Analysis of coronary intramural hematomas after coronary artery stent implantation / 中国介入心脏病学杂志

Objective To analyze the rates of occurrence,presentations and treatment of coronary intramural hematomas(IMH)after coronary artery stent implantation.Methods Retrospective analysis was carried out in non-chronic total occlusion patients who developed coronary intramural hematomas after coronary artery stent implantation between January 1,2011 to December 31,2016.Statistical analysis was made in the fields clinical data,coronary angiography features,treatment provided,and postoperative follow-up date of the patients.Results Among the 26 IMH patients,the male gender(15/26,57.7％)and existiing hypertension(17/26,65.4％)were more common risk factors for IMH after coronary artery stent implantation.Fourteen patients developed coronary dissection.The coronary intramural hematomas presented as new non-spasm and non-thrombus coronary stenosis.The coronary intramural hematomas were found to have involved the distal segment to the stents in 16 patients.Two patients received balloon dilation,five patients had stents implantation after balloon dilation,13 patients(50.0％)were treated with direct stent implantation and the other 6 patients did not have further intervention.The follow up period after hospital discharge was(2.39±1.68)years.No adverse cardiovascular event occurred.Five patients received follow-up angiography examination.Two patients and another one patient were found to have coronary intramural hematomas fully resolved at three months and one year with coronary angiographic follow up,respectively.Two patients had IMH on angiography at 1 year follow up.Conclusions Coronary intramural hematomas after coronary artery stent implantation often involved the distal segment to the stent in hypertensive patients presenting as new non-spasm and non-thrombus coronary stenosis.Patients at low risk of acute coronary occlusion could receive conservative treatment.Patients with extentsive length of intramural hematomas should consider stent implantation for treatment.

Establishment of a Novel Mouse Model of Coronary Microembolization / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Exenatide Reduces Tumor Necrosis Factor-α-induced Apoptosis in Cardiomyocytes by Alleviating Mitochondrial Dysfunction / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Effects of intracoronary administration of nitroglycerin and verapamil for treatment of coronary slow flow phenomenon / 中华心血管病杂志

<p><b>OBJECTIVE</b>To assess the efficacy of intracoronary nitroglycerin and verapamil for patients with the coronary slow flow phenomenon (CSFP).</p><p><b>METHODS</b>Sixty-four patients with CSFP without stenotic lesions during diagnostic coronary angiography were enrolled and divided into the nitroglycerin group (n = 35) and verapamil group (n = 29), 29 patients with normal coronary flow served as normal control. CSFP was defined when 4 or more heart beats were needed for contrast media to opacify the distal vasculature. Intracoronary injection of 100 - 400 microg nitroglycerin or verapamil through the diagnostic catheter was applied to patients with CSFP to improve coronary flow. The coronary blood flow was evaluated by thrombolysis in myocardial infarction (TIMI) frame count (TFC) method.</p><p><b>RESULTS</b>Clinical characteristics were similar among the three groups. The basic TFCs of left anterior descending artery (LAD), left circumflex artery (LCX) and right coronary artery (RCA) were 78.3 +/- 19.4, 57.2 +/- 14.6, 56.9 +/- 12.5 in the verapamil group, and were 70.8 +/- 21.7, 55.3 +/- 12.5, 51.1 +/- 15.4 in the nitroglycerin group, respectively, which were significantly higher than those in the normal controls (LAD 29.2 +/- 4.4, LCX 23.1 +/- 3.5 and RCA 19.7 +/- 1.8, respectively). After the administration of drugs, the TFCs of LAD, LCX and RCA were 42.3 +/- 8.9, 36.7 +/- 6.8, 30.3 +/- 5.9 respectively (all P < 0.01 vs. baseline) in the nitroglycerin group and 37.7 +/- 9.3, 31.5 +/- 11.3, 24.6 +/- 4.4 respectively (all P < 0.01 vs. baseline) in the verapamil group. The TFCs after drug administration in both therapy groups were significantly higher than that in normal controls (all P < 0.05). The TFCs decrease in the verapamil group were more significant than that in the nitroglycerin group (all P < 0.05).</p><p><b>CONCLUSION</b>Intracoronary administration of verapamil could result in more coronary flow improvement in patients with CSFP than nitroglycerin, although the post therapy coronary flow was still slower than normal.</p>

Acute hyperenhancement on delayed contrast-enhanced magnetic resonance imaging is the characteristic sign after coronary microembolization / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Detection of coronary microembolization is of clinical importance for patient management and prediction of long-term outcome. However, there are few studies of the changes of magnetic resonance imaging after coronary microembolization. This study was designed to investigate the imaging of the left ventricle using delayed contrast enhanced magnetic resonance imaging as well as the left ventricular ejection fraction after coronary microembolization in animal models.</p><p><b>METHODS</b>Eight miniswine, of either sex (body weight 21-25 kg), were used to make the coronary microembolization model. After coronary angiography, a 2.8F infusion catheter was placed in the left anterior descending artery with the tip located between the second and third diagonal branches. Microspheres with the diameter of 42 microm and mean dosage of 1.2 x 10(5) were selectively infused into the left anterior descending artery. First pass and stressed first pass perfusion scan were performed after cine images were acquired. Then a second bolus of 0.15 mmol/kg gadolinium DTPA was given at a rate of 2 ml/s. Ten minutes later, delayed contrast enhanced magnetic resonance images of the left ventricular wall were evaluated. Serum changes of tumor necrosis factor alpha (TNF-alpha) were evaluated by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>Hypoenhancement was not observed at first pass perfusion at the anterior wall of the left ventricle. Hyperenhancements of the anterior-septal and anterior wall of the left ventricle was in evidence on delayed enhancement images 6 hours after microembolization and disappeared one week later. The characteristic change of coronary microembolization on delayed contrast enhanced magnetic imaging was non-enhanced regions within the hyperenhancement zone. Left ventricular ejection fraction measured by magnetic resonance imaging decreased significantly from 0.451 +/- 0.063 at baseline to 0.362 +/- 0.070 at the sixth hour (P < 0.01), and recovered to 0.431 +/- 0.053 one week later (P < 0.01 vs 6th hour). Compared with baseline values, the left ventricular end systolic volume enlarged significantly at 6th hour and at one week after microembolization (P < 0.05 and P < 0.01 respectively). Serum TNF-alpha increased significantly at 6th hour (22.62 +/- 6.96) pg/ml compared with baseline (16.83 +/- 3.45) pg/ml (P < 0.05) and it further increased to (27.44 +/- 3.97) pg/ml at one week after coronary microembolization and was significantly higher than that at baseline (P < 0.01).</p><p><b>CONCLUSIONS</b>On delayed contrast enhanced magnetic resonance imaging, hyperenhancement of the anterior-septal and anterior wall of the left ventricle show at 6th hour but not at one week after coronary microembolization. This might represent the characteristic imaging after coronary microembolization. The left ventricular ejection fraction decreased at 6th hour and recovered one week later after coronary microembolization. Although impairment of left ventricular function could be recovered at 1 week after coronary microembolization, the left ventricular remodeling process still continued in concert with continuously elevation of serum TNF-alpha.</p>