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Biomedical subjects

A S Tang

Publications and source records attributed to A S Tang.

At least 19 recordsLinked to original sources
PubMed2001

Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial.

BACKGROUND: Survival rates for cardiac arrest patients, both in and out of hospital, are poor. Results of a previous study suggest better outcomes for patients treated with vasopressin than for those given epinephrine, in the out-of-hospital setting. Our aim was to compare the effectiveness and safety of these drugs for the treatment of in-patient cardiac arrest. METHODS: We did a triple-blind randomised trial in the emergency departments, critical care units, and wards of three Canadian teaching hospitals. We assigned adults who had cardiac arrest and required drug therapy to receive one dose of vasopressin 40 U or epinephrine 1 mg intravenously, as the initial vasopressor. Patients who failed to respond to the study intervention were given epinephrine as a rescue medication. The primary outcomes were survival to hospital discharge, survival to 1 h, and neurological function. Preplanned subgroup assessments included patients with myocardial ischaemia or infarction, initial cardiac rhythm, and age. FINDINGS: We assigned 104 patients to vasopressin and 96 to epinephrine. For patients receiving vasopressin or epinephrine survival did not differ for hospital discharge (12 [12%] vs 13 [14%], respectively; p50.67; 95% CI for absolute increase in survival 211.8% to 7.8%) or for 1 h survival (40 [39%] vs 34 [35%]; p50.66; 210.9% to 17.0%); survivors had closely similar median mini-mental state examination scores (36 [range 19-38] vs 35 [20-40]; p50.75) and median cerebral performance category scores (1 vs 1). INTERPRETATION: We failed to detect any survival advantage for vasopressin over epinephrine. We cannot recommend the routine use of vasopressin for inhospital cardiac arrest patients, and disagree with American Heart Association guidelines, which recommend vasopressin as alternative therapy for cardiac arrest.

Aged↗
PubMed2001

Relationship between pacemaker dependency and the effect of pacing mode on cardiovascular outcomes.

BACKGROUND: A recently completed trial, the Canadian Trial of Physiological Pacing (CTOPP), showed that physiological pacing did not significantly reduce mortality, stroke, or heart failure hospitalization, but it did show that atrial fibrillation occurred less frequently in patients with physiological pacing. Many pacemaker patients experience only transient bradyarrhythmias with an adequate unpaced heart rate (UHR) and are not pacemaker-dependent. The purpose of the present analysis was to determine if pacemaker-dependent patients have an increased benefit from physiological pacing compared with non-pacemaker-dependent patients. METHODS AND RESULTS: Of 2568 patients included in the CTOPP trial, 2244 patients had a pacemaker dependency test performed at the first follow-up visit. The yearly event rate of cardiovascular death or stroke steadily increased with decreasing UHR in the ventricular pacing group, but it remained constant in the physiological pacing group. When the patients were subdivided to UHR </=60 bpm or >60 bpm, there was an interaction between pacing mode treatment and UHR subgroup. The Kaplan-Meier plot confirmed a physiological pacing advantage only in the UHR </=60 bpm subgroup. This differential effect was also present for the outcomes of cardiovascular death and total mortality. CONCLUSIONS: This study demonstrated that UHR at first follow-up has an important influence on how pacing mode selection affects cardiovascular death and total mortality. Pacemaker-dependent patients with low UHR will probably be paced frequently and will likely benefit from physiological pacing. In contrast, non-pacemaker-dependent patients will likely be paced infrequently and may not benefit from physiological pacing.

Aged↗
PubMed2001

Identification of a gene responsible for familial Wolff-Parkinson-White syndrome.

BACKGROUND: The Wolff-Parkinson-White syndrome, with a prevalence in Western countries of 1.5 to 3.1 per 1000 persons, causes considerable morbidity and may cause sudden death. We identified two families in which the Wolff-Parkinson-White syndrome segregated as an autosomal dominant disorder. METHODS: We studied 70 members of the two families (57 in Family 1 and 13 in Family 2). The subjects underwent 12-lead electrocardiography and two-dimensional echocardiography. Genotyping mapped the gene responsible to 7q34-q36, a locus previously identified to be responsible for an inherited form of Wolff-Parkinson-White syndrome. Candidate genes were identified, sequenced, and analyzed in normal and affected family members to identify the disease-causing gene. RESULTS: A total of 31 members (23 from Family 1 and 8 from Family 2) had the Wolff-Parkinson-White syndrome. Affected members of both families had ventricular preexcitation with conduction abnormalities and cardiac hypertrophy. The maximal combined two-point lod score was 9.82 at a distance of 5 cM from marker D7S636, which confirmed the linkage of the gene in both families to 7q34-q36. Haplotype analysis indicated that there were no alleles in common in the two families at this locus, suggesting that the two families do not have a common founder. We identified a missense mutation in the gene that encodes the gamma2 regulatory subunit of AMP-activated protein kinase (PRKAG2). The mutation results in the substitution of glutamine for arginine at residue 302 in the protein. CONCLUSIONS: The identification of this genetic defect has important implications for elucidating the pathogenesis of ventricular preexcitation. Further understanding of how this molecular defect leads to supraventricular arrhythmias could influence the development of specific therapies for other forms of supraventricular arrhythmia.

AMP-Activated Protein Kinases↗
PubMed2001

Circadian variation of paroxysmal atrial fibrillation. PA3 Investigators. Atrial Pacing Peri-ablation for Prevention of Atrial Fibrillation Trial.

The circadian variation of paroxysmal atrial fibrillation (AF) was studied in 67 patients who received a dual-chamber pacemaker 3 months before a planned atrioventricular node ablation. A distinct circadian variation of AF was observed with 2 time peaks in initiation (1 in the early morning and 1 in the early evening hours), which was modulated by atrial pacing, the duration of AF, and the use of beta-adrenergic blocking agents.

Amiodarone↗
PubMed2001

Dynamic changes of QT interval and QT dispersion in non-Q-wave and Q-wave myocardial infarction.

QT interval and QT dispersion both prolong early postinfarction. Non-Q wave (NQMI) and Q-wave myocardial infarction (QMI) differ in the extent of transmural necrosis, which may influence these measures of myocardial repolarization. This study compared dynamic changes in QT interval and QT dispersion early postinfarction between NQMI and QMI. In 40 patients with NQMI and 69 patients with QMI, maximum QTc (QTc(max)) and QT dispersion (QTD) were measured during the first 4 days postinfarction. Infarct size was assessed daily by using the Selvester QRS score. In both infarct types, QTc(max) and QTD were prolonged on day 1 of infarction, peaking over the next 2 days before returning toward baseline by day 4. NQMI patients had significantly longer QTc(max) and QTD by days 2 to 3 when compared with QMI patients. Multivariable linear regression identified "infarct type x QRS score" as the only independent predictor of QTc(max) (R(2) =.32, P <.0001) and QTD (R(2) =.19, P <.0001) on day 2. In conclusion, dynamic changes of QTc(max) and QTD occur in both infarct types. Large NQMI is associated with greater prolongation of QTc(max) and QTD, which may be due to greater M cell uncoupling and exposure when compared with QMI.

Aged↗
PubMed2000

Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of Physiologic Pacing Investigators.

BACKGROUND: Evidence suggests that physiologic pacing (dual-chamber or atrial) may be superior to single-chamber (ventricular) pacing because it is associated with lower risks of atrial fibrillation, stroke, and death. These benefits have not been evaluated in a large, randomized, controlled trial. METHODS: At 32 Canadian centers, patients without chronic atrial fibrillation who were scheduled for a first implantation of a pacemaker to treat symptomatic bradycardia were eligible for enrollment. We randomly assigned patients to receive either a ventricular pacemaker or a physiologic pacemaker and followed them for an average of three years. The primary outcome was stroke or death due to cardiovascular causes. Secondary outcomes were death from any cause, atrial fibrillation, and hospitalization for heart failure. RESULTS: A total of 1474 patients were randomly assigned to receive a ventricular pacemaker and 1094 to receive a physiologic pacemaker. The annual rate of stroke or death due to cardiovascular causes was 5.5 percent with ventricular pacing, as compared with 4.9 percent with physiologic pacing (reduction in relative risk, 9.4 percent; 95 percent confidence interval, -10.5 to 25.7 percent [the negative value indicates an increase in risk]; P=0.33). The annual rate of atrial fibrillation was significantly lower among the patients in the physiologic-pacing group (5.3 percent) than among those in the ventricular-pacing group (6.6 percent), for a reduction in relative risk of 18.0 percent (95 percent confidence interval, 0.3 to 32.6 percent; P=0.05). The effect on the rate of atrial fibrillation was not apparent until two years after implantation. The observed annual rates of death from all causes and of hospitalization for heart failure were lower among the patients with a physiologic pacemaker than among those with a ventricular pacemaker, but not significantly so (annual rates of death, 6.6 percent with ventricular pacing and 6.3 percent with physiologic pacing; annual rates of hospitalization for heart failure, 3.5 percent and 3.1 percent, respectively). There were significantly more perioperative complications with physiologic pacing than with ventricular pacing (9.0 percent vs. 3.8 percent, P<0.001). CONCLUSIONS: Physiologic pacing provides little benefit over ventricular pacing for the prevention of stroke or death due to cardiovascular causes.

Aged↗
PubMed2000

Interatrial conduction of atrial tachycardia in heart transplant recipients: potential pathophysiology.

Surgical suture lines formed at the site of anastamosis have been considered to be electrically inert and thus present a line of block to conduction. However, a number of reports have suggested that conduction is occasionally possible across suture lines. Most of these cases have reported conduction between donor and recipient atria following cardiac transplantation. We report an illustrative case successfully treated with radiofrequency ablation, and present pathology findings that may give insight into the pathophysiology.

Adult↗
PubMed2000

Permanent pacing from a left ventricular vein in a patient with persistent left and absent right superior vena cava.

Persistent left superior vena cava with coexisting absent right superior vena cava is rare with less than 150 cases in the literature. Various techniques for pacemaker implantation have been described in this situation. We report a 40-year-old man with sinus and atrioventricular nodal dysfunction who underwent dual chamber pacemaker implantation. We elected to implant the ventricular electrode down a left ventricular branch of the coronary sinus and the lead is stable at 4-month follow-up.

Adult↗
PubMed2000

Radiofrequency ablation of atrial tachycardia originating from the triangle of Koch.

Atrial tachycardia (AT) originating in the triangle of Koch is reported rarely and presents a potential risk of atrioventricular (AV) block during radiofrequency (RF) catheter ablation. Eight patients with AT in the triangle of Koch undergoing RF ablation are presented. There were five women and three men, ranging in age from 32 to 74 years. One patient had bicuspid aortic valve disease, and the other seven patients had no structural heart disease. At electrophysiological study, AT was inducible in all eight patients. In one patient, AV nodal re-entrant tachycardia was also inducible. The site of AT was located by recording the earliest atrial activation during AT and successful RF ablation. Fluoroscopy confirmed the corresponding site to the region of the triangle of Koch. The earliest atrial activation was 35+/-9 ms before the surface P wave, and was recorded at the apex of the triangle of Koch near the bundle of His in six patients and midway between the bundle of His and coronary sinus os in two patients. At the successful RF application site, His potential was not recorded in any patient. The mean AV ratio was 5:1 (range 1:1 to 12:1). RF ablation at the successful site resulted in accelerated junctional rhythm in four of the eight patients and successfully terminated AT in all eight patients, with first-degree AV block in one patient. In conclusion, AT from the triangle of Koch is a distinct entity and RF ablation can be successfully performed; however, a potential risk of AV block remains.

Adult↗
PubMed1999

Dofetilide enhances shock-induced extension of refractoriness and lowers defibrillation threshold.

OBJECTIVE: To explore the hypothesis that class III antiarrhythmics reduce defibrillation threshold (DFT) by prolonging postshock refractoriness. ANIMALS AND METHODS: The effect of a new selective potassium channel blocker, dofetilide (DOFlow 2.5 micrograms/kg bolus plus 0.9 microgram/kg/h; DOFmed 10 micrograms/kg bolus plus 3.6 micrograms/kg/h; and DOFhigh 25 micrograms/kg bolus plus 9 micrograms/kg/h), on DFT was compared with that of placebo in anesthetized open chest dogs (n = 6 per group). The effects of dofetilide on refractory period extension (RPE) were assessed by using DFT strength shocks delivered at various stages of repolarization. RESULTS: DFT was significantly decreased in the DOFhigh group, whether expressed as shock peak voltage or energy (P < 0.05 compared with changes in placebo). At baseline, a shock timing of ventricular effective refractory period of 25 ms resulted in RPE of 100 +/- 24 ms, 80 +/- 11 ms, 91 +/- 14 ms and 90 +/- 20 ms in the placebo, DOFlow, DOFmed, and DOFhigh groups, respectively. After infusion, these RPE values were unchanged in the placebo group but tended to increase in the dofetilide treatment groups. DOFhigh significantly increased RPE by 20 +/- 18 ms (P < 0.05 compared with baseline values and changes in placebo). Dofetilide-induced changes in RPE and DFT were significantly correlated when expressed as voltage (r2 = 0.78, P < 0.01), current (r2 = 0.80, P < 0.01) and energy (r2 = 0.53, P < 0.01). CONCLUSIONS: These results show that dofetilide prolonged RPE at a plasma level that reduced DFT, thus providing support for the hypothesis that selective prolongation of refractoriness may synergize with shock-induced RPE to decrease the energy requirements for defibrillation.

Animals↗
PubMed1998

Ventriculophasic modulation of atrioventricular nodal conduction in humans.

BACKGROUND: Baroreceptor-mediated phasic changes in vagal tone have been hypothesized to cause ventriculophasic sinus arrhythmia (VPSA). The objectives of this study were to demonstrate ventriculophasic modulation of AV nodal conduction and to substantiate the role of the baroreflex on ventriculophasic AV nodal conduction (VPAVN) by pharmacological perturbation of parasympathetic tone. METHODS AND RESULTS: Twelve patients with infra-Hisian second-degree heart block and VPSA were studied. Incremental atrial pacing was performed until AV nodal Wenckebach block at baseline, after phenylephrine infusion, and after atropine. AV nodal conduction curves were constructed for each phase and compared. At baseline, VPAVN was present in 9 of 12 patients on the steep portion of the AV nodal conduction curves. Phenylephrine increased systolic blood pressure from 149+/-33 to 177+/-22 mmHg (P<0.001) and sinus cycle length from 844+/-169 to 1010+/-190 ms (P<0.001) and shifted the AV nodal conduction curves up and to the right. Phenylephrine induced VPAVN in 2 of 3 patients in whom it was not present at baseline and in 11 of 12 total. Atropine abolished both VPSA and VPAVN in all patients. CONCLUSIONS: VPAVN was demonstrated in patients with infra-Hisian second-degree AV block. It was accentuated by phenylephrine and abolished by atropine, suggesting a baroreflex mechanism for VPSA and VPAVN.

Aged↗
PubMed1997

Atrioventricular nodal reentrant tachycardia with atrioventricular block.

Atrioventricular block (AVB) during atrioventricular nodal reentrant tachycardia (AVNRT) has been well documented, although it is not a common phenomenon. The mechanism for the initiation and resolution of AVB during AVNRT have been postulated. However, the site of AVB and its implication on the reentrant circuit in AVNRT is not clear. We illustrate two examples of AVNRT with AVB and offer further clarification on the site and mechanism of AVB.

Adult↗