The MAPH (mean platelet volume, age, total protein and hematocrit) score is a newly developed simple scoring system for patients with STEMI that has been associated with satisfactory predictive values to determine thrombus burden in STEMI patients. Therefore, the aim of our study was to determine the relationship between the MAPH risk score and TIMI flow in patients with STEMI.

The study included 260 patients who underwent primary percutaneous coronary intervention between December 2019 to July 2022, and had TIMI 0 flow in the responsible coronary artery due to STEMI. According to the TIMI flow score after stent implantation, the patients were classified into either the no-reflow group (n = 59) or the normal flow group (n = 201). In order to calculate the MAPH score, ROC analysis was performed to find the cutoff point for each component of the MAPH score. MAPH scores were calculated (MPV + Age + Protein + Hematocrit) for both groups. Our study was a retrospective, observational study.

In the multivariable regression analysis, the MAPH score (OR: 0.567; 95%CI: 0.330-0.973, P = 0.04) and glycoprotein IIb/IIIa inhibitors (OR: 0.249; 95%CI: 0.129-0.483, P < 0.001) were parameters found to be independent predictors of TIMI flow. An MAPH score value > 2.5 predicted the presence of low TIMI coronary flow in patients with STEMI, with 78% specificity and 45% sensitivity (ROC area under curve: 0.691, 95% CI: 0.617-0.766, P < 0.001).

The MAPH risk score is simple, inexpensive, and quick to calculate. A high MAPH score may be an indicator of coronary no-reflow in patients with STEMI.

Renal dysfunction greatly influences decision-making for emergency percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). This observational study investigated renal function changes and risk factors for renal injury in patients with AMI with reduced estimated glomerular filtration rate (eGFR) who underwent emergency PCI. The study included 85 patients with AMI with decreased eGFR who underwent emergency PCI, categorized into stage 2, 3, and 4 chronic kidney disease groups. Baseline data, laboratory indicators, coronary characteristics, and serum creatinine concentration were monitored at multiple time points. Renal injury was defined using two criteria: an increase in serum creatinine level by 0.3 mg/dL or a 50% increase from baseline. During the 1-year follow-up, renal injury incidence varied from 1.18% to 15.29%. The pattern showed an increasing trend in the 1st week after PCI, peaking at 1 week, followed by a decrease at 3 months, and another increase at one year. Low basal eGFR, high contrast agent dosage, and diabetes were associated with renal injury according to logistic regression analysis. The eGFR cutoff value of 35.475 mL/minute·1.73 m² had a sensitivity of 83.05% and specificity of 57.69% for predicting renal injury based on receiver operating characteristic curve analysis. In summary, patients with AMI with basal eGFR lower than 35.475 mL/minute·1.73 m² have a higher risk of renal injury after PCI. These findings emphasize the importance of assessing renal function and considering associated risk factors when deciding on emergency PCI for AMI with reduced eGFR.

Dyslipidemia has been widely recognized as a significant risk factor for coronary atherosclerosis disease (CAD). In fact, lipid variability has emerged as a more reliable predictor of cardiovascular events. In this study, we aimed to examine the variability in plasma lipids under two different lipid-lowering regimens (intensive statin therapy versus the combination of conventional-dose statins with ezetimibe). In total, we have retrospectively examined 1275 patients with CAD from January 2009 to April 2019 and divided them into two groups: intensive statin group and conventional-dose statins combined with ezetimibe group. All patients were followed up for at least 1 year. Lipid variability was verified by standard deviation (SD), coefficient of variation (CV), and variability independent of mean (VIM) triple methods. Multiple linear regression and subgroup analyses were performed. In the overall participants, the mean age was 62.3 ± 10.4 years old, and 72.8% were male. Multivariate linear regression analysis indicated that the intensive statin group had lower variability in terms of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C) in all SD, CV, and VIM triple methods than statins combined with ezetimibe group (P for all <0.05). Similar results were established in the subgroup analyses based on atorvastatin or rosuvastatin, diabetes mellitus or not, and hypertension or not (P for all < 0.05). Thus, we can conclude that intensive statin therapy could contribute in lowering lipid variability than conventional-dose statins combined with ezetimibe therapy among patients with CAD.

Subjects with coronary artery disease (CAD) have myocardial ischemia and associated abnormal left ventricular ejection fraction (EF). Heart failure with mildly reduced EF (41-49%) (HFmrEF) is a new subgroup of EF for heart failure. Although prognostic factors for CAD and HF with reduced EF are well known, fewer studies have been conducted on factors related to the survival of CAD and HFmrEF. We recruited study subjects with significant CAD and HFmrEF from our cardiac catheterization data bank. Data were recorded from traceable chart records from our hospital. All-cause and cardiovascular mortality were recorded until December 2019 and served as a follow-up outcome. A total of 348 subjects with CAD and HFmrEF were analyzed. The median duration of follow-up was 37 months. Seventy-eight subjects died during the follow-up period and 30 of them were due to cardiovascular causes. In univariate analyses, those who died were of older ages, and with a lower estimated glomerular filtration rate (eGFR) (47 ± 30 versus 71 ± 30 mL/minute/1.73 m², P < 0.001), and lower usage of percutaneous coronary intervention (PCI) and beta blockers. In the Cox survival regression analysis, a higher eGFR (hazard ratio 0.980, P < 0.001) was protective, while older age and a higher serum total cholesterol (hazard ratio 1.006, P = 0.048) were related to all-cause mortality for CAD with HFmrEF. Furthermore, a higher eGFR was also associated with less cardiovascular mortality. In conclusion, for subjects with CAD and HFmrEF, a higher eGFR was protective and associated with a lower all-cause and cardiovascular mortality.

Dynamic coronary roadmap (DCR) is a novel technology that creates a real-time overlay of the coronary arteries in percutaneous coronary intervention (PCI) and has the potential to reduce the contrast volume. However, the efficacy of DCR in terms of clinical outcomes in patients with chronic kidney disease (CKD) remains to be fully elucidated.

This single center retrospective study enrolled 275 patients with CKD who underwent PCI, and divided them into a DCR group (n = 124) and Non-DCR group (n = 151). Propensity score matching was performed to minimize the differences in baseline characteristics in 113 patient pairs. The primary endpoint was a composite outcome of all-cause death, hospitalization for heart failure, nonfatal myocardial infarction, or the introductory rate of dialysis within 2 years. The secondary endpoints were contrast medium volume, the incidence of contrast-induced acute kidney injury (CI-AKI), and the introductory rate of dialysis within 2 years.

Although there was no significant difference in the success rate (DCR group: 99.1% versus Non-DCR group: 98.2%; P = 0.561), contrast volume (92.20 mL versus 115.97 mL; P = 0.002) was significantly lower in the DCR group. CI-AKI incidence was 0.9% versus 6.2% in the DCR and Non-DCR groups, respectively (P = 0.031). The composite outcome defined as primary endpoint occurred in 10 patients in the DCR group and 20 patients in the Non-DCR group (8.8% versus 17.7%; P = 0.049).

From the perspective of acute and long-term clinical outcomes, DCR use may be effective for patients with CKD.

Comparison of the bleeding risk for long-term oral anticoagulation (OAC) in patients with nonvalvular atrial fibrillation (AF) with and without cancers has been inconsistent. This study aimed to clarify the differences in the bleeding risk in patients with AF with cancers and those without cancers during the long-term OAC.

The CODE-AF prospective registry enrolled 5,902 consecutive patients treated for AF at 10 tertiary referral centers in Korea. Of the enrolled patients, 464 (7.8%) were diagnosed with cancers and were followed for all stroke and bleeding events (net composite events).

The age, CHA₂DS₂-VASC, and HAS-BLED scores were similar between AF patients with and without cancers. Male population greatly comprised patients with AF with cancers. They were equally prescribed with direct OAC compared to those without cancers. The incidence rate for clinically relevant nonmajor (CRNM) bleeding events was higher in the patients with AF with cancers than in those without cancers (4.4 per 100 person-years versus 2.8 per 100 person-years, P = 0.023), and net composite events were also more frequent in patients with AF with cancers than in those without cancers (6.4 per 100 person-years versus 4.0 per 100 person-years, P = 0.004). Patients with AF with cancers showed a significantly higher rate of CRNM bleeding (hazard ratio [HR] 1.54, confidence interval [CI] 1.05-2.25, P = 0.002) than those without cancers.

Based on the AF cohort, AF with cancers could face a significantly higher risk for CRNM bleeding events in the long-term OAC than those without cancers.

The best cardiac phases in retrospective ECG-gated CT for detecting an intimal tear (IT) in aortic dissection (AD) and an ulcer-like projection (ULP) in an intramural hematoma (IMH) have not been established. This study aimed to compare the detection accuracy of diastolic-phase and systolic-phase ECG-gated CT for IT in AD and ULP in IMH, with subsequent surgical or angiographical confirmation as the reference standard.

In total, 81 patients (67.6 ± 11.8 years; 41 men) who underwent emergency ECG-gated CT and subsequent open surgery or thoracic endovascular aortic repair for AD (n = 52) or IMH (n = 29) were included. The accuracies of detecting IT and ULP were compared among only diastolic-phase, only systolic-phase, and both diastolic-phase and systolic-phase methods of retrospective ECG-gated CT; surgical or angiographical findings were used as the reference standard. The detection accuracy for IT and ULP using only diastolic-phase, only systolic-phase, and both diastolic-phase and systolic-phase methods of ECG-gated CT was 93% [95% CI: 87-97], 94% [95% CI: 88-97], and 95% [95% CI: 90-97], respectively. There were no significant differences in detection accuracy among the 3 acquisition methods (P = 0.55). Similarly, there were no significant differences in the accuracy of detecting IT in AD (P = 0.55) and ULP in IMH (P > 0.99) among only diastolic-phase, only systolic-phase, and both diastolic- and systolic-phase ECG-gated CT.

Retrospective ECG-gated CT for detecting IT in AD and ULP in IMH yields highly accurate findings. There were no significant differences seen among only diastolic-phase, only systolic-phase, and both diastolic-phase and systolic-phase ECG-gated CT.

Atherosclerotic plaque rupture and subsequent cardiovascular complications threaten the population's health worldwide. The polymorphism of miR-146a rs2910164 was significantly associated with the risk of vulnerable plaques. However, it remains unclear whether the circulating miR-146a is differentially expressed in stable and vulnerable plaques and thus, serves as a potential biomarker.

This study aims to analyze the differential expression of circulating miR-146a between patients with stable and vulnerable plaques to explore the potential molecular mechanisms.

Public databases were searched from their inception up to November 2022. A study reporting the specific circulating miR-146a levels between patients with stable and vulnerable plaques was included. The study quality was assessed using the modified genetic 8-stars Newcastle-Ottawa scale. The differential expression levels of miR-146a were evaluated using the standardized mean difference (SMD).

Eight studies with 978 patients were included and analyzed. The results showed that miR-146a expression levels were significantly higher in the vulnerable plaque population than in the stable plaque population (SMD: 1.91; 95% confidence interval: 1.35, 2.47; P < 0.01). A similar statistical significance was found in subgroup analyses regarding sample source, disease type, and vulnerable plaque characteristics. Sensitivity analysis suggested the robustness of the results. Analysis of downstream genes suggested that miR-146a-targeted regulation of ACTN4, SARM1, and ULK2 may affect intraplaque hemorrhage.

Patients with vulnerable plaque have higher circulating miR-146a levels than those with stable plaque. However, based on the limitations of this study, high-quality studies are still needed to confirm the results.

Acute aortic syndromes (AAS) are a series of life-threatening conditions of the aorta. To improve predictability and prevention, we investigated the daily, weekly, monthly, and seasonal variations in the onset of AAS in Liaoning Province, Northeast China.

We collected the clinical data of 1,197 patients treated for AAS at the General Hospital of Northern Theater Command between June 2002 and June 2021. Chi-square goodness-of-fit testing was used to determine whether AAS uniformly occurred.

The average age was 54.93 ± 12.32 years, and 614 patients (51.29%) aged below or equal to 55 years. Nine-hundred-and-five patients (75.61%) were male. The proportions of patients comorbid with hypertension and diabetes were 80.37% and 4.09%, respectively. The peak time of the day for the onset of AAS was between 12:00 and 17:59 (P < 0.001). Furthermore, we found that patients with hypertension had obvious circadian rhythm. AAS had a weekly distribution (P = 0.032), with Sunday and Monday being two troughs. The incidence rate of AAS was low in warmer periods, such as July and August in summer (P < 0.001). The correlation analysis revealed a negative association between the incidence of AAS and the monthly average temperature (P < 0.05).

Our results revealed that AAS displayed circadian and seasonal rhythms in northeast China. AAS peaked between 12:00 and 17:59. Patients with AAS with hypertension had obvious circadian rhythm. Summer was trough season for the onset of AAS. The incidence rate of AAS was negatively correlated with the monthly average temperature.

Remote dielectric sensing (ReDS) is a non-invasive, electromagnetic energy-based technology to quantify pulmonary congestion. However, the accuracy of ReDS values in patients with a variety of physiques has not been fully validated.

Prospective successive measurements of ReDS values and body mass index (BMI) were performed on admission in consecutive hospitalized patients with cardiovascular diseases. Patients were stratified into 4 groups according to the WHO classification: underweight (BMI < 18.5), normal weight (18.5 ≤ BMI < 24.9), pre-obese (25.0 ≤ BMI < 29.9), and obese (30.0 ≤ BMI). The indexed ReDS value was defined as a ReDS value divided by the modified congestion score index (the severity of pulmonary congestion on chest X-ray). The indexed ReDS values were compared among the 4 stratified groups.

A total of 436 patients (76 [69, 82] years old and 254 men) were included. The median indexed ReDS values were 21.3 (19.1, 23.8), 25.7 (21.0, 29.5), 25.7 (20.3, 31.0), and 28.0 (21.1, 34.0) in underweight, normal weight, pre-obese, and obese patients, respectively, highlighting the underweight group had the lowest values (P < 0.001).

ReDS values may be underestimated and specific caution should be paid in its interpretation in underweight patients.

Participation in clinical research has served clinicians to develop academic careers, as well as to deepen clinical insights, implement evidence-based medicine practices, and even inspire new clinical questions. Early engagement in academic pursuits may better prepare clinicians to maintain long-term research productivity, rather than starting later in their careers.

We included medical doctors who graduated from a medical university and retrospectively followed them for 10 years after graduation. The impact of at least one publication within the first 5 years on the achievement of ≥ 5 publications within 10 years was evaluated.

A total of 79 medical doctors, including 60 (76%) men, were included. During the first 5 years, 21 (27%) published at least one paper. Overall, 25 (32%) achieved the primary outcome. At least one publication during the first 5 years was an independent predictor of the primary outcome (odds ratio 30.4, 95% confidence interval 2.68-251, P = 0.002). Medical doctors with at least one publication within the first 5 years had significantly higher cumulative 10-year publications compared to no publications within the first 5 years (9 [5, 13] versus 0 [0, 3], P < 0.001).

In this retrospective study, we demonstrated that an early involvement in research defined by academic output was associated with higher odds of multiple publications later in a career. Prospective studies to validate our findings by involving young medical doctors in academic pursuits are needed to understand the longitudinal effects of early career academic productivity.

Two key echocardiographic parameters, left ventricular mass index (LVMI) and left atrial volume index (LAVI), are important in assessing structural myocardial changes in heart failure (HF) with preserved ejection fraction (HFpEF). However, the differences in clinical characteristics and outcomes among groups classified by LVMI and LAVI values are unclear.

We examined the data of 960 patients with HFpEF hospitalized due to acute decompensated HF from the PURSUIT-HFpEF registry, a prospective, multicenter observational study. Four groups were classified according to the cut-off values of LVMI and LAVI [LVMI = 95 g/m² (female), 115 g/m² (male) and LAVI = 34 mL/m²]. Clinical endpoints were the composite of HF readmission and all-cause death. Study endpoints among the 4 groups were evaluated. The composite endpoint occurred in 364 patients (37.9%). Median follow-up duration was 445 days. Kaplan-Meier analysis revealed significant differences in the composite endpoint among the 4 groups (P < 0.001). Cox proportional hazards analysis demonstrated that patients with increased LAVI alone were at significantly higher risk of HF readmission and the composite endpoints than those with increased LVMI alone (P = 0.030 and P = 0.024, respectively). Age, male gender, systolic blood pressure at discharge, atrial fibrillation (AF) hemoglobin, renal function, and LAVI were significant determinants of LVMI and female gender, AF, hemoglobin, and LVMI were significant determinants of LAVI.

In HFpEF patients, increased LAVI alone was more strongly associated with HF readmission and the composite of HF readmission and all-cause death than those with increased LVMI alone.

A total of 69 patients were enrolled in the study, including 23 patients with hypertrophic cardiomyopathy (HCM), 26 patients with Left Ventricle (LV) enlargement comprising 16 dilated cardiomyopathy (DCM) patients and 10 ischemic cardiomyopathy (ICM) patients, and 20 control subjects. All patients underwent 2DE, contrast-enhanced 2DE (Contrast-2DE), 3DE, Contrast-3DE, and single photon emission computed tomography (SPECT) examinations. The 2DE-AL and 3DE methods measured the left ventricular mass (LVM). The results were compared with those measured by SPECT. The measured LVM of the 69 patients was systematically overestimated by 2DE-AL (177.4 ± 56.2 g), Contrast-2DE-AL (174.5 ± 55.5 g), 3DE (167.3 ± 59.2 g), and Contrast-3DE (154.2 ± 46.7 g) when compared with SPECT (148.5 ± 52.4 g) (P < 0.05), while Contrast-3DE provided the best agreement with SPECT in LVM measurement (r = 0.898, P < 0.001) and had the smallest deviation (5.7 ± 23.1 g). 3DE overestimated LVM more compared to Contrast-3DE in LV hypertrophy group (165.5 ± 37.9 g versus 153.5 ± 27.6 g, P = 0.003) and LV enlargement group (204.5 ± 69.3 g versus 183.5 ± 53.5 g, P = 0.006). For 2DE methods, there was no significant difference between the LVM obtained with or without contrast enhancement in control group (132.3 ± 23.6 g versus 128.4 ± 23.3 g), LV hypertrophy group (177.7 ± 38.6 versus 178.3 ± 30.9 g, P = 0.889), and LV enlargement group (211.9 ± 63.2 g versus 206.5 ± 66.0 g, P = 0.386). The difference between LVM measured by 2DE-AL and SPECT was the greatest (27.9 ± 34.0 g), especially in LV hypertrophy group and LV enlargement group (LV hypertrophy group 39.7 ± 26.0 g; LV enlargement group 24.2 ± 42.8 g). To conclude, Contrast-3DE and SPECT show greater consistency in LVM measurement, especially in cardiomyopathy, when compared with 2DE. Administering contrast can effectively reduce the overestimation of LVM by non-contrast DE.

Whether a nodular calcification (NC), which is the precursor to intracoronary thrombosis, is focally or diffusely distributed in the coronary tree has major implications for ongoing efforts to identify. This study aimed to investigate the frequency and spatial distribution patterns of sheet calcification (SC) and NC in a 3-vessel examination of autopsied human hearts.

A total of 323 coronary artery specimens from 110 cadavers were obtained from autopsy cases. After fixation and decalcification, the coronary artery trees were cut every 5 mm into 4-μm transverse cross-sections for histological assessment. An SC was defined as a plate-like calcification of > 1 quadrant of the vessel or > 3 mm in diameter, and NC as nodular calcium deposits separated by fibrin, and a deposit size > 1 mm in diameter.

Of the 6,306 histological cross-sections, SCs and NCs were identified in 1,627 (26%) and 233 (4%) cross-sections, respectively. SCs and NCs had a similar distribution pattern in all 3 coronary arteries. In the left anterior descending artery (LAD), NCs were predominantly located in the proximal segment: the first 45 mm from the LAD ostium (72%) and the first 60 mm from the LAD ostium (84%), respectively. However, NCs were evenly distributed throughout the length of the coronary artery in the right coronary artery (RCA) and left circumflex artery (LCX).

NCs coexisted with SCs, and tended to cluster in predictable parts within the proximal segments of the LAD, but were evenly distributed throughout the RCA and LCX in coronary arteries from cadavers.

Left ventricular assist device in combination with clenbuterol has been demonstrated to significantly improve heart function in patients with advanced heart failure. However, the roles of clenbuterol in mechanical unloading and its underlying mechanism are poorly understood. A rat abdominal heart transplantation model has been developed to mimic mechanical unloading of the heart. The recipient rats were randomly segregated into experimental groups for the daily administration of either saline (the "Trans" group; n = 13) or clenbuterol (2 mg/kg, the "Trans + CB" group; n = 12). Another group of 10 rats served as a treatment mimic control/sham animals (the "Sham" group). All interventions were performed via intraperitoneal injections once daily for 4 weeks. The Trans group animals exhibited myocardial atrophy and dysfunction with decreased expression levels of transient receptor potential channel 3 (TRPC3) and phospholipase C-β1 (PLC-β1) at 4 weeks post-transplantation. Administration of clenbuterol improved cardiac function, prevented myocardial atrophy, and restored expression of TRPC3 and PLC-β1 in the unloaded hearts of the "Trans + CB" animals at 4 weeks post-transplantation. Silencing of the TRPC3 gene by siRNA inhibited the pro-hypertrophic effect of clenbuterol in the rat primary cardiomyocytes in vitro. Furthermore, U73122, an inhibitor of the PLC-β1/diacylglycerol (DAG) pathway, significantly attenuated clenbuterol-induced upregulation of TRPC3 in cardiomyocytes. These findings suggest that the anti-atrophic effect of clenbuterol may be dependent on the upregulation of TRPC3 through the activation of the PLC-β1/DAG pathway during mechanical unloading. The results of our study reveal a potential target for the prevention and treatment of mechanical unloading-induced myocardial atrophy.

As a kind of anthracycline, doxorubicin (DOX) is commonly used as an antitumor drug, but its clinical application has been greatly hindered due to its severe cardiotoxicity. Hence, in this study, we investigated the role of catalpol (CTP) and its effect on DOX-induced cardiotoxicity.

The cardiac function of mice was evaluated by assessing lactate dehydrogenase, creatine kinase isoenzyme, heart weight to body weight, and heart weight/tibia length levels. Histopathological changes were observed using hematoxylin and eosin staining, and the terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to examine myocardial apoptosis. Superoxide dismutase (SOD) activity, glutathione (GSH), and malondialdehyde (MDA) levels were measured to confirm the changes in oxidative stress. Western blotting showed the levels of autophagy- and pathway-related proteins. Expression of autophagy marker LC3 was examined using immunofluorescence staining.

CTP alleviated DOX-induced cardiac damage in mice. We further observed upregulated SOD and GSH levels, and downregulated MDA level after the CTP treatment in DOX-treated mice, indicating the protective role of CTP against oxidative injury. DOX-induced myocardial apoptosis was also inhibited by CTP treatment in mice. In addition, CTP decreased the levels of Beclin1 and LC3II/LC3I, increased the levels of P62, and activated the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in DOX-treated mice.

CTP ameliorated DOX-induced cardiotoxicity by inhibiting oxidative stress, myocardial apoptosis, and autophagy via the AKT-mTOR pathway.

Circular RNAs (circRNAs) are known to play a crucial role in the progression of atherosclerosis (AS). In this study, we aim to explore the function of oxidized low-density lipoprotein (ox-LDL)-induced macrophage-derived exosomal circ_100696 in AS.

THP-1 macrophages were induced by ox-LDL to mimic AS cell model. A quantitative real-time polymerase chain reaction (qRT-PCR) assay was applied to determine the expression of circ_100696, microRNA-503-5p (miR-503-5p), and pregnancy-associated plasma protein A (PAPPA). The morphology and size distribution of exosomes were examined by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). Western blot assay was performed for protein levels. Cell proliferation was assessed using 5-ethynyl-2'-deoxyuridine (EdU) assay. Flow cytometry analysis was performed to analyze the cell cycle. Wound-healing assay and transwell assay were done to examine cell migration. RNA pull-down assay, dual-luciferase reporter assay, and RNA immunoprecipitation (RIP) assay were employed to analyze the relationship among circ_100696, miR-503-5p, and PAPPA.

Circ_100696 level was increased in ox-LDL-induced THP-1 macrophages and ox-LDL-treated THP-1 macrophage-derived exosomes (OM-Exo). OM-Exo promoted the proliferation, cell cycle, and migration of vascular smooth muscle cells (VSMCs). Circ_100696 was upregulated in VSMCs cocultured with OM-Exo. Circ_100696 knockdown reversed the effects of OM-Exo on VSMC proliferation and migration. Circ_100696 was demonstrated to function as the sponge for miR-503-5p, and miR-503-5p directly targeted PAPPA. Circ_100696 overexpression facilitated VSMC proliferation and migration, with miR-503-5p upregulation or PAPPA silencing reversing these effects. Moreover, circ_100696 overexpression promoted PAPPA expression by targeting miR-503-5p.

OM-Exo promoted VSMC growth and migration by regulating the circ_100696/miR-503-5p/PAPPA axis, thereby promoting AS progression.

This study aims to examine the changes in myocardial microcirculation in rats in a high-altitude hypoxic environment via computed tomography (CT) myocardial perfusion imaging technology. Rats in two groups were raised in different environments from 4 weeks of age for a period of 24 weeks. At 28 weeks of age, both groups underwent CT myocardial perfusion scanning, and the following myocardial perfusion parameters were measured: time to peak (TTP), mean transit time (MTT), blood flow (BF), and blood volume (BV). Following the scan, the rats were sacrificed, the cardiac index and right ventricular hypertrophy index were obtained, and hematoxylin-eosin (HE) staining was utilized to observe the pathological changes in the myocardium. In the group of rats that are subject to a high-altitude hypoxic environment for 24 weeks (the high-altitude group), the TTP and MTT values were increased (P < 0.05), the BF and BV values were lower (P < 0.05), the right heart mass was higher (P < 0.05) than that in the low-altitude group. As shown by the pathological results of HE staining, the gap between cardiomyocytes in the high-altitude group was widened, the arrangement of cardiomyocytes was irregular, and the cells were filled with a few fat vacuoles. The myocardial microcirculation is altered in a high-altitude hypoxic environment. In particular, the myocardium is in a state of inadequate perfusion, the BF in the myocardium slows down, and the right heart displays compensatory hypertrophy.

A certain dosage of cyclophosphamide (CYP) in clinical applications contributes to severe cardiotoxicity. Herein, this study explored the impact of adipose-derived mesenchymal stem cell (AdMSC)-exosomes (Exos) on CYP-induced cardiotoxicity.

AdMSCs and AdMSCs-Exos were isolated and identified. CYP was utilized for developing a cardiotoxicity rat model, after which blood was collected and then the serum contents of cardiac injury-related indexes (creatine kinase-MB, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase) were detected with enzyme-linked immunosorbent assay kits. Oxidative stress (OS)-related indicators were measured with the corresponding kits. Myocardial pathological changes and collagen fibrosis were tested with hematoxylin-eosin and Masson staining, and apoptosis-related and autophagy-related proteins in rat cardiac tissues with immunohistochemistry and Western blot assays, respectively.

AdMSCs and AdMSCs-Exos were successfully isolated. AdMSCs-Exos could target rat hearts. AdMSCs-Exos improved cardiac function and diminished the content of the cardiac injury-related indexes in CYP rats. In addition, AdMSCs-Exos reduced CYP-induced cardiac fibrosis, OS, apoptosis, and autophagy in rats.

AdMSCs-Exos alleviated CYP-induced cardiotoxicity in rats via the repression of OS, apoptosis, and autophagy.

Tanshinone IIA (Tan IIA), the core ingredient of Salvia miltiorrhiza, is commonly used for treating cardiovascular diseases. However, its underlying mechanism in regulating autophagy in atherosclerosis (AS) remains unclear. An in vivo model of AS was constructed using Apolipoprotein E-deficient (ApoE^−/−) mice fed with a high-fat diet. Histopathologic changes and lipid accumulation were evaluated by hematoxylin and eosin (HE) and Oil red O staining, respectively. The inflammatory cytokine levels were evaluated by Enzyme-linked immunosorbent assay (ELISA). An oxidized low-density lipoprotein (ox-LDL) was used to induce foam cells in RAW264.7 cells. Cholesterol uptake and efflux assay were used to assess changes in intracellular and extracellular cholesterol levels. The expression levels of autophagy-related protein-16-like protein 1 (ATG16L1) and miR-214-3p in the samples and cells derived from mice were assessed by quantitative real-time polymerase chain reaction (qRT-PCR), and the protein levels of the mitogen-activated protein kinase (MAPK)/mammalian target of rapamycin (mTOR) and autophagy-related markers were detected using western blot. The binding site of miR-214-3p on ATG16L1 was determined using a dual-luciferase reporter assay. We observed a decrease in ATG16L1 and increase in miR-214-3p expression level in the AS mice and ox-LDL stimulated RAW264.7 cells. However, the miR-214-3p and ATG16L1 expression could be reversed by Tan IIA. In vivo experiments showed that Tan IIA alleviated AS by reducing lipid accumulation and inflammatory factor levels and promoting autophagy. The in vitro assays demonstrated that Tan IIA regulated lipid levels and autophagy via the miR-214-3p/ATG16L1 axis to inhibit foam cell formation. Additionally, Tan IIA inhibited the MAPK/mTOR pathway by reducing miR-214-3p expression and promoting autophagy. Findings from this study suggested that Tan IIA regulated the MAPK/mTOR signal-mediated autophagy to alleviate AS through the miR-214-3p/ATG16L1 axis.

Coronary artery malformations are rare in the clinic. When with severe atherosclerosis, there is an additional risk. Specific coronary artery malformations, such as single right coronary artery, may be involved in the arteriosclerotic process, especially when accompanied by significant coronary artery tortuosity. It will remarkably challenge the treatment. We report a case of a single right coronary artery with severe stenosis and heart valve disease. She successfully underwent coronary artery bypass grafting and aortic valve replacement.

Mitral valve aneurysm (MVA) is a relatively rare but life-threatening condition that may occur as a complication of an infective endocarditis (IE) involved aortic valve. Rupture of the valve aneurysm is one of the most serious complications, which could result in severe mitral regurgitation and cause rapid hemodynamic deterioration, especially in heart failure patients. Timely diagnosis using echocardiography and appropriate treatments, such as invasive surgical repair or replacement of the valve, can effectively prevent catastrophic complications. Here, we present a 57-year-old male patient with MVA after IE and emphasize the key role of echocardiography in the early diagnosis and management of these kinds of conditions.

Several errors (shown with underlines) in the following list appeared in the article entitled "Silencing of Hsa_circ_0055440 Alleviates Hypoxia-Induced Cardiomyocyte Injury by Regulating the MiR-499b-5p/ACSL1 Axis" by Lianhua Yan, Haijun Qi, and Wei Zhou (Vol. 64 No.2, 274-282, 2023).