Search PubMed⌕ Search

Biomedical subjects

Kun-Tai Lee

Publications and source records attributed to Kun-Tai Lee.

52 records · Page 3Linked to original sources
PubMed2004

Effect of electrophysiologic character of ventricular premature beat on heart rate turbulence.

Heart rate turbulence (HRT) has been described as a predictor of high-risk patients with cardiac diseases. The purpose of this study is to determine how the degree of prematurity of a ventricular premature beat (VPB%) and retrograde ventriculoatrial (VA) conduction of VPBs affect HRT. We studied 30 patients without organic heart disease. We calculated turbulent slope (TS) and turbulent onset (TO) from VPBs induced by programmed stimulation from the right ventricular apex. TS was inversely and TO was positively correlated to VPB%. Without retrograde VA conduction of VPBs, TS was inversely and TO was positively correlated to VPB%. In VPBs with retrograde VA conduction, there were no significant correlations between TO and TS with VPB%. In conclusion, TS and TO calculated from VPBs with different degrees of prematurity varied widely. Both VPB% and characteristics of retrograde VA conduction may affect HRT.

Adult↗
PubMed2004

Ankle-brachial pressure index measured using an automated oscillometric method as a predictor of the severity of coronary atherosclerosis in patients with coronary artery disease.

Ankle-brachial pressure index (ABI) measured using a conventional Doppler method is an independent predictor of the number of coronary vessels affected in coronary artery disease (CAD). Recently, a new clinical device has been developed to measure ABI using an oscillometric method. It is unclear whether ABI measured using this device is a significant predictor of the severity of coronary atherosclerosis. We retrospectively included 87 patients from our outpatient clinic who had ever undergone coronary angiography. ABI was determined in all subjects using the new ABI-form device. The lower value of ABI in either limb was used for analysis. We divided our subjects into two groups, with either ABI less than 0.9 or at least 0.9, and compared basal characteristics between groups. We analyzed the relationship between ABI and the severity of CAD. In addition, we calculated the sensitivity, specificity, and positive and negative predictive values of ABI less than 0.9 in predicting multivessel (two-vessel + three-vessel) involvement in our patients. There were 15 patients with ABI less than 0.9 and 72 with ABI at least 0.9. Patients with ABI less than 0.9 were older and had higher plasma levels of uric acid. The prevalence of diabetes mellitus, hypertension, smoking, and diuretic use was significantly higher in patients with ABI less than 0.9. In addition, the group with ABI less than 0.9 had a lower prevalence of one-vessel CAD and higher prevalence of three-vessel or multivessel CAD. The sensitivity, specificity, and positive and negative predictive values of ABI less than 0.9 in predicting multivessel CAD were 22%, 96%, 93%, and 34%, respectively. In conclusion, ABI measured using the automated oscillometric method can be used to predict the severity of coronary atherosclerosis in patients with CAD.

Aged↗
PubMed2004

A case of subarahnoid hemorrhage with persistent shock and transient ST elevation simulating acute myocardial infarction.

Electrocardiographic changes in neurovascular disease are not rare. Patients with subarachnoid hemorrhage have electrocardiographic (ECG) abnormalities that may mimic ischemic heart disease and acute myocardial infarction. Outflow of catecholamines in the early stage of subarachnoid hemorrhage contributes to elevated blood pressure in most patients. Hypotension is a rare presentation in subarachnoid hemorrhage. We report a case of subarachnoid hemorrhage with transient ST elevation and intractable shock simulating acute myocardial infarction, and review the mechanism of ECG changes in subarachnoid hemorrhage.

Aged↗
PubMed2004

Terlipressin-related acute myocardial infarction: a case report and literature review.

Acute ST-segment elevation myocardial infarction after the administration of terlipressin in patients with hemorrhagic esophageal varices is a rare but life-threatening complication. We report the case of a 73-year-old female patient with esophageal variceal bleeding complicated with acute ST-segment elevation myocardial infarction after intravenous injection of terlipressin. We discuss the underlying mechanisms of terlipressin-related acute myocardial infarction and review the literature.

Aged↗
PubMed2004

Mechanism of repolarization change during initiation of supraventricular tachycardia.

INTRODUCTION: Previous literature has documented the association between narrow QRS supraventricular tachycardia (SVT) and pronounced ST-T segment change. The aim of this study was to evaluate repolarization changes during SVT initiation and demonstrate the possible mechanism. METHODS AND RESULTS: Fifty-one consecutive patients (20 men and 31 women; mean age 46.1 +/- 16.4 years) with narrow QRS SVT (32 patients with AV nodal reentrant tachycardia and 19 patients with AV reentrant tachycardia) were included. We retrospectively analyzed the intracardiac recordings and ST-T segment changes on 12-lead surface ECGs during SVT initiation. Twenty-six (51%) patients developed ST segment repolarization changes during SVT initiation. Patients with shorter baseline sinus cycle length, shorter tachycardia cycle length, elevated systolic blood pressure before tachycardia induction, and greater reduction of systolic blood pressure had a higher incidence of repolarization changes. However, multivariate analysis showed that reduction of systolic blood pressure after SVT induction was the only independent predictor of repolarization changes. Furthermore, the maximal degree of ST segment depression during SVT correlated with the reduction of systolic blood pressure (r = 0.75, P < 0.001). CONCLUSION: Repolarization changes during SVT initiation were caused mainly by concurrent hemodynamic change after SVT initiation with abrupt cycle length shortening.

Adult↗
PubMed2004

Mechanism of adenosine-induced termination of focal atrial tachycardia.

INTRODUCTION: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. METHODS AND RESULTS: The study consisted of 7 patients (4 men and 3 women; age 44 +/- 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3-12 mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 +/- 11.7 msec vs 4.7 +/- 4.5 msec, P < 0.001) and standard deviation of normalized AT cycle length (0.033 +/- 0.014 vs 0.011 +/- 0.005, P < 0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (-27.2 +/- 15.3%, P < 0.01), preferential conduction (proximal: -32.1 +/- 18.7, mid: -28.4 +/- 22.8, distal portion: -29.6 +/- 21.4%, P < 0.01), and breakout (-31.4 +/- 12.5%, P < 0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 +/- 1.5 (range 1-4), with maximum shifting distance of 15.0 +/- 3.1 (range 10-19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50% of total shifting origins, without late recurrence. CONCLUSION: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.

Adenosine↗
PubMed2004

Electrophysiological mechanisms and catheter ablation of complex atrial arrhythmias from crista terminalis:.

Paroxysmal atrial fibrillation (PAF) can be initiated by ectopic activation from the crista terminalis. The crista terminalis conduction gap is also a critical isthmus in atrial reentrant arrhythmias like upper and lower loop reentry. The aim of this study was to investigate the mechanism and results of catheter ablation for complex atrial arrhythmias originating from the crista terminalis using the noncontact mapping system (NCM). The study population consisted of six patients (5 men, 1 woman; 70 +/- 9 years) with drug refractory PAF and typical/atypical atrial flutter. NCM identified the earliest ectopic activation originating from the crista terminalis in these six patients. The reentry circuit of atypical atrial flutter propagated around the upper crista terminalis in five patients, and lower crista terminalis in one patient. The reentry circuit of atypical atrial flutter and the initial reentry circuit of AF conducted through the crista terminalis gap in all patients. Radiofrequency applications were delivered on the sites of ectopy, which initiated AF. Substrate modification was also performed over the crista terminalis gap (six patients) and cavotricuspid isthmus (three patients) responsible for the reentry. During a mean follow-up of 9 +/- 5 months (range 5-18 months), five patients were free of AF without antiarrhythmic drugs, and one patient did not have AF or atrial flutter using propafenone. NCM demonstrated the mechanism of crista terminalis ectopy-initiating AF and associated typical/atypical atrial flutter. Catheter ablation of crista terminalis ectopy and substrate for the reentry guided by NCM successfully eliminated these atrial arrhythmias.

Aged↗
PubMed2003

Acute thrombosis after elective direct intracoronary stenting in primary antiphospholipid syndrome: a case report.

Antiphospholipid syndrome (APS) is an uncommon prothrombotic disorder that has been increasingly recognized in recent years. The diagnosis of APS must be associated with venous or arterial thrombosis or both. Patients with APS usually present with recurrent deep vein thrombosis, pulmonary thromboembolism, thromboembolic stroke, or myocardial infarction. Here, we report a case of a 61-year-old female who presented with a 3-month history of increasingly frequent retrosternal chest tightness. After treadmill test and thallium-201 myocardial perfusion scan, she was admitted and underwent elective coronary angiography but developed acute thrombosis after direct intracoronary stenting. She was successfully rescued with repeat percutaneous transluminal coronary angioplasty and prolonged heparin and glycoprotein IIb/IIIa antagonist use. Laboratory data showed prolongation of partial thromboplastin time and positive anti-cardiolipin antibody. These findings satisfied the criteria for APS; the patient was diagnosed with primary APS because she had neither typical symptoms nor signs of systemic lupus erythematosus or other immunologic disorders. Thereafter, long-term oral anticoagulant appeared to be effective. To our knowledge, this is the first report of acute stent thrombosis in a patient with primary APS.

Acute Disease↗
PubMed2003

Spontaneous left main coronary artery dissection: a case report.

Coronary artery dissection is a devastating disease, but spontaneous left main coronary artery dissection is extremely rare. We present the case of a 58-year-old diabetic man who was found to have primary spontaneous left main coronary artery dissection during a coronary angiography examination. Although the dissecting lesion persisted, he had no peri-procedural chest discomfort or electrocardiographic change. We performed urgent coronary artery bypass grafting, which was uneventful. The patient received regular cardiovascular follow-up and did not complain of any postoperative chest discomfort. He had an uneventful recovery.

Aortic Dissection↗
PubMed2003

Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.

BACKGROUND: Increased oxidative stress in end-stage renal disease (ESRD) patients may oxidize macromolecules and consequently lead to cardiovascular events during chronic hemodialysis. Electrolyzed reduced water (ERW) with reactive oxygen species (ROS) scavenging ability may have a potential effect on reduction of hemodialysis-induced oxidative stress in ESRD patients. METHODS: We developed a chemiluminescence emission spectrum and high-performance liquid chromatography analysis to assess the effect of ERW replacement on plasma ROS (H2O2 and HOCl) scavenging activity and oxidized lipid or protein production in ESRD patients undergoing hemodialysis. Oxidized markers, dityrosine, methylguanidine, and phosphatidylcholine hydroperoxide, and inflammatory markers, interleukin 6 (IL-6), and C-reactive protein (CRP) were determined. RESULTS: Although hemodialysis efficiently removes dityrosine and creatinine, hemodialysis increased oxidative stress, including phosphatidylcholine hydroperoxide, and methylguanidine. Hemodialysis reduced the plasma ROS scavenging activity, as shown by the augmented reference H2O2 and HOCl counts (Rh2o2 and Rhocl, respectively) and decreased antioxidative activity (expressed as total antioxidant status in this study). ERW administration diminished hemodialysis-enhanced Rh2o2 and Rhocl, minimized oxidized and inflammatory markers (CRP and IL-6), and partly restored total antioxidant status during 1-month treatment. CONCLUSION: This study demonstrates that hemodialysis with ERW administration may efficiently increase the H2O2- and HOCl-dependent antioxidant defense and reduce H2O2- and HOCl-induced oxidative stress.

Adult↗
PubMed2002

Differential effects of adenosine on antegrade fast pathway, antegrade slow pathway, and retrograde fast pathway in atrioventricular nodal reentry.

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 +/- 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 +/- 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 +/- 0.5, 4.2 +/- 1.6, and 8.5 +/- 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.

Adenosine↗
PubMed2002

Cold effect on qt dispersion in healthy subjects.

Thirty-one healthy subjects, aged 35 +/- 6 (21 to 48) years, were included in the study to evaluate the effect of ice water immersion on QT dispersion. There was no difference in the age between females (n = 11) and males (n = 20). Baseline, stress (at the end of ice water immersion, 4 degrees C, for 3 minutes) and recovery 12-lead electrocardiograms (ECGs) were recorded on each subject. During the test, a significant variability developed in both the QT dispersion (52 +/- 17, 68 +/- 25 and 59 +/- 21 ms; p = 0.015) and the corrected QT dispersion (56 +/- 17, 76 +/- 27 and 64 +/- 23 ms; p = 0.005), but not in the heart rate (74 +/- 11, 76 +/- 9, and 74 +/- 9 bpm, respectively; p = 0.447). There was no inter-sex difference in the baseline heart rate or QT dispersion, or in their response to ice water immersion. Age significantly correlated with the variation of QT dispersion to ice water immersion (r = 0.380, p = 0.035). With 37 years of age as a separation point, the variation of QT dispersion to ice water immersion was more obvious in the older group (28 +/- 22 vs. 10 +/- 19 ms, p = 0.023). In conclusion, cold may increase QT dispersion in healthy subjects, with a more obvious effect in the older ones.

Adult↗
PubMed2002

Changes of coronary risk factors after eradication of Helicobacter pylori infection.

Several epidemiological studies have shown a positive correlation between chronic gastric infection with Helicobacter pylori (HP) and coronary artery disease. A number of reports also claimed that there are strong relationships between HP infection and coronary risk factors. However, clinical studies concerning the changes of coronary risk factors after eradication of HP infection are few and contradictory. We conducted a prospective study aiming to compare sugar, lipid and fibrinolytic profiles before HP eradication with those after HP eradication. HP infection was confirmed by endoscope-based examinations and eradicated by a standard OAC (omeperazole-amoxicillin-clarithromycin) regimen. We measured and compared pre- and post-eradication blood sugar, lipid profiles (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride) and fibrinolytic profiles (tissue-plasminogen activator, plasminogen activator inhibitor-1, fibrinogen, and D-dimer levels). Forty-eight patients (male:female, 25:23; mean age, 50.8 +/- 11.3 years) with gastric HP infection were enrolled in this study. Although HP infection was confirmed to have been successfully eradicated, no significant changes of blood fasting sugar, lipids or fibrinolytic profiles were found in patients after treatment. Coronary risk factors including fasting sugar, lipid and fibrinolytic profiles were not changed after successful HP eradication treatment. The relationship between HP infection and coronary artery disease needs to be clarified.

Adult↗
PubMed2002

Arrhythmogenic right ventricular cardiomyopathy: three cases.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare disease characterized by replacement of myocardium with fibrofatty tissue. It mainly involves the right ventricle (RV) and causes abnormal RV performance. ARVC is the most common cause of sudden cardiac death in young Italian athletes because it induces malignant ventricular tachyarrhythmias. Clinical manifestations of ARVC may be different between Chinese and Western patients. In this paper, we share our experience of the clinical manifestations of ARVC and review previous reports of ARVC.

Aged↗