BACKGROUND: It is well known that intracoronary thrombolysis during the early period of acute myocardial infarction leads to the limitation of myocardial necrosis, preserves left ventricular function, and improves survivals. The recanalization rate of intracoronary rrokinase infusion into infarct-related coronary artery was known as 62-94 percents in previos studies. The various factors influence the outcome of intracoronary thrombolysis, including total dose of urokinase, time from onsrt of chest pain to thrombolysis. The purpose of this study was to evaluate whether the occlusion site morphology influences recanalization rates of intracoronary thrombolysis. METHODS: We evaluated infarct-related coronary artery morphology of 56 acute mycardial infarction patients who performed intracoronary thrombolytic therapy within 6-12 hours after the onset of acute myocardial infarction. Intracoronary urokinase infusion was performed at a rate of 25000 IU/minute. The presence of calcification, collaterals, side branches and the stump site morphologies(thrombus type, pencil type, cutting type) were identified on magnified 35mm cine frames. RESULTS: Reperfusion was successed in 34 patients and failed in 22 patients. There were no statistically significant difference in the pressure of calcification, collaterals, and side branches between success and failure groups. Intracoronary thrombus was identified in 21 percent of success group, but not in failure group. The reperfusion rates according to stump site morphology were 76% in thrombus type, 58% in cutting type, and 42% in pencil type(p<0.05). CONCLUSION: Our study indicates the presence of intracoronary thrombus and the morphology of thrombus type is more effective in intracoronary thrombolysis in acute myocardial infarction. The identification of types of the coronary obstruction will be helpful for the selection of intracoronary thrombolysis in acute myocardial infarction patients. And the results suggest that the difference of stump composition show different stump morphologies.
Chest Pain ; Coronary Vessels* ; Humans ; Infarction ; Myocardial Infarction* ; Necrosis ; Reperfusion ; Thrombolytic Therapy ; Thrombosis ; Urokinase-Type Plasminogen Activator ; Ventricular Function, Left

BACKGROUND AND OBJECTIVES: The myocardial protective effect of ischemic preconditioning is well known. However, the mechanism is remains unclear. The purpose of this study is to determine the role of adenosine, protein kinase C, KATP channel and the change of monophasic action potential duration on cardioprotective effect of ischemic preconditioning in cat. Materials AND METHODS: In this experiment, 66 cats were allocated into 7 groups:control (n=10), ischemic preconditioning (n=10), adenosine pre-treated (n=10), SPT (8-p-sulfophenyl theophylline) pre-treated (n=9), polymyxin B pre-treated (n=9), glibenclamide pre-treated (n=9) and nicorandil pre-treated (n=9) groups. Ischemic preconditioning was performed in ischemic preconditioning, SPT pre-treated, polymyxin B pre-treated and glibenclamide pre-treated groups by 3 episodes of 5 minutes ischemia and 10 minutes reperfusion. All animals were subjected to 40 minutes of ischemia and 40 minutes reperfusion. Monophasic action potential duration at 50% repolarization (MAP50) was measured in the ischemic and non-ischemic area respectively by epicardial probe throughout the experiment. The effect of ischemic preconditioning was determined by infarct size (% area at risk). RESULTS: Ischemic preconditioning, adenosine pre-treatment and nicorandil pre-treatment groups demonstrated a significant reduction in infarct size (26+/-4%, 25+/-4% and 34+/-8% infarction of the risk zone, respectively, p<0.01, p<0.01 and p<0.05 vs. control) with respect to control (41+/-8% infarction of the risk zone). However, pretreatment with SPT, polymyxin B or glibenclamide abolished the effect of ischemic preconditioning. Ischemic preconditioning group exhibited a significant reduction of MAP50 duration in the ischemic area during preconditioning;at the first preconditioning 128+/-11 msec vs. 144+/-10 msec control, at the second preconditioning 110+/-10 msec vs.147+/-10 msec control (p<0.01), at the third preconditioning 114+/-10 msec vs. 145+/-11 msec control (p<0.05). But, pretreatment with SPT, polymyxin B and glibenclamide prevented the reduction of MAP50 in the ischemic area during ischemic preconditioning. During 40 minutes ischemia, the shortening of MAP50 was more pronounced in the preconditioned group than in control group;at 5 minutes 112+/-13 msec vs. 124+/-10 msec control, at 10 minutes 89+/-12 msec vs. 133+/-11 msec control (p<0.05 ), at 20 minutes 93+/-12 msec vs. 136+/-11 msec control (p<0.05), and at 30 minutes 107+/-19 msec vs. 144+/-14 msec control (p<0.05). In adenosine pre-treated group, the MAP50 was significantly shortened than control group throughout 40 minutes occlusion period;at 5 minutes 90+/-8 msec (p<0.05), at 10 minutes 77+/-9 msec (p<0.05), at 20 minutes 92+/-8 msec (p<0.05), and at 30 minutes 103+/-8 msec (p<0.05). Nicorandil pretreatment pronounced the ischemic shortening of MAP50 in ischemic area and the effect was significant during early ischemic period;at 10 minutes 98+/-22 msec (p<0.05 vs. control). In pretreatment groups with SPT, polymyxin B or glibenclamide, the ischemic preconditioning of MAP50 measured in non-ischemic area was not significantly different compared with control group. MAP50 measured in ischemic area during reperfusion was not significantly different between groups. CONCLUSION: Based on this study, adenosine receptor-protein kinase C-KATP channel activation and monophasic action potential duration shortening during ischemia play an important role in myocardial protection during ischemic injury.
Action Potentials* ; Adenosine* ; Animals ; Cats* ; Glyburide ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Nicorandil ; Phosphotransferases ; Polymyxin B ; Protein Kinase C* ; Protein Kinases* ; Receptors, Purinergic P1* ; Reperfusion

BACKGROUNG AND OBJECTIVES: To evaluate the clinical and prognostic significance of precordial ST segment depression in precordial leads on admission electrocardiogram (ECG) in acute inferior myocardial infarction treated with intravenous thrombolytic therapy. We analysed about clinical and angiographic characters. MATERIALS AND METHOD: ECG findings in 50 patients with acute inferior myocardial infarction were retrospectively studied with results of coronary angiography and clinical informations. We classified all patients in two group according to the admissional ECG. Twenty nine patients (Group A) had no or <1.0 mm ST depression in precordial lead and Twenty one patients (Group B) had > or =1.0 mm ST depression in two or more precordial (V1-V6) leads were included in this group. RESULTS: In precordial ST segment depression in acute inferior myocardial infarction patients had higher plasma peak mean CK levels (1945+/-1419 vs 3547+/-2728 IU/L, p=0.027) and lower LV ejection fraction (62+/-10% vs 53+/-11%, p=0.008) and lower left ventricle global chordal shortening (0.89+/-0.71 vs -1.39+/-0.94, p=0.046) and inferior wall chordal shortening (-1.68+/-1.11 vs -2.43+/-0.74, p=0.014) and higher Killip class (1.3+/-0.8 vs 2.4+/-1.4, p=0.002) than without precordial ST segment depression patients. CONCLUSION: In conclusion acute inferior myocardial infarction with precordial ST depression patients had more extensive myocardial damage with global and inferior left ventricle severe wall motion dysfunction. Therefore, this suggests a worse prognosis in acute inferior myocardial infarction with precordial ST depression than without precordial ST depression patients. We need more aggressive diagnosis and treatment in this patients to prevent extending myocardial damage.
Coronary Angiography ; Depression* ; Diagnosis ; Electrocardiography ; Heart Ventricles ; Humans ; Inferior Wall Myocardial Infarction* ; Plasma ; Prognosis ; Retrospective Studies ; Thrombolytic Therapy

BACKGROUND AND OBJECTIVES: QT dispersion (QTd) is defined as the difference between the maximum and minimum QT interval in any of the 12 leads of the surface ECG. QTd has been shown to reflect regional variations in ventricular repolarization. Ischemic dilated cardiomyopathy (DCM) may lead to more spatial and temporal dispersion in ventricular repolarization than idiopathic DCM. The purpose of this study was to determine the difference of QTd between patients who had ischemic and idiopathic DCM. MATERIALS AND METHODS: The study population included 30 patients with ischemic DCM and 30 with idiopathic DCM. All standard 12-lead ECGs were examined prospectively by two observers who were unware of the patient's details. RESULTS: QTd in ischemic DCM was significantly higher than that in idiopathic DCM (63+/-32 vs. 44+/-26 msec, p=0.012) and JTd in ischemic DCM was significantly higher than that in idiopathic DCM (48+/-21 vs. 36+/-22 msec, p=0.036). Results did not change when Bazett's QTc and JTc was substituted for QT (QTcd:69+/-33 vs. 52+/-28 p=0.039) and JT (JTcd:56+/-21 vs. 41+/-25 p=0.043). CONCLUSION: Ischemic DCM has increased spatial inhomogeneity of repolarization probably due to more regional myocardial damages compared with idiopathic DCM. The value of QT dispersion as an easily accessible, non-invasive method in predicting the risk of life threatening arrhythmia and overall mortality in patients with dilated cardiomyopathy must be confirmed in prospective trials.
Arrhythmias, Cardiac ; Cardiomyopathy, Dilated* ; Electrocardiography ; Heart Failure ; Humans ; Mortality ; Prospective Studies

Recently, there have been many changes in the area of healthcare. There is no certainty how these changes will affect the healthcare system and public health. However, to at least have these changes positively implemented, it is clear that evaluation through continuous monitoring is necessary. The enforcement of the Medical Institution Accreditation and Medical Dispute Mediation Law as well as legal revisions regarding the public healthcare system are changes to improve the quality of healthcare, while at the same time, provide penalties for infractions of the new law such as medicine/medical device rebates; moreover, legal revisions regarding telemedicine are anticipated to impartially vitalize technical development as well as the pharmaceutical industry. For these changes to have a positive effect on the medical field and people's lives, an accurate comprehension of the system and understanding of the details is necessary to be able to respond sensitively to any changes in the future. Therefore, this paper examined the background information on the current discussion on the changes in the healthcare system, examined the detailed content of the system, and reviewed the areas that were in dispute as well as the main issues to contemplate the expected effects of the changes and future tasks that may be generated as a result. These considerations will act as foundation for an in depth understanding of recent trends in the healthcare system.
Accreditation/legislation & jurisprudence ; Delivery of Health Care/*legislation & jurisprudence ; Health Care Reform ; Humans ; Quality of Health Care ; Telemedicine

BACKGROUND/AIMS: Inflammation plays a key role in the pathogenesis and progression of cardiovascular disease (CAD). A small number of recent studies reported anti-inflammatory therapy achieved a reduction of CAD progression. The aim of the present study was to explore the roles of inflammatory markers and the conventional risk factors for CAD progression. METHODS: One hundred and fifty patients (58+/-10 years, 112 men) who underwent percutaneous coronary intervention and follow-up angiography (mean duration, 7.5+/-2.0 months) were enrolled in this study. On comparison of the coronary angiographic findings, the patients were divided into the progression and non-progression groups. The serologic inflammatory markers were angiography measured at the time of follow up. The clinical characteristic and inflammatory markers were compared between the two groups and the independent predictors of CAD progression were analyzed. CAD progression was defined as more than 30% diameter reduction of a pre-existing luminal stenosis. RESULTS: CAD progression occurred in 32 patients (21.3%). The frequency of diabetes mellitus (37.5% versus 19.5%, respectively, p=0.033) and the number of the disease vessels (p=0.003) were higher in the CAD progression group. In terms of the inflammatory markers, the progression patients had higher hsCRP (p=0.023), MCP-1 (p=0.036), sVCAM-1 (p=0.000), sP-selectin (p=0.000) and sCD40L (p=0.001) levels. Multiple logistic regression analysis of the variables showed that the logCRP (relative risk (RR) 5.016, CI=1.384-18.177, p=0.014) logVCAM-1 (RR 11.854, CI=1.883-74.614, p=0.008) and triple vessel disease of the coronary arteries (RR 5.037, CI=1.550-16.350, p=0.007) were independent predictors of CAD progression. CONCLUSION: In the present study, the extent of coronary artery disease and inflammatory markers like hsCRP and VCAM-1 were independent predictors for the progression of atherosclerotic lesions.
Angiography ; Atherosclerosis ; Cardiovascular Diseases ; Cell Adhesion Molecules ; Constriction, Pathologic ; Coronary Artery Disease ; Coronary Disease ; Coronary Vessels ; Diabetes Mellitus ; Follow-Up Studies ; Glycosaminoglycans ; Humans ; Inflammation ; Logistic Models ; Percutaneous Coronary Intervention ; Phenobarbital ; Risk Factors ; Vascular Cell Adhesion Molecule-1

BACKGROUND: Patients with acute non-traumatic chest pain are among the most challenging patients for care by emergency physicians, so the correct diagnosis and triage of patients with chest pain in the emergency department(ED) becomes important. To avoid discharging patients with acute myocardial infarction(AMI) without medical care, most emergency physicians attempt to admit almost all patients with acute chest pain and order many laboratory tests for the patients. But in practice, many patients with non-cardiac pain can be discharged with simple tests and treatment. These patients occupy expensive intensive care beds, substantially increasing financial cost and time of stay at ED for the diagnosis and treatment of myocardial ischemia and AMI. Despite vigorous efforts to identify patients with ischemic heart disease, approximately 2% to 5% of patients presented to the ED with AMI and chest pain are inadvertently discharged. If the cause for the chest pain is known, rapid and accurate diagnosis can be implemented, preventing wastes in time and money and inadvertent discharge. Methods and Results: The medical records of 488 patients from Jan. 1 to Dec. 31, 1997 were reviewed. There were 320(angina pectoris 140, AMI 128) cases of cardiac diseases, and 168(atypical chest pain 56, pneumothorax 47) cases of non-cardiac diseases. The number of associated symptoms were 1.1+/-0.9 in non-cardiac diseases, 1.4+/-1.1 in cardiac diseases and 1.7+/-1.1 in AMI(p<0.05). In laboratory finding the sensitivity of electrocardiography(EKG) was 96.1%, while the sensitivity of myoglobin test ranked 45.1%. Admission rate was 71.6% in for cardiac diseases and 50.6% for non-cardiac diseases(p<0.01). Mortality rate was 8.8% in all cases, 13.8% in cardiac diseases, 0.6% in non-cardiac diseases, and 28.1% especially in AMI. CONCLUSION: In conclusion, all emergency physicians should have thorough knowledge of the clinical characteristics of the diseases which cause non-traumatic chest pain, because a patient with any of these life-threatening diseases would require immediate treatment. Detailed history on the patient should be taken and physical examination performed. Then, the most simple diagnostic approach should be used to make an early diagnosis and to provide treatment.
Chest Pain* ; Diagnosis ; Early Diagnosis ; Emergencies* ; Emergency Service, Hospital* ; Heart Diseases ; Humans ; Critical Care ; Medical Records ; Mortality ; Myocardial Ischemia ; Myoglobin ; Physical Examination ; Pneumothorax ; Thorax* ; Triage

A 21-year-old woman found to be hypertensive was referred for hypertension. On examination, blood pressure was 170/110mmHg in the right arm, 160/100mmHg in left arm,and 120/70mmHg in legs. A grade 2/6 systolic ejection murmur was present at the left upper sternal border, and a chest x-ray revealed a rib notching on the inferior margin of 4th rib. Two-dimensional echocardiogram showed the coarctation of aorta beyound the origin of the left subclavian artery. Biplane TEE demonstrated a discrete narrowing of the descending aorta at the site of coarctation. The blood pressure was 169/86mmHg in ascending aorta and 118/84mmHg in descending aorta. Aortogram showed a localized coarcted aortic segment of 7mm in diameter and 5mm long just distal to the left subclavian artery. Balloon coarctation angioplasty was performed with 7F 30x15mm pediatric balloon dilatation catheter. Balloon position was confirmed on fluoroscopy by the hourglass appearance of the balloon inflation and thereafter, the balloon was inflated until the waist of the balloon disappeared. After procedure, a pull back pressure tracing across the coarctation of aorta revealed no pressure gradient between ascending and descending aorta with 141/90mmHg. Aortogram showed an increase in diameter of the coarctation of aorta to 18mm with aneurysmal formation. 3 months later, follow up aortogram showed no significant change in diameter of coarctation of aorts or aneurysmal formation. Nonsurgical balloon coarctation angioplasty appears to be an alternative therapy for the coarctation of aorta in adults.
Adult* ; Aneurysm ; Angioplasty* ; Angioplasty, Balloon ; Aorta ; Aorta, Thoracic ; Aortic Coarctation* ; Arm ; Blood Pressure ; Catheters ; Dilatation ; Female ; Fluoroscopy ; Follow-Up Studies ; Humans ; Hypertension ; Inflation, Economic ; Leg ; Ribs ; Subclavian Artery ; Systolic Murmurs ; Thorax ; Young Adult

BACKGROUND: Cryopreservation can cause mechanical and chemical stress, ultimately leading to the formation of reactive oxygen species (ROS) and oxidative stress. ROS inhibits the expression of antioxidant enzymes in cells, resulting in increased DNA fragmentation and apoptosis. In this paper, we used a vitrification method that has the advantage of producing less ice crystal formation, cost-effectiveness, and time efficiency during cryopreservation. The objective of this paper is to evaluate the degree of protection of ovarian tissue against oxidative stress when N-acetylcysteine (NAC) and Klotho proteins are treated in the vitrification process of ovarian tissue. METHODS: The control group and the cryopreservation groups were randomly assigned, and treated NAC, Klotho, or the combination (NAC ? Klotho). The cell morphological change, DNA damage, senescence, and apoptosis of each group after the freeze–thaw process were compared using transmission electron microscopy, immunohistochemistry, and western blot analysis. RESULTS: Both NAC and Klotho were found to be more effective at protecting against DNA damage than the control;however, DNA damage was greater in the NAC ? Klotho group than in the group treated with NAC and Klotho, respectively. DNA damage and cellular senescence were also reduced during the vitrification process when cells were treated with NAC, Klotho, or the combination (NAC ? Klotho). NAC increased apoptosis during cryopreservation, whereas Klotho inhibited apoptosis and NAC-induced apoptosis. CONCLUSION This study highlights Klotho’s benefits in inhibiting DNA damage, cell senescence, and apoptosis, including NAC-induced apoptosis, despite its unclear role in vitrification.

We report on a case of ischemic dysfunction of the sinus node as a complication after percutaneous transluminal coronary angioplasty of the distal left circumflex artery. After local thrombolytic therapy in the sinus node artery, sinus node arterial flow was re-established and sinus node function normalized over the period of a week. Our experience suggests that immediate reperfusion of a totally occluded nodal artery can be re-established. Ischemic dysfunction of the sinus node, as a complication of angioplasty, is generally transient and requires a prolonged period for recovery. Therefore the decision to implant a permanent pacemaker should be delayed for at least one week after the ischemic insult.
Urinary Plasminogen Activator/administration & dosage/*therapeutic use ; Thrombolytic Therapy/*methods ; Sinoatrial Node/*physiopathology ; Myocardial Ischemia/*complications/radiography/therapy ; Middle Aged ; Male ; Infusions, Intravenous ; Humans ; Follow-Up Studies ; Fibrinolytic Agents/administration & dosage/*therapeutic use ; Electrocardiography ; Coronary Angiography ; Arrhythmia/diagnosis/*drug therapy/etiology ; Angioplasty, Transluminal, Percutaneous Coronary/adverse effects