No abstract available.
Aged* ; Blood Platelets* ; Glycoproteins* ; Humans ; Myocardial Infarction* ; Percutaneous Coronary Intervention*

BACKGROUND: The high concentration of plasma total homocysteine is recently considered an independent risk factor for atherosclerosis. The purpose of this study was to provide reference ranges for plasma homocysteine levels and to investigate the relationship between plasma homocysteine and cardiovascular risk factors in healthy Korean men. METHODS: Anthropometric parameters, alcohol intake, cigarette use and nutrient intake were determined in 166 healthy men within a wide age range(30-69 yr). Serum levels of lipids, glucose and insulin levels during oral glucose tolerance test(OGTT), plasma amino acid concentrations and levels of antioxidant nutrients and enzymes were also measured. Hyperhomocysteinemia was defined as plasma homocysteine levels above the 90th percentile(> or =15micromol/L) of respective plasma homocysteine distribution in study subjects. Characteristics of hyperhomocysteinemic men(n=16) were compared to normohomocys- teinemic men(n=16) matched for age and body mass index. RESULTS: Plasma total homocysteine values ranged from 2.4 to 38.1micromol/L, a skewed, right-tailed distribution. The homocysteine levels of 25th, 50th and 75th percentile were 7.02, 9.61 and 12.4micromol/L, respectively. The mean concentration of plasma total homocysteine was 10.7micromol/L. Plasma total homocysteine level was positively correlated to body mass index, serum cholesterol and triglyceride levels and alcohol intake, but negatively correlated to serum bata-carotene concentration. In multivariate analysis, serum triglyceride level was the strongest determinant of plasma total homocysteine concentration. There were no significant differences between two groups in waist to hip ratio, alcohol intake, cigarette use, blood pressure and serum levels of glucose and insulin during OGTT. Hyperhomocysteinemic men had significantly higher mean values of serum triglyceride(258mg/dl), total cholesterol(226mg/dl), and LDL-cholesterol(140mg/dl) than normohomocysteinemic men. Hyperhomocysteinemic men showed a decrease in lipid corrected values of serum bata-carotene and alpha-tocopherol and plasma concentrations of serine and taurine, when compared to normohomocysteinemic men. The mean intakes of vitamin B6, folate, vitamin B12 and bata-carotene tended to decline by 25-30% in hyper- homocysteinemic group, when compared to normohomocysteinemic group. CONCLUSION: Our results indicate that healthy Korean men with hyperhomocys- teinemia show signs of hyperlipidemia and decreased antioxidants nutrients and these factors increase risk for coronary artery disease. In addition, hyperhomocysteinemia may affect amino acid metabolism related to homocysteine.
alpha-Tocopherol ; Antioxidants ; Atherosclerosis ; Blood Pressure ; Body Mass Index ; Cholesterol ; Coronary Artery Disease ; Folic Acid ; Glucose ; Glucose Tolerance Test ; Homocysteine* ; Humans ; Hyperhomocysteinemia ; Hyperlipidemias ; Insulin ; Male ; Metabolism ; Multivariate Analysis ; Plasma* ; Reference Values ; Risk Factors* ; Serine ; Taurine ; Tobacco Products ; Triglycerides ; Vitamin B 12 ; Vitamin B 6 ; Waist-Hip Ratio

Thrombomodulin (TM) is thrombin receptor present on the luminal surface of endothelial cells. Because the thrombin-TM complex acts as an anticoagulant, the functional variants or deficiency of TM may lead to increment of thrombotic tendency. In this study, we screened the genetic variants of the TM gene in patients with myocardial infarction (MI) and analyzed the genotype to elucidate the effects of genetic variations of TM gene on the development of the MI. We screened a promoter region and coding sequence of the TM gene using single strand conformation polymorphism-heteroduplex analysis and identified three common genetic variants: those were TM G-33A, TM Ala455Val, and TM C1922T. The genotype frequencies were investigated in the patients with MI (n=234) and control subjects (n=291) by the method of allele-specific oligomer hybridization. The frequencies of mutant genotypes (TM -33A, TM 455Val, and TM 1922T) were higher in patient group compared to the control subjects in males while there were no significant differences in females. In the multiple logistic regression analysis, TM 455Val and TM 1922T alleles were independent risk factors for MI (OR[95% CI: 1.799[1.125-2.878] p=0.014 and 5.624[1.019-31.025], p=0.048, respectively) in males. However, the genetic variations were not independent risk factors for MI in females. There were significant linkage disequilibriums among three genetic variants. These linkage disequilibriums explain the similar effects of three genetic variants on the development of MI. To investigate the effect of the TM G-33A mutation on TM promoter activity, the two TM promoter constructs (pTM-355 and pTM-125, bearing TM -33G or TM -33A) containing of firefly luciferase gene were transfected into HepG2, BAE, and CHO cells. The promoter activities were higher in the promoter constructs with TM -33G compared to the constructs with TM -33A in pTM-355. These results suggest the possibility of the positive predisposing effect of TM -33A allele on MI in males. The functional study for TM Ala455Val and TM C1922T should be followed to elucidate the genotype effects of these mutations on the development of MI. In this study, we identified three genetic variants of TM gene and showed the significant associations between genetic variants and MI in males. These results proposed that TM gene is an attractive candidate for genetic risk factor for MI in Koreans.
Alleles ; Animals ; CHO Cells ; Clinical Coding ; Cricetinae ; Endothelial Cells ; Female ; Fireflies ; Genetic Variation ; Genotype ; Humans ; Linkage Disequilibrium ; Logistic Models ; Luciferases ; Male ; Myocardial Infarction* ; Phenobarbital ; Promoter Regions, Genetic ; Receptors, Thrombin ; Risk Factors* ; Thrombomodulin

BACKGROUND: The real incidence of atherosclerotic lesions in carotid and peripheral arteries in coronary artery disease patients is not well known in Korea. The aim of this study was to prospectively evaluate the prevalence of atherosclerotic involvement of the coronary, carotid, and peripheral arteries in each arterial disease patients. This study was also designed to evaluate the risk factors, the clinical characteristics of associated carotid artery stenosis in patients with coronary artery disease, and associated peripheral vascular disease in patients with coronary artery disease. METHODS: Between June 1996 and March 1998, 475 patients (369 males, 106 females, mean age 60+/-10 years) were studied. Three hundred and seventy-three patients who presented with ischemic symptoms were enrolled in the coronary artery disease group, 81 patients were enrolled in the peripheral vascular disease group due to presenting claudications, and 21 patients were enrolled in the carotid stenosis group due to presenting cerebrovascular symptoms. Coronary angiography was done by the routine method. Carotid angiography was performed at the aortic arch by the digital subtraction angiography method. Peripheral vascular angiography was taken from the suprarenal abdominal aorta to both femoral arteries. RESULTS: 1) Risk factors for coronary stenosis, peripheral vascular disease, and carotid stenosis: The risk factors were not different between coronary stenosis, peripheral vascular disease, and carotid stenosis groups, but smoking was more frequent among patients with peripheral vascular disease than in patients with coronary stenosis (p-value=0.001). 2) Coronary artery stenosis and carotid artery stenosis: The mean age of coronary artery patients with carotid stenosis was significantly older (p-value=0.006) than for patients without carotid stenosis. The prevalence of peripheral vascular disease was more common in patients with carotid stenosis than in patients without carotid stenosis. 3) Coronary artery stenosis and peripheral vascular disease: Carotid stenosis was more common inpatients with peripheral vascular disease than in patients without peripheral vascular disease in the coronary stenosis group. 4) Prevalence of coronary, carotid, and peripheral artery disease: In patients with coronary stenosis, the prevalence of carotid stenosis was 13.9% and that of peripheral vascular disease was 29.2%. In patients with peripheral artery stenosis, the prevalence of coronary stenosis was 45.7% and that of carotid artery disease was 33.3%. In patients with carotid stenosis, the prevalence of coronary stenosis was 81.0% and that of peripheral vascular disease was 52.4%. CONCLUSION: Carotid artery disease and peripheral vascular disease developed concurrently with coronary artery disease in a significant proportion of patients. Therefore, routine angiography of peripheral and carotid arteries in patients with coronary artery disease is considered, especially in old age.
Angiography* ; Angiography, Digital Subtraction ; Aorta, Abdominal ; Aorta, Thoracic ; Arteries ; Carotid Arteries* ; Carotid Artery Diseases ; Carotid Stenosis ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease ; Coronary Stenosis ; Coronary Vessels ; Female ; Femoral Artery ; Humans ; Incidence ; Inpatients ; Korea ; Male ; Peripheral Arterial Disease ; Peripheral Vascular Diseases ; Prevalence ; Prospective Studies ; Risk Factors ; Smoke ; Smoking

After coronary stent implantation, neointima formation resembles the wound healing process as it involves the sequential processes of inflammation, granulation, and remodeling. Because antiproliferative drugs and polymers of drug-eluting stents (DESs) delay vascular healing compared with bare metal stents, fibrin deposition can remain long after stent implantation, or inflammation can be excessive. Delayed vascular healing can be associated with adverse clinical outcomes including DES thrombosis or restenosis, and poor endothelization of DES neointima can accelerate neoatherosclerotic change inside the neointima, further contributing to luminal restenosis or neointimal instability. Despite the lack of correlation between pathologic and optical coherence tomography (OCT) findings, OCT assessments of neointima under various circumstances can reveal vascular responses to stent therapy. Homogeneous, heterogeneous, and layered neointima patterns can be recognized by OCT and can change with time. Homogeneous neointima might be associated with better clinical outcomes after DES implantation, whereas non-homogeneous neointima or neoatherosclerotic change can be associated with poorer clinical outcomes. However, limited data are currently available, and further studies are required to comprehensively address these questions.
Coronary Artery Disease ; Drug-Eluting Stents* ; Fibrin ; Inflammation ; Neointima* ; Phenobarbital ; Polymers ; Stents ; Thrombosis ; Tomography, Optical Coherence ; Wound Healing

BACKGROUND AND OBJECTIVES: Perfluorocarbon exposed sonicated dextrose albumin (PESDA) microbubbles has been suggested to facilitate thrombus disruption under the transcutaneous ultrasound (US). Thus, we investigated whether such a noninvasive approach could augment thrombolytic effect of fibrinolytic agent in an experimental thrombotic model. MATERIALS AND METHODS: Thrombus formation was induced with electrical injury in the rabbit iliofemoral arteries (n=20): Thrombus occlusion was documented by angiography in all arteries. In the control group, only tissue plasminogen activator (t-PA, 3 mg/kg) was administered intrav-enously in five rabbits. In the Group 1 (n=9), injured arteries were exposed to transcutaneous US (20 kHz, 30 W/cm2, continuous mode) with t-PA (3 mg/kg). In the Group 2 (n=6), the same treatment was given while administering PESDA continuously (10 ml/min, intravenous). Angiographic results were evaluated at 10 minute interval for 1 hour respectively. RESULTS: In the control group, two of five iliofemoral arteries (40.0%) were recanalized and one of nine iliofemoral arteries (11.1%) was recanalized in Group 1. In contrast, four of six iliofemoral arteries (66.7%) were recanalized angiographically in Group 2 (p=0.392 vs. control group: p=0.047 vs. Group 1). However, late reocclusion occurred in all iliofemoral arteries of Group 2. CONCLUSION: Although PESDA with transcutaneous US significantly enhanced initial angiographic patency rate of t-PA, it was associated with high rate of reocclusion. Further studies will be necessary for clinical application of this noninvasive method in acute arterial occlusion.
Angiography ; Arteries ; Glucose* ; Microbubbles ; Rabbits ; Thrombolytic Therapy* ; Thrombosis ; Tissue Plasminogen Activator ; Ultrasonography*

BACKGROUND: Plaque compression (and/or redistribution) and vessel expansion are important mechanisms of percutaneous coroanry balloon angioplasty. We investigated the mechanisms of balloon angioplasty according to plaque characteristics by intravascular ultrasound and assessed the time-sequencing morphometric changes of target vessel after balloon dilation without catheter change using intravascular ultrasound balloon catheter. METHOD: We studied balloon angioplasty in 10 patients (eight male, average age of 55.3 years). Quantitative coronary angiography and intravascular ultrasound images were attained at baseline and at timed intervals of 0sec, 60sec and 180sec post-balloon angioplasty. The following categories were attained : reference diameter, minimal lumen diameter, cross sectional area (CSA) of lumen (L), external elastic membrane (EEM), and plaque + media (P+M). We also assessed the plaque morphology of target lesion and classified them into two groups according to intravascular ultrasound imaging : a soft plaque group versus a group characterized by fibrous and/or mildly calcified plaque. RESULTS: The proportions of plaque compression in the total luminal gain were 80% in the soft plaque group and 70% in the other ; the absolute amount of plaque compression was 26.9% in soft plaque and 24.0% in the other group. The time sequencing changes of target lesion EEM CSA of both group were 14.4+/-2.9mm2, 14.3+/-3.8mm2 (baseline) 15.1+/-2.5mm2, 15.4+/-3.7mm2 (immediate) 15.0+/-2.8mm2, 14.5+/-3.9mm2 (180sec), those of P+M CSA (target lesion) were 10.4+/-3.3mm2, 10.7+/-2.4mm2 (baseline) 7.6+/-2.7mm2, 8.1+/-2.4mm2 (immediate) 7.9+/-2.9mm2, 8.5+/-3.4mm2 (180sec). Target lesion lumen CSA were 4.0+/-1.1mm2, 3.6+/-2.0mm2 (baseline) 7.5+/-1.1mm2, 7.3+/-3.2mm2 (immediate) 7.1+/-1.3mm2, 6.0+/-1.7mm2 (180sec) respectively. CONCLUSION: Plaque compression (and/or redistribution) is the predominant mechanism of luminal gain in both groups. The absolute amounts of P+M CSA changes and time sequencing increment of target lesion were similar in both groups. In the non-soft group, the immediate increment and time sequencing reduction of EEM CSA in target lesion were greater than those of the soft plaque group.
Angioplasty ; Angioplasty, Balloon ; Angioplasty, Balloon, Coronary* ; Catheters ; Coronary Angiography ; Humans ; Male ; Membranes ; Phenobarbital ; Ultrasonography

BACKGROUND: A stenosis of left main coronary artery has critical prognostic importance. Recent reports on successful left main stenting are now challenging traditional treatment patterns for this lesion. We evaluated recent four-year trends in incidence, clinical, angiographic findings and treatment modalities in patients with left main coronary artery stenosis(LMS). METHODS: Patients who were diagnosed as a significant LMS at Yonsei cardiovascular hospital between 1996 and 1999 were analyzed retrospectively. RESULTS: The incidence of LMS during the period of 1996 to 1999 was 3.3%(n=24) and it was significantly higher than that of previous 15 years before 1996(p<0.01). The incidence of isolated ostial lesion was 0.28% and this lesion was more prevalent in young female patients with less risk factors compared with other types of LMS(p<0.01). After exclusion of the patients with an isolated ostial lesion, patients were grouped according to the lesion site: ostium, shaft, and shaft lesion extended to distal vessels. There were no differences in clinical and hemodynamic findings among these groups. Coronary artery bypass graft was performed in 141 patients(63%) and stent implantation in 16 patients(14%). CONCLUSION: The incidence of LMS has been increased. There was no difference in clinical and hemodynamic findings according to the types of LMS. Surgery is still a standard treatment, but in selected patients percutaneous coronary intervention can be another treatment option.
Constriction, Pathologic ; Coronary Artery Bypass ; Coronary Stenosis* ; Coronary Vessels* ; Female ; Hemodynamics ; Humans ; Incidence ; Percutaneous Coronary Intervention ; Retrospective Studies ; Risk Factors ; Stents ; Transplants

BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.
Antifibrinolytic Agents ; Fibrinogen ; Fibrinolytic Agents ; Humans ; Myocardial Infarction* ; Plasma ; Protein C ; Protein S ; Thrombolytic Therapy ; Tissue Plasminogen Activator* ; Urokinase-Type Plasminogen Activator*

BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.
Antifibrinolytic Agents ; Fibrinogen ; Fibrinolytic Agents ; Humans ; Myocardial Infarction* ; Plasma ; Protein C ; Protein S ; Thrombolytic Therapy ; Tissue Plasminogen Activator* ; Urokinase-Type Plasminogen Activator*