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Y G Li

Publications and source records attributed to Y G Li.

At least 37 records · Page 2Linked to original sources

Atrial flutter in the recipient atrium induced by premature beats arising from the donor atrium 10 years after orthotopic heart transplantation.

BACKGROUND: Several mechanisms for the genesis of supraventricular arrhythmias in patients after orthotopic heart transplantation have been reported. METHODS AND RESULTS: We describe a 58-year-old male patient in whom atrial flutter occurred 10 years after orthotopic heart transplantation. During an electrophysiological study, bidirectional conduction between the recipient and donor atria was found. Atrial flutter in the recipient atrium was induced by programmed stimulation of the donor atrium using a single extrastimulus. The clinical symptoms were caused by atrial flutter arising from the recipient atrium with 1:1 to 3:1 conduction to the donor atrium. Mapping the anastomosis between the two atria indicated fragmented potentials at a discrete site of conduction. Delivery of radiofrequency energy at this site terminated conduction in both directions. Subsequent atrial pacing of the donor and recipient atria, respectively, demonstrated bidirectional conduction block. CONCLUSION: Symptomatic arrhythmias in patients after heart transplantation can indirectly originate from the donor atrium via bidirectional recipient-donor atrial conduction. This type of arrhythmia can be successfully treated with radiofrequency ablation.

Atrial Flutter↗

Pharmacological therapy of atrial fibrillation.

Pharmacological treatment of atrial fibrillation aims at reducing symptoms and possible complications of this frequently encountered arrhythmia. Prevention of embolic events by means of oral vitamin K antagonists is therefore mandatory in most patients presenting with atrial fibrillation. Whereas in paroxysmal atrial fibrillation reduction in frequency and duration of episodes is the treatment goal, symptomatic relief of persistent atrial fibrillation can be achieved by two treatment strategies: 1) restoration of sinus rhythm, referred to as rhythm control, and 2) limitation of the average and maximal ventricular heart rate, referred to as rate control. This review provides data from relevant clinical studies addressing the effectiveness and limitations of currently available drug therapy according to the two treatment approaches.

Anti-Arrhythmia Agents↗

Randomized comparison of slow pathway modification within the posteroseptal versus the midseptal area in patients with atrioventricular nodal reentrant tachycardia.

A total of 332 local electrogram recordings including 62 successful and 270 unsuccessful sites were analyzed. Univariate analysis revealed that there was a longer duration and more peaks of the atrial electrogram with a lower atrioventricular ratio and a higher incidence and shorter onset time of junctional ectopy during energy delivery at successful than at unsuccessful target sites.

Adult↗

T wave alternans as a predictor of recurrent ventricular tachyarrhythmias in ICD recipients: prospective comparison with conventional risk markers.

INTRODUCTION: The current standard for arrhythmic risk stratification is electrophysiologic (EP) testing, which, due to its invasive nature, is limited to patients already known to be at high risk. A number of noninvasive tests, such as determination of left ventricular ejection fraction (LVEF) or heart rate variability, have been evaluated as additional risk stratifiers. Microvolt T wave alternans (TWA) is a promising new risk marker. Prospective evaluation of noninvasive risk markers in low- or moderate-risk populations requires studies involving very large numbers of patients, and in such studies, documentation of the occurrence of ventricular tachyarrhythmias is difficult. In the present study, we identified a high-risk population, recipients of an implantable cardioverter defibrillator (ICD), and prospectively compared microvolt TWA with invasive EP testing and other risk markers with respect to their ability to predict recurrence of ventricular tachyarrhythmias as documented by ICD electrograms. METHODS AND RESULTS: Ninety-five patients with a history of ventricular tachyarrhythmias undergoing implantation of an ICD underwent EP testing, assessment of TWA, as well as determination of LVEF, baroreflex sensitivity, signal-averaged ECG, analysis of 24-hour Holter monitoring, and QT dispersion from the 12-lead surface ECG. The endpoint of the study was first appropriate ICD therapy for electrogram-documented ventricular fibrillation or tachycardia during follow-up. Kaplan-Meier survival analysis revealed that TWA (P < 0.006) and LVEF (P < 0.04) were the only significant univariate risk stratifiers. EP testing was not statistically significant (P < 0.2). Multivariate Cox regression analysis revealed that TWA was the only statistically significant independent risk factor. CONCLUSIONS: Measurement of microvolt TWA compared favorably with both invasive EP testing and other currently used noninvasive risk assessment methods in predicting recurrence of ventricular tachyarrhythmias in ICD recipients. This study suggests that TWA might also be a powerful tool for risk stratification in low- or moderate-risk patients, and needs to be prospectively evaluated in such populations.

Adult↗

[Combined therapy with transvenous cardioverter/defibrillator and anti-bradycardia pacemaker systems].

Implantable cardioverter/ defibrillators (ICD) represent in many patients with ventricular tachyarrhythmias the first line treatment. Up to 15% of the patients requiring an ICD need concomitant permanent cardiac pacing for bradyarrhythmias resulting in the need of simultaneous ICD- and antibradycardic pacemaker-therapy. We present four patients with successful implantation of a transvenous ICD-system (Medtronic Jewel 7220 and Micro Jewel 7221; electrode: Medtronic 6939), all of which had an antibradycardic pacemaker (2 unipolar, 2 bipolar) implanted prior to ICD-implantation. Meticulous intraoperative testing in order to avoid adverse interactions between the two systems has been carried out successfully in all cases. Possible adverse interactions comprise oversensing of pacemaker signals by the ICD with subsequent inadequate therapy, inhibition of defibrillation therapy during ventricular fibrillation caused by false detection of pacemaker spikes by the ICD as well as reprogramming of the pacemaker after shock delivery. A review of the published literature yielded 91 reported cases of combined ICD- and pacemaker-therapy. In 16% of the patients, one or more of the mentioned complications have been observed. Those occurred more frequently with unipolar than with bipolar pacemaker-systems. Thus, combined therapy with antibradycardic pacemaker and transvenous ICD-systems can be performed safely.

Aged↗

Slow sodium-dependent potential oscillations contribute to ectopic firing in mammalian demyelinated axons.

Ectopic action potentials can arise at regions of axonal demyelination, and are believed to contribute to a range of symptoms in patients with demyelinating conditions such as multiple sclerosis. The mechanism(s) by which the ectopic impulses are generated are uncertain. We have previously shown that such ectopic activity can result from inward potassium currents. Paradoxically, the potassium channel blocking agent 4-aminopyridine (4AP) can sometimes cause ectopic activity in demyelinating lesions. To study this phenomenon we have made intra-axonal recordings of ectopic activity in demyelinated axons, both in the presence and absence of 5 mM 4AP. 4AP promoted a pattern of firing which was observed, albeit less frequently, in demyelinated axons in the absence of this drug, namely trains of single impulses, or trains of short, high-frequency bursts of impulses. When recorded close to the demyelinated lesion, the impulses were generated by an underlying, almost sinusoidal oscillation of the membrane potential. This oscillation was abolished by the sodium channel blocking agent tetrodotoxin (0.1-1 microM). We conclude that the ectopic spiking induced by 4AP is generated by membrane potential oscillations associated with the site of demyelination. The sodium-dependent current underlying these oscillations, together with the prolonged inward potassium currents which we have previously described, may contribute to the generation of ectopic discharges in a range of disorders of myelinated axons.

4-Aminopyridine↗

Drug treatment of atrial fibrillation: what have we learned?

Pharmacologic treatment continues to be the mainstay of therapy in patients with atrial fibrillation (AF). Over the past few years, considerable progress has been made in establishing the role of antiarrhythmic drug therapy for restoration and subsequent maintenance of sinus rhythm as well as for the control of ventricular rate in permanent AF. For pharmacologic cardioversion, intravenous or oral administration of class IC drugs is associated with success rates of 60% to 80% depending mainly on the duration of the arrhythmia. In persistent AF of longer than 1 week's duration, electrical cardioversion is recommended because this method is more effective and safer than drug therapy. For maintenance of sinus rhythm following successful cardioversion, class I drugs continue to be used often. However, there is increasing awareness of their proarrhythmic risk, particularly in the case of quinidine. Sotalol, a class III agent with beta-receptor antagonism, is as effective as quinidine but better tolerated. In patients with so-called refractory AF, amiodarone has been proven to be effective in approximately 60% to 70% of treatment attempts. For control of ventricular rate, digoxin, beta-blockers, and calcium-channel antagonists are widely used. In these patients, chronic anticoagulation with warfarin aiming at international normalized ratios between 2.0 and 3.5 has been documented to significantly reduce thromboembolic risk.

Anti-Arrhythmia Agents↗

Heart rate variability used as an arrhythmia risk stratifier after myocardial infarction.

Heart rate variability (HRV) is considered to represent a noninvasive tool to assess cardiac autonomic tone at the level of the sinus node. It has been shown to have predictive power for risk assessment in patients surviving acute myocardial infarction. For this purpose, HRV should be assessed from 24-hour Holter recordings obtained 7-10 days following the infarction. Although there is some recovery of HRV during the first 3 months after infarction, HRV remains reduced in postinfarction patients compared to values obtained in healthy individuals. Compared to assessment of left ventricular function as a risk marker, HRV is superior with respect to prediction of arrhythmic events and sudden death whereas both parameters yield comparative power for prediction of total cardiac mortality. Since the predictive power of HRV analysis alone is relatively low, the combined use of HRV measurements together with traditional risk markers (such as ventricular ectopic beats, signal-averaged ECG, or left ventricular function) results in improved risk prediction with positive predictive accuracy in the range of 30%-50%.

Arrhythmias, Cardiac↗

T wave alternans during exercise and atrial pacing in humans.

INTRODUCTION: Evidence is accumulating that microvolt T wave alternans (TWA) is a marker of increased risk for ventricular tachyarrhythmias. Initially, atrial pacing was used to elevate heart rate and elicit TWA. More recently, a noninvasive approach has been developed that elevates heart rate using exercise. METHODS AND RESULTS: In 30 consecutive patients with a history of ventricular tachyarrhythmias, the spectral method was used to detect TWA during both atrial pacing and submaximal exercise testing. The concordance rate for the presence or absence of TWA using the two measurement methods was 84%. There was a patient-specific heart rate threshold for the detection of TWA that averaged 100 +/- 14 beats/min during exercise compared with 97 +/- 9 beats/min during right atrial pacing (P = NS). Beyond this threshold, there was a significant and comparable increase in level of TWA with decreasing pacing cycle length and increasing exercise heart rates. CONCLUSIONS: The present study is the first to demonstrate that microvolt TWA can be assessed reliably and noninvasively during exercise stress. There is a patient-specific heart rate threshold beyond which TWA continues to increase with increasing heart rates. Heart rate thresholds for the onset of TWA measured during atrial pacing and exercise stress were comparable, indicating that heart rate alone appears to be the main factor of determining the onset of TWA during submaximal exercise stress.

Adult↗

Electrophysiologic features of torsades de pointes: insights from a new isolated rabbit heart model.

INTRODUCTION: The exact electrophysiologic mechanism of torsades de pointes (TdP) is under intense investigation. No isolated animal heart model of this particular arrhythmia exists. METHODS AND RESULTS: In isolated rabbit hearts, TdP was induced by means of bradycardia in the presence of a high concentration of d-sotalol (10(-4) M) and shortly after lowering the concentration of potassium and magnesium in the perfusate. Multiple simultaneous epicardial and endocardial monophasic action potentials (MAPs) and volume-conducted 12-lead ECGs were recorded. d-Sotalol prolonged repolarization and increased dispersion of ventricular repolarization compared to baseline recordings. With the onset of low potassium and magnesium concentrations, repolarization was further prolonged and dispersion of repolarization was further increased followed by the occurrence of early afterdepolarizations (EADs) in the majority of MAP recordings, i.e., at both endocardial and epicardial locations of both ventricles. Upon increase of EAD amplitude, triggered arrhythmias with TdP of up to 42 beats ensued in 10 of 11 hearts studied. MAP duration at 90% repolarization (APD90), dispersion of APD90, and the incidence of EADs as well as dispersion of the QT interval and T wave area were significantly higher in beats triggering bigemini, couplets, or runs of TdP. CONCLUSION: TdP observed in this new isolated heart model was associated with markedly increased dispersion of ventricular repolarization and the occurrence of EADs in multiple locations of the heart. TdP is initiated when the amplitude of an EAD reaches threshold for initiation of the first beat of an episode.

Action Potentials↗

Radiofrequency catheter ablation of atrial flutter after orthotopic heart transplantation.

INTRODUCTION: Antiarrhythmic drug refractory recurrent atrial flutter occurred in a 39-year-old man who had undergone successful orthotopic heart transplantation 3 months ago. METHODS AND RESULTS: At electrophysiologic study, the transplanted right atrium showed type I atrial flutter. The recipient right atrium was in sinus rhythm with complete atrioatrial dissociation of electrical activity. Mapping demonstrated double-spike electrograms in the low posterior region of the donor right atrium. During radiofrequency current application near this site, the double potentials were dissociated progressively and atrial flutter was terminated immediately. Thereafter, both the recipient and the transplanted atria were in sinus rhythm of different cycle lengths with continued electrical dissociation. CONCLUSION: This is the first report of successful radiofrequency catheter ablation of atrial flutter in a transplanted heart. Although mapping of the arrhythmia is more difficult due to the large circumference of the right atrium, which consists of parts of the recipient right atrium and the transplanted atrium, ablation should be considered in those patients with drug refractory supraventricular tachyarrhythmias.

Adult↗

Changes in plasma epinephrine concentration and in heart rate during head-up tilt testing in patients with neurocardiogenic syncope: correlation with successful therapy with beta-receptor antagonists.

INTRODUCTION: Tilt table testing is widely used in the management of patients with neurocardiogenic syncope. However, the exact pathophysiologic mechanism of this disorder is still under debate. Likewise, therapy of these patients continues to represent a challenge in many cases. Therefore, the present study aimed to gain further insight into the pathophysiology of this syndrome and to examine easily accessible clinical parameters that can improve therapy selection. METHODS AND RESULTS: In 16 patients with neurocardiogenic syncope, changes in endogenous catecholamine concentrations were determined during repeated tilt table testing before and during treatment with metoprolol. Tachycardia preceded syncope in 8 of 10 responders compared to only 1 of 6 nonresponders (P < 0.05). In responders, the relative increase in epinephrine levels averaged 197% +/- 51% during drug-free tilting and 75% +/- 33% during repeated testing while on beta-blocker therapy (P < 0.05). In nonresponders, there was a smaller relative increase in epinephrine averaging 137% +/- 35% at baseline tilt. During repeated tilt testing, a similar increase was observed in these patients with recurrent syncope (156% +/- 104%; P = NS compared to baseline). CONCLUSION: In patients with neurocardiogenic syncope who show both an increase in epinephrine concentration during tilt test and sinus tachycardia prior to the onset of symptoms, beta-blocker treatment is very effective. These findings confirm the major role of sympathetic activation as a trigger of syncope. Particularly, heart rate changes at the onset of syncope may allow early identification of patients responding to antiadrenergic therapy.

Adrenergic beta-Antagonists↗

Inactivation and conformation changes of the glycated and non-glycated D-glyceraldehyde-3-phosphate dehydrogenase during guanidine-HCl denaturation.

The glycated D-glyceraldehyde-3-phosphate dehydrogenases have been isolated from rabbit muscle and erythrocytes (He et al. (1995) Biochem. J. 309, 133-139). The circular dichroism spectrum in the near-ultraviolet of gGAPDH was different from that of GAPDH. Changes in intrinsic protein fluorescence and in the 410 nm fluorescence of the NAD derivatives introduced at the active sites of both the glycated and non-glycated GAPDH from rabbit were compared on inactivation during denaturation in GuHCl. Complete inactivation for the non-glycated enzyme occurred in 0.5 M GuHCl solution, however, that for the glycated enzyme occurred in the 0.35 M solution. The kinetic inactivation of gGAPDH was a biphasic process (the fast and slow phases). The fast phase for gGAPDH was faster than that of GAPDH. The kinetic exposure of the fluorescent NAD derivatives at the active sites of both enzymes was also biphasic with fast phase rates which approach those of the inactivation. It appears that glycation of the enzyme may disturb the spatial geometry of the functional groups responsible for the catalytic mechanism and affect the activity.

Animals↗

[The biological significance of endocrine cells in pancreatic carcinoma].

Endocrine cells (EC) were found in 19 out of 42 cases of the pancreas carcinoma (42.5%). Among them, 4 cases had a positive rate of EC more than 50%. The positive rate of EC in the well differentiated carcinomas (5/20) was lower than that of the poorly-differentiated ones (12/19) or mucinous carcinoma (2/2), and the positive rate in histologic grade I cases (5/18) was significantly lower than that of the grade III cases (7/8). The number of mast cells infiltrating in the matrix in EC positive cases was significantly higher than that of the negative ones. The positive rate of EC in the cases with metastasis (8/14) was higher than that of the non-metastasis cases (7/21). Immunocytochemical staining showed that GN (8), SS(4), HCG(5), CK(12), EMA(13) and CEA(9) were positive in 19 EC positive cases.

Adenocarcinoma↗

A report on selective radiofrequency ablation of dual atrioventricular node pathways in 34 cases.

Selective ablation of slow pathway by radiofrequency (RF) current in 34 patients with atrioventricular (AV) node pathways and tachycardia was performed with two methods in our section; posterior approach was used in the first 12 patients, the slow pathways were ablated successfully. Inferior approach was performed in the other 22 patients. Slow pathways were interrupted in 14 patients. Retrograde fast pathways and/or slow pathways were ablated in 6 patients. Retrograde fast pathways and slow pathways were abolished and antegrade fast pathways were injured transitorily in 2 cases. The total procedure time was shorter, RF applications were fewer by inferior approach than by posterior approach (P < 0.05). Both antegrade and retrograde conduction of fast pathways had not been affected after slow pathways were ablated (P > 0.05). After a mean of 8 months follow-up, two patients recurred and were ablated successfully again. We come to the conclusion that inferior approach might be a preferable method compared with posterior approach; the slow pathways is the compact node and its posterior input of transitional cells; the retrograde fast pathway may be the anterior superficial group of transitional cells and is not always in the same location of antegrade fast pathway.

Adult↗

Failure to induce long-term depression by an anti-correlation procedure in area CA1 of the rat hippocampal slice.

We have independently in our two laboratories re-examined the report by Stanton and Sejnowski (Nature, 339, 215-218, 1989) that single stimuli to a test pathway in area CA1 of the hippocampal slice, when delivered between short bursts of stimuli to a second, convergent pathway, produce an associative long-term depression (LTD) in the test pathway. While robust associative LTP was observed when stimuli to the two inputs were correlated in time, the anti-correlation procedure failed to induce LTD; rather, a trend towards potentiation was observed. This result was obtained using both submerged and interface chambers, and in two different strains of rat. A transient depression lasting for a few minutes could usually be elicited by strong tetanic stimulation; this depression was not restricted to activated pathways.

Animals↗