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

No abstract available.
Humans ; Peritoneal Dialysis* ; Spinal Cord*

Pacemaker malfunctions are secondary to alterations of the preset pacing rate, irregular pacing failure of sensing, failure of cardiac capture or depolarization, and various combinations of these events. A 76 years old male patients was admitted due to pacemaker malfunction. 2 years ago, he was diagnosed as complete atrioventricular block. And then bipolar permanent pacemaker was implanted. Since then syncopal attack developed repetitivly. 12 lead ECG and 24 hour holter moniter monitoring, revealed pacing and sensing failure, thus we converted bipolar system into unipolar system. since then syncopal attack did not developed again.
Atrioventricular Block* ; Electrocardiography ; Humans ; Male

BACKGROUND: Despite extensive investigation, the clinical features and prognostic significance of the non-Q wave myocardial infarction, when compared with Q wave myocardial infarction, remain controversial. And no definite relationship between EKG findings and infarct related arteries has been reported. METHOD: A retrospective analysis was done on 205 patient with acute myocardial infarction who were undergone coronary angiography and left ventriculography. Among them, 30 patient with non-Q wave myocardial infarction and 175 patients with Q wave myocardial infarction. RESULTS: 1) There was no significant difference between the two groups in risk factors, prevalence of preinfarct angina and preinfarct heart failure. 2) The faction of patients with non-Q wave myocardial infarction who received thromobolytic therapy was significantly less, compared to patient with Q wave myocardial infarction(p<0.0001). 3) The patients with non-Q wave myocardial infarction had a smaller infarct size estimated by peak creatine phosphokinase(p<0.01). But there was no difference in Killip's classification and left ventricular ejection fraction. 4) In patients with non-Q wave myocardial infarction, 87% of the patients had one or more abnormal EKG finding other than Q wave, and the most frequent abnormal finding was primary T wave change. 5) The location of infarct-related artery was significantly different between group(p<0.0001). The most frequently involved coronary artery in non-Q wave myocardial infarction was left circumflex coronary artery, especially in patients with normal EKG findings. 6) There was no significant difference between the two groups in the prognosis. CONCLUSION: There were significant differences between non-Q wave and Q wave myocardial infarction in the infarct size and the location of infarct related arteries. but not in the risk factors, the prevalence of previous coronary artery disease and prognsis. Further prospective and collaborative studies should be performed to define conclusion.
Arteries* ; Classification ; Coronary Angiography ; Coronary Artery Disease ; Coronary Vessels ; Creatine ; Electrocardiography* ; Heart Failure ; Humans ; Myocardial Infarction* ; Prevalence ; Prognosis ; Retrospective Studies ; Risk Factors ; Stroke Volume

BACKGROUND: Coronary artery spasm plays an important role in the pathogenesis of not only variant angina but also other forms of angina,acute myocardial infarction, and sudden death. However precise mechanisms by which coronary spasms occur remains unknown. The role of increased coronary artery tone as a part of pathogenesis of conary spasm and relation to the severity of coronary artery disease are still controversial. Thus we underwent this study to investigate the role of increased coronary artery tone as a part of pathogenesis of conary spasm and realtion to the severity of coronary artery disease. METHODS: Intracoronary acetylcholine and isosorbide dintrate were used as a spasm-provocative agent and vasodilator respectively. We analyzed 176 vessels(69 right coronary artery, 58 left anterior descending coronary artery, 49 left circumflex coronary artery) of 75 patients admitted for evaluation of chest pain syndrome. Among the 176 vessels, spasm occurred in 39 vessels of 25 patients. RESULTS: 1)Coronary artery spasm occured in 30.4%(21/69), 17.2%(10/58), 16.3%(8/49) of right coronary artery, left anterior descending coronary artery, left circumflex coronary artery respectively. 2) There is no relationship between angiographically visible minimal coronary artery disease and occurrence of spasm provoked by acetylcholine. 3) There was no significant difference of coronary risk factor predicting coronary spasm between two groups. 4) There is more significant % vasodilation by isosorbide dintrate(ISDDN) occurred din both the spastic and nonspastic arterial segment of vasospastic angina group than no spasm group(30.2%, 28.4% vs 14.2%, p<0.05). 5) Degree of % vasodilation by ISDN was more significantly larger in vasospastic angina group than no spasm group despite the presence of same amount of angiographically visible minimal coronary artery disease(38.3% vs 12.5%, p<0.05). CONCLUSION: These findings suggests that the occurrence of conronary artery spasm is not related to minimal coronary artery disease. Increased coronary artery tone observed only in vasospastic angina group may be part of pathogenesis of coronary spasm.
Acetylcholine* ; Arteries ; Chest Pain ; Coronary Artery Disease ; Coronary Vessels* ; Death, Sudden ; Humans ; Isosorbide ; Muscle Spasticity ; Myocardial Infarction ; Risk Factors ; Spasm ; Vasodilation

BACKGROUND: Among the various mechanisms of Myocardial reperfusion injuries, neutrophil is thought to be one of them. Endogenous coronary vasodilator adenosine is known to have myocardial protective effect through variable pharmacologic action, influencing the function of several cell types involved in the pathogenesis of myocardial reperfusion injury. This study was designed to determine the beneficial effect of adenosine on the left ventricular function during reperfusion and whether this effect is due to the adenosine on the role of neutrophil. METHODS: 27 open-chest cats were randomly divided into 3 groups. 6 cats received ischemic injury without reperfusion(group 1). 21 cats were subjected to 60 minutes of proximal left anterior descending coronary artery occlusion followed by a 60-minute reperfusion. 11 of 21 cats received intravenous adenosine(0.15mg/Kg/min) infusion starting 5 minutes before reperfusion throughout the entire period(group 3). 10 cats received equal volume of saline instead of adenosine(group 2). RESULTS: 1) During the experimental period, significant decrease of heart rate, blood pressure, RPI, negative dP/dT and increase of LVEDP were noted in group 2 and 3 with no difference between the two groups. The reduction of positve dP/dT was more significant in group 2 at 30 and 60 minute of reperfusion than the preocclusion value(1404+/-111, 1631+/-161 vs 1832+/-169mmHg/sec at baseline, p<0.05). In contrast, positive dP/dT in group 3 at 30 and 60 minute of reperfusion were similar to baseline values(1890+/-92, 2052+/-112 vs 2025+/-227mmHg/sec at baseline, p=NS). These were significantly higher(p<0.05) than untreated group 2. 2) Infarct size was significantly reduced in adenosine-treated group 3, when expressed as a percentage of the area at risk(28.4+/-3.3% vs 44.5+/-3.2% of group 2, p<0.05). The significant increase in myeloperoxidase activity observed after reperfusion was not detected in adenosine treated group 3.(0.18+/-0.05 vs 0.46+/-0.09 unit/100mg wet tissue weight, p<0.05). A significant correlation was present between infarct size (% of left ventricle) and myeloperoxidase activity(r=0.72, p<0.01). 3) Light microscopic examination demonstrated the decreased acute interstitial and intra vascular inflammatory infiltration and capillary plugging together with decreased tendency of incidence of contraction band necrosis in adenosine treated group 3. CONCLUSION: These findings suggest that intravenous administration of adenosine during the early reperfusion period significantly reduces infarct size, improving the early recovery of global ventricular function. The probable cause is the effect of adenosine on neutrophil as one of the various protective mechanisms of adenosine in feline heart model subjected to coronary occlusion and reperfusion, 60 minutes each.
Adenosine* ; Administration, Intravenous ; Animals ; Blood Pressure ; Capillaries ; Cats ; Coronary Occlusion ; Coronary Vessels ; Heart Rate ; Heart* ; Incidence ; Myocardial Reperfusion Injury* ; Myocardial Reperfusion* ; Necrosis ; Neutrophils ; Peroxidase ; Reperfusion ; Reperfusion Injury ; Ventricular Function ; 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

OBJECTIVE: Restenosis after successful PTCA remains the main limitation of this technique. Restenosis is a response to injury of the vessel wall, platelet aggregation, thrombus formation, liberation of growth factors, cellular hyperplasia involving predominantly smooth muscle proliferation and migration, and intercellular matrix formation. The identification of risk factors for restenosis could help to prevent and reduce the impact of this phenomenon. We undertook this study to evaluate retrospectively the association between risk factors and restenosis after PTCA METHODS: We studied 123 patients and 174 lesions that underwent successful PTCA and the follow-up period (from PTCA to follow-up angiography) was 8.2+/-5.8 months in all patients. They were divided into two groups according to the restenosis. Clinical feature, lesional feature, PTCA procedural feature, and other risk factors were compared. Restenosis was defined as the cutoff point of >50% in diameter stenosis at angiographic follow-up. RESULTS: 1) Restenosis was found in 68 lesions after successful PTCA(39.1%). 2) Clinical features of restenosis group are similar to no restenosis group 3) Thrombus (p=0.002), total occlusion(p=0.001), severity of stenosis in the initial lesion(p=0.013) and residual stenosis(p=0.001) were found to be independently associated with restenosis, whereas other lesional characteristics were not. 4) Balloon inflation duration(p=0.017) and dissection(p=0.002) were found to be independently associated with restenosis, whereas other procedural characteristics were not. CONCLUSION: Thrombus, total occlusion, dissection, severity of stenosis in the initial lesion, balloon inflation time, residual stenosis were found to be associated with restenosis after PTCA in our study.
Angioplasty, Balloon, Coronary* ; Constriction, Pathologic ; Follow-Up Studies ; Humans ; Hyperplasia ; Inflation, Economic ; Intercellular Signaling Peptides and Proteins ; Muscle, Smooth ; Platelet Aggregation ; Retrospective Studies ; Risk Factors ; Thrombosis