-
[show abstract]
[hide abstract]
ABSTRACT: BACKGROUND: Previously developed techniques for pacemaker lead introduction usually require some form of image guidance to facilitate the axillary vein puncture process. The existing blind vein puncture methods have not gained widespread acceptance. We aimed to investigate whether our blind vein puncture approach is effective and safe. METHODS: We compared the patient characteristics and clinical outcomes of 600 consecutive patients who underwent different blind axillary vein puncture procedures. In group I, a steep needle puncture method was used, whereas in group II a shallow needle puncture technique was used. RESULTS: The shallow needle puncture method was associated with a higher success rate than the steep needle puncture method (94% vs 54%, P < 0.00001). The shallow needle puncture method was also associated with a much shorter puncture and lead insertion time (7 ± 2 minutes vs 10 ± 3 minutes, P = 0.02). CONCLUSION: Our shallow needle puncture technique does not require any extra equipment. In addition, this method is effective and safe and may be used as the initial attempt for venous access during pacemaker implantation.
Pacing and Clinical Electrophysiology 05/2013; · 1.35 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: As reported in the literature, the worldwide 5-year overall survival rate for patients with gastric cancer receiving surgical treatment in the progressive stage is less than 25%. Therefore, there is an urgent need for the development of novel therapeutic strategies. Our preliminary studies demonstrated that proliferin-related protein (PRP) inhibits the proliferation of TM3 Leydig testicular cells. To evaluate whether PRP has antitumor effects in vitro and in vivo, we stably expressed PRP in SGC-7901 gastric carcinoma cells. PRP inhibited the proliferation and cell cycle progression of SCG-7901 cells, as determined by cell growth and cell cycle assays. Transwell experiments demonstrated that PRP inhibited the cell migration and invasion of SCG-7901 cells. Western blotting demonstrated that PRP-overexpressing cells had upregulated matrix metalloproteinase 9 (MMP-9) and downregulated tissue inhibitor of metalloproteinases-1 (TIMP-1). In a xenograft tumor formation assay using nude mice, tumors formed by PRP-overexpressing cells had significantly lower weights than those formed by control cells, and the tumor inhibitory rate reached 71.9%. We demonstrated for the first time that PRP inhibits gastric carcinoma cell proliferation, motility, and tumorigenicity in vivo, suggesting that PRP may become an important target for the development of gastric cancer gene therapy.
Oncology Reports 04/2013; · 1.84 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: BACKGROUND: Although left ventricular pacing (LVP) leads to a greater acute hemodynamic response than does biventricular pacing (BVP), the long-term effects are diverse. We aimed to assess the efficacy of LVP and BVP in patients undergoing cardiac resynchronization therapy and determine which patients would benefit more from LVP or BVP. METHODS: Randomized controlled trials that compared left and biventricular pacing were retrieved from MEDLINE and analyzed for changes in cardiac function and dimensions, cardiac resynchronization therapy response, and electromechanical effects. RESULTS: A total of 811 patients were included from 9 trials. After a mean follow-up, a shorter QRS duration (-40.92 milliseconds; 95% confidence interval [CI], -64.50 to -17.34; P = 0.0007), and improved left ventricular dimensions were observed in the BVP group compared with the LVP group. Moreover, the BVP group had a longer 6-minute hall walk (6MHW) test (37.19 m; 95% CI, 4.72 to 69.67; P = 0.02). CONCLUSION: Our results indicate that BVP results in a better electromechanical effect and leads to a better 6MHW test. For all other test criteria, LVP showed a benefit equal to that of BVP. Thus, there is currently insufficient evidence to advocate for LV-only pacing.
The Canadian journal of cardiology 02/2013; · 3.36 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: OBJECTIVES: We used virtual histology intravascular ultrasound (VH-IVUS) to investigate plaque composition of chronic total occlusions (CTO). BACKGROUND: There are limited data on the composition of CTOs, especially in vivo. METHODS: VH-IVUS was performed in 50 CTO lesions (49 patients) after guidewire crossing or pre-dilation using a 1.5-2 mm balloon. Plaque composition in the proximal reference, distal reference, and CTO segment (subsequently divided into proximal, middle, and distal subsegments) was analyzed and reported as median and interquartile range. VH-IVUS phenotype was also assessed. The definition of a fibroatheroma was >10% confluent necrotic core (NC) in more than three consecutive frames. RESULTS: Overall, the maximum NC within the CTO [35.5% (28.7, 44.3%)] was similar to the proximal reference [35.6% (24.1, 42.1%)] and greater than the distal reference [31.5% (22.6, 35.2%), P < 0.01]. There was no difference in maximum NC observed among proximal [31.4% (25.2, 10.4%)], middle [31.0% (23.3, 38.3%)], and distal CTO subsegments [30.4% (22.0, 39.5%)]. Overall, 42/50 CTOs contained a VH-fibroathroma; and 8/50 did not. CTOs containing a VH-fibroatheroma had more NC and dense calcium while CTOs not containing a fibroatheroma had more fibrotic and fibrofatty plaque. Importantly, 60.5% of VH-fibroatheroma-containing CTOs had a thin-cap fibroatheroma (NC abutted to the lumen) in the proximal reference. CONCLUSIONS: Using VH-IVUS, CTO morphology can be divided into two patterns: (1) CTO with VH-fibroatheroma or (2) CTO without VH-fibroatheroma. This suggests two mechanisms of CTO formation-the majority evolving from acute coronary syndrome and thrombosis and the minority from atherosclerosis progression. © 2012 Wiley Periodicals, Inc.
Catheterization and Cardiovascular Interventions 03/2012; · 2.29 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: AimsEmerging evidence indicates that nuclear receptors play a critical regulatory role in cardiovascular physiology/pathology. Recently, farnesoid-X-receptor (FXR), a member of the metabolic nuclear receptor superfamily, has been demonstrated to be expressed in vascular cells, with important roles in vascular physiology/pathology. However, the potential cardiac function of FXR remains unclear. We investigated the cardiac expression and biological function of FXR.Methods and resultsFarnesoid-X-receptor was detected in both isolated neonatal rat cardiac myocytes and fibroblasts. Natural and synthetic FXR agonists upregulated cardiac FXR expression, stimulated myocyte apoptosis, and reduced myocyte viability dose- and time-dependently. Mechanistic studies demonstrated that FXR agonists disrupted mitochondria, characterized by mitochondrial permeability transition pores activation, mitochondrial potential dissipation, cytochrome c release, and both caspase-9 and -3 activation. Such mitochondrial apoptotic responses were abolished by siRNA-mediated silencing of endogenous FXR or pharmacological inhibition of mitochondrial death signalling. Furthermore, low levels of FXR were detected in the adult mouse heart, with significant (∼2.0-fold) upregulation after myocardial ischaemia/reperfusion (MI/R). Pharmacological inhibition or genetic ablation of FXR significantly reduced myocardial apoptosis by 29.0-53.4%, decreased infarct size by 23.4-49.7%, and improved cardiac function in ischaemic/reperfused myocardium.ConclusionThese results demonstrate that nuclear receptor FXR acts as a novel functional receptor in cardiac tissue, regulates apoptosis in cardiomyocytes, and contributes to MI/R injury.
European Heart Journal 02/2012; · 10.48 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Numerous studies have demonstrated that Bisphenol A (BPA) can cause reproductive toxicity. Ginseng has wide range of pharmacological actions and, more importantly, has proven its worth with respect to reproductive function in several reports. We have suggested that ginsenosides, the main active components of ginseng, may protect against BPA-induced cell damage. Therefore, an in vitro culture model of 15P-1 Sertoli cells was employed to investigate whether ginsenosides have protective effects on BPA-stimulated 15P-1 Sertoli cells. The results revealed that ginsenosides (75 μg/ml) significantly inhibited BPA-induced decreases in cell viability and increases in apoptosis. Immunofluorescence staining showed that BPA exposure-induced collapse of vimentin intermediate filaments was prevented by the application of ginsenosides. Ginsenosides also inhibited extracellular signal-regulated kinase (ERK1/2) phosphorylation and BPA-induced alterations of Bcl-2 and Bax protein expression in 15P-1 Sertoli cells. Furthermore, the alterations of T-AOC, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione and malondialdehyde levels in BPA-stimulated cells were partially prevented with pre-treatment with ginsenosides. Taken together, these results suggest that ginsenosides have protective effects against BPA-induced cell damage and that these effects are mediated by preventing ERK1/2 phosphorylation and through the enhancement of cellular antioxidant capacity. Ginsenosides may therefore be beneficial in the prevention of environmental BPA-induced, reproduction-related toxicity.
Basic & Clinical Pharmacology & Toxicology 01/2012; 111(1):42-9. · 2.18 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To identify the common inhibition types, the putative decision system is unsatisfactory. In a new decision system, Michaelis-Menten constants and maximal reaction rates were plotted versus inhibitor concentrations for deriving K(ik) and K(iv) as the inhibition constants, respectively; their difference was quantified as the ratio of the larger one to the smaller one. Such ratios below 2.0 suggested uncompetitive inhibitors, over 5.0 suggested noncompetitive or competitive inhibitors, and from 2.0 to 5.0 suggested mixed inhibitors. By the new decision system, (i) the simulation recovery of uncompetitive inhibitors under CVs of 2% or 5% was improved by four times, but that of competitive or noncompetitive inhibitors was improved slightly; (ii) the recovery of L-phenylalanine as an uncompetitive inhibitor of intestinal alkaline phosphatase reached 38%, while the putative decision system lost all; the recovery of xanthine as a competitive inhibitor of uricase was improved slightly. Therefore, the new decision system was better.
Journal of Enzyme Inhibition and Medicinal Chemistry 01/2012; · 1.62 Impact Factor
-
Ling-hong Shen,
Fang Wan,
Long Shen,
Song Ding,
Xin-rong Gong,
Zhi-qing Qiao,
Yong-ping Du,
Wei Song,
Jie-yan Shen,
Shu-xuan Jin, Jun Pu,
Tian-bao Yao,
Li-sheng Jiang,
Wei-zhen Li,
Guo-wei Zhou,
Shao-wen Liu,
Ya-ling Han,
Ben He
[show abstract]
[hide abstract]
ABSTRACT: Most patients with acute ST-elevation myocardial infarction (STEMI) cannot receive timely primary percutaneous coronary intervention (PCI) because of lack of facilities or delays in patient transfer or catheterization team mobilization. In these patients, early routine post-thrombolysis PCI might be a reasonable, useful strategy. This study investigated feasibility and safety of early PCI after successful half-dose alteplase reperfusion in a Chinese population. Patients with STEMI received half-dose alteplase if expected time delay to PCI was ≥90 min. Patients who reached clinical criteria of successful thrombolysis reperfusion were recommended to undergo diagnostic angiography within 3-24 h after thrombolysis. Patients with residual stenosis ≥70% in the infarct-related artery underwent PCI, regardless of flow or patency status. Epicardial arterial flow was assessed using thrombolysis in myocardial infarction (TIMI) flow grade and TIMI frame count (CTFC). Myocardial perfusion was assessed using myocardial blush grade (MBG) and TIMI myocardial perfusion frame count (TMPFC). Forty-nine patients were enrolled and underwent diagnostic angiography 3-11.3 h (median 6.5 h) after thrombolysis. Forty-six patients underwent PCI. No procedure-related complications occurred, except two patients who had no reflow after PCI. Twenty-two (47.8%) patients had TIMI grade 3 flow before PCI and 33 (71.7%) after PCI. CTFC was significantly improved after PCI (48.5 ± 32.1 vs. 37.9 ± 25.6, P = 0.01). MBG and TMPFC exhibited a similar improving trend after PCI, and the best myocardial perfusion tended to be achieved 3-12 h after lysis. During the 30-day follow-up, there were two deaths. The composite end point of death, cardiogenic shock, heart failure, reinfarction, and recurrent ischemia occurred in four patients. TIMI minor bleeding occurred in four patients. No TIMI major bleeding and stroke occurred. Early routine PCI after half-dose alteplase thrombolysis in Chinese population appears feasible. A larger clinical trial should be designed to further elucidate its efficacy and safety. Early PCI after thrombolysis in STEMI: The EARLY-PCI pilot feasibility study, ChiCTR-TNC-11001363.
Journal of Thrombosis and Thrombolysis 11/2011; 33(1):101-8. · 1.48 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Macrophages crosstalk with oxidized low-density lipoprotein (oxLDL), play a critical role in the initiation, progression, and subsequently stability of atherosclerotic plaques. Statins, inhibitors of HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, reduce the expression of inflammatory proteins in addition to their lipid-lowering action. However, the effect and detailed anti-inflammation mechanisms of statins in macrophages induced by oxLDL remain unclearly. In the present study, we investigated the effect of atorvastatin on inflammatory response upon oxLDL stimulation in murine macrophages and analyzed the underlying mechanisms. Tumor necrosis factor (TNF)α and monocyte chemoattractant protein-1 (MCP-1) mRNA levels were assayed by real-time PCR. The expression of cyclooxygenases-2 (COX-2) was detected by real-time PCR and Western blotting. While mitogen-activated protein kinase (MAPK) phosphorylation and IκBα degradation were determined by Western blotting. Our results showed that exposure of RAW264.7 cells to oxLDL, substantially changed the morphology of the cells and increased TNFα and MCP-1 secretion. While pretreatment with atorvastatin resulted in a significant inhibition of oxLDL-induced morphological alteration and inflammatory cytokines expression in a dose-dependent fashion. Further investigation of the molecular mechanism revealed that oxLDL upregulated the transcription and protein expression of COX-2 in a time-dependent manner. Whereas, pretreatment with atorvastatin suppressed COX-2 expression, MAPK activation and IκBα degradation. Thus, we conclude that the anti-inflammatory effect of atorvastatin is mediated through the inhibition of proinflammatory COX-2. Furthermore, suppression of ERK phosphorylation and IκBα degradation is involved in this regulation. Our findings provide a novel evidence that statins suppress inflammatory response, exert its anti-atherogenic actions via against inflammation beyond cholesterol-lowing effect.
Journal of Cellular Biochemistry 09/2011; 113(2):611-8. · 2.87 Impact Factor
-
International journal of cardiology 09/2011; 153(1):87-8. · 7.08 Impact Factor
-
Jun Pu,
Pei-ren Shan,
Song Ding,
Zhi-qin Qiao,
Li-sheng Jiang,
Wei Song,
Yong-ping DU,
Jie-yan Shen,
Lin-hong Shen,
Shu-xuan Jin,
Ben He
[show abstract]
[hide abstract]
ABSTRACT: Myocardial tissue-level perfusion failure is associated with adverse outcomes following ST-elevation myocardial infarction (STEMI) despite successful epicardial recanalization. We have developed a new quantitative index-thrombolysis in myocardial infarction (TIMI) myocardial perfusion frame count (TMPFC)--for assessing myocardial tissue level perfusion. However, factors affecting this novel index of myocardial perfusion are currently unknown.
A total of 255 consecutive STEMI patients undergoing primary angioplasty were enrolled. Myocardial tissue level perfusion was assessed by TMPFC, which measures the filling and clearance of contrast in the myocardium using cine-angiographic frame counting. We differentiate three groups with two cut off values for TMPFC: a TMPFC of 90 frames was the upper boundary of the 95% confidence interval (CI) for the TMPFC observed in normal arteries, and a TMPFC of 130 was the 75th percentile of TMPFC.
STEMI patients with TMPFC > 130 frames (68 patients, 26.7%) had higher clinical and angiographic risk factor profiles as well as a higher 30-day MACE rate compared with those with TMPFC ≤ 90 frames and those with TMPFC > 90 and ≤ 130 frames. Multivariable analysis identified that the independent predictors of TMPFC > 130 frames were age ≥ 75 years (OR 2.08, 95%CI 1.21 to 3.58, P = 0.007), diabetes (OR 1.37, 95%CI 1.01 to 1.86, P = 0.042), Killip class ≥ 2 (OR 1.52, 95%CI 1.05 to 2.21, P = 0.027), and prolonged pain-to-balloon time (OR 1.73, 95%CI 1.07 to 2.79, P = 0.013). TMPFC > 130 frames was identified as the strongest independent predictor of 30-day major adverse cardiac event (MACE) (OR 2.77, 95%CI 1.21 to 6.31, P = 0.008), along with age ≥ 75 years (OR 2.19, 95%CI 1.11 to 4.33, P = 0.016), female gender (OR 1.67, 95%CI 1.03 to 2.70, P = 0.038), and Killip class ≥ 2 (OR 1.83, 95%CI 1.07 to 3.14, P = 0.021).
STEMI patients with poor myocardial perfusion assessed by TMPFC had higher risk factor profiles. Advanced age, diabetes, higher Killip class, and longer ischemia time were independent predictors of impaired TMPFC after primary percutaneous coronary intervention. These results emphasize that particular attention should be paid on myocardial microvascular reperfusion in STEMI patients with these risk factors.
Chinese medical journal 03/2011; 124(6):873-8. · 0.86 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Pulmonary arterial hypertension (PAH) is characterized by increasing pulmonary pressure, right ventricular failure, and death. The typical pathological changes include medial hypertrophy, intimal fibrosis and in situ thrombosis. Serotonin (5-HT) and other factors contribute to the development of pathologic lesions. Aspirin (ASA), a platelet aggregation inhibitor, inhibits 5-HT release from platelets. The aim of this study was to determine the efficacy of ASA in preventing or attenuating PAH. Sprague-Dawley rats injected with monocrotaline (MCT) developed severe PAH within 31 days. One hundred forty rats were randomized to receive either vehicle or ASA (0.5, 1, 2, or 4 mg/kg/day). The pre-ASA group was treated with ASA (1 mg/kg/day) for 30 days before the MCT injection. Thirty-one days after the injection (day 61 for the pre-ASA group), pulmonary arterial pressure (PAP), right ventricular hypertrophy and pulmonary arteriole thickness were measured. Plasma 5-HT was measured by high-performance liquid chromatography. Aspirin suppressed PAH and increased the survival rate compared with the control group (84 vs. 60%, P < 0.05). Aspirin treatment also reduced right ventricular hypertrophy and pulmonary arteriole proliferation in ASA-treated PAH model. In addition, plasma 5-HT was decreased in our ASA-treated PAH model. The degree of 5-HT reduction was associated with systolic PAP, right ventricular hypertrophy and wall thickness of pulmonary arterioles in rats. These results showed that ASA treatment effectively attenuated MCT-induced pulmonary hypertension, right ventricular hypertrophy, and occlusion of the pulmonary arteries. The effects of ASA was associated with a reduction of 5-HT.
Cell biochemistry and biophysics 02/2011; 61(1):23-31. · 3.34 Impact Factor
-
Catheterization and Cardiovascular Interventions 12/2010; 76(7):1073-5. · 2.29 Impact Factor
-
Jun Pu,
Peiren Shan,
Song Ding,
Zhiqin Qiao,
Lisheng Jiang,
Wei Song,
Yongping Du,
Jieyan Shen,
Linhong Shen,
Shuxuan Jin,
Ben He
[show abstract]
[hide abstract]
ABSTRACT: The impact of gender on clinical course after ST-elevation myocardial infarction (STEMI) is not fully understood. We prospectively investigated whether there are gender-related differences in epicardial and myocardial tissue-level perfusion, both of which represent important prognostic determinants in STEMI patients undergoing primary percutaneous coronary intervention (PPCI).
A total of 594 consecutive non-selected STEMI patients undergoing PPCI were prospectively enrolled. Primary end-point of the study was post-procedural epicardial and myocardial perfusion. Secondary end-points were the 30-day and 6-month composite occurrence of major adverse cardiac events (MACE).
Women with STEMI had higher risk factor profiles than men. Although PPCI achieved equal rates of successful epicardial reperfusion, women tended to have impaired microvascular reperfusion as reflected by lower rates of normal TIMI myocardial perfusion grade (P=0.007) and complete ST-segment resolution (P=0.079). After adjustment for the risk profiles, multivariable analysis showed that gender itself was not an independent predictor of impaired microvascular reperfusion. Both female gender and impaired myocardial reperfusion were independent predictors of 30-day MACE, whereas gender lost its prognostic significance for 6-month MACE. Multivariable analysis restricted to female patients identified incomplete ST-segment resolution as the strongest determinant of 30-day MACE.
The differences in microvascular reperfusion after PPCI between women and men are attributed to higher risk profiles in women. Both female gender and impaired myocardial reperfusion were independent predictors of 30-day outcomes after PPCI, emphasizing the importance of successful microvascular reperfusion in the women with STEMI.
Atherosclerosis 11/2010; 215(1):203-8. · 3.79 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Oxidized low-density lipoprotein (oxLDL) cross-talks with macrophages, and both play a crucial role in the initiation and progression of atherosclerosis. Orphan nuclear receptor Nur77 is potently induced in macrophages by diverse stimuli, suggesting that it may be a key regulator of inflammation in vascular cells. The detailed mechanism of Nur77 activation and subsequent function in macrophages induced by oxLDL remains unclearly. In this study, we demonstrated that Nur77 is upregulated in a dose and time-dependent fashion by oxLDL stimulation in murine macrophages, as detected by real-time PCR and Western blotting. OxLDL activated the phosphorylation ERK1/2 and p38 MAPK, inhibition of p38 MAPK but not ERK1/2 attenuated Nur77 expression. Importantly, overexpression of Nur77 suppressed oxLDL-induced proinflammatory cytokines and chemokines secretion including tumor necrosis factor (TNF)alpha and monocyte chemoattractant protein-1(MCP-1). While knockdown Nur77 expression by specific small interfering RNA (siRNA) resulted in the enhancement of the secretion. Furthermore, exposure of macrophages to oxLDL significantly upregulated cyclooxygenase-2(COX-2) expression. However, this could be markedly inhibited by Nur77 overexpression. Also, Nur77 siRNA increased oxLDL-induced COX-2 expression and 6-mercaptopurine (6-MP) attenuated the increase. The results indicated that Nur77 is induced by oxLDL via p38 MAPK signal pathway and subsequently protects against inflammation by the inhibition of proinflammatory COX-2 pathway in activated macrophages. Specifically modifying transcription activity of Nur77 may represent a potential molecular target for the prevention and treatment of atherosclerosis.
Journal of Molecular and Cellular Cardiology 04/2010; 49(2):304-11. · 5.17 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The endocannabinoid system has recently been attracted interest for its anti-inflammatory and anti-oxidative properties. In this study, we investigated the role of the endocannabinoid system in regulating the oxidized low-density lipoprotein (oxLDL)-induced inflammatory response in macrophages. RAW264.7 mouse macrophages and peritoneal macrophages isolated from Sprague-Dawley (SD) rats were exposed to oxLDL with or without the synthetic cannabinoid WIN55,212-2. To assess the inflammatory response, reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF- alpha) levels were determined, and activation of the mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappa B signaling pathways were assessed. We observed that: i) oxLDL strongly induced ROS generation and TNF- alpha secretion in murine macrophages; ii) oxLDL-induced TNF- alpha and ROS levels could be lowered considerably by WIN55,212-2 via inhibition of MAPK (ERK1/2) signaling and NF-kappa B activity; and iii) the effects of WIN55212-2 were attenuated by the selective CB2 receptor antagonist AM630. These results demonstrate the involvement of the endocannabinoid system in regulating the oxLDL-induced inflammatory response in macrophages, and indicate that the CB2 receptor may offer a novel pharmaceutical target for treating atherosclerosis.
The Journal of Lipid Research 03/2010; 51(8):2181-90. · 5.56 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Patients aged ≥75 years compose a high-risk subgroup for acute myocardial infarction (AMI). It is unknown whether myocardial perfusion in these patients is decreased compared with younger ones after primary percutaneous coronary intervention (PPCI), which may contribute to their worse prognosis. We compared epicardial and myocardial perfusions as well as short-term outcomes between elderly and younger patients undergoing PPCI.
A total of 547 consecutive PPCI patients were prospectively enrolled; of these, 106 were elderly (≥75 yrs). Epicardial perfusion was evaluated by the Thrombolysis in Myocardial Infarction (TIMI) flow grade and corrected TIMI frame count (CTFC), and myocardial perfusion was evaluated by the TIMI myocardial perfusion grade (TMPG) and ST-segment resolution (STR).
Despite comparable epicardial perfusion pre- and post-PPCI, elderly patients had impaired myocardial perfusion after PPCI, as measured by reduced TMPG (35.9% vs 14.5%, p=0.001) and absent STR (18.9% vs 9.8%, p=0.009). After adjusting for clinical and angiographic risk profiles, multivariate analysis showed that age ≥75 years remained independently associated with reduced TMPG or absent STR. In the whole population, multivariate analysis revealed that both age ≥75 years and absent STR were independently associated with 3-month major adverse cardiac events (MACE). In the elderly subgroup, multivariate analysis identified absent STR as the strongest determinant of 3-month MACE.
Age is associated with impaired myocardial perfusion, but not epicardial perfusion, after PPCI for AMI. To further improve the outcome of elderly AMI patients, efforts should be aimed at improving myocardial perfusion beyond epicardial recanalization.
Aging clinical and experimental research 12/2009; 22(4):295-302. · 1.55 Impact Factor
-
Song Ding, Jun Pu,
Zhi-qing Qiao,
Peiren Shan,
Wei Song,
Yongping Du,
Jie-Yan Shen,
Shu-xuan Jin,
Yu Sun,
Long Shen,
Yean-leng Lim,
Ben He
[show abstract]
[hide abstract]
ABSTRACT: We sought to develop a new quantitative method to evaluate the degree of myocardial perfusion.
Currently available methods for assessing myocardial perfusion, both TIMI myocardial perfusion grading (TMPG) and myocardial blush grading (MBG), are subjective.
TIMI Myocardial Perfusion Frame Count (TMPFC), an objective method that measures the filling and clearance of contrast in the myocardium using cine-angiographic frame-counting, was developed to quantify myocardial perfusion. Myocardial perfusion of 45 normal coronary arteries in 15 patients, and 137 culprit arteries in 137 patients immediately after primary angioplasty, was successfully assessed with TMPFC.
The mean TMPFC in the normal arteries was 83.47 +/- 17.96 frames (95% CI: 78.07 frames <or= TMPFC <or= 88.86 frames). Therefore, TMPFC < 90 frames, a value representing the upper bound of the 95% CI for the TMPFC observed in normal arteries, was defined as normal myocardial perfusion. In 137 culprit arteries, the mean TMPFC values after primary angioplasty for the right coronary artery (RCA), left anterior descending artery (LAD), and left circumflex artery (LCX) were 141 +/- 82.6, 112 +/- 80.3, and 102 +/- 37.5 frames, respectively. Patients with suboptimal myocardial perfusion (ex: TMPG <or= 2 or MBG <or= 2 grade) had higher levels of TMPFC. Furthermore, multivariate analysis shows that the TMPFC was an independent predictor for 30-day (P = 0.0261) and 6-month incidence of MACE (P = 0.0207).
TMPFC is a quantitative index for the assessment of myocardial perfusion; it allows quantification of TMPG and may serve as a discerning tool to predict prognosis in patients undergoing primary angioplasty.
Catheterization and Cardiovascular Interventions 10/2009; 75(5):722-32. · 2.29 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Monocyte/macrophage differentiation is an essential process during atherosclerosis development. The retinoid X receptor (RXR) is a member of the nuclear hormone receptor superfamily, which plays an important regulatory role in many metabolic disorders, including atherosclerosis. The purpose of this study was to investigate the effect of RXR agonist on monocyte/macrophage differentiation in vitro. The THP-1 cell line was differentiated into a macrophage-like phenotype by incubation with phorbol-12-myristate-13-acetate (PMA) in the presence or absence of RXR agonist. The viability of adherent differentiated THP-1 cells was determined by MTT assay. Macrophage surface marker CD11b and CD36 was analyzed by flow cytometry. Phagocytosis was measured by fluorescence-labeled latex beads. The production of Cytokine Tunlornecrosisfactor-alpha (TNF-alpha), Interlaken-12p70 (IL-12p70), and Matrix metalloproteinase-9 (MMP-9), each of which was analyzed by ELISA. In the presence of the RXR agonists 9-cis retinoic acid or SR11237, PMA-induced THP-1 cells became less adherent, showed decreased macrophage-like morphological changes, decreased cell surface antigen CD11b and CD36 expression, and down regulated the phagocytosis of latex beads and the production of TNF-alpha and MMP-9. These data suggest that RXR agonists inhibit PMA-induced THP-1 cell differentiation into macrophage-like cells, which may be helpful in understanding the anti-atherosclerotic effect of RXR and its agonists.
Molecular and Cellular Biochemistry 09/2009; 335(1-2):283-9. · 2.06 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Evidence from recent studies suggests that the endocannabinoid system participates in the regulation of lipid metabolism and body composition. We hypothesize that the system is activated by oxidized low-density lipoprotein (oxLDL) and regulates cellular cholesterol metabolism in macrophages.
Primary peritoneal macrophages isolated from Sprague-Dawley rats and RAW264.7 mice macrophages were cultured. A liquid chromatography/mass spectrometry (LC/MS) system was used to measure the endocannabinoid anandamide (AEA), 2-arachidonoylglycerol (2-AG), and cellular cholesterol levels in macrophages. The regulatory mechanisms of cellular cholesterol metabolism were also investigated by molecular biology methods. The results showed that the endocannabinoid system in macrophages was activated by oxLDL through elevation of the AEA and 2-AG levels and the up-regulation of the cannabinoid CB1 and CB2 receptor expression. Win55,212-2, a synthetic cannabinoid, promotes cellular cholesterol accumulation in macrophages, which was associated with an increase in the expression of CD36 and a decrease in the expression of ATP-binding cassette protein A1 (ABCA1) as mediated by an up-regulated peroxisome proliferator-activated receptor gamma (PPARgamma). AM251, a selective cannabinoid CB1 receptor antagonist, impaired the abilities of Win55,212-2-treated macrophages to accumulate cholesterol by down-regulating CD36 receptor expression and up-regulating ABCA1 expression.
We have demonstrated, for the first time, that the endocannabinoid system in macrophages is activated by oxLDL and that the activated endocannabinoid system promotes cellular cholesterol accumulation in macrophages. The results also indicate that selectively blocking the CB1 receptor can reduce oxLDL accumulation in macrophages, which might represent a promising therapeutic strategy for atherosclerosis.
Cardiovascular research 01/2009; 81(4):805-13. · 5.80 Impact Factor
