths and unfavorable discharge than those with hematologic malignancies (6.4% versus 3.2%, P < 0.001; 14.0% versus 11.2%, P = 0.01, respectively). Acute PE patients with hematologic malignancies had a lower risk of in-hospital death (aOR: 0.43, 95% CI: 0.31-0.60), unfavorable discharge (aOR: 0.76, 95% CI: 0.63-0.92), and prolonged LOS (aOR: 0.83, 95% CI: 0.71-0.98) than those with solid tumors. Stratified analysis showed that male patients aged <60 years with hematologic malignancies had a lower risk of prolonged LOS (aOR: 0.70, 95% CI: 0.52-0.94; aOR: 0.85, 95% CI: 0.68-1.05) and unfavorable discharge (aOR: 0.40, 95% CI: 0.22-0.71; aOR: 0.65, 95% CI: 0.50-0.85) than those with solid tumors. In the comparison of the outcomes of acute PE with hematologic malignancies and solid tumors, patients with hematologic malignancy had a lower risk of in-hospital deaths, prolonged LOS, and unfavorable discharge than those with solid tumors.

Emerging evidence uncovers the important involvement of circular RNAs (circRNAs) in the dysfunction of cardiomyocytes under hypoxia conditions. However, no studies proved whether circTRRAP (hsa_circ_0081241) can participate in cardiomyocyte injury evoked by hypoxia.

A qRT-PCR or immunoblotting method was used to evaluate the expression of circTRRAP, miR-761, and mitogen-activated protein kinase kinase kinase 2 (MAP3K2). The direct relationships of circTRRAP/miR-761 and miR-761/MAP3K2 were confirmed by RNA immunoprecipitation (RIP) assay, dual-luciferase reporter assay, and RNA pull-down assay. The effects of the circTRRAP/miR-761/MAP3K2 axis on cell functional behaviors were examined by 5-ethynyl-2'-deoxyuridine (EdU) assay, CCK-8 assay, and flow cytometry. The production levels of proinflammatory cytokines (IL-1β, TNF-α, and IL-6) were evaluated by enzyme-linked immunosorbent assay.

CircTRRAP and MAP3K2 were overexpressed but miR-761 was downregulated in AC16 cardiomyocytes under hypoxia and in the serum of patients with acute myocardial infarction. Silencing circTRRAP attenuated hypoxia-evoked inflammation, apoptosis, and oxidative stress in human AC16 cardiomyocytes. CircTRRAP targeted miR-761, and miR-761 directly targeted and suppressed MAP3K2. CircTRRAP involved the post-transcriptional regulation of MAP3K2 through miR-761, indicating its competing endogenous RNA (ceRNA) activity. Moreover, miR-761 inhibition abolished the effects of circTRRAP depletion in hypoxia-induced cell injury. MAP3K2 silencing phenocopied miR-761 increase in attenuating hypoxia-evoked cardiomyocyte inflammation, apoptosis, and oxidative stress.

Our study demonstrates that circTRRAP can protect AC16 cardiomyocytes from hypoxia-evoked injury through the miR-761/MAP3K2 axis.

The effects of recombinant semaphorin 3A (Sema3A) on myocardial contractility and electrical remodeling in mice with isoproterenol (ISP) -induced heart failure were investigated.

C57BL/6J mice intraperitoneally received ISP (480 mg/kg/day, ISP group; n = 24) or saline (control group; n = 31) for 14 days. Twenty-one ISP-treated mice received 0.5 mg/kg Sema3A intravenously on days 7 and 11 (ISP+Sema3A group). The sympathetic nervous system was activated upon ISP treatment, but was reduced upon Sema3A administration. Greater myocardial tissue fibrosis was observed in the ISP group than in the control group. However, fibrosis was not significantly different between the ISP+Sema3A and control groups. Fractional shortening of the left ventricle was lower in the ISP group than in the control group and was restored in the ISP+Sema3A group (control, 53 ± 8%; ISP, 37 ± 7%; ISP+Sema3A, 48 ± 3%; P < 0.05). Monophasic action potential duration at 20% repolarization (MAPD₂₀) was prolonged in the ISP group (compared to control group), but this was reversed upon Sema3A administration (control, 29 ± 3 ms; ISP, 35 ± 6 ms; ISP+Sema3A, 29 ± 3 ms; P < 0.05). qPCR revealed Kv4.3, KChIP2, and SERCA2 downregulation in the ISP group and upregulation in the ISP+Sema3A group; however, Western blotting revealed similar changes only for Kv4.3 (P < 0.05).

Intravenous Sema3A may maintain myocardial contractility by suppressing the sympathetic innervation of the myocardium and reducing myocardial tissue damage, in addition to restoring MAPD via Kv4.3 upregulation.

The research aimed to study the mechanism of how trimethylamine N-oxide (TMAO) regulates autophagy to promote atherosclerosis (AS). The AS in vitro model was constructed with vascular smooth muscle cells (VSMCs) treated with ox-LDL. The Cell Counting Kit-8 (CCK-8) trial was chosen to examine VSMCs' absorbance (OD) value. A transmission electron microscope (TEM) was selected for monitoring autophagosomes. Western blotting (WB) was adopted for examining the expression of Beclin-1, p62, LC3, α-SMA, SM22-α, OPN, PI3K, AKT, mTOR, p-PI3K, p-AKT, and p-mTOR proteins. Real-time fluorescent quantitative PCR (RT-qPCR) was accepted for testing the expression of α-SMA, SM22-α, OPN, PI3K, AKT, mTOR, Beclin-1, p62, and LC3 genes. The transwell assay was employed to examine the ability of migration in VSMCs. Oil red O staining assay was accepted to stain lipid droplets in VSMCs. TMAO noticeably promoted autophagy inhibition and the phenotypic transformation of AS. Protein expressions of p-PI3K/PI3K, p-AKT/AKT, p-mTOR/mTOR, and p62 of the TMAO+ox-LDL group were higher than the ox-LDL group, while Beclin-1 and LC3 were lower than the ox-LDL group. Gene expressions of PI3K, AKT, mTOR, and p62 of the TMAO+ox-LDL group were higher than the ox-LDL group, while Beclin-1 and LC3 were lower than the ox-LDL group. The intervention of LY294002 reversed the regulation of the corresponding proteins and genes. The study proved that TMAO could promote autophagy inhibition of AS via activating the PI3K/AKT/mTOR pathway. It supplied a reliable basis for improving clinical diagnostic methods and developing targeted AS drugs.

Long noncoding RNAs (lncRNAs) can serve as treatment targets for abdominal aortic aneurysms (AAAs). Nonetheless, the exact role of FGD5 antisense RNA 1 (FGD5-AS1) in AAAs is unclear. Therefore, this study investigated the contribution of FGD5-AS1 to AAA growth regulated by vascular smooth muscle cells (VSMCs) and its potential mechanisms. ApoE^-/- mice were used to establish the angiotensin II (Ang II)-elicited AAA model. RNA pull-down assay and dual luciferase reporter assay (DLRA) in human VSMCs were used in examining the interactions between FGD5-AS1 and its downstream proteins or miRNA targets. FGD5-AS1 expression in the mouse Ang II perfusion group was dramatically increased relative to the PBS-infused group. In the mouse AAA model, FGD5-AS1 overexpression induced SMC apoptosis, thereby promoting AAA growth. miR-195-5p acts as a potential FGD5-AS1 downstream target, whereas FGD5-AS1 promotes MMP3 expression by inhibiting miR-195-5p expression, thereby inhibiting proliferation and promoting apoptosis of smooth muscle cells. LncRNA FGD5-AS1 is detrimental to the proliferation and survival of SMCs during AAA growth. Therefore, FGD5-AS1 could be a novel treatment target for AAA.

Primary cardiac sarcomas are rare diseases with very poor prognoses. In this report, we present a case of coronary artery intimal sarcoma in a patient who survived for a long time after diagnosis. A 57-year-old female underwent percutaneous coronary intervention of the right coronary artery due to acute myocardial infarction caused by thrombotic occlusion and was diagnosed as having coronary artery intimal sarcoma. She underwent surgical resection and coronary artery bypass surgery of the artery, cryothermy coagulation, and postoperative adjuvant chemotherapy for 1 year. After 3 years, focal recurrence was detected in the caudal region of the left ventricular inferior wall. Radiotherapy was performed. The tumor shrank significantly after radiotherapy. Four years later, there was no significant abnormal uptake on positron-emission tomography/computed tomography. At 7 years after diagnosis, when this case report was submitted, the patient was alive and her performance had maintained a good status. Intimal sarcoma occurring in a coronary artery is extremely rare. The efficacy of treatments for cardiac intimal sarcoma, which include surgical resection, chemotherapy and radiotherapy, has been reported to be limited. To the best of our knowledge, this is the first report of a case of coronary artery intimal sarcoma with long-term survival after comprehensive therapies including surgical resection and radiotherapy.

For complex aortic root lesions, the flanged Bentall procedure has more advantages than the traditional one. Here, we report two patients with complex root lesions treated with the flanged Bentall and Cabrol procedure: one was a 25-year-old male with interventricular septal dissection with Behçet's disease, and the other was a 4-year-old female with a very large ascending aortic aneurysm with a small annulus and Loeys-Dietz syndrome. Both patients recovered uneventfully and obtained good short-term results.

Intracardiac thrombosis formation in patients in sinus rhythm is a rare phenomenon. An 84-year-old woman was admitted because of worsening dyspnea on exertion. An electrocardiogram showed sinus rhythm, left atrial overload, marked left axis deviation, low voltage, and poor r-wave progression in leads V1-4. An echocardiogram showed relatively preserved left ventricular ejection fraction with minimal wall thickening. Her serum level of B-type natriuretic peptide (931 pg/mL) was markedly elevated and a diagnosis of worsening heart failure was made. During the course of treatment for heart failure, she was complicated by acute abdominal aortic thromboembolism together with left atrial thrombus. An emergency abdominal aortic thrombectomy was followed by the removal of a left atrial thrombus 2 days later. Left ventricular biopsy performed during the surgery revealed amyloid deposits in the myocardial interstitium. Immunohistochemical study confirmed the diagnosis of transthyretin cardiac amyloidosis. It is postulated that the risk of intracardiac thrombosis and systemic embolism is increased even in sinus rhythm in patients with cardiac amyloidosis.

Tako-tsubo syndrome (TTS) can be triggered by emotional or physical stress and is characterized by transient left ventricular dysfunction with apical ballooning. Some neurologic disorders and pheochromocytoma serve as triggers for TTS, however, its association with primary aldosteronism (PA) is not well known. Pulmonary vein isolation (PVI) with catheter ablation for atrial fibrillation (AF) has been performed worldwide, and TTS following PVI has been reported as a rare complication. Sympathetic stimulation can play an important role in TTS development, however, its mechanism and risk factors are not yet understood.

We describe a 72-year-old woman with PA who developed TTS after PVI with radiofrequency catheter ablation (RFCA) for symptomatic paroxysmal AF. Complete isolation of the pulmonary vein was carried out without any complications, however, she complained of epigastric discomfort 7 hours after the procedure. An electrocardiogram showed recurrent AF with a new negative-T wave and prolonged QT interval. Transthoracic echocardiography revealed apical ballooning and basal hypercontraction, characteristic of TTS, and coronary angiography showed no significant stenosis. She was diagnosed with TTS following RFCA for AF and managed well with conservative therapy.

The present case suggests that TTS should be recognized as a complication associated with AF ablation. Moreover, PA may be involved in TTS development by increasing sympathetic activity. Further studies on the mechanism and characteristics of TTS are required.

Fabry disease is an X-linked lysosomal storage disorder caused by defective enzyme activity of α-galactosidase A and treated with enzyme replacement therapy (ERT) with recombinant α-galactosidase. ERT reduces left ventricular mass assessed by echocardiography or magnetic resonance imaging. However, electrocardiogram changes during ERT have not been fully elucidated. In the present case, ERT with agalsidase alfa for 4 years decreased QRS voltage and negative T depth along with a reduction of left ventricular mass and wall thickness and improvement of symptoms in a female patient with Fabry disease. Long-term observation of electrocardiogram changes might be useful for determining the efficacy of ERT in this case.

Tetralogy of Fallot (ToF) is the most common cyanotic congenital heart disease. Cyanotic spells occur more frequently after infancy in unrepaired cases. Acute esophageal necrosis (AEN) is a rare disease that causes circumferential mucosal necrosis in the distal esophagus. We report the case of a 26-year-old man who was admitted due to coffee-ground emesis, black stools, and decreased oxygen saturations. The patient had an unrepaired ToF and a congenital portosystemic venous shunt. An upper gastrointestinal endoscopy revealed AEN, which could be due to unstable hemodynamics of cyanotic spells. This is the first adult case presenting these 2 conditions occurring simultaneously.

Coronary periarteritis with aneurysms has been reported as a cardiovascular manifestation of immunoglobulin G4 (IgG4) -related disease. We report a 10-year clinical observation of a patient with IgG4-related coronary periarteritis (IgG4-rCP) characterized by multiple thickening of periarterial tissue and coronary artery aneurysms (CAAs).

A 60-year-old man with a history of IgG4-related autoimmune pancreatitis had an incidental detection of a total of 5 tumor-like lesions surrounding the right and left coronary arteries on coronary computed tomography angiography (CCTA) in 2012. Among them, 3 lesions were located at the middle to the distal portions of the right coronary artery (RCA) and the most proximal lesion was accompanied by a CAA. Although corticosteroid therapy was continued, 4-year follow-up of CCTA in 2016 showed the most proximal lesion gradually increased from 33 to 45 mm and the CAA enlarged from 9 to 22 mm. In order to avoid aneurysmal rupture, the patient underwent resection of the most proximal lesion with an enlarged aneurysm concomitant with coronary artery bypass grafting (CABG). Histopathological findings were coincident with IgG4-rCP. CCTA in 2018, however, showed the remaining distal tumor-like lesion of RCA had slightly enlarged and a new CAA developed despite the corticosteroid therapy. Follow-up CCTA in 2022 revealed the CAA increased to 13 mm, which showed rapid enlargement by 4 mm/year. A second operation through a re-median sternotomy was planned. The residual lesions with the CAA were resected followed by CABG. The other lesions at the left coronary artery remained stable without aneurysmal change, but careful follow-up has been continued.

An error appeared in the article entitled "Epidemiology of Heart Valve Disease in Taiwan: A Population-Based Cohort Study" by Ching-Hu Chung, Yu-Jen Wang, and Chia-Ying Lee (Vol. 62 No.5, 1026-1034, 2021). Figure 1 on page 1029 should be replaced by the following.