Identification of High-Risk Coronary Lesions by 3-Vessel Optical Coherence Tomography.

BACKGROUND: Optical coherence tomography (OCT) may provide a method for detecting histologically defined high-risk plaques in vivo. OBJECTIVES: The authors aimed to investigate the prognostic value of OCT for identifying patients and lesions that are at risk for adverse cardiac events. METHODS: Between January 2017 and May 2019, OCT of all the 3 main epicardial arteries was performed in 883 patients with acute myocardial infarction (MI) who were referred for primary percutaneous coronary intervention. The primary endpoint was the composite of cardiac death, nonculprit lesion-related nonfatal MI, and unplanned coronary revascularization. Patients were followed for up to 4 years (median 3.3 years). RESULTS: The 4-year cumulative rate of the primary endpoint was 7.2%. In patient-level analysis, thin-cap fibroatheroma (TCFA) (adjusted HR: 3.05; 95% CI: 1.67-5.57) and minimal lumen area (MLA) <3.5 mm2 (adjusted HR: 3.71; 95% CI: 1.22-11.34) were independent predictors of the primary endpoint. In lesion-level analysis, nonculprit lesions responsible for subsequent events were not angiographically severe at baseline (mean diameter stenosis 43.8% ± 13.4%). TCFA (adjusted HR: 8.15; 95% CI: 3.67-18.07) and MLA <3.5 mm2 (adjusted HR: 4.33; 95% CI: 1.81-10.38) were predictive of events arising from each specific lesion. TCFAs with an MLA <3.5 mm2 carried a higher risk and were sufficient for identifying patients at risk for the composite of cardiac death and nonculprit lesion-related nonfatal MI. CONCLUSIONS: OCT imaging of angiographically nonobstructive territories in patients with acute MI can aid in identifying patients and lesions at increased risk for adverse cardiac events.

Dendrophthoe falcata (L.f.) Ettingsh. and Dendrophthoe pentandra (L.) Miq.: A review of traditional medical uses, phytochemistry, pharmacology, toxicity, and applications.

Dendrophthoe falcata (L.f.) Ettingsh. (DF) and Dendrophthoe pentandra (L.) Miq. (DP) have been traditionally used for the treatment of various ailments, such as cancer, ulcers, asthma, paralysis, skin diseases, tuberculosis, and menstrual troubles, in the ethnomedicinal systems of India and Indonesia. Currently, the chemical structures of 46 compounds have been elucidated from DF and DP, including flavonoids, triterpenes, tannins, steroids, open-chain aliphatics, benzyl derivates, and cyclic chain derivatives. In vitro assays have revealed their anti-tumor and anti-microbial activities. In vivo studies have unraveled their pharmacological properties against tumors, depression, fertility disorders, inflammatory responses, and so on. Additionally, their weak toxicity to rats and brine shrimp, as well as their promising applications for pharmaceutical preparations and combined medication, were also revealed. Herein, we not only recapitulated traditional medical uses, phytochemistry, pharmacology, toxicity, and applications of DF and DP but also discussed current research limitations and future perspectives, which are instructive for those interested in them and are committed to advancing parasitic plants to the Frontier of phytomedicine. We highlighted that DF and DP will become promising medical plants rather than being discarded as notorious pests, provided that more and deeper research is undertaken.

Predictors of Adverse Prognosis in Patients With Acute Coronary Syndrome Caused by Plaque Erosion With a Nonstent Strategy.

Background The EROSION (Effective Anti-Thrombotic Therapy Without Stenting: Intravascular Optical Coherence Tomography-Based Management in Plaque Erosion) study demonstrated that antithrombotic therapy without stenting was safe and feasible in selected patients with acute coronary syndrome caused by plaque erosion. However, the factors related to the prognosis of these patients are not clear. This study aimed to explore the predictors of an adverse prognosis of a nonstent strategy in a larger sample size. Methods and Results A total of 252 (55 patients were from the EROSION study) patients with acute coronary syndrome with plaque erosion who met the inclusion criteria of the EROSION study and completed clinical follow-up were enrolled. Patients were divided into 2 groups according to the occurrence of major adverse cardiovascular events (MACE), which were defined as the composite of cardiac death, recurrent myocardial infarction, ischemia-driven target lesion revascularization, rehospitalization because of unstable or progressive angina, major bleeding, and stroke. Among 232 patients with acute coronary syndrome included in the final analysis, 50 patients (21.6%) developed MACE at a median follow-up of 2.9 years. Compared with patients without MACE, patients with MACE were older and had a higher degree of percentage of area stenosis (72.2%±9.4% versus 64.2%±15.7%, P<0.001) and thrombus burden (24.4%±10.4% versus 20.4%±10.9%, P=0.010) at baseline. Multivariate Cox regression analysis confirmed that age, percentage of area stenosis, and thrombus burden were predictors of MACE. The best cutoff values of predictors were age ≥60 years, percentage of area stenosis ≥63.5%, and thrombus burden ≥18.5%, respectively, and when they were all present, the rate of MACE rose to 57.7%. Conclusions The nonstent treatment strategy of patients with acute coronary syndrome caused by plaque erosion was heterogeneous, and patients aged ≥60 years, percentage of area stenosis ≥63.5%, and thrombus burden ≥18.5% may predict a worse clinical outcome.

Clinical Outcomes of Different Calcified Culprit Plaques in Patients with Acute Coronary Syndrome.

Background: Previous studies have found that coronary artery calcification is closely associated with the occurrence of major adverse cardiac events (MACE). This study aimed to investigate the characteristics and clinical outcomes of different calcified plaques in patients with acute coronary syndrome (ACS) by using optical coherence tomography (OCT). Methods: 258 ACS patients with calcified culprit plaques who underwent OCT-guided stent implantation were enrolled. They were divided into three subtypes based on the calcified plaque morphology, including eruptive calcified nodules, calcified protrusion, and superficial calcific sheet. Results: Compared with superficial calcific sheet and calcified protrusion, eruptive calcified nodules had the greatest calcium burden and a higher rate of stent edge dissection (p < 0.001) and incomplete stent apposition (p < 0.001). In a median follow-up period of 2 years, 39 (15.1%) patients experienced MACE (a composite event of cardiac death, target-vessel myocardial infarction, ischemia-driven revascularization), with a significantly higher incidence in the eruptive calcified nodules group (32.1% vs. 10.1% vs. 13.0%, p = 0.001). A multivariate Cox analysis demonstrated that the eruptive calcified nodules (hazard ratio 3.14; 95% confidence interval, 1.64−6.02; p = 0.001) were an independent predictor of MACE. Conclusions: MACE occurred more frequently in ACS patients with eruptive calcified nodules, and the eruptive calcified nodules were an independent predictor of MACE.

Optical Coherence Tomographic Features of Pancoronary Plaques in Patients With Acute Myocardial Infarction Caused by Layered Plaque Rupture Versus Layered Plaque Erosion.

Atherosclerotic plaque instability could occur on the basis of healed plaque which has a layered appearance on optical coherence tomography. This study aimed to investigate pancoronary plaque features of layered plaque rupture (LPR) and layered plaque erosion (LPE) in patients with acute myocardial infarction. Among 388 patients with acute myocardial infarction who underwent preintervention optical coherence tomography imaging of three coronary arteries, 190 patients with layered culprit plaque (49.0%) were identified and further divided into 2 groups: LPR group and LPE group. Clinical characteristics, pancoronary plaque features and clinical outcomes were compared between the 2 groups. Patients with LPR were older, less often male and current smoker, and had a lower coronary flow grade than those with LPE. At the culprit lesion, LPR group had a higher prevalence of lipid plaque, thin-cap fibroatheroma (TCFA), macrophage, and microchannel, and presented with more severe lumen area stenosis than LPE group. At nonculprit lesions, LPR group had a higher prevalence of TCFA and had greater layered tissue thickness and area than LPE group. The ischemia-driven revascularization rate was higher in LPR group. Moreover, we found that TCFA, diameter stenosis >56.5%, and mean lipid arc >179.1° were predictors for layered culprit plaque. In conclusion, patients with LPR had more vulnerable plaque features at culprit and nonculprit lesions and had higher incidence of ischemia-driven revascularization than those with LPE. TCFA, diameter stenosis >56.5%, and mean lipid arc >179.1° were predictors of layered culprit plaque.

Culprit and Non-Culprit Plaque Characteristics With vs. Without a Healed Phenotype in Patients With Acute Myocardial Infarction Caused by Plaque Erosion　- A 3-Vessel OCT Study.

BACKGROUND: Plaque erosion can occur quietly without causing clinical symptoms, followed by a healing process resulting in healed plaque. This study aimed to assess culprit and non-culprit plaque characteristics of patients with acute myocardial infarction (AMI) caused by plaque erosion with vs. without healed phenotype at the culprit plaque using optical coherence tomography (OCT).Methods and Results: A total of 117 AMI patients caused by plaque erosion who underwent OCT imaging of 3 coronary arteries were included. Patients were divided into 2 groups based on presence or absence of a healed phenotype at the culprit site. Culprit and non-culprit plaque characteristics were compared between the 2 groups. A healed phenotype at the culprit lesion was identified in 47.9% of AMI patients caused by plaque erosion. Patients with a healed phenotype at the culprit site were more frequently with hyperlipidemia, and had a higher prevalence of macrophage infiltration, microchannels, cholesterol crystals, and calcification at the culprit lesion. Moreover, patients with a healed phenotype at the culprit site had more non-culprit plaques and more characteristics of plaque vulnerability at the non-culprit lesion. In addition, patients with a healed phenotype at the culprit site presented with more severe luminal stenosis at both the culprit and non-culprit lesion. CONCLUSIONS: A healed phenotype was identified in 47.9% of AMI patients caused by plaque erosion at the culprit site. A healed phenotype within eroded culprit plaque was associated with signs of pancoronary vulnerability and advanced atherosclerosis.

In vivo evidence of atherosclerotic plaque erosion and healing in patients with acute coronary syndrome using serial optical coherence tomography imaging.

BACKGROUND: The EROSION study (Effective Anti-Thrombotic Therapy Without Stenting: Intravascular Optical Coherence Tomography-Based Management in Plaque Erosion) allowed us to observe the healing process of coronary plaque erosion in vivo. The present study aimed to investigate the incidence of newly formed healed plaque and different baseline characteristics of acute coronary syndrome (ACS) patients caused by plaque erosion with or without newly formed healed plaque using optical coherence tomography (OCT). METHODS: A total of 137 ACS patients with culprit plaque erosion who underwent pre-intervention OCT imaging and received no stent implantation were enrolled. Patients were stratified according to the presence or absence of newly formed healed phenotype at 1-month (137 patients) or 1-year OCT follow-up (52 patients). Patient's baseline clinical, angiographic, OCT characteristics and outcomes were compared. RESULTS: There were 55.5% (76/137) of patients developed healed plaque at 1 month, and 69.2% (36/52) of patients developed healed plaque at 1 year. Patients with newly formed healed plaque had larger thrombus burden, and lower degree of area stenosis (AS%) at baseline than those without, and thrombus burden and AS% were predictors of plaque healing. The healing process was accompanied by the significant increase of AS% and incidence of microchannels, and greater inflammatory response. The outcomes appeared to be similar between the two groups. CONCLUSIONS: Newly formed healed plaque was found in more than half of ACS patients with plaque erosion without stenting. Patients with newly formed healed plaque had lower luminal stenosis and larger thrombus burden. During healing process, luminal stenosis increased gradually.

[Role of mimecan in development of atherosclerosis induced by increased blood pressure variability].

OBJECTIVE: To examine the changes of mimecan protein expression in development of atherosclerosis induced by sinoaortic denervation, and to explore the effects of mimecan knock down on the proliferation and migration of vascular smooth muscle cells.
 Methods: The animals were randomly divided into a sham group and a model group (n=8 in each group). The rat model of blood pressure variability was established by sinoaortic denervation, and the hemodynamic indexes were recorded 20 weeks after the surgery to confirm the success of the model. The thoracic aorta was excised and stained with immunohistochemistry to observe the pathological changes of smooth muscle tissues and the changes of mimecan expression. The mice vascular smooth muscle cells were isolated, and which were treated with mimecan siRNA to knock down the mimecan expression. The cell proliferation was observed by 5-ethynyl-2'-deoxyuridine (Edu) in corporation test and the changes of cell migration was observed by wound healing test.
 Results: Twenty weeks after sinoaortic denervation, the blood pressure variability in the model group was significantly increased compared with that in the sham group, suggesting the model was successfully established. In addition, the increased blood pressure variability in the model group promoted the proliferation and migration of the vascular smooth muscle cells in thoracic aorta, while the expression of mimecan protein was significantly decreased. In in vitro assays, the knock down of mimecan in mice vascular smooth muscle cells could promote the cell proliferation and migration.
 Conclusion: Mimecan plays a protective role in the development of sinoaortic denervation induced atherosclerosis through amechanism involving suppression of the proliferation and migration of vascular smooth muscle cells.

Interaction between interleukin­6 and angiotensin II receptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure.

The association between interleukin­6 (IL­6) and angiotensin II receptor 1 (AT1­R) in modulating the progression of heart failure (HF) remains to be fully elucidated. The aim of the present study was to investigate the mechanism of IL­6 and AT1­R in a model of HF induced by surgery. Male Sprague­Dawley rats were randomly divided into five groups, including sham surgery and vehicle groups. The animals were treated for 4 weeks via paraventricular nucleus infusion with either vehicle, losartan (LOS; 200 µg/day), IL­6 (1 µg/day) or LOS and IL­6 together (LOS+IL­6). The rats with HF had higher levels of IL­6, corticotropin­releasing hormone (CRH) and norepinephrine (NE), and a lower level of neuronal nitric oxide synthase (nNOS), compared with the rats in the sham surgery group. Treatment with LOS attenuated the decrease in nNOS and the increases in IL­6, CRH and NE; whereas treatment with IL­6 facilitated the lower expression of nNOS and higher expression levels of IL­6, CRH and NE. No differences in the expression levels of nNOS, CRH or NE were found between the LOS group and LOS+IL­6 group. The results of the study demonstrated that IL­6 contributed to the progression of HF via the AT1­R pathway.

A novel rat model of heart failure induced by high methionine diet showing evidence of association between hyperhomocysteinemia and activation of NF-kappaB.

Heart failure is one of the most serious diseases worldwide, and can be caused by many factors, among them hyperhomocysteinemia can increase the risk for development of heart failure. In this study, we treated rats with high methionine diet (HMD), which can be conversed to homocysteine in human body, to induce a novel model of heart failure. We proved the successful establishment of this model by echocardiography and pathological evaluation at the termination of treatment. Ejection fraction and fractional shortening were significantly deceased after HMD treatment, while left ventricular volume in systole was increased. HMD treatment caused hypertrophy of cardiomyocytes, disarrangement of myofibers, and infiltration of inflammatory cells, as well as abundant apoptotic cells appeared after HMD treatment. Plasmatic homocysteine level was elevated after HMD treatment. Furthermore, through electrophoretic mobility shift assay and chromatin immunoprecipitation, the activity of NF-κB in nuclear extract was also significantly elevated, showing evidence of positive relationship between hyperhomocysteinemia and activation of NF-κB in HMD-induced heart failure. The successful development and validation of this model have made it a new tool for translational medical research of metabolic disorders-related cardiovascular disease.

Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats.

OBJECTIVE: To explore the effect and mechanism of microRNA-208a (miR-208a) in the mitochondrial apoptosis of cardiomyocytes of neonatal rats. METHODS: The primary cultured cardiomyocytes of neonatal rats were added into the hypoxia incubator for the hypoxia induction. The overexpression system for miR-208a of cardiomyocytes of neonatal rats was built. The flow cytometry assay was employed to detect the incidence of apoptosis in the over-expressed miR-208a. The mitochondrial staining technique was used to detect the change in the mitochondrial morphology of over-expressed miR-208a. The bioinformatic analysis was chosen to analyze and predict the target gene of miR-208a. RESULTS: Firstly, the primary culture system of cardiomyocytes of neonatal rats was successfully built. The miR-208a was over-expressed in cardiomyocytes of neonatal rats by miR-208a Mimics. Results of flow cytometry assay showed that the over-expressed miR-208a could significantly reduce the incidence of apoptosis; while results of mitochondrial staining indicated the change in the mitochondrial morphology of over-expressed miR-208a and the mitochondrial fission process was inhibited. In conclusion, it was supposed that miR-208a could inhibit the activation of mitochondrial fission process to keep the cardiomyocytes from apoptosis. CONCLUSIONS: The over-expressed miR-208a can reduce the incidence of apoptosis in the cardiomyocytes of neonatal rats, significantly change the mitochondrial morphology and inhibit the mitochondrial fission process.

Diffuse triple-vessel coronary spasm as a cause of asystole and syncope.

Vasospasm plays an important role in the pathogenesis of ischemic heart disease, including unstable angina, myocardial infarction, and sudden death. Coronary artery spasm rarely involves different coronaries in the same time. Three-vessel spasm may be accompanied by ST-segment elevation, lethal arrhythmias, and syncope due to the wide extent of ischemia. In the present case, a patient with syncope secondary to documented diffuse vasospasm involving 3 major coronary arteries was reported. This case report indicated that in case of unexplained syncope, asystole secondary to coronary artery spasm should be considered as a possible cause.

Coronary Revascularization Improves QT Dispersion in Patients with Chronic Coronary Artery Total Occlusion.

As an important parameter of cardiac functions, QT interval is usually irregular in patients with chronic coronary artery total occlusion (CTO). We sought to determine the effect of coronary revascularization (CRV) on QT interval dispersion in patients with CTO. To this end, we used electrocardiogram of 12 leads to record changes in the QT interval dispersion in 22 patients with CTO treated with percutaneous coronary intervention (PCI) and 24 patients treated with coronary artery bypass grafting (CABG). Our data showed that QTd and QTcd diminished markedly (P < 0.01) after PCI or CABG. No significant difference was observed between the postoperative groups (P > 0.05) or between PCI and CABG groups. We concluded that CRV could diminish QTd and QTcd in patients with CTO with no distinguishable differences with PCI and CABG procedures. Therefore, CRV can revitalize the existing functional myocardium and resume the myocardial electrophysiological functions in patients with CTO.

Interaction between interleukin-1 beta and angiotensin II receptor 1 in hypothalamic paraventricular nucleus contributes to progression of heart failure.

The central mechanisms by which interleukin-1 beta (IL-1ß) and angiotension II receptor 1 (AT1-R) contribute to sympathoexcitation in heart failure (HF) are unclear. In this study, we determined whether an interaction between IL-1ß and AT1-R in the paraventricular nucleus (PVN) contributes to progression of HF. Rats were implanted with bilateral PVN cannulae and subjected to coronary artery ligation or sham surgery (Sham). Subsequently, animals were treated for 4 weeks through PVN infusion with either vehicle, losartan (LOS, 200 µg/day), IL-1ß (IL, 1 µg/day), or IL-1ß along with LOS (LOS+IL). HF rats had higher levels of corticotropin-releasing hormone (CRH), norepinephrine (NE), and glutamate (Glu); lower levels of gamma-aminobutyric acid (GABA); and more positive fra-like activity in PVN when compared with Sham rats. HF rats also had higher levels of NE, epinephrine (EPI), and IL-1ß in plasma. PVN infusion of LOS attenuated the decreases in GABA and the increases in CRH, NE, and Glu in the PVN of HF rats. IL-1ß could further increase the expression of CRH, NE, Glu, EPI, and IL-1ß and decrease GABA expression. Treatment with IL-1ß along with LOS could eliminate the effects of IL-1ß. These findings suggest that an interaction between AT1-R and IL-1ß in the PVN contributes to progression in HF.

Analysis of heart rate variability in masked hypertension.

To investigate heart rate variability (HRV) in patients with masked hypertension (MH), participants were classified based on clinic and 24-h ambulatory blood-pressure monitoring: essential hypertension (EH, n = 40; MH, n = 36) and normotension (NT, n = 48). The HRV parameters were observed using a 24-h Holter monitor. Compared with NT controls, the parameters of HRV (SDNN, SDANN, SDNN Index, RMSSD, HF) and parameters in EH and MH patients had significantly decreased. No statistically significant difference in the HRV parameters was found between the EH and MH groups. The changes in HRV parameters show cardiac autonomic nerve dysfunction in patients with MH.

Electrocardiogram for predicting cardiac functional recovery.

To investigate if the 12-lead resting electrocardiogram (ECG) is a predictor of left ventricular (LV) functional recovery after revascularization of chronic total coronary artery occlusions (CTO). Revascularization was performed in 58 CTO patients who had impaired regional wall motion. The 12-lead resting ECG was used to evaluate Q-wave, QT dispersion, and other parameters. Pre- and postoperative LV regional wall motions were evaluated by real-time three-dimensional echocardiography (RT-3DE). In patients with non-Q-wave, the wall motion score index (WMSI) was dropped from 1.56 ± 0.31 to 1.12 ± 0.21 (P < 0.05), while there was no significant changes (1.73 ± 0.12 and 1.59 ± 0.23, P > 0.05) for WMSI in patients with Q-wave. Preoperative non-Q-wave at baseline was predicted recovery with 88 % sensitivity and 68 % specificity. Positive predictive value for recovery was 67 % in patients with non-Q-wave. The presence of Q-wave can predict non-recovery of the regional wall motion with 68 % sensitivity and 88 % specificity. For CTO patients treated by revascularization, recovery can be predicted reliably through the analysis of pathological Q-wave on the 12-lead resting ECG.

Correlation of echocardiographic epicardial fat thickness with severity of coronary artery disease in patients with acute myocardial infarction.

The aim of this study was to test the hypotheses that epicardial adipose tissue (EAT) can be a marker of severe coronary artery disease in patients with acute myocardial infarction. Overall, 373 cases who underwent coronary angiography were classified into 2 groups by SYNTAX score: low-score and high-score group. EAT was measured by transthoracic echocardiography. Obtained data were compared using Pearson correlation analyses and univariate and multiple logistic regression analysis. The results showed that EAT in the high-score group was significantly greater than in the normal group (5.6 ± 1.1 vs. 4.1 ± 1.0 mm, P < 0.01). EAT had a positive correlation with SYNTAX score (r = 0.61, P < 0.01). Receiver operating characteristic (ROC) curve analyses showed that EAT could reliably discriminate patients with high SYNTAX score (≥ 33) [AUC: 0.86, 95% confidence interval (CI): 0.822-0.898, P < 0.01]. Multivariate regression analyses showed that EAT was an independent predictor for major in-hospital events. These data showed an association between EAT and SYNTAX score.

Mean platelet volume predicts left descending artery occlusion in patients with non-ST-elevation myocardial infarction.

Platelets play an important role in atherothrombosis. As the most common site plaque occurs, left anterior descending artery (LAD) infarct location always associate with poor prognosis. We sought to assess whether mean platelet volume (MPV) could predict LAD infarct location and short-term clinical outcome. In this study, 190 consecutive patients with non-ST-elevation myocardial infarction (NSTEMI) were enrolled. Clinical, electrocardiography and laboratory characteristics were measured. All patients underwent coronary angiography examination and had definite culprit vessel during hospitalization. The results showed that MPV was smaller in patients with a LAD infarct location than that of left circumflex artery or right coronary artery (9.0 ± 1.5 versus 9.8 ± 1.6, p<0.001). Multivariate analysis also showed that MPV was the only independent factor to predict LAD infarct location [Odds ratio (OR)=0.65, 95% confidence interval (CI) 0.53-0.80, p<0.0001] in patients with NSTEMI. B-type natriuretic peptide and electrocardiography were unreliable predictive factors to locate culprit vessel. Receiver operating characteristic curve analysis showed MPV (area under the curve: 0.65, 95% CI 0.56-0.74, p<0.01) could reliably discriminate those patients with NSTEMI who had a major in-hospital event. Multivariate regression analyses also showed that MPV (OR=1.46, 95% CI 1.15-1.86, p<0.01) were predictors of major in-hospital events. In conclusion, MPV was the only factor independently associated with LAD infarct location in patients with non-ST-elevation myocardial infarction.

Assessment of recanalization of chronic total occlusions on left ventricular function in patients with or without previous myocardial infarction by real-time three-dimensional echocardiography.

The changes of left ventricular ejection fraction (LVEF) were assessed after successful recanalization of chronic total occlusions (CTO) with or without previous myocardial infarction (MI) by real-time three-dimensional echocardiography (RT3DE). 32 patients with a successfully recanalyzed CTO were included in the present prospective study. The patients were divided into group 1 without previous MI and group 2 with previous MI in the territories of total occlusion vessel that was recanalized. In addition, there was a subgroup composed of 14 patients with collateral flow or retrograde flow in group 2. In all patients, LVEF was determined by RT3DE at baseline and after 6 weeks. In group 1, the evolution of LVEF increased significantly from 59.9 ± 7.2-67.5 ± 8.7% (P < 0.05). In group 2, the evolution of LVEF increased from 48.6 ± 6.1-50.1 ± 6.4%, however, it was without statistic significance (P > 0.05). The evolution of LVEF increased from 46.8 ± 7.1-53.0 ± 7.2% (P < 0.05) in the subgroup of group 2. Left ventricular function in patients with CTO can be feasibility and actually evaluated by RT3DE. The influence of recanalization of CTO on the improvement of left ventricular function was different between MI and non-MI patients. The left ventricular function did not improve in MI patients, but improved significantly in the patients having rich collateral circulation.