Association of elevation of anti-Helicobacter pylori antibody with myocardial ischemic events in coronary artery disease.
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Antibodies, Bacterial↗
Biomedical subjects
L J Lin
Publications and source records attributed to L J Lin.
Properties and substrate of slow pathway exposed with a compact node targeted fast pathway ablation in rabbit atrioventricular node.
INTRODUCTION: The properties and substrates of slow and fast AV nodal pathway remain unclear. This applies particularly to the slow pathway (SP), which is largely concealed by fast pathway (FP) conduction. We designed a new FP ablation approach that exposes the SP over the entire cycle length range and allows for its independent characterization and ablation. METHODS AND RESULTS: Premature stimulation was performed before and after FP ablation with 5.4 +/- 1.9 lesions (300-microm diameter each; overall lesion size 1.4 +/- 0.5 mm) targeting the junction between perinodal and compact node tissues in seven rabbit heart preparations. The resulting SP recovery curve and control curve had the same maximum nodal conduction time (165 +/- 22 msec vs 164 +/- 24 msec; P = NS) and effective refractory period (101 +/- 10 msec vs 100 +/- 9 msec; P = NS). The two curves covered the same cycle length range. However, the SP curve was shifted up with respect to control one at intermediate and long cycle lengths and thus showed a longer minimum nodal conduction time (81 +/- 15 msec vs 66 +/- 10 msec; P < 0.01) and functional refractory period (180 +/- 11 msec vs 170 +/- 12 msec; P < 0.05). The SP curve was continuous and closely fitted by a single exponential function. Small local lesions (2 +/- 1) applied to the posterior nodal extension resulted in third-degree nodal block in all preparations. CONCLUSION: The posterior nodal extension can sustain effective atrial-His conduction at all cycle lengths and account for both the manifest and concealed portion of SP. Slow and FP conduction primarily arise from the posterior extension and compact node, respectively.
Animals↗
Correlation of homocytsteine levels with the extent of coronary atherosclerosis in patients with low cardiovascular risk profiles.
Elevation of homocysteine is now known as an independent risk factor for vascular diseases. However, influences of homocysteine to the extent of coronary atherosclerosis in patients with different coronary risk profiles have not been studied. In this study, we used angiographic "diffuse score" and "clinical vessel score" to evaluate the extent of coronary atherosclerosis, and examined the correlation between levels of serum total homocysteine and angiographic scores among patients with high- and low-risk profiles. Seventy consecutive patients (58 men and 12 women, mean age 50 years) undergoing selective coronary angiography for the first time were recruited for this study. Patients were divided into high-risk (risk factor > or =3, n = 35) and low-risk (risk factor <3, n = 35) groups. Linear regression analysis revealed that levels of serum homocysteine were only significantly correlated with diffuse (r = 0.217, p = 0.007) and clinical vessel (r = 0.078, p = 0.037) scores in low-risk patients. These correlations could not be observed in diffuse (r = 0.070, p = 0.319) and clinical vessel (r = -0.001, p = 0.970) scores in the high-risk group. In conclusion, levels of homocysteine correlated with the extent of coronary atherosclerosis only among patients with low cardiovascular risk profiles.
Coronary Angiography↗
Distal end of the atrioventricular nodal artery predicts the risk of atrioventricular block during slow pathway catheter ablation of atrioventricular nodal re-entrant tachycardia.
OBJECTIVE: To search for a reliable anatomical landmark within Koch's triangle to predict the risk of atrioventricular (AV) block during radiofrequency slow pathway catheter ablation of AV nodal re-entrant tachycardia (AVNRT). PATIENTS AND METHODS: To test the hypothesis that the distal end of the AV nodal artery represents the anatomical location of the AV node, and thus could be a useful landmark for predicting the risk of AV block, 128 consecutive patients with AVNRT receiving slow pathway catheter ablation were prospectively studied in two phases. In phase I (77 patients), angiographic demonstration of the AV nodal artery and its ending was performed at the end of the ablation procedure, whereas in the subsequent phase II study (51 patients), the angiography was performed immediately before catheter ablation to assess the value of identifying this new landmark in reducing the risk of AV block. Multiple electrophysiologic and anatomical parameters were analysed. The former included the atrial activation sequence between the His bundle recording site (HBE) and the coronary sinus orifice or the catheter ablation site, either during AVNRT or during sinus rhythm. The latter included the spatial distances between the distal end of the AV nodal artery and the HBE and the final catheter ablation site, and the distance between the HBE and the tricuspid border at the coronary sinus orifice floor. RESULTS: In phase I, nine of the 77 patients had complications of transient (seven patients) or permanent (two patients) complete AV block during stepwise, anatomy guided slow pathway catheter ablation. These nine patients had a wider distance between the HBE and the distal end of the AV nodal artery, and a closer approximation of the catheter ablation site to the distal end of the AV nodal artery, which independently predicted the risk of AV block. In contrast, none of the available electrophysiologic parameters were shown to be reliable. When the distance between the distal end of the AV nodal artery and the ablation target site was more than 2 mm, the complication of AV block virtually never occurred. In phase II, all 51 patients had successful elimination of the slow pathways without complication when the ablation procedure was guided by preceding angiography with identification of the distal end of the AV nodal artery. CONCLUSIONS: The distal end of the AV nodal artery shown by angiography serves as a useful landmark for the prediction of the risk of AV block during slow pathway catheter ablation of AVNRT.
Adolescent↗
Effect of atrial fibrillation on pulmonary venous flow patterns assessed by Doppler transesophageal echocardiography.
STUDY OBJECTIVES: To investigate the effect of atrial fibrillation (AF) on pulmonary venous flow (PVF) patterns in a cohort with nonrheumatic AF. DESIGN AND SETTINGS: A prospective and controlled study undertaken at a tertiary referral medical center. PATIENTS AND MEASUREMENTS: The echocardiographic parameters of left superior PVF as assessed by Doppler transesophageal echocardiography in 40 patients with chronic AF (group 1) were compared to those of 33 volunteers with sinus rhythm (group 2) and well-matched baseline characteristics. RESULTS: : All group 1 patients presented with single systolic forward flow (SFF) patterns. In contrast, single and double SFF patterns were found equally in group 2. With regard to reverse flow (RF), most group 1 patients (33 of 40) had an early systolic RF and none had atrial RF; however, most group 2 subjects (29 of 33) had an atrial RF. Some of the group 1 patients (17%) had a late systolic RF in the absence of significant mitral regurgitation. In group 1, the SFF appeared later and disappeared earlier than in group 2. The mean systolic peak velocity and time-velocity integral (TVI) of the SFF were significantly lower in group 1 compared to group 2. The diastolic peak velocity and TVI were not significantly different between groups. CONCLUSIONS: : Our data indicate that AF independently and significantly affects the PVF and leads to characteristic flow patterns different from sinus rhythm. The presence of AF reduces SFF in addition to the absence of atrial RF. These changes in the flow patterns should be taken into account while interpreting the implications of PVF in the presence of AF.
Aged↗
Decreased left atrial appendage function is an important predictor of elevated left ventricular filling pressure in patients with congestive heart failure.
OBJECTIVE: The aim of this study was to investigate whether left atrial (LA) appendage function, as indicated by LA appendage blood flow velocities and its ejection fraction, could identify elevated left ventricular filling pressure in patients with chronic congestive heart failure. METHODS: Using transesophageal echocardiography, adequate pulsed Doppler LA appendage active emptying and filling velocities could be recorded in 25 consecutive patients (16 men and 9 women, aged 57+/-10 years) with chronic congestive heart failure (symptom duration > or =1 year). LA appendage ejection fraction calculated as (LA appendage maximal area)-(LA appendage minimal area)/(LA appendage maximal area) x 100 was also determined in these patients. Left ventricular end-diastolic pressure was recorded during cardiac catheterization performed within 24 h of echocardiographic study. RESULTS: Left ventricular end-diastolic pressure was 2 to 47 mm Hg. There were close negative correlations of LA appendage emptying velocity (r=-0.508; P<0.01), filling velocity (r=-0.429; P<0.05) and LA appendage ejection fraction (r=-0.523; P<0.005) with left ventricular end-diastolic pressure. LA appendage active emptying velocity <30 cm/s predicted left ventricular end-diastolic pressure >25 mm Hg with a sensitivity of 72.7%, a specificity of 92.9% and a positive and negative predictive value of 88.9 and 81.3%. CONCLUSIONS: The findings suggest that measurement of LA appendage blood flow velocities and contractile function by transesophageal echocardiography can be used to predict elevated left ventricular filling pressure in patients with congestive heart failure.
Atrial Function, Left↗
Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction.
OBJECTIVES: The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND: Increased plasma hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical data concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS: Blood samples were obtained from 64 patients (mean age 67 +/- 11 years; 49 male) with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasma concentrations of fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS: The follow-up time was 27 +/- 17 months, and 19 patients died of cardiac causes during the follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86; 95% confidence interval [CI] 1.55-15.19), left ventricular ejection fraction (hazard ratio 0.94; 95% CI 0.90-0.99), FPA (hazard ratio 1.54; 95% CI 1.13-2.10), F1+2 (hazard ratio 2.03; 95% CI 1.17-3.53) and TAT (hazard ratio 1.88; 95% CI 1.27-2.79) as significant factors associated with cardiac mortality. In multivariate analyses, only FPA level (hazard ratio 1.84; 95% CI 1.03-3.30) and left ventricular ejection fraction (hazard ratio 0.93; 95% CI 0.88-0.98) were independent predictors of cardiac mortality. CONCLUSIONS: Elevated FPA in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction.
Adult↗
O- and N-methylation in the biosynthesis of staurosporine.
The feeding of (13)C- and (2)H-enriched methionine to Streptomyces staurosporeus established that the methyl carbon and proton source of both the 3'-O- and 4'-N-methyl groups of staurosporine (1) was methionine and that all three methyl protons from methionine were retained on 1. In the presence of the methyltransferase inhibitor, sinefungin, the biosynthesis of staurosporine was blocked at the last step, O-methylation. An intermediate, 3'-demethoxy-3'-hydroxystaurosporine (2), was efficiently accumulated in the medium. Other general methyltransferase inhibitors failed to produce any other staurosporine intermediates or analogues.
Chromatography, High Pressure Liquid↗
Role of the compact node and its posterior extension in normal atrioventricular nodal conduction, refractory, and dual pathway properties.
INTRODUCTION: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. METHODS AND RESULTS: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (approximately 300 microm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 +/- 16 ms to 123 +/- 11 msec (P < 0.01) and prolonged the effective refractory period from 104 +/- 6 msec to 119 +/- 11 msec (P < 0.01) without affecting A2H2min (55 +/- 9 msec vs 55 +/- 8 msec; P = NS) and functional refractory period (174 +/- 7 msec vs 175 +/- 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. CONCLUSION: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.
Animals↗
Characteristics, circuit, mechanism, and ablation of reentry in the rabbit atrioventricular node.
INTRODUCTION: The circuitry underlying AV nodal reentry remains debated. We developed a model of AV nodal reentry and assessed the role of nodal inputs, compact node, and its posterior nodal extension (PNE) in this phenomenon. METHODS AND RESULTS: A fine scanning of short coupling interval range with an atrial premature beat consistently initiated slow-fast AV nodal reentrant beats that occurred 37+/-31 msec (mean+/-SD) after His-bundle activation in 11 of 16 consecutive rabbit heart preparations. The repeated testing (>40 times) of a chosen coupling interval within reentry window (6+/-9 msec, n = 11) yielded reentrant intervals that varied by 2+/-1 msec (mean SD for 40 beats+/-SD, n = 11). The breakthrough point of reentrant activation, as assessed from four perinodal sites, varied in different preparations from diffuse (4) to anterior (1), medial (3), or posterior (3); mean reentrant interval did not differ between perinodal sites. Antegrade perinodal activation pattern did not differ at reentrant versus nonreentrant coupling intervals and thus was not a primary determinant of reentry. A PNE ablation (n = 4) interrupted the slow pathway conduction and prevented reentry without affecting antegrade perinodal activation or fast pathway conduction. CONCLUSION: A reproducible model of AV nodal reentrant beats was developed and used to study underlying circuitry. The AV nodal reentry involves unaltered antegrade perinodal activation, slow PNE conduction and retrograde broad invasion of perinodal tissues starting at a preparation-dependent breakthrough point. A PNE ablation abolishes the reentry.
Animals↗
Electrophysiological determinant for induction of isthmus dependent counterclockwise and clockwise atrial flutter in humans.
OBJECTIVE: To investigate the electrophysiological determinant underlying the electrical induction of counterclockwise and clockwise isthmus dependent atrial flutter. PATIENTS AND METHODS: The isthmus bordered by the inferior vena caval orifice-tricuspid annulus-coronary sinus ostium (IVCO-TA-CSO) has been assumed to be the site of both slow conduction and unidirectional block critical to the initiation of atrial flutter. Trans-isthmus and the global atrial conduction were studied in 25 patients with isthmus dependent atrial flutter (group A) and in 21 patients without atrial flutter (group B), by pacing at the coronary sinus ostium and the low lateral right atrium (LLRA) and mapping with a 20 pole Halo catheter in the right atrium. RESULTS: Mean (SD) fluoroscopic isthmus length between the coronary sinus ostium and LLRA sites was 28.1 (4.0) mm in group A and 28.0 (3.9) mm in group B (p = 0.95), but the trans-isthmus conduction velocity of both directions at various pacing cycle lengths was nearly halved in group A compared with group B (mean 0.39-0.46 m/s v 0.83-0.89 m/s, p < 0.0001). Pacing at coronary sinus ostium directly induced counterclockwise atrial flutter in 14 patients and pacing at LLRA induced clockwise atrial flutter in 11 patients, following abrupt unidirectional trans-isthmus block. Transient atrial tachyarrhythmias preceded the onset of atrial flutter in 10 counterclockwise and six clockwise cases of atrial flutter. None of the group B patients had inducible atrial flutter even in the presence of trans-isthmus block. The intra- and interatrial conduction times, as well as the conduction velocities at the right atrial free wall and the septum, were similar and largely within the normal range in both groups. CONCLUSIONS: Critical slowing of the trans-IVCO-TA-CSO isthmus conduction, but not the unidirectional block or the global atrial performance, is the electrophysiological determinant of the induction of counterclockwise and clockwise isthmus dependent atrial flutter in man.
Adult↗
Prognostic value of Doppler-derived mitral deceleration time in postinfarction patients with left ventricular ejection fractions of 35% or more.
Short Doppler-derived mitral deceleration time of early filling has been proved to be an independent predictor of poor prognosis in patients with left ventricular dysfunction. However, the prognostic value of Doppler-derived mitral deceleration time in postinfarction patients without overt left ventricular dysfunction is poorly understood. A total of 27 survivors of acute myocardial infarction with left ventricular ejection fractions of 35% or more, as determined by radionuclide ventriculography, were prospectively studied. Doppler study was performed 5 to 7 days after the index infarction. The patients were divided into two groups. Group A included 10 patients whose mitral deceleration time was 125 msec or less and group B consisted of 17 patients whose mitral deceleration time was 125 msec or more. The two groups were similar in terms of age and gender distribution and there were no statistically significant differences in coronary risk factors, peak creatine kinase concentration, location of infarction, Killip classification, thrombolytic therapy, left ventricular ejection fraction, or medications. After a mean follow-up period of 30 months, the rate of congestive heart failure (New York Heart Association, NYHA, class II or above) was significantly higher in group A (5/10) than in group B (1/17) (p < 0.01). These results suggest that a short mitral deceleration time could be a useful early predictor of the potential development of future congestive heart failure in postinfarction patients with left ventricular ejection fractions of 35% or more.
Blood Flow Velocity↗
Prognostic determinants of infective endocarditis in the 1990s.
The clinical profiles of infective endocarditis (IE) might have changed in recent years, owing to the advent of transesophageal echocardiography, the introduction of new diagnostic criteria, and the increased frequency of intravenous drug abuse. In this retrospective study, we sought to identify factors affecting the in-hospital outcome of IE patients in a single tertiary referral center in the 1990s (1990-1997). Eighty-eight episodes of IE in 80 consecutive patients admitted from January 1990 through June 1997 were evaluated. Clinical variables that were significantly associated with in-hospital mortality in univariate analyses were entered into a multiple logistic regression model. A total of 22 patients (25%) died. Fatal episodes were significantly more likely than non-fatal episodes to involve older patients (> or = 50 years), use of coumadin, short interval between symptom onset and hospitalization (< 15 days), noncardiac shock, and complications of the heart, central nervous system, and kidneys. White blood cell counts and C-reactive protein concentrations were also significantly higher in fatal than in non-fatal episodes of IE. Multivariate analysis showed that in-hospital mortality was associated with noncardiac shock, neurological complications, cardiac complications, and older age (> or = 50 years). Compared with previous reports, our findings suggest that the clinical profiles of IE have undergone some changes in the 1990s. The most important prognostic predictors of in-hospital mortality in patients with IE were noncardiac shock and neurologic complications.
Adolescent↗
Images in cardiovascular medicine. Unusual manifestation of subaortic membrane.
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Aortic Valve↗
Venous access thrombosis detected by transcutaneous vascular ultrasound in patients with single-polyurethane-lead permanent pacemaker.
In order to assess the incidence of significant venous thrombosis after transvenous permanent pacemaker implantation, transcutaneous ultrasound studies were performed in 109 consecutive patients with single-polyurethane-lead pacemakers. Ultrasonic evaluation was found to be a good noninvasive method in assessing the veins. Six patients (5.5%) were found to have significant venous obstruction in the subclavian vein. However, none of them were symptomatic. No difference in the incidence of venous obstruction was found, based on the age, duration of implantation, operative technique, potentially thrombogenic factors including atrial fibrillation, diabeties mellitus, hypertension, heart failure and end-stage renal disease.
Adult↗
Effects of pharmacological autonomic blockade on dual atrioventricular nodal pathways physiology in patients with slow-fast atrioventricular nodal reentrant tachycardia.
The purpose of this study was to investigate the atrioventricular AV nodal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 +/- 17 years) with clinical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71%) of 17 patients still demonstrated AV nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 +/- 105 ms vs 630 +/- 80 ms, P < 0.005) and AV blocking cycle length (365 +/- 64 ms vs 338 +/- 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and functional refractory period of the fast pathway (369 +/- 67 ms vs 305 +/- 73 ms, P < 0.005; 408 +/- 56 ms vs 350 +/- 62 ms, P < 0.005) and the slow pathway (271 +/- 30 ms vs 258 +/- 27 ms, P < 0.01; 344 +/- 60 ms vs 295 +/- 50 ms, P < 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 +/- 94 ms vs 326 +/- 89 ms, NS) and effective refractory period of retrograde fast pathway (228 +/- 38 ms vs 240 +/- 80 ms, NS) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the decreased inducibility of clinical AVNRT.
Adrenergic beta-Agonists↗
New electrocardiographic criteria for the differentiation between counterclockwise and clockwise atrial flutter: correlation with electrophysiological study and radiofrequency catheter ablation.
OBJECTIVE: To develop new electrocardiographic (ECG) criteria for the differentiation between counterclockwise and clockwise atrial flutters. BACKGROUND: Traditionally, the ECG differentiation between counterclockwise and clockwise atrial flutters is based on the flutter wave polarity in the inferior leads. However, determination of flutter wave polarity is subjective and sometimes difficult, especially in flutter waves of undulating pattern. PATIENTS: The study comprised 37 consecutive patients with drug resistant atrial flutter; 30 had counterclockwise and 17 had clockwise atrial flutter (10 had both forms of atrial flutter). The isthmus dependence was confirmed by entrainment study and catheter ablation. The ECG patterns of both types of atrial flutter were compared and the flutter wave polarity in the inferior leads was determined by four independent cardiologists. RESULTS: The flutter wave polarity in the inferior leads appeared negative in 24, positive in one, and equivocal in five of the counterclockwise atrial flutters; polarity appeared negative in one, positive in 10, and equivocal in six of the clockwise atrial flutters. However, the aVF/lead I flutter wave amplitude ratio was > 2.5 in all counterclockwise but < 2.5 in all clockwise atrial flutters. The flutter wave nadirs in the inferior leads corresponded to the upstrokes in V1 in all counterclockwise atrial flutters, but corresponded to the downstrokes in V1 in all clockwise atrial flutters. CONCLUSIONS: The flutter wave polarity in the inferior leads does not correlate well with the flutter wave rotating direction. However, counterclockwise and clockwise atrial flutters can be differentiated by new ECG criteria with high accuracy.
Adult↗
Amebic liver abscess complicated with cardiac tamponade and mediastinal abscess.
Amebic pericarditis is an extremely rare complication of liver abscess and an uncommon etiology of sterile pericardial effusion with cardiac tamponade. The association of mediastinal abscess in this clinical setting has not been reported in the literature. Herein, we describe a case of amebic liver abscess complicated with mediastinal abscess and amebic pericarditis with cardiac tamponade. A 44-year-old man was admitted to our hospital because of shortness of breath for the previous 2 days. Cardiac tamponade was diagnosed and emergency pericardiectomy was performed. Chocolate-like pus was found in the pericardial sac and mediastinal space during surgery. Abdominal computed tomography revealed an ill-defined hypodense lesion over the left lobe of the liver, suggesting a liver abscess. Amebic liver abscess and pericarditis were diagnosed on the basis of a high serum titer of amebic antibodies on hemagglutination test. The patient was treated with metronidazole for 2 weeks and discharged in good condition. This case should alert clinicians to the possibility of amebic pericarditis in patients with cardiac tamponade associated with chocolate-like sterile pus in the pericardium and mediastinum. To establish the diagnosis of amebic pericarditis, one should investigate the presence of a liver abscess, a high serum titer of amebic hemagglutination antibodies, and the presence of Entamoeba histolytica trophozoites in the pericardium or pericardial aspirate.
Abscess↗