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1.  Different contribution of extent of myocardial injury to left ventricular systolic and diastolic function in early reperfused acute myocardial infarction 
Background
We sought to investigate the influence of the extent of myocardial injury on left ventricular (LV) systolic and diastolic function in patients after reperfused acute myocardial infarction (AMI).
Methods
Thirty-eight reperfused AMI patients underwent cardiac magnetic resonance (CMR) imaging after percutaneous coronary revascularization. The extent of myocardial edema and scarring were assessed by T2 weighted imaging and late gadolinium enhancement (LGE) imaging, respectively. Within a day of CMR, echocardiography was done. Using 2D speckle tracking analysis, LV longitudinal, circumferential strain, and twist were measured.
Results
Extent of LGE were significantly correlated with LV systolic functional indices such as ejection fraction (r = -0.57, p < 0.001), regional wall motion score index (r = 0.52, p = 0.001), and global longitudinal strain (r = 0.56, p < 0.001). The diastolic functional indices significantly correlated with age (r = -0.64, p < 0.001), LV twist (r = -0.39, p = 0.02), average non-infarcted myocardial circumferential strain (r = -0.52, p = 0.001), and LV end-diastolic wall stress index (r = -0.47, p = 0.003 with e’) but not or weakly with extent of LGE. In multivariate analysis, age and non-infarcted myocardial circumferential strain independently correlated with diastolic functional indices rather than extent of injury.
Conclusions
In patients with timely reperfused AMI, not only extent of myocardial injury but also age and non-infarcted myocardial function were more significantly related to LV chamber diastolic function.
doi:10.1186/1476-7120-12-6
PMCID: PMC3922533  PMID: 24512272
Acute myocardial infarction; Diastolic function; Cardiac magnetic resonance; Speckle tracking echocardiography
2.  Usefulness of metabolic syndrome score in the prediction of angiographic coronary artery disease severity according to the presence of diabetes mellitus: relation with inflammatory markers and adipokines 
Background
It is a matter of debate whether metabolic syndrome (MS) improves cardiovascular risk prediction beyond the risk associated with its individual components. The present study examined the association of MS score with high sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), resistin, adiponectin, and angiographic coronary artery disease (CAD) severity according to the presence of DM. In addition, the predictive value of various clinical and biochemical parameters were analyzed, including the MS score for angiographic CAD.
Methods
The study enrolled 363 consecutive patients (196 men, 62 ± 11 years of age) who underwent coronary angiography for evaluation of chest pain. Blood samples were taken prior to elective coronary angiography. MS was defined by the National Cholesterol Education Program criteria, with MS score defined as the numbers of MS components. CAD was defined as > 50% luminal diameter stenosis of at least one major epicardial coronary artery. CAD severity was assessed using the Gensini score.
Results
Of the 363 patients studied, 174 (48%) had CAD and 178 (49%) were diagnosed with MS. When the patients were divided into 4 subgroups according to MS score (0–1, 2, 3, 4–5), IL-6 levels and the CAD severity as assessed by the Gensini score increased as MS scores increased. In contrast, adiponectin levels decreased significantly as MS scores increased. When subjects were divided into two groups according to the presence of DM, the relationships between MS score and IL-6, adiponectin, and Gensini score were maintained only in patients without DM. Age, smoking, DM, MS score, and adiponectin independently predicted angiographic CAD in the whole population. However, age is the only predictor for angiographic CAD in patients with DM.
Conclusions
In the presence of DM, neither adipokines nor MS score predicted angiographic CAD. However, in non-diabetic patients, IL-6 and adiponectin showed progressive changes according to MS score, and MS score was an independent predictor of CAD in patients without DM.
doi:10.1186/1475-2840-12-140
PMCID: PMC3850730  PMID: 24088407
Metabolic syndrome; Adipokines; Coronary artery disease; Diabetes mellitus
3.  A Case of Acute Ventricular Capture Threshold Rise Associated with Flecainide Acetate 
Yonsei Medical Journal  2006;47(1):152-154.
Antiarrhythmic agents may increase capture threshold, but this is rarely of clinical significance. Flecainide acetate, a class IC agent, is reported to have a significant effect on the myocardial capture threshold. In this presentation, we report the case of a 72-year-old male, with a previously implanted VVI pacemaker due to sick sinus syndrome, who was treated with flecainide acetate for paroxysmal atrial arrhythmia control. During the fifteenth day of treatment, an abrupt rise in the ventricular capture threshold with ventricular pacing failure was noted. The capture threshold decreased two days after discontinuation of flecainide acetate.
doi:10.3349/ymj.2006.47.1.152
PMCID: PMC2687576  PMID: 16502500
Flecainide acetate; capture threshold; pacing failure
4.  Effect of Abciximab on the Levels of Circulating Microparticles in Patients with Acute Myocardial Infarction Treated by Primary Angioplasty 
Korean Circulation Journal  2013;43(9):600-606.
Background and Objectives
We investigated the effect of the additional use of abciximab during percutaneous coronary intervention (PCI) on the level of procoagulant microparticles (MPs) in patients with ST-segment elevation myocardial infarction (STEMI) who had undergone primary PCI.
Subjects and Methods
In this study, we studied 86 patients with STEMI (72 men, age 58±13) who had undergone primary PCI. The decision to administer abciximab immediately prior to PCI was left to the discretion of the operator. Blood samples for analysis of MPs were obtained from the femoral artery before and after PCI. MPs with procoagulant potential were measured using a commercial kit. The cellular origins of MPs were determined by antigenic capture with specific antibodies.
Results
Procoagulant MPs captured onto annexin V were not changed significantly after PCI {13.4±13.2 nM vs. 13.2±16.1 nM phosphatidylserine equivalent (PS eq), p=0.479}. Abciximab was used in 30 of 86 patients (35%) immediately prior to PCI. In patients who had undergone PCI without abciximab, no significant change in the level of MPs was observed after PCI. However, in the abciximab group, the level of circulating MPs was significantly decreased after PCI (12.0±10.7 nM vs. 7.8±11.7 nM PS eq, p=0.018). Levels of endothelial- and platelet-derived MPs also showed a significant reduction after PCI in the abciximab group.
Conclusion
Primary PCI with additional abciximab significantly reduced the level of procoagulant MPs regardless of their cellular origins in patients with STEMI.
doi:10.4070/kcj.2013.43.9.600
PMCID: PMC3808855  PMID: 24174960
Cell-derived microparticles; Myocardial infarction; Platelet aggregation inhibitors
5.  Correction with blood T1 is essential when measuring post-contrast myocardial T1 value in patients with acute myocardial infarction 
Background
Post-contrast T1 mapping by modified Look-Locker inversion recovery (MOLLI) sequence has been introduced as a promising means to assess an expansion of the extra-cellular space. However, T1 value in the myocardium can be affected by scanning time after bolus contrast injection. In this study, we investigated the changes of the T1 values according to multiple slicing over scanning time at 15 minutes after contrast injection and usefulness of blood T1 correction.
Methods
Eighteen reperfused acute myocardial infarction (AMI) patients, 13 cardiomyopathy patients and 8 healthy volunteers underwent cardiovascular magnetic resonance with 15 minute-post contrast MOLLI to generate T1 maps. In 10 cardiomyopathy cases, pre- and post-contrast MOLLI techniques were performed to generate extracellular volume fraction (Ve). Six slices of T1 maps according to the left ventricular (LV) short axis, from apex to base, were consecutively obtained. Each T1 value was measured in the whole myocardium, infarcted myocardium, non-infarcted myocardium and LV blood cavity.
Results
The mean T1 value of infarcted myocardium was significantly lower than that of non-infarcted myocardium (425.4±68.1 ms vs. 540.5±88.0 ms, respectively, p< 0.001). T1 values of non-infarcted myocardium increased significantly from apex to base (from 523.1±99.5 ms to 561.1±81.1 ms, p=0.001), and were accompanied by a similar increase in blood T1 value in LV cavity (from 442.1±120.7 ms to 456.8±97.5 ms, p<0.001) over time. This phenomenon was applied to both left anterior descending (LAD) territory (from 545.1±74.5 ms to 575.7±84.0 ms, p<0.001) and non-LAD territory AMI cases (from 501.2±124.5 ms to 549.5±81.3 ms, p<0.001). It was similarly applied to cardiomyopathy patients and healthy volunteers. After the myocardial T1 values, however, were adjusted by the blood T1 values, they were consistent throughout the slices from apex to base (from 1.17±0.18 to 1.25±0.13, p>0.05). The Ve did not show significant differences from apical to basal slices.
Conclusion
Post-contrast myocardial T1 corrected by blood T1 or Ve, provide more stable measurement of degree of fibrosis in non-infarcted myocardium in short- axis multiple slicing.
doi:10.1186/1532-429X-15-11
PMCID: PMC3564738  PMID: 23331480
Cardiovascular magnetic resonance; T1 mapping; Myocardium
6.  Spontaneous Sinus Conversion of Permanent Atrial Fibrillation During Treatment of Hyperkalemia 
Korean Circulation Journal  2012;42(1):65-68.
Hyperkalemia is a common adverse effect of treatment for heart failure and is associated with high mortality and morbidity. The cardiac manifestations of hyperkalemia include various electrocardiogram changes. We describe a case of a 74-year-old woman with heart failure and permanent atrial fibrillation who reverted to normal sinus rhythm during recovery from hyperkalemia.
doi:10.4070/kcj.2012.42.1.65
PMCID: PMC3283759  PMID: 22363388
Hyperkalemia; Atrial fibrillation; Electrocardiography
7.  Impact of Metabolic Syndrome and Its Individual Components on the Presence and Severity of Angiographic Coronary Artery Disease 
Yonsei Medical Journal  2010;51(5):676-682.
Purpose
Metabolic syndrome (MS) has been reported as a potential risk factor of coronary artery disease (CAD). The aims of this study were to assess whether there was a relationship between MS score and CAD angiographic severity, and to assess the predictive value of individual components of MS for CAD.
Materials and Methods
We retrospectively enrolled 632 patients who underwent coronary angiography for suspected CAD (394 men, 61.0 ± 10.6 years of age). MS was defined by the National Cholesterol Education Program criteria with the waist criterion modified into a body mass index (BMI) of more than 25 kg/m2. The MS score defined as the number of MS components. CAD was defined as > 50% luminal diameter stenosis of at least one major epicardial coronary artery. CAD angiographic severity was evaluated with a Gensini scoring system.
Results
Of the patients, 497 (78.6%) had CAD and 283 (44.8%) were diagnosed with MS. The MS score was significantly related to the Gensini score. High fasting blood glucose (FBG) was the only predictive factor for CAD. A cluster including high FBG, high blood pressure (BP), and low high-density lipoprotein cholesterol (HDL-C) showed the highest CAD risk.
Conclusion
The MS score correlates with the angiographic severity of CAD. The predictive ability of MS for CAD was carried almost completely by high FBG, and individual traits with high BP and low HDL-C may act synergistically as risk factors for CAD.
doi:10.3349/ymj.2010.51.5.676
PMCID: PMC2908873  PMID: 20635441
Metabolic syndrome; coronary artery disease; coronary angiography
8.  Evaluation of Reperfused Myocardial Infarction by Low-Dose Multidetector Computed Tomography Using Prospective Electrocardiography (ECG)-Triggering: Comparison with Magnetic Resonance Imaging 
Yonsei Medical Journal  2010;51(5):683-691.
Purpose
To evaluate the potential of prospective electrocardiography (ECG)-gated 64-slice multidetector computed tomography (MDCT) for evaluation of myocardial enhancement, infarct size, and stent patency after percutaneous coronary intervention (PCI) with stenting in patients with myocardial infarction.
Materials and Methods
Seventeen patients who were admitted with acute myocardial infarction were examined with prospective ECG-gated 64-slice cardiac MDCT and magnetic resonance (MR) imaging after reperfusion using PCI with stenting. Cardiac MDCT was performed with two different phases: arterial and delayed phases. We evaluated the stent patency on the arterial phase, and nonviable myocardium on the delayed phase of computed tomography (CT) image, and they were compared with the results from the delayed MR images.
Results
Total mean radiation dose was 7.7 ± 0.5 mSv on the two phases of CT images. All patients except one showed good patency of the stent at the culprit lesion on the arterial phase CT images. All patients had hyperenhanced area on the delayed phase CT images, which correlated well with those on the delayed phase MR images, with a mean difference of 1.6% (20 ± 10% vs. 22 ± 10%, r = 0.935, p = 0.10). Delayed MR images had a better contrast-to-noise ratio (CNR) than delayed CT images (27.1 ± 17.8% vs. 4.3 ± 2.1%, p < 0.001).
Conclusion
Prospective ECG-gated 64-slice MDCT provides the potential to evaluate myocardial viability on delayed phase as well as for stent patency on arterial phase with an acceptable radiation dose after PCI with stenting in patients with myocardial infarction.
doi:10.3349/ymj.2010.51.5.683
PMCID: PMC2908876  PMID: 20635442
Prospective ECG-gated MDCT; magnetic resonance imaging; myocardial infarction; delayed enhancement imaging
9.  Potential role of HMG CoA reductase inhibitor on oxidative stress induced by advanced glycation endproducts in vascular smooth muscle cells of diabetic vasculopathy 
Experimental & Molecular Medicine  2009;41(11):802-811.
Advanced glycation endproducts (AGEs)-induced vascular smooth muscle cell (VSMCs) proliferation and formation of reactive oxygen species (ROS) are emerging as one of the important mechanisms of diabetic vasculopathy but little is known about the antioxidative action of HMG CoA reductase inhibitor (statin) on AGEs. We hypothesized that statin might reduce AGEs-induced intracellular ROS of VSMCs and analyzed the possible mechanism of action of statin in AGEs-induced cellular signaling. Aortic smooth muscle cell of Sprague-Dawley rat (RASMC) culture was done using the different levels of AGEs stimulation in the presence or absence of statin. The proliferation of RASMC, ROS formation and cellular signaling was evaluated and neointimal formation after balloon injury in diabetic rats was analyzed. Increasing concentration of AGEs stimulation was associated with increased RASMC proliferation and increased ROS formation and they were decreased with statin in a dose-dependent manner. Increased NF-κB p65, phosphorylated ERK, phosphorylated p38 MAPK, cyclooxygenase-2, and c-jun by AGEs stimulation were noted and their expression was inhibited by statin. Neointimal formation after balloon injury was much thicker in diabetic rats than the sham-treated group but less neointimal growth was observed in those treated with statin after balloon injury. Increased ROS formation, subsequent activation of MAPK system and increased VSMC proliferation may be possible mechanisms of diabetic vasculopathy induced by AGEs and statin may play a key role in the treatment of AGEs-induced diabetic atherosclerosis.
doi:10.3858/emm.2009.41.11.086
PMCID: PMC2788734  PMID: 19641377
cyclooxygenase 2; diabetes mellitus; extracellular signal-regulated MAP kinases; hydroxymethylglutaryl-CoA reductase inhibitors; muscle, smooth, vascular; NFκB; p38 mitogen-activated protein kinases; proto-oncogene proteins c-jun; reactive oxygen species
10.  Pathobiological role of advanced glycation endproducts via mitogen-activated protein kinase dependent pathway in the diabetic vasculopathy 
Experimental & Molecular Medicine  2008;40(4):398-406.
Advanced glycation endproducts (AGEs) have been reported to play a role in neointimal formation and increase the rate of in-stent restenosis (ISR) in the diabetic coronary artery disease patients treated with stents, but the potential pathogenic mechanisms of AGEs in vascular smooth muscle cell proliferation remain unclear. We sought to determine the AGEs related pathobiological mechanism of diabetic vasculopathy. Rat aortic smooth muscle cell (RAoSMC) culture was done with different concentrations of AGEs and proliferation was assessed. Immunohistochemistry for receptor of AGEs (RAGE) was performed with human carotid atheroma. Western blotting was performed to assess the activation of MAP kinase system in the cultured RAoSMC. AGEs increased RAoSMC proliferation and were associated with increased phosphorylation of ERK and p38 kinase by time and dose dependent manner. The MAP kinase activity was decreased by RNA interference for RAGE. AGEs stimulation increased reactive oxygen species (ROS) generation in cultured RAoSMC. From this study it is concluded that AGEs played a key role in RAoSMC proliferation via MAP kinase dependent pathways. Activation of vascular smooth muscle cell (VSMC) proliferation by MAP kinase system and increased formation of ROS may be the possible mechanisms of AGEs induced diabetic vasculopathy.
doi:10.3858/emm.2008.40.4.398
PMCID: PMC2679265  PMID: 18779652
atherosclerosis; blood vessels; diabetes mellitus; glycation end products, advanced; mitogen-activated protein kinases
11.  A Case of Noncompaction of the Ventricular Myocardium Combined with Situs Ambiguous with Polysplenia 
Yonsei Medical Journal  2007;48(6):1052-1055.
A 33-year-old man was admitted to our hospital with chest pain and exertional dyspnea. Two-dimensional echocardiography showed prominent trabeculations and deep intertrabecular recesses, findings consistent with noncompaction of the ventricular myocardium. Thoracoabdominal CT and cardiac magnetic resonance imaging (CMR) revealed situs ambiguous with polysplenia and noncompaction of the left ventricular myocardium. CMR also demonstrated delayed enhancement of the trabeculations located at the apical portion of the left ventricle. The coronary angiogram was normal. This is the first case of noncompaction of the ventricular myocardium associated with situs ambiguous with polysplenia.
doi:10.3349/ymj.2007.48.6.1052
PMCID: PMC2628179  PMID: 18159602
Noncompaction of the ventricular myocardium (NVM); situs ambiguous with polysplenia
12.  Percutaneous Coronary Intervention Versus Coronary Artery Bypass Grafting in Patients with Coronary Artery Disease and Diabetic Nephropathy: A Single Center Experience 
Background
Patients with diabetic nephropathy (DN) and coronary artery disease (CAD) represent a subset of patients with high cardiovascular morbidity and mortality. The optimal revascularization strategy using either percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) remains controversial. The purpose of this study was to compare the clinical outcomes of PCI to CABG in DN patients with CAD.
Methods
The clinical and angiographic records of DN patients with CAD who underwent either CABG (n=52) or PCI (n=48) were retrospectively analyzed.
Results
The baseline characteristics were similar in the two groups except for the severity of the CAD. At 30 days, the death rate (PCI: 2.1% vs. CABG: 9.6%, p=0.21) and major adverse cardiac events (MACE) rate (PCI: 2.1% vs. CABG: 9.6%, p=0.21) were similar in comparisons between the PCI and CABG groups. At three years, the death rate (PCI: 18.8% vs. CABG: 19.2%, p=0.94) was similar between the PCI and CABG groups but the MACE rate (PCI: 47.9% vs. CABG: 21.2%, p=0.006) was higher in the PCI group compared to the CABG group. In addition, the repeat revascularization rate was higher in the PCI group compared to the CABG group (PCI: 12.5% vs. CABG: 1.9%, p=0.046).
Conclusions
The CABG procedure was associated with a lower incidence of MACE and repeat revascularization for up to three years of follow-up in DN patients with CAD. However, the overall survival rate was similar in the CABG and PCI groups. Therefore, CABG may be superior to PCI with regard to MACE and repeat revascularization.
doi:10.3904/kjim.2007.22.3.139
PMCID: PMC2687692  PMID: 17939329
Diabetic Nephropathy; Coronary Artery Disease; Coronary Artery Bypass Grafting; Percutaneous Transluminal Coronary Angioplasty
13.  Significance of Small Dense Low-Density Lipoprotein as a Risk Factor for Coronary Artery Disease and Acute Coronary Syndrome 
Yonsei Medical Journal  2006;47(3):405-414.
Small dense LDL (sd-LDL) has recently emerged as an important coronary artery disease (CAD) risk factor. This study was performed to investigate how LDL particle size is related to CAD and acute coronary syndrome (ACS). Blood samples were collected from 504 patients that underwent coronary angiography to evaluate chest pain. The LDL particle size of these samples was measured. The mean LDL particle size was smaller in patients with angiographically proven CAD than in the controls (26.41 ± 0.95 vs 26.73 ± 0.64 nm, p < 0.001), and was negatively correlated with the Framingham risk score (r = -0.121, p = 0.007). Patients with more extensive CAD had smaller LDL particles. LDL particle size was also smaller in patients with acute coronary syndrome as compared to non-ACS patients (26.09 ± 1.42 vs 26.54 ± 0.63 nm, p = 0.011). These results suggest that sd-LDL is independently associated with the incidence and extent of CAD, and can be a risk factor for the development of ACS in the Korean population.
doi:10.3349/ymj.2006.47.3.405
PMCID: PMC2688162  PMID: 16807992
Small dense LDL; coronary artery disease
14.  Serum Levels of Advanced Glycation End Products Are Associated with In-Stent Restenosis in Diabetic Patients 
Yonsei Medical Journal  2005;46(1):78-85.
The formation of advanced glycation end products (AGEs), in various tissues has been known to enhance immunoinflammatory reactions and local oxidant stresses in long standing diabetes. Recently, AGEs have been reported to play a role in neointimal formation in animal models of arterial injury. We attempted to determine whether the serum levels of AGEs are associated with coronary restenosis in diabetic patients. Blood samples were collected from diabetic patients with coronary artery disease undergoing stent implantation and the serum levels of AGEs were analyzed by the fluorescent intensity method. The development of in-stent restenosis (ISR) was evaluated by a 6-month follow-up coronary angiography. A total of 263 target lesions were evaluated, in 203 patients. The ISR rate in the high-AGE (>170 U/ml) group (40.1%) was significantly higher than in the low-AGE group (≤170 U/ml) (19.6%) (p<0.001). Furthermore, multivariate analysis revealed that a high level of serum AGEs is an independent risk factor for the development of ISR (odds ratio, 2.659; 95% CI, 1.431-4.940; p=0.002). The serum levels of AGEs constitute an excellent predictive factor for ISR, and should be one of the guidelines for medical therapy and interventional strategy to prevent ISR in diabetic patients.
doi:10.3349/ymj.2005.46.1.78
PMCID: PMC2823061  PMID: 15744809
Diabetes mellitus; coronary artery disease; angioplasty; restenosis
15.  Spontaneous disruption of mycotic aneurysm involving innominate artery. 
Journal of Korean Medical Science  2003;18(4):589-591.
We report a case of ruptured mycotic aneurysm involving innominate artery requiring an urgent surgical treatment. A 62-yr-old woman presented with fever and dyspnea. Previously, she was diagnosed with colon cancer and received right hemicolectomy and one cycle of adjuvant chemotherapy. On echocardiogram, pericardial effusion was noted and emergency pericardiocentesis was performed. CT scan revealed aortic aneurysm involving ascending aorta and innominate artery, and thrombi surrounding those structures. Patch repair of the defect in the ascending aorta and ringed Goretex graft to bypass the innominate and ascending aorta were performed. We believe that this is the first case of ruptured mycotic aneurysm involving innominate artery.
PMCID: PMC3055067  PMID: 12923339

Results 1-15 (15)