The Key Laboratory of Myocardial Ischemia

Harbin, China

The Key Laboratory of Myocardial Ischemia

Harbin, China
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Hu S.,Harbin Medical University | Hu S.,The Key Laboratory of Myocardial Ischemia | Zhu Y.,Harbin Medical University | Zhu Y.,The Key Laboratory of Myocardial Ischemia | And 24 more authors.
Journal of the American Heart Association | Year: 2017

Background-Plaque rupture and erosion are the 2 most common mechanisms for acute coronary syndromes. However, the outcome of these 2 distinct pathologies in patients with acute coronary syndromes has never been studied. Methods and Results-We retrospectively studied 141 patients with acute coronary syndromes who underwent optical coherence tomography (OCT) imaging of the culprit lesion prior to stenting from the Massachusetts General Hospital OCT Registry. Management (stent versus no stent), poststent OCT findings, and outcomes were compared. Among the 141 culprit lesions, rupture was found in 79 (56%) patients and erosion in 62 (44%). Stent implantation was performed in 77 (97.5%) patients with rupture versus 49 (79.0%) in those with erosion (P < 0.001). Immediately after percutaneous coronary intervention, OCT showed a higher incidence of malapposition (37.5% versus 7.3%, P < 0.001), thrombus (59.4% versus 14.6%, P < 0.001), and protrusion (93.8% versus 73.2%, P = 0.008) in the rupture group compared with the erosion group. Plaque rupture was associated with a higher incidence of no reflow or slow flow and distal embolization. Although cardiac event rates were comparable between the two groups at the 1-year follow-up, none of the erosion patients who were treated conservatively without stenting had adverse cardiac events. Conclusions-Unfavorable poststent OCT findings were more frequent in rupture patients compared with erosion patients. A subset of erosion patients who were treated conservatively without stenting remained free of adverse cardiac events for up to 1 year. © 2017 The Authors.

Jia H.,Harbin Medical University | Jia H.,The Key Laboratory of Myocardial Ischemia | Hu S.,Harbin Medical University | Hu S.,The Key Laboratory of Myocardial Ischemia | And 16 more authors.
Catheterization and Cardiovascular Interventions | Year: 2017

Objectives: To compare stent coverage and malapposition in patients with chronic total occlusion (CTO) lesions and non-CTO lesions (including lipid-rich plaque [LRP] and non-lipid-rich plaque [non-LRP]) after drug-eluting stent (DES) implantation by optical coherence tomography (OCT). Background: Different initial lesion characteristics may be related to heterogeneous vessel responses after DES implantation. However, the vessel response in patients with CTO and non-CTO lesions after stenting is unclear. Methods We retrospectively enrolled 64 patients with 68 target lesions. All of the patients underwent OCT imaging immediate after stenting and 6 months after stenting. LRP was defined as the plaque with lipid content in ≥2 quadrants. Non-LRP consisted of fibrous, fibrocalcific plaque, and lipid plaque with less than 2 quadrants lipid content. Results: The malapposition (3.0%, 2.6% vs. 0.6%, P = 0.022), tissue protrusion (15.0% vs. 11.0% vs. 6.4%, P < 0.001), and intrastent thrombus (3.8% vs. 2.4% vs. 1.1%, P = 0.012) were more frequent in the CTO and LRP groups. At 6-month follow-up, malapposition (5.0% vs. 1.0% and 0.4%, P = 0.002) and cross sections with uncovered struts (23.4% vs. 8.2% and 6.6%, P < 0.001) were most frequently observed in the CTO group. Although the incidence of stent thrombosis was non-significantly higher in the CTO group than the other two groups, no events were observed in patients with CTO. Conclusions: Patients with CTO lesions showed unfavorable responses to DES in the acute phase as well as at the 6-month follow-up, indicating the important pathological link between the original lesion morphology underneath the stents and heterogeneous artery healing. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.

Liu Q.,The Key Laboratory of Myocardial Ischemia | Liu Q.,Harbin Medical University | Du G.Q.,The Key Laboratory of Myocardial Ischemia | Du G.Q.,Harbin Medical University | And 14 more authors.
Journal of Translational Medicine | Year: 2015

Background: Skeletal myoblasts (SkMs) has provided a promising treatment for myocardial infarction (MI). Functioning as posttranscriptional regulators, microRNAs (miRNAs) play important roles in cardiac repairment and stem cell regulation. However, the correlation between miRNAs and their targeted genes in SkM cell therapy for MI was not fully understood. Methods: We explored the cardioprotection by SkMs in infracted rats and determined cardiac functions at 4weeks. In addition, we compared the expression profiles of miRNAs and mRNAs in post-MI rats with or without SkM cell therapy using microarray. The concordance between miRNA expression and mRNA levels of potential target genes was confirmed by quantitative real-time PCR. Results: Quantitative echocardiography and histology showed improved cardiac function, attenuated heart infarcted area and inhibited cardiomyocyte apoptosis in the SkM group, compared with MI group. We identified that 160 miRNAs were differentially expressed in MI group as compared to the control group and 78 miRNAs were differentially expressed in the SkM treated group as compared to the untreated post-MI. We focused on a novel set of apoptosis-associated miRNAs and their target genes, among which 4 miRNAs (miR-30a-5p, miR-30c-5p, miR-145-5p, miR-140-3p), except one (miR-143-3p), were downregulated in the SkM treated group as compared to the untreated group. Furthermore, we found seven genes including Angptl4, Dpep1, Egr1, Eif5a, Tsc22d3, Irs2 and Cebpb that showed a linear correlation with which miRNAs. Conclusions: The downregulation of apoptosis-regulatory miRNAs and in turn upregulation of target genes may partially account for rescue effect of SKM therapy for MI. © 2015 Liu et al.

Li N.,Harbin Medical University | Li N.,The Key Laboratory of Myocardial Ischemia | Zhang S.,Harbin Medical University | Zhang S.,The Key Laboratory of Myocardial Ischemia | And 5 more authors.
Heart Lung and Circulation | Year: 2012

Since its invention, optical coherence tomography (OCT) has been primarily used for the diagnosis of coronary artery disease. A few feasibility studies of OCT to visualise the pulmonary arteries were reported. However, OCT findings in the pulmonary arteries have not been validated using histology as the gold standard. To validate OCT findings for pulmonary arterial imaging, we selected 27 pulmonary arteries from 11 cadavers (6 males, 5 females, mean age 39.6 ± 21.3 years). Comparison of OCT images and histology was performed. Each histological sample was examined using three types of stains, and the quantified results were analysed by statistics. In conclusion, there was a strong correlation between histology and OCT measurements of the pulmonary arterial wall thickness, the pulmonary arterial wall has a single-layered structure with an average thickness of 0.162. mm. We propose that OCT is probably a useful tool of diagnosing pulmonary artery hypertension and may provide a means to study the pulmonary remodelling process. © 2012.

PubMed | Harbin Medical University, The Key Laboratory of Myocardial Ischemia and VA Boston Healthcare System
Type: | Journal: Blood | Year: 2017

Despite routine treatment of unselected acute promyelocytic leukemia (APL) with all-trans-retinoic acid (ATRA), early death due to hemorrhage remains unacceptably common and the mechanism underlying this complication remains elusive. We have recently demonstrated that APL cells undergo a novel cell death program, termed ETosis, which involves release of extracellular chromatin. However, the role of promyelocytic extracellular chromatin in APL-associated coagulation remains unclear. Our objectives were to identify the novel role of ATRA-promoted extracellular chromatin in inducing a hypercoagulable and hyperfibrinolytic state in APL and to evaluate its interaction with fibrin and endothelial cells (ECs). Results from a series of coagulation assays have shown that promyelocytic extracellular chromatin increases thrombin and plasmin generation, causes a shortening of plasma clotting time of APL cells, and increases fibrin formation. DNase I but not anti-tissue factor antibody could inhibit these effects. Immunofluorescence staining showed that promyelocytic extracellular chromatin and phosphatidylserine on APL cells provide platforms for fibrin deposition and render clots more resistant to fibrinolysis. Additionally, co-incubation assays revealed that promyelocytic extracellular chromatin is cytotoxic to ECs, converting them to a procoagulant phenotype. This cytotoxity was blocked by DNase I by 20% or activated protein C (APC) by 31%. Our current results thus delineate the pathogenic role of promyelocytic extracellular chromatin in APL coagulopathy. Furthermore, the remaining coagulation disturbance in high-risk APL patients after ATRA administration may be treatable by intrinsic pathway inhibition via accelerating extracellular chromatin degradation.

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