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Biomedical subjects

S A Chen

Publications and source records attributed to S A Chen.

At least 37 records · Page 2Linked to original sources
PubMed2001

Atypical atrial flutter involving the isthmus between the right pulmonary veins and fossa ovalis.

Typical atrial flutter, counterclockwise or clockwise movement around the tricuspid annulus, has been well studied. However, the reentrant circuits in atypical atrial flutter are not well defined. A patient without a prior history of cardiac surgery who presented with incessant atypical atrial flutter is described. Activation mapping demonstrated a circular movement around the fossa ovalis in the interatrial septum. Entrainment mapping demonstrated a protected isthmus between the right pulmonary veins and the fossa ovalis. Radiofrequency ablation of this isthmus terminated atrial flutter without recurrence during the follow-up period.

Aged↗
PubMed2001

Acute and long-term effects of atrioventricular junction ablation and VVIR pacemaker in symptomatic patients with chronic lone atrial fibrillation and normal ventricular response.

INTRODUCTION: The precise role of irregular ventricular response in atrial fibrillation (AF) has not been fully elucidated. This study examined the independent effects of rhythm regularity in patients with chronic AF. METHODS AND RESULTS: This study included 50 patients who had chronic lone AF and a normal ventricular rate. Among these patients, 21 who underwent AV junction ablation and implantation of a VVIR pacemaker constituted the ablation group; the other 29 patients were the medical group. Acute hemodynamic findings were measured in 21 ablation patients before ablation (during AF, baseline) and 15 minutes after ablation (during right ventricular pacing). Compared with baseline data, ablation and pacing therapy increased cardiac output (4.7 +/- 0.8 vs 5.2 +/- 0.9 L/min; P = 0.05), decreased pulmonary capillary wedge pressure (16 +/- 5 vs 13 +/- 4 mmHg; P = 0.001), and decreased left ventricular end-diastolic pressure (14 +/- 4 vs 11 +/- 3 mmHg; P < 0.05). After 12 months, the ablation group patients showed lower scores in general quality of life (-20%; P < 0.001), overall symptoms (-24%; P < 0.001), overall activity scale (-23%; P = 0.004), and significant increase of left ventricular ejection fraction (44% +/- 6% vs 49% +/- 5%; P = 0.02) by echocardiographic examination. CONCLUSION: AV junction ablation and pacing in patients with chronic AF and normal ventricular response may confer acute and long-term benefits beyond rate control by eliminating rhythm irregularity.

Aged↗
PubMed2001

Pulmonary vein dilation in patients with atrial fibrillation: detection by magnetic resonance imaging.

INTRODUCTION: The positive relationship between left atrial (LA) size and atrial fibrillation (AF) is well recognized; however, there is little information on the association of pulmonary vein (PV) diameter and AF. The purpose of this study was to investigate by magnetic resonance angiography the change of PV and LA size in patients with no history of AF, patients with paroxysmal AF (PAF), and patients with chronic AF (CAF). METHODS AND RESULTS: The study included 47 patients. Group I included 15 patients with normal sinus rhythm and no history of documented AF. Group II included 24 patients with drug-refractory PAF who underwent electrophysiologic study and radiofrequency ablation of PV foci. Group III included 8 patients with CAF who were converted to sinus rhythm by external electrical cardioversion. Age and concomitant heart diseases were similar among the three groups. We measured the diameter of each PV at its junction with the LA in addition to LA dimensions by gadolinium-enhanced magnetic resonance angiography with three-dimensional reconstruction. Significant dilation of both superior PVs (P < 0.01) and transverse diameter of LA (P < 0.01) was seen in the three groups. There were no significant changes of both inferior PVs, corrected PV (PV/LA) diameter, or longitudinal diameter of LA among the three groups. Only 28% patients showed arrhythmogenic foci from the largest PV. CONCLUSION: Significant dilation of both superior PVs with simultaneous LA enlargement was demonstrated i

Aged↗
PubMed2001

Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology.

Regular atrial tachycardias classically are classified into flutter or tachycardia, depending on the rate and presence of a stable baseline on the ECG. However, current understanding of electrophysiology atrial tachycardias makes this classification obsolete, because it does not correlate with mechanisms. The proposed classification is based on electrophysiologic mechanisms, defined by mapping and entrainment. Radiofrequency ablation of a critical focus or isthmus can afford proof. Focal tachycardias are characterized by radial spread of activation and endocardial activation not covering the whole cycle. Ablation of the focus of origin interrupts the tachycardia. The mechanism of focal firing is difficult to ascertain by clinical methods. Macroreentrant tachycardias are characterized by circular patterns of activation that cover the whole cycle. Fusion can be shown during entrainment on the ECG or by multiple endocardial recordings. Ablation of a critical isthmus interrupts the tachycardia. Macroreentry can occur around normal structures (terminal crest, eustachian ridge) or around atrial lesions. The anatomic bases of these tachycardias must be defined, to guide appropriate treatment. Atrial flutter is a mere description of continuous undulation on the ECG, and only some strictly defined typical flutter patterns correlate with right atrial macroreentry bounded by the tricuspid valve, terminal crest, and caval vein orifices. This classification should be considered open, as some classically described tachycardias, such as reentrant sinus tachycardia, inappropriate sinus tachycardia, and type II atrial flutter, cannot be classified accurately. Furthermore, the possibility of fibrillatory conduction makes the limits with atrial fibrillation still ill defined.

Animals↗
PubMed2001

Acquired pulmonary vein stenosis after radiofrequency catheter ablation of paroxysmal atrial fibrillation.

INTRODUCTION: Elimination of the initiating focus within the pulmonary vein (PV) using radiofrequency (RF) catheter ablation is a new treatment modality for treatment of drug-refractory atrial fibrillation. However, information on the long-term safety of RF ablation within the PV is limited. METHODS AND RESULTS: In 102 patients with drug-refractory atrial fibrillation and at least one initiating focus from the PV, series transesophageal echocardiography was performed to monitor the effect of RF ablation on the PV. There were 66 foci in the right upper PV and 65 foci in the left upper PV. Within 3 days of ablation, 26 of the ablated right upper PVs (39%) had increased peak Doppler flow velocity (mean 130+/-28 cm/sec, range 106 to 220), and 15 of the ablated left upper PVs (23%) had increased peak Doppler flow velocity (mean 140+/-39 cm/sec, range 105 to 219). Seven patients had increased peak Doppler flow velocity in both upper PVs. No factor (including age, sex, site of ablation, number of RF pulses, pulse duration, and temperature) could predict PV stenosis after RF ablation. Three patients with stenosis of both upper PVs experienced mild dyspnea on exertion, but only one had mild increase of pulmonary pressure. There was no significant change of peak and mean flow velocity and of PV diameter in sequential follow-up studies up to 16 (209+/-94 days) months. CONCLUSION: Focal PV stenosis is observed frequently after RF catheter ablation applied within the vein, but usually is without clinical significance. However, ablation within multiple PVs might cause pulmonary hypertension and should be considered a limiting factor in this procedure.

Adult↗
PubMed2001

Hyperventilation facilitates induction of supraventricular tachycardia: a novel method and the possible mechanism.

INTRODUCTION: Hyperventilation has been demonstrated to alter autonomic function. Sympathomimetic drugs (isoproterenol) and parasympatholytic drugs (atropine) may be needed to facilitate induction of supraventricular tachycardia (SVT). The aim of this study was to test the clinical utility and mechanisms of hyperventilation to facilitate SVT initiation. METHODS AND RESULTS: Fourteen patients with clinically documented SVT (9 AV nodal reentrant tachycardia and 5 AV reciprocating tachycardia) but noninducible during baseline electrophysiologic study were included. Immediately after hyperventilation test (at least 30 respirations/min) for 2 minutes, systolic blood pressure, sinus cycle length, anterograde and retrograde 1:1 conduction, and induced SVT were measured. Arterial blood gas, pH, and heart rate variability before and after hyperventilation were measured. Seven of nine patients with AV nodal reentrant tachycardia and 3 of 5 patients with AV reciprocating tachycardia could be induced immediately after the hyperventilation test. After hyperventilation, anterograde AV and retrograde VA 1:1 conduction were improved, sinus cycle length was decreased, and heart rate variability were decreased in both groups. CONCLUSION: Hyperventilation can facilitate induction of SVT. Improvement of conduction properties and changes of autonomic function are the possible mechanisms.

Accessory Nerve↗
PubMed2001

Mechanisms of transition between double paroxysmal supraventricular tachycardias.

INTRODUCTION: Coexistence of double tachycardias in one patient has been infrequently reported. Furthermore, the mechanisms of transition between double paroxysmal supraventricular tachycardias have not been well studied. METHODS AND RESULTS: Thirty-five patients with two paroxysmal supraventricular tachycardias were studied. Group IA consisted of 3 patients with spontaneous transition between AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). Group IB consisted of 13 patients without spontaneous transition between AVRT and AVNRT. Group IIA consisted of 5 patients with spontaneous transition between AVNRT and atrial tachycardia (AT). Group IIB consisted of 14 patients without spontaneous transition between AVNRT and AT. The absolute values of differences between the two tachycardia cycle lengths were significantly smaller in patients with than in those without transition between the two tachycardias (25+/-8 msec vs 90+/-46 msec, P < 0.05, IA vs IB; 21+/-25 msec vs 99+/-57 msec, P < 0.01, IIA vs IIB). The cutoff point of 25 msec had 80% positive predictive value for transition between the two tachycardias. Transition between two tachycardias occurred due to a spontaneous premature atrial complex (30%), conduction block at one limb of tachycardia (20%), or tachycardia-induced tachycardia (50%). Absence of transition between two tachycardias might be explained by the absence of a spontaneous premature atrial complex, longer cycle length of the first tachycardia, larger difference between two tachycardia cycle lengths, or induction of each tachycardia under different situations. CONCLUSION: Double supraventricular tachycardias with similar tachycardia cycle lengths are vulnerable to transition between different tachycardias.

Adolescent↗
PubMed2001

Role of right middle pulmonary vein in patients with paroxysmal atrial fibrillation.

INTRODUCTION: Elimination of the ectopic foci from pulmonary veins (PVs) has proved to be a curative therapy for focal atrial fibrillation (AF). However, information about the importance of the right middle PV (RMPV) in initiation of AF and radiofrequency ablation of AF is limited. METHOD AND RESULTS: Forty-three patients (34 men and 9 women; age 65+/-12 years) with drug-refractory paroxysmal AF underwent electrophysiologic study and catheter ablation for treatment of AF. Three-dimensional magnetic resonance angiography (MRA) of the PVs and left atrium (LA) was performed to determine the anatomic patterns of RMPV. Diameter of PV ostium was measured at the junction of the LA and each PV. MRA findings showed the following: (1) 36 (84%) of 43 patients had a discrete RMPV; (2) there are three drainage patterns of RMPV, including joining the proximal part (<1 cm from the ostium) of the right superior PV (RSPV), joining the right inferior PV (RIPV), and a separate RMPV ostium in the LA wall; and (3) the ostial diameter of RMPV was significantly smaller than RSPV and RIPV (P < 0.01). Electrophysiologic studies demonstrated that five AF foci arose from RMPV. The coupling interval between the ectopic beat of AF and sinus beat was longer in RMPV than RSPV (262+/-45 msec vs 212+/-47 msec; P = 0.043). All AFs from RMPV were ablated successfully. PV stenosis or AF recurrence from RMPV was not found during follow-up of 10+/-4 months. CONCLUSION: RMPV was detected by MRA in >80% of paroxysmal AF patients. Ectopy from RMPV can initiate AF, and radiofrequency ablation of RMPV foci is feasible and safe.

Adult↗
PubMed2001

Effect of nitric oxide on strophanthidin-induced ventricular tachycardia.

Nitric oxide (NO) has been demonstrated to have several effects on the heart. Through the stimulation of guanylate cyclase, NO increases cyclic GMP and decreases intracellular calcium. The purpose of this study was to evaluate the effects of NO on ventricular arrhythmia induced by strophanthidin in guinea pigs and dogs. In experiment 1, after strophanthidin-induced ventricular tachycardia, guinea pigs received different doses of L-arginine (0, 25, 50, 100, 200, and 400 mg/kg; n = 10 for each dose), 200 mg/kg L-arginine combined with 100 mg/kg N(G)-nitro-L-arginine methylester (L-NAME, n = 10), or 200 mg/kg D-arginine (n = 10). In experiment 2, after strophanthidin-induced ventricular tachycardia, dogs (n = 7) received 200 mg/kg L-arginine. By 12-lead ECG, monophasic action potentials in left and right ventricles were recorded throughout the study. In experiment 1, guinea pigs which received 200 mg/kg or 400 mg/kg L-arginine had greater incidences of ventricular tachycardia termination (60 and 80%, respectively) than those which received 0, 25, 50, and 100 mg/kg L-arginine (0, 0, 20, and 30%, respectively), those which received L-arginine with L-NAME (0%), and those which received D-arginine (0%). In experiment 2, 5 (71%) of the dogs had successful termination of ventricular tachycardia. These findings suggest that L-arginine was effective in treating strophanthidin-induced ventricular tachycardia in vivo and that the underlying mechanism is through a NO pathway.

Animals↗
PubMed2001

Linkage and mutation analysis in two Taiwanese families with long QT syndrome.

Long QT syndrome (LQT) is a cardiovascular disorder causing syncope and sudden death from arrhythmias. Mutations in KCNQ1, KCNH2, KCNE1, KCNE2, and SCN5A genes encoding cardiac potassium and sodium ion channels cause LQT. Two Taiwanese LQT families were screened for mutations in these ion channel genes. In family H87, the diagnosis was made in the 25-year-old female proband and six family members based on recurrent syncope and/or a prolonged QT interval. Genotyping revealed a novel nonsense mutation, R744X (C to T transition in codon 744), in the KCNH2 potassium channel gene, resulting in truncation of the putative cyclic nucleotide-binding domain and C-terminal region of the HERG K(+)-channel in all affected family members. The mutation was confirmed by DdeI endonuclease digestion of the DNA from each family member. The 26-year-old female proband in family L89 developed repeated syncope with QTc of 0.61 seconds. After linkage and mutation analysis, the syndrome in this family was associated with a novel KCNQ1 missense mutation, T309I, causing the substitution of a threonine residue at position 309, in the pore region of the KvLQT1 K(+)-channel, with an isoleucine. By Tsp45I restriction analysis, the mutation was noted in the proband and the proband's asymptomatic brother, but was not detected in 100 unrelated normal individuals. Identification of a mutation has clinical implications for presymptomatic diagnosis and therapy.

Adult↗
PubMed2000

Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava: electrophysiological characteristics and results of radiofrequency ablation.

BACKGROUND: The superior vena cava (SVC) has cardiac musculature extending from the right atrium. However, no previous study in humans has given details regarding the ectopic foci that initiate paroxysmal atrial fibrillation (PAF), which may originate from the SVC. METHODS AND RESULTS: A total of 130 patients with frequent attacks of PAF initiated by ectopic beats were included. Eight patients (6%) had spontaneous AF initiated by a burst of rapid ectopic beats from the SVC (located 19+/-7 mm above the junction of the SVC and right atrium), which was confirmed by multiplane angiographic and intracardiac echocardiographic visualization and was marked by a sharp SVC potential preceding atrial activity. During initial repetitive discharges, the group with SVC ectopy had a higher incidence of intravenous conduction block than the group with pulmonary vein ectopy (75% versus 37%; P=0.03). The activation time of the earliest intracardiac ectopic activities relative to ectopic P wave onset was significantly shorter in the SVC ectopy than the pulmonary vein ectopy group (37+/-15 versus 84+/-32 ms; P<0. 001). After 5+/-3 applications of radiofrequency energy, AF was eliminated. SVC angiography after ablation revealed a local indentation of the venous wall in one patient. Two patients manifested coexisting sinus rhythm and a "focal" fibrillating activity confined inside the SVC after radiofrequency ablation. During a follow-up period of 9+/-3 months, all 8 patients were free of antiarrhythmic drugs, without tachycardia recurrence or symptoms of SVC obstruction. CONCLUSIONS: Ectopic beats initiating PAF can originate from the SVC. A radiofrequency current delivered to eliminate these ectopies is a highly effective and safe way to prevent PAF.

Adult↗
PubMed2000

Pulmonary vein morphology in patients with paroxysmal atrial fibrillation initiated by ectopic beats originating from the pulmonary veins: implications for catheter ablation.

BACKGROUND: Successful ablation of ectopic beats originating from the pulmonary veins (PV) could eliminate paroxysmal atrial fibrillation (PAF). However, information about the structure of the PV in patients with PAF that is initiated by PV ectopic beats has not been reported. METHODS AND RESULTS: We studied the morphology of the PVs and measured their diameters in 3 groups of patients. Group I included 52 patients (aged 66+/-14 years; 44 men) with focal atrial fibrillation (AF) from the PVs. Group II included 8 patients (aged 50+/-10 years; 3 men) with focal AF from the superior vena cava or cristal terminalis. Group III included 23 control patients (aged 55+/-16 years; 17 men). Of the control patients, 11 had AV node and 12 had AV reentrant tachycardia. After an atrial transseptal procedure, selective PV angiography using a biplane system with a right anterior oblique view of 30 degrees, a left anterior oblique view of 60 degrees, and a cranial angle of 20 degrees was performed. The ostial and proximal portions of the right and left superior PVs (RSPV and LSPV) were significantly dilated in group I patients compared with those in groups II and III. Furthermore, the ostia of the RSPV and LSPV were significantly dilated in group II compared with group III patients. However, the mean diameters of the inferior PVs were similar between the 3 groups. Comparisons of the individual PV diameters among the 3 subgroups of group I (which was divided according to where the ectopic focus was located) showed nonselective dilatation of the PV. CONCLUSIONS: Nonspecific dilatation of the ostia and proximal portion of superior PVs were found in patients with PAF initiated by ectopic beats from the superior PVs.

Adult↗
PubMed2000

Effect of verapamil on long-term tachycardia-induced atrial electrical remodeling.

BACKGROUND: The effect of verapamil on long-term tachycardia-induced atrial electrical remodeling has not been reported. METHODS AND RESULTS: Forty-eight dogs were randomly divided into verapamil and control groups. The dogs in the verapamil group received verapamil 120 mg every day, those in the control group did not receive verapamil. Atrial effective refractory period (AERP), inducibility of atrial fibrillation (AF), and duration of AF were assessed before and after complete atrioventricular junction ablation with 1-day, 1-week, or 6-week rapid atrial pacing (780 bpm). AERP shortening, AERP dispersion, AERP maladaptation, and inducibility of AF after 1-day pacing was significantly attenuated by verapamil. However, verapamil did not have any significant effect on these parameters in the dogs with 1-week or 6-week pacing. Verapamil did not have any significant effect on the conduction velocity in the dogs with 1-day, 1-week, or 6-week pacing. Before rapid atrial pacing, verapamil significantly prolonged the duration of AF. In the dogs with 1-day pacing, the duration of AF measured immediately after termination of pacing was similar between the control and verapamil groups. However, in the dogs with 1-week or 6-week pacing, the duration of AF after pacing was significantly longer in the verapamil group. CONCLUSIONS: Verapamil cannot prevent long-term (1 and 6 weeks, respectively) tachycardia-induced changes of atrial electrophysiological properties. Furthermore, verapamil increases the duration of AF in the dogs either before or after long-term rapid atrial pacing.

Adaptation, Physiological↗