Virtual reality-based cognitive-behavioural therapy for the treatment of anxiety in patients with acute myocardial infarction: a randomised clinical trial.

Background: The presence of mental health conditions is pervasive in patients who experienced acute myocardial infarction (AMI), significantly disrupting their recovery. Providing timely and easily accessible psychological interventions using virtual reality-based cognitive-behavioural therapy (VR-CBT) could potentially improve both acute and long-term symptoms affecting their mental health. Aims: We aim to examine the effectiveness of VR-CBT on anxiety symptoms in patients with AMI who were admitted to the intensive care unit (ICU) during the acute stage of their illness. Methods: In this single-blind randomised clinical trial, participants with anxiety symptoms who were admitted to the ICU due to AMI were continuously recruited from December 2022 to February 2023. Patients who were Han Chinese aged 18-75 years were randomly assigned (1:1) via block randomisation to either the VR-CBT group to receive VR-CBT in addition to standard mental health support, or the control group to receive standard mental health support only. VR-CBT consisted of four modules and was delivered at the bedside over a 1-week period. Assessments were done at baseline, immediately after treatment and at 3-month follow-up. The intention-to-treat analysis began in June 2023. The primary outcome measure was the changes in anxiety symptoms as assessed by the Hamilton Anxiety Rating Scale (HAM-A). Results: Among 148 randomised participants, 70 were assigned to the VR-CBT group and 78 to the control group. The 1-week VR-CBT intervention plus standard mental health support significantly reduced the anxiety symptoms compared with standard mental health support alone in terms of HAM-A scores at both post intervention (Cohen's d=-1.27 (95% confidence interval (CI): -1.64 to -0.90, p<0.001) and 3-month follow-up (Cohen's d=-0.37 (95% CI: -0.72 to -0.01, p=0.024). Of the 70 participants who received VR-CBT, 62 (88.6%) completed the entire intervention. Cybersickness was the main reported adverse event (n=5). Conclusions: Our results indicate that VR-CBT can significantly reduce post-AMI anxiety at the acute stage of the illness; the improvement was maintained at the 3-month follow-up. Trial registration number: The trial was registered at www.chictr.org.cn with the identifier: ChiCTR2200066435.

Role of collateral flow in infarct border zone extent and contractile function in patients with chronic coronary total occlusion.

PURPOSE: There is a paucity of data regarding the border zone parameters in patients with chronic coronary total occlusion (CTO). We investigated the border zone extent and contractile function and their associations with collateral flow. METHODS: CTO patients (n = 47) and sex- and age-matched volunteers (n = 15) were prospectively enrolled and underwent cardiac MRI examinations to acquire cine and late-gadolinium enhancement (LGE) images. Myocardial peak strain (PS) and the time to PS were determined at the segmental level and global level. Infarct, border zone, adjacent, and remote regions were defined according to the transmural extent of infarction (TEI) by LGE at each segment. Angiographic collateral flow was evaluated using the Rentrop grading system. RESULTS: CTO patients with well-developed collateral flow had a higher TEI in border zone regions compared to patients with poorly developed collateral flow (p = 0.02). Conversely, CTO patients with poorly developed collaterals showed a higher TEI in infarct regions (p < 0.01). Enhanced border function, characterized by greater PS and earlier time to PS, was noted in well-developed collaterals (all p < 0.05). In the multivariate linear analyses, the level of collateral flow was an independent predictor of the border zone extent (ß = 0.40, p = 0.02) and contractile function (radial: ß = -0.42, p = 0.02; circumferential: ß = 0.39, p = 0.02; and longitudinal: ß = 0.47, p < 0.01). CONCLUSIONS: In CTO patients, the presence of well-developed collateral flow was closely linked to a greater extent of LGE and contractile function in border zone regions. Our findings shed light on the cardiac MRI-based pathophysiological underpinning in border zone regions, which could offer complementary and prognostic information in clinical practice.

Poor cardiovascular health status among Chinese women.

BACKGROUND: Systematic investigation and analysis of cardiovascular health status (CVHS) of Chinese women is rare. This study aimed to assess CVHS and atherosclerotic cardiovascular disease (ASCVD) burden in the Chinese women physicians (CWP) and community-based non-physician cohort (NPC). METHODS: In this prospective, multicenter, observational study, CVHS using the American Heart Association (AHA) defined 7 metrics (such as smoking and fasting glucose) and ASCVD risk factors including hypertension, hyperlipidemia and type-2 diabetes were evaluated in CWP compared with NPC. RESULTS: Of 5832 CWP with a mean age of 44 ± 7 years, only 1.2% achieved the ideal CVHS and 90.1% showed at least 1 of the 7 AHA CVHS metrics at a poor level. Total CVHS score was significantly decreased and ASCVD risk burden was increased in postmenopausal subjects in CWP although ideal CVHS was not significantly influenced by menopause. Compared to 2596 NPC, fewer CWP had ≥ 2 risk factors (8% vs. 27%, P < 0.001); CWP scored significantly higher on healthy factors, a composite of total cholesterol, blood pressure, fasting glucose (P < 0.001), but, poorly on healthy behaviors (P < 0.001), specifically in the physical activity component; CWP also showed significantly higher levels of awareness and rates of treatment for hypertension and hyperlipidemia, but, not for type-2 diabetes. CONCLUSION: Chinese women's cardiovascular health is far from ideal and risk intervention is sub-optimal. Women physicians had lower ASCVD burden, scored higher in healthy factors, but, took part in less physical activity than the non-physician cohort. These results call for population-specific early and improved risk intervention.

An unexpected electrocardiogram sign of subacute left ventricular free wall rupture: Its early awareness may be lifesaving.

BACKGROUND: Post-infarct left ventricular free wall rupture (LVFWR) is not always an immediately catastrophic complication. The rupture can be subacute, allowing time for diagnosis and intervention. Accordingly, early recognition of the entity may be lifesaving. METHODS: We present an electrocardiogram (ECG) change pattern in two cases, which was erroneously attributed to ischemia. Two women in their 80s were admitted to our institute after experiencing the sudden onset of chest pain. They were managed as anterior ST-segment elevation myocardial infarction without reperfusion treatment. Unfortunately, they experienced a recurrence of severe chest pain with cardiogenic shock during hospitalisation. The ECG recorded at that time showed a ST-segment re-elevation in infract-related leads. RESULTS: The two cases were regrettably received a misjudgement of reinfarction at first, and one of the patients even was administrated with tirofiban. Afterwards the diagnosis of subacute LVFWR was made through antemortem echocardiography. CONCLUSION: New ST-segment elevation (STE) in infarct-associated leads, coupled with recurrence of chest pain and new-onset hypotension, may constitute the premonitory signs of a subacute LVFWR.

Residual platelet reactivity is preferred over platelet inhibition rate in monitoring antiplatelet efficacy: insights using thrombelastography.

Although thrombelastography (TEG) has been widely implemented in the clinical setting of endovascular intervention, consensus on the optimal parameter for defining high ischemic risk patients is lacking due to the limited data about the relationship between various TEG parameters and clinical outcomes. In this article, we report a post hoc analysis of a prospective, single-center cohort study, including 447 patients with acute coronary syndrome (ACS). Arachidonic acid (AA)- or adenosine diphosphate (ADP)-induced platelet-fibrin clot strength (MAAA or MAADP) was indicative of the net residual platelet reactivity after the treatment with aspirin or clopidogrel, respectively. AA% or ADP% was indices of the relative platelet inhibition rate on AA or ADP pathway. We found that each parameter alone was predictive of the risk of 6-month ischemic event, even after adjusting for confounding factors. However, the association between AA% and clinical outcome disappeared when further adjusted for MAAA. Likewise, inclusion of MAADP changed the significant relation between ADP% and clinical outcome. MAADP > 47.0 mm and MAAA > 15.1 mm were identified as the optimal cutoffs by receiver operating characteristic analysis. High MAAA (HR = 3.963; 95% CI: 1.152-13.632; P = 0.029) and high MAADP (HR = 5.185; 95% CI: 2.228-12.062; P < 0.001) were independent predictors when both were included in multivariable Cox regression hazards model. Interestingly, an even higher risk was found for the coexisting high MAAA and high MAADP (HR = 7.870; 95% CI: 3.462-17.899; P < 0.001). We conclude that when performing TEG to predict clinical efficacy, residual platelet reactivity has superiority over platelet inhibition rate as a measure of thrombotic risk in patients treated with aspirin and clopidogrel after ACS.

Impact of multi-vessel therapy to the risk of periprocedural myocardial injury after elective coronary intervention: exploratory study.

BACKGROUNDS: Periprocedural myocardial injury (PMI) after elective percutaneous coronary intervention (PCI) significantly influences the prognosis of coronary artery disease (CAD). However, it was unclear whether the occurrence of PMI was associated with a series of controllable factors, such as PCI strategy or severity of CAD. METHODS: A total of 544 consecutive stable CAD patients underwent elective PCI were enrolled. The main outcome is PMI, defined as troponin T after PCI was at least one value above the 99th percentile upper reference limit. Major adverse cardiac events (MACE), including all-cause death, repeat myocardial infarction and target vessel revascularization were record in the period of follow-up. Univariate and multivariate analysis was applied to assess predictors for the occurrence of PMI. RESULTS: The incidence of PMI was 38.8% in the study. Compared with non-PMI patients (n = 333), PMI patients (n = 211) had more diseased vessels, higher Gensini and Syntax score. Meanwhile, there were higher incidence of MACE in PMI groups (9.5% vs. 3.2%, P < 0.01). We found that PMI patients underwent higher proportion of multi-vessel PCI simultaneously (32.2% vs. 10.5%, P < 0.01) and had more stents implanted (1.8 ± 0.8 vs. 1.4 ± 0.6, P < 0.01). Importantly, after simultaneously adjusted by other factors (such as age, diabetes, total cholesterol, number of diseased vessels, Gensini score and stent length), the risk of PMI was still increased 84% by multi-vessel PCI independently (OR = 1.654, 95% CI = 1.004-2.720, P < 0.05). CONCLUSIONS: The phenomenon of PMI occurred more commonly in stable CAD patients underwent multi-vessel PCI. Multi-vessel international therapy could increase the risk of PMI in elective PCI.

Establishment of a Novel Mouse Model of Coronary Microembolization.

BACKGROUND: Coronary microembolization (CME) has been frequently seen in acute coronary syndromes and percutaneous coronary intervention. Small animal models are required for further studies of CME related to severe prognosis. This study aimed to explore a new mouse model of CME. METHODS: The mouse model of CME was established by injecting polystyrene microspheres into the left ventricular chamber during 15-s occlusion of the ascending aorta. Based on the average diameter and dosage used, 30 C57BL/6 male mice were randomly divided into five groups (n = 6 in each): 9 µm/500,000, 9 µm/800,000, 17 µm/200,000, 17 µm/500,000, and sham groups. The postoperative survival and performance of the mice were recorded. The mice were sacrificed 3 or 10 days after the surgery. The heart tissues were harvested for hematoxylin and eosin staining and Masson trichrome staining to compare the extent of inflammatory cellular infiltration and fibrin deposition among groups and for scanning transmission electron microscopic examinations to see the ultrastructural changes after CME. RESULTS: Survival analysis demonstrated that the cumulative survival rate of the 17 µm/500,000 group was significantly lower than that of the sham group (0/6 vs. 6/6, P = 0.001). The cumulative survival rate of the 17 µm/200,000 group was lower than those of the sham and 9 µm groups with no statistical difference (cumulative survival rate of the 17 µm/200,000, 9 µm/800,000, 9 µm/500,000, and sham groups was 4/6, 5/6, 6/6, and 6/6, respectively). The pathological alterations were similar between the 9 µm/500,000 and 9 µm/800,000 groups. The extent of inflammatory cellular infiltration and fibrin deposition was more severe in the 17 µm/200,000 group than in the 9 µm/500,000 and 9 µm/800,000 groups 3 and 10 days after the surgery. Scanning transmission electron microscopic examinations revealed platelet aggregation and adhesion, microthrombi formation, and changes in cardiomyocytes. CONCLUSION: The injection of 500,000 polystyrene microspheres at an average diameter of 9 µm is proved to be appropriate for the mouse model of CME based on the general conditions, postoperative survival rates, and pathological changes.

Atorvastatin antagonizes the visfatin-induced expression of inflammatory mediators via the upregulation of NF-κB activation in HCAECs.

The present study investigated whether atorvastatin antagonizes the visfatin-induced expression of inflammatory mediators in human coronary artery endothelial cells (HCAECs). Several analysis methods, such as reverse transcription-quantitative polymerase chain reaction, western blot analysis and H2DCFDA incubation, were used in the present study. The data showed that atorvastatin decreased the visfatin-induced expression of interleukin (IL)-6 and IL-8 in HCAECs. In addition, atorvastatin inhibited the visfatin-induced expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in HCAECs. In addition, the present study found that atorvastatin inhibited the visfatin-activated nuclear factor-κB (NF-κB) signal pathway by preventing extracellular signal-regulated kinase phosphorylation in HCAECs. Atorvastatin significantly inhibited visfatin-induced NF-κB activity via the upregulation of reactive oxygen species production. Atorvastatin, a visfatin antagonist (FK866) and an NF-κB inhibitor (BAY11-7082) decreased the visfatin-induced expression of inflammatory mediators via the upregulation of NF-κB activation in HCAECs. These results suggest that atorvastatin may inhibit the visfatin-induced upregulation of inflammatory mediators through blocking the NF-κB signal pathway. The findings of the present study provide a potential use for atorvastatin and visfatin in the pathogenesis of HCAEC dysfunction. This knowledge may contribute to the development of novel therapies for atherosclerosis.

Suppression of Bim by microRNA-19a may protect cardiomyocytes against hypoxia-induced cell death via autophagy activation.

Microvascular obstruction (MO), one of unfavorable complications of percutaneous coronary intervention (PCI), is responsible for the lost benefit of reperfusion therapy. Determination of microRNA-19a, a member of the miR-17-92 cluster, using quantitative real-time polymerase chain reaction (PCR) revealed notably down-regulated microRNA-19a, in myocardium with MO. Nonetheless, the role of miR-19a in MO and the underlying mechanism remains to be elucidated. To this end, an in vitro microembolization model in cardiomyocytes was used. Our data revealed that hypoxic exposure prompted cardiomyocyte apoptosis in a time-dependent manner accompanied by reduced miR-19a. miR-19a overexpression clearly ameliorated hypoxia-induced cell death (necrosis and apoptosis), at least in part, through switching on autophagy. Further dual-luciferase reporter assay and immunoblotting studies demonstrated that miR-19a-induced cytoprotection might be achieved in part through modulation of the specific target Bcl-2 interacting mediator of cell death, Bim, an apoptotic activator. Bim sufficiently interfered with miR-19a-induced LC3 conversion and increased cardiomyocyte apoptosis under hypoxia. Moreover, cardiomyocytes pretreated with 3-methyladenine conferred resistance to the cytoprotective effect of miR-19a and displayed notably increased TUNEL staining and caspase-3 activity. In conclusion, miR-19a protected cardiomyocytes against hypoxia-induced lethality at least in part via Bim suppression and subsequently autophagy activation.

Myocardial extracellular volume fraction measurement in chronic total coronary occlusion: Association with myocardial injury, angiographic collateral flow, and functional recovery.

PURPOSE: To investigate whether myocardial extracellular volume fraction (ECV) measurement by cardiac MR is indicative of myocardial injury, angiographic collateral flow, and functional recovery in patients with chronic total coronary occlusion (CTO). MATERIALS AND METHODS: A total of 50 CTO patients undergoing 1.5 Tesla MR were prospectively enrolled, and 28 underwent a second MR 6 months after revascularization. T1-mapping based indices, including pre- and postcontrast T1 values and ECV, were obtained from infarcted and non-infarcted myocardium, myocardial segments, and coronary territory. The severity of myocardial injury was rated by transmurality extent of infarction (TEI) and regional wall motion abnormalities (RWMA) score. Angiographic collateral flow was evaluated using Rentrop classification. Improvement in segmental wall motion at 6 months was also assessed. RESULTS: ECV and postcontrast T1 value significantly outperformed precontrast T1 value for identifying myocardial infarction (area under the receiver operating characteristic curve [AUC]: 0.998 and 0.953 versus 0.824, all P < 0.02). Myocardial ECV was strongly correlated with TEI (P = 0.000), RWMA score (P = 0.000), and collateral classification (P = 0.007 for left anterior descending artery [LAD] territory, P = 0.001 for non-LAD territory). Furthermore, the likelihood of functional recovery was better predicted by ECV than by late gadolinium enhancement (LGE) (AUC: 0.76 versus 0.68, P < 0.02). CONCLUSION: Myocardial ECV may be a useful surrogate to assess myocardial injury and angiographic collateral flow in CTO, and ECV provides incremental value to LGE in assessing functional recovery after revascularization. J. MAGN. RESON. IMAGING 2016;44:972-982.

Trends in the prevalence of heart diseases over a ten-year period from single-center observations based on a large echocardiographic database.

There is a paucity of data regarding trends in the incidence of heart disease in China during recent years. Using a large echocardiography database in our center, we analyzed trends in the prevalence of several common heart diseases from Dec. 2003. This study retrospectively analyzed the echocardiographic database in our Department from 2003 to 2012. A total of 385 682 cases were included in the study. The prevalence of rheumatic heart disease decreased over the 10-year period, from 4.04% in 2003 to 3.06% in 2012 (P<0.01). Infective endocarditis also decreased, from a mean prevalence of 0.37% in July 2003 to 0.27% in Dec. 2008 (P<0.001). The prevalence of hypertrophic cardiomyopathy, which includes 20% apical hypertrophic cardiomyopathy and 20% hypertrophic obstructive cardiomyopathy, was about 1.8%. The prevalence of the three most common adult congenital heart diseases (CHDs) decreased by about 10% from July 2003 to Dec. 2008 (all P<0.001). The prevalence of moderate pulmonary arterial hypertension (PAH) or left ventricular systolic dysfunction (LVSD) decreased during the 10-year period (P<0.001), but there was no change in the prevalence of severe PAH or LVSD (P>0.05). The present study indirectly demonstrates that the prevalence of several common heart diseases in China has declined in recent years.

Rapid predictors for the occurrence of reduced left ventricular ejection fraction between LAD and non-LAD related ST-elevation myocardial infarction.

BACKGROUNDS: Reduced left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI), which implies the occurrence of cardiac dysfunction, impacts cardiac prognosis, even after primary percutaneous coronary intervention (PCI). This study was designed to clarify the difference of clinical and angiographic predictors for reduced LVEF in ST-elevation myocardial infarction (STEMI) patients with left anterior descending artery (LAD) or non-LAD vessel as culprit artery. METHODS: This was a retrospective study to review a total of 553 patients of STEMI underwent primary PCI in our hospital. All patients underwent echocardiography. Univariate analysis, multivariate analysis and classification and regression tree (CART) were performed between LAD related AMI and non-LAD related STEMI. The primary outcome was the occurrence of reduced LVEF 4-6 days after PCI. RESULTS: In this study, culprit arteries of STEMI were 315 in LAD system (6 in left main artery, 309 in LAD) and 238 in non-LAD system (63 in left circumflex and 175 in right coronary artery). Compared with non-LAD group, post-MI LVEF was significantly reduced in LAD related STEMI group (52.4 ± 9.3% vs. 57.1 ± 7.8%, P < 0.01). Multivariate analysis indicated that elder (>65 years), time to hospital and proximal occlusion were associated with reduced LVEF (<55%) in LAD related STEMI patients. However, in non-LAD patients, time to hospital, multivessel stenosis and post-PCI blood pressure predicted the occurrence of reduced LVEF. Furthermore, CART analysis also obtained similar findings. CONCLUSIONS: Patients with LAD or non-LAD related STEMI could suffer reduced LVEF, while the clinical and angiographic predictors for the occurrence were different.

Exenatide Reduces Tumor Necrosis Factor-α-induced Apoptosis in Cardiomyocytes by Alleviating Mitochondrial Dysfunction.

BACKGROUND: Tumor necrosis factor-α (TNF-α) plays an important role in progressive contractile dysfunction in several cardiac diseases. The cytotoxic effects of TNF-α are suggested to be partly mediated by reactive oxygen species (ROS)- and mitochondria-dependent apoptosis. Glucagon-like peptide-1 (GLP-1) or its analogue exhibits protective effects on the cardiovascular system. The objective of the study was to assess the effects of exenatide, a GLP-1 analogue, on oxidative stress, and apoptosis in TNF-α-treated cardiomyocytes in vitro. METHODS: Isolated neonatal rat cardiomyocytes were divided into three groups: Control group, with cells cultured in normal conditions without intervention; TNF-α group, with cells incubated with TNF-α (40 ng/ml) for 6, 12, or 24 h without pretreatment with exenatide; and exenatide group, with cells pretreated with exenatide (100 nmol/L) 30 mins before TNF-α (40 ng/ml) stimulation. We evaluated apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and flow cytometry, measured ROS production and mitochondrial membrane potential (MMP) by specific the fluorescent probes, and assessed the levels of proteins by Western blotting for all the groups. RESULTS: Exenatide pretreatment significantly reduced cardiomyocyte apoptosis as measured by flow cytometry and TUNEL assay at 12 h and 24 h. Also, exenatide inhibited excessive ROS production and maintained MMP. Furthermore, declined cytochrome-c release and cleaved caspase-3 expression and increased bcl-2 expression with concomitantly decreased Bax activation were observed in exenatide-pretreated cultures. CONCLUSION: These results suggested that exenatide exerts a protective effect on cardiomyocytes, preventing TNF-α-induced apoptosis; the anti-apoptotic effects may be associated with protection of mitochondrial function.

The influence of aortic valve calcification on the risk of periprocedural myocardial injury after elective coronary intervention.

BACKGROUND: Aortic valve calcification (AVC) is a common progressive condition that involves several inflammatory and atherosclerotic mediators. However, it is unclear whether the occurrence of periprocedural myocardial injury (PMI) after elective coronary intervention is associated with AVC in stable coronary artery disease (CAD) patients. METHODS: A total of 530 stable CAD patients who underwent elective coronary intervention were enrolled in this clinical study. High sensitive cardiac troponin T (hs-cTnT) was detected before and after the procedure. PMI was defined as hs-cTnT after coronary intervention higher than 99th percentile upper reference limit (URL). All patients underwent echocardiography to detect the occurrence of AVC. Univariate and multivariate analyses were applied to analyze risk factors of PMI. RESULTS: A total of 210 patients (39.6 %) were diagnosed with PMI after elective coronary intervention. Compared with non-AVC patients (n = 386), AVC patients (n = 144) had higher rate of PMI (64.6 vs. 30.3 %, P < 0.01). CAD patients with AVC had higher Gensini score (39.9 ± 26.6 vs. 34.2 ± 22.1, P < 0.05) and more number of implanted stents (1.7 ± 0.8 vs. 1.5 ± 0.7, P < 0.05). After stratification by classic risk factors of CAD (such as age, male gender and diabetes) in subgroup analyses, we found that AVC patients had increased risk of PMI compared with non-AVC patients. Importantly, even after being adjusted by multivariate analysis, AVC still independently increased the risk of PMI (OR = 3.329, 95 % CI = 2.087-5.308, P < 0.01). CONCLUSION: AVC significantly increased the risk of PMI after elective coronary intervention. It could be one of the independent predictors for PMI in stable CAD patients.

Nine-month angiographic and two-year clinical follow-up of novel biodegradable-polymer arsenic trioxide-eluting stent versus durable-polymer sirolimus-eluting stent for coronary artery disease.

BACKGROUND: Despite great reduction of in-stent restenosis, first-generation drug-eluting stents (DESs) have increased the risk of late stent thrombosis due to delayed endothelialization. Arsenic trioxide, a natural substance that could inhibit cell proliferation and induce cell apoptosis, seems to be a promising surrogate of sirolimus to improve DES performance. This randomized controlled trial was to evaluate the efficacy and safety of a novel arsenic trioxide-eluting stent (AES), compared with traditional sirolimus-eluting stent (SES). METHODS: Patients with symptoms of angina pectoris were enrolled and randomized to AES or SES group. The primary endpoint was target vessel failure (TVF), and the second endpoint includes rates of all-cause death, cardiac death or myocardial infarction, target lesion revascularization (TLR) by telephone visit and late luminal loss (LLL) at 9-month by angiographic follow-up. RESULTS: From July 2007 to 2009, 212 patients were enrolled and randomized 1:1 to receive either AES or SES. At 2 years of follow-up, TVF rate was similar between AES and SES group (6.67% vs. 5.83%, P = 0.980). Frequency of all-cause death was significantly lower in AES group (0 vs. 4.85%, P = 0.028). There was no significant difference between AES and SES in frequency of TLR and in-stent restenosis, but greater in-stent LLL was observed for AES group (0.29 ± 0.52 mm vs. 0.10 ± 0.25 mm, P = 0.008). CONCLUSIONS: After 2 years of follow-up, AES demonstrated comparable efficacy and safety to SES for the treatment of de novo coronary artery lesions.