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International journal of cardiology 04/2013; · 7.08 Impact Factor
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ABSTRACT: BACKGROUND: The mechanism by which vascular regeneration declines with aging is not fully understood. An interaction between integrin and vascular endothelial growth factor receptor-2 (VEGFR-2) plays a substantial role in angiogenesis. Here, we investigated whether aging impairs this interaction in endothelial progenitor cells (EPCs) under hypoxia. METHODS AND RESULTS: Aging reduced the blood flow and vessel density in ischemic muscles in mice. Levels of phosphorylated Src (p-Src), p-β3, and p-VEGFR-2 in acute ischemia were reduced in the muscles of aged mice compared to young mice. The hypoxia-inducible factor (HIF)-1α stabilizer deferoxamine improved the age-related impairment of angiogenesis, but this effect was diminished by LY290004, an inhibitor of phosphatidylinositol 3-kinase. Deferoxamine improved the reduction in chronic ischemia-induced β3-integrin and VEGFR-2 phosphorylation in the muscles of aged mice; this effect was also diminished by LY290004. In EPCs, we identified the molecular requirements for VEGF-mediated β3-integrin and VEGFR-2 cross-activation in vitronectin-induced cell adhesion under acute hypoxia. We demonstrated that c-Src controlled the adhesion- and VEGF-induced β3 tyrosine phosphorylation in hypoxia. Aging enhanced the hypoxia-induced EPC apoptosis and impaired several c-Src-related VEGF-induced receptor events, including β3 tyrosine activation, ligand binding, cell adhesion, and tubulogenesis in cultured EPCs of animals and those of humans. CONCLUSIONS: These data suggest that the aging-related decline in angiogenic action in response to ischemia is mediated by the impairment of cross-activation between β3 and VEGFR-2 in EPCs, which is partially associated with decreased HIF-1α stability.
International journal of cardiology 02/2013; · 7.08 Impact Factor
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Heart (British Cardiac Society) 11/2012; · 4.22 Impact Factor
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ABSTRACT: Passage failure of guidewire is still remained most common reason for percutaneous coronary intervention (PCI) failure in chronic total occlusion (CTO). Intravascular ultrasound study (IVUS) and cardiac CT angiography can help identify features that most influence current success rates of PCI. We report our experience using the reverse controlled antegrade and retrograde subintimal tracking technique under the aid of IVUS, cardiac CT angiography for an ambiguous CTO of proximal right coronary artery.
Korean Circulation Journal 09/2012; 42(9):625-8.
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International journal of cardiology 07/2012; · 7.08 Impact Factor
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ABSTRACT: Mitochondrial dysfunction plays a central role in mediating both the necrotic and apoptotic components of reperfusion injury. Because mitochondrial swelling is one of the most important indicators of the beginning of mitochondrial permeability transition, quantification of morphological changes in mitochondria would be useful in evaluating the degree of IR injury, as well as the protective effects of various therapies. In this study, we characterized the morphological changes in heart mitochondria caused by the duration and severity of ischemia utilizing particle shape analysis on atomic force microscopy (AFM) topographic images. We also simultaneously investigated the nano-mechanical changes in rat heart mitochondria by injury using force-distance curve measurements. Rats were randomly divided into 3 groups: control group (n=3), myocardial ischemia without reperfusion (PI group, n=3), and myocardial ischemia with reperfusion (IR group, n=4). Normal mitochondria appeared ellipsoidal with a mean area of 3551±1559nm(2) and mean perimeter of 217.54±52.09nm (n=60). The mean area and perimeter of mitochondria in the IR groups increased to 28,181±21,248nm(2) and 595.74±234.29nm (n=40, p<0.0001 vs. control group, respectively), maintaining oval in shape. But, in the PI group, all parameters showed significant differences compared to parameters of the control group (n=35, p<0.0001). In particular, the mean axial ratio and roundness were significantly different from those in the IR group. Mitochondria in the PI group looked more spherical than those of control and IR groups. Adhesion force is the force before the last event on the retraction half of force-distance curve measurements, corresponding to the point where the tip and the surface loose contact. The adhesion forces of heart mitochondria in the IR and PI groups significantly decreased to 19.56±1.08nN (n=30, p<0.0001) and 18.65±3.18nN (n=30, p<0.0001), compared to normal mitochondria which had an adhesion force of 27.64±0.88nN (n=30). Adhesion force is governed by the attractive portion of the interacting forces between the surface atoms of the contacts. From the morphological and nano-mechanical changes in heart mitochondria, we suggested that the outer membranes of mitochondria were broken by myocardial ischemic injury before they became swollen, and the swelling might be correlated with the ischemic injury. We inferred that the breakage of membranes leads to uptake of water and matrix swelling. As a result, shape measurement parameters for the quantitative analysis of mitochondrial swelling could be very effective for evaluating the myocardial injury.
Micron 06/2012; · 1.53 Impact Factor
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American heart journal 05/2012; 163(5):e33. · 4.65 Impact Factor
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The Korean Journal of Internal Medicine 03/2012; 27(1):107-10.
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ABSTRACT: Below the knee (BTK) interventions are increasing in patients with rest pain or critical limb ischemia, and these interventions are frequently successful in facilitating limb salvage. New intervention techniques and devices allow successful recanalization of occluded BTK arteries. Here, we report a case of successful recanalization of BTK arteries using multidisciplinary methods, including an antegrade approach and retrograde approach without the use of a sheath, but with simple balloon angioplasty, and plaque excision using Silverhawk atherectomy device.
Korean Circulation Journal 02/2012; 42(2):125-8.
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International journal of cardiology 12/2011; 154(3):369-70. · 7.08 Impact Factor
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ABSTRACT: The purpose of this study was to evaluate whether exenatide administration can prevent impairment in endothelium-dependent vasodilatation induced by ischemia-reperfusion (IR) injury and whether this effect is mediated by K(ATP) channel opening.
In a double-blind, placebo-controlled, crossover design, 20 volunteers were randomly assigned to 2 groups: subcutaneous exenatide (10 μg) or placebo administration. At 30 minutes after the study drug administration, endothelium-dependent flow-mediated dilatation (FMD) of the radial artery was measured before and after IR (15 minutes of ischemia at the level of the brachial artery followed by 15 minutes of reperfusion) injury. Seven days later, both groups were crossed over and received the other treatment (ie, placebo or exenatide) and underwent the same protocol. Pre-IR radial artery diameter, FMD, and baseline radial artery diameter after IR injury were similar between 2 groups (P=no significant difference). After placebo administration, IR significantly blunted FMD (before IR: 12.0±6.23%; after IR: 4.6±3.57%, P=0.02). Exenatide prevented this impairment (FMD before IR: 15.0±7.14%; FMD after IR: 15.0±5.96%, P=no significant difference; P<0.001 compared with placebo). In a separate protocol, this protective effect was completely abolished by pretreatment with glibenclamide (glyburide, 5 mg), a blocker of K(ATP) channels (n=7; FMD before IR: 12.0±2.2%; after IR: 3.2±2.1%, P<0.001).
The present study demonstrates that subcutaneous exenatide protects IR-induced endothelial dysfunction through opening of K(ATP) channels in human IR injury model.
Arteriosclerosis Thrombosis and Vascular Biology 12/2011; 32(2):474-80. · 6.37 Impact Factor
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ABSTRACT: Chronic kidney disease (CKD) is a factor of low response to clopidogrel. We sought to assess the functional impact of cilostazol in CKD patients with undergoing hemodialysis.
Seventy-four patients with CKD undergoing hemodialysis and percutaneous coronary intervention were enrolled. Patients were randomly assigned to receive clopidogrel (75 mg/d [group 1, n = 24]), high-maintenance dose of clopidogrel (150 mg/d [group 2, n = 25]), or clopidogrel (75 mg/d) with cilostazol (200 mg/d [group 3, n = 25]) for 14 days. Another 50 patients with normal renal function undergoing percutaneous coronary intervention were treated with 75 mg of clopidogrel and served as the control group. Platelet function was evaluated before and after antiplatelet therapy with light transmittance aggregometry and with VerifyNow P2Y12 assay (Accumetrics, San Diego, CA). Platelet activation markers (soluble CD40 ligand and soluble P-selectin) were also assessed.
The baseline platelet function measurements were similar in the 3 groups of patients; however, the CKD groups had significantly higher platelet aggregation activity compared with the control groups. The rate of high on-treatment platelet reactivity was significantly lower in group 3 than in groups 1 and 2 (10% vs 43% vs 32%, respectively; P < .05). After 14 days of antiplatelet therapy, the changes in plasma soluble CD40 ligand and soluble P-selectin levels were significantly higher in group 3 compared with groups 1 and 2 (P < .01); however, there were no significant differences in platelet function and activation markers between groups 1 and 2.
Adjunctive cilostazol improves platelet inhibition compared with 75 or 150 mg of clopidogrel in CKD patients undergoing hemodialysis.
American heart journal 12/2011; 162(6):1018-25. · 4.65 Impact Factor
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ABSTRACT: A 42-year-old male patient presented with refractory hypertension and congestive heart failure. He had taken hydrochlorthiazide 50 mg, carvedilol 25 mg, diltiazem 180 mg, and losartan 100 mg per day. Aortogram revealed a severe luminal narrowing in the distal thoracic aorta with a peak systolic pressure gradient of 60 mmHg across the lesion. Endovascular management was performed with 22 × 80 mm self-expandable Nitinol-S stent after predilation with 10 × 40 mm balloon. After endovascular management, the patient's blood pressure, left ventricular ejection fraction (LVEF) and dilated LV dimension were remarkably improved.
Journal of cardiovascular ultrasound 09/2011; 19(3):144-7.
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International journal of cardiology 07/2011; 151(3):377-8. · 7.08 Impact Factor
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ABSTRACT: A pulmonary thromboembolism (PTE) causes a dramatic pressure overload to the right heart. Previous case reports have shown that elevated right atrial pressure secondary to a PTE can cause right-to-left shunting in the presence of an atrial septal aneurysm (ASA). A 57-year-old female with diabetes, hypertension, and an old cerebral infarction was admitted to our hospital with acute PTE. Initial transthoracic echocardiography (TTE) showed an ASA swing from the right side to the left side, and right-to-left shunting was detected immediately in the agitated saline test. However, definite signs of pressure overload of the right heart were not detected in the TTE. This educational case shows that right-to-left shunting via a patent foramen ovale in the ASA can cause normal right atrial pressure, thus masking the pressure overload of the right heart in a patient with PTE.
Chonnam medical journal. 04/2011; 47(1):54-6.
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Hyun Kuk Kim,
Young Joon Hong,
Myung Ho Jeong, Weon Kim,
Sung Soo Kim,
Jum Suk Ko,
Min Goo Lee,
Doo Sun Sim,
Keun Ho Park,
Nam Sik Yoon,
Hyun Ju Yoon,
Kye Hun Kim,
Hyung Wook Park,
Ju Han Kim,
Youngkeun Ahn,
Jeong Gwan Cho,
Jong Chun Park,
Jung Chaee Kang
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ABSTRACT: Carvedilol is an antioxidant that inhibits smooth muscle cell proliferation and migration. The aim of this study was to investigate the beneficial effects of carvedilol-loaded stents on 2-year clinical outcomes after stent implantation in patients with coronary artery disease.
We performed a prospective trial with male subjects to compare the safety and effects of carvedilol-loaded BiodivYsio® stents implanted into 20 patients with those of bare-metal BiodivYsio® stents implanted into 21 patients for de novo coronary lesions. The primary end point was the degree of neointimal hyperplasia, which was measured by intravascular ultrasound (IVUS) 6 months after the procedure; the secondary end point was major adverse cardiac events (MACE) at 2 years after implantation. All carvedilol and control stents were deployed successfully.
A 2-year follow-up was completed for 19 patients (95%) in the carvedilol stent group and 20 patients (95%) in the control stent group. IVUS showed a trend toward a larger luminal area (6.86 ± 2.59 vs. 5.47 ± 1.52 mm², p = 0.267), smaller neointimal area (1.34 ± 0.70 vs. 2.40 ± 1.73 mm², p = 0.18), and reduced net decrease in luminal area (-0.78 ± 0.97 vs. -1.89 ± 1.78 mm², p = 0.106) in the carvedilol stent group compared with the control stent group, respectively. There were no significant differences in the incidence of MACE (10.5 vs. 30.0%, respectively, p = 0.132) between the groups at 2 years after stent implantation. Stent thrombosis did not occur in either group after 2 years.
The carvedilol-loaded stents tended to inhibit neointimal hyperplasia without the occurrence of cardiac death, myocardial infarction, or stent thrombosis at 2-year follow-up.
The Korean Journal of Internal Medicine 03/2011; 26(1):41-6.
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Seung-Ju Kim, Weon Kim,
Jong-Shin Woo,
Sang-Jin Ha,
Won-Yu Kang,
Sun-Ho Hwang,
Dong-Gu Kang,
Seung-Uk Lee,
Sang-Ki Cho,
Jeong-Soo Im,
Wan Kim
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ABSTRACT: Several studies have demonstrated that adenosine and nicorandil protect the myocardium against angioplasty-related myocardial injury. We conducted a prospective study to investigate the myocardial protective effects of combination therapy with intracoronary adenosine and nicorandil.
We enrolled 213 consecutive patients with stable or unstable angina who were scheduled for non-urgent PCI for de-novo coronary lesions. Patients were randomized into group I (control saline, n=55), group II (adenosine 50 μg, n=54), group III (nicorandil 4 mg, n=54), or group IV (adenosine-nicorandil combination, n=50). Serial assessments of CK-MB were used to assess myocardial necrosis before and after PCI. The primary endpoint was the incidence of myocardial necrosis (elevation of CK-MB), and the secondary endpoints were the changes in serum CK-MB and cTnI levels and the incidence of post-procedural myocardial infarction (MI).
No significant differences were observed among the four groups with regard to baseline or angiographic characteristics. No major adverse events related to adenosine and nicorandil were observed. There were no significant differences in the incidence of post-procedural myocardial necrosis among the four groups (10.9, 14.8, 14.8, and 14.0%, respectively, p=0.9). There were no significant differences in the incidence of post-procedural MI among groups (p=0.6). In multivariate regression analysis, multivessel stenting, median stent length, and the presence of a compromised side branch were independent predictors of myonecrosis.
Pretreatment with intracoronary adenosine, nicorandil, or the combination of the two drugs did not reduce the incidences of myocardial necrosis or MI after non-urgent PCI in patients with low-risk angina pectoris.
International journal of cardiology 01/2011; 158(1):88-92. · 7.08 Impact Factor
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International journal of cardiology 12/2010; 145(3):516-8. · 7.08 Impact Factor
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ABSTRACT: The purpose of this study was to determine the clinical and laboratory characteristics in patients with acute myocardial infarction (AMI) associated with coronary vasospasm.
Consecutive 231 patients with documented coronary vasospasm by ergonovine provocation test but with a normal-appearing coronary angiogram were divided into two groups, variant angina pectoris (VAP) patients (group I; n=202, 49.5 ± 11.1 years) and AMI patients (group II; n=29, 47.4 ± 11.2 years). Matched control patients were 84 AMI patients with significant stenosis (>50%) (group III; n=84, 61.2 ± 11.8 years). Although, the incidence of hypertension, diabetes mellitus, and smoking were lower in group I than in group III, there was no difference between group II and III (diabetes, 7.9% vs. 13.8% vs. 29.8%; hypertension, 19.8% vs. 24.1% vs. 41.7%; smoking 48% vs. 48.3% vs. 61.9%; respectively, p<0.01). Measured high-sensitivity C-reactive protein (hsCRP) and fibrinogen level were higher (respectively, p<0.001, p<0.001) in groups II and III (group II, 1.88 ± 2.9 mg/dl, 317.5 ± 51.2mg/dl; group III, 2.92 ± 3.9 mg/dl, 326.8 ± 107.7 mg/dl) than those in group I (0.68 ± 1.5mg/dl, 263.2 ± 70.3mg/dl). A correlation was clearly seen between fibrinogen and hsCRP (r=0.472, p<0.001).
The clinical characteristics of patients with AMI associated with spasm were similar to those with VAP, but laboratory findings were similar to those of AMI in patients with significant stenosis.
Journal of Cardiology 11/2010; 56(3):320-5. · 1.28 Impact Factor
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ABSTRACT: We have developed a porcine model of acute myocardial infarction (AMI) and ischemic heart failure by transcatheter intracoronary injection of ethyl alcohol and observed pathologic changes induced in the alcohol-injured coronary artery and infarcted myocardium. In a total of 12 female pigs, anteroseptal AMI was induced by transcatheter delivery of 1 mL of 99.9% ethyl alcohol using a 2.5 mm diameter over-the-wire balloon catheter in the left anterior descending artery (LAD). Another five pigs underwent the sham operation, and the differences in left ventricular (LV) dimension and LV ejection fraction between these pigs and those injected with ethyl alcohol were evaluated. Follow-up coronary and LV angiography, echocardiography and histopathology were performed at 4 weeks after the procedure. Myocardial SPECT using (201)Tl (and (99m)Tc-MIBI) and triphenyl tetrazolium chloride (TTC) stain were performed and compared. Procedure-related death occurred in two pigs with proximal LAD occlusion. Four pigs suffered from ventricular tachycardia, which converted to sinus rhythm by DC cardioversion. Follow-up coronary angiography at 4 weeks revealed persistent total occlusion in all pigs. Echocardiogram showed decreased apicoanteroseptal wall motion with an ejection fraction of 46.5 ± 3.3% and nonsignificantly changed LV dimensions. Myocardial SPECT revealed a perfusion defect in the apicoanterior wall in all subjects (percent area of the perfusion defect = 22.1 ± 2.50%). The percentage of myocardium not stained by TTC was 23.1 ± 2.25%. Histologic examination revealed severe fibrosis in the infarcted myocardium and massive thrombus with organization and calcification in the alcohol-injured coronary artery. The porcine model of AMI obtained by intracoronary alcohol injection provides a safe and reproducible method for the research and development of new therapeutic modalities for MI and end-stage heart failure.
Heart and Vessels 10/2010; 26(3):342-8. · 2.05 Impact Factor
