Biomedical subjects

Win-Kuang Shen

Publications and source records attributed to Win-Kuang Shen.

40 records · Page 3Linked to original sources

PubMed2002

Modification and ablation for inappropriate sinus tachycardia: current status.

Inappropriate sinus tachycardia is an ill-defined clinical syndrome with diverse clinical manifestations. Clinical symptoms can range from intermittent palpitations to multisystem complaints. Although there is a general consensus that when the heartbeat exceeds 100 beats per minute at rest or with minimal physiologic challenge, it is considered "inappropriate," this quantitative differentiation is quite arbitrary, while validation of the reproducibility of the heart rate/activity correlation can be challenging. Once the clinical diagnosis of inappropriate sinus tachycardia is expected, other supraventricular tachyarrhythmias and medical conditions causing sinus tachycardia should be excluded. The underlying mechanism of inappropriate sinus tachycardia is not well understood. "Intracardiac" mechanisms such as enhanced intrinsic automaticity, enhanced sympathetic tone, increased sympathetic receptor sensitivity, and blunted parasympathetic tone have been proposed. Evidences for "extracardiac" mechanisms such as length-dependent autonomic neuropathy, excessive venous pooling, beta-receptor hypersensitivity, alpha-receptor hyposensitivity, altered sympathovagal balance, and brainstem dysregulation have also been reported. Currently, our ability to differentiate primary (intracardiac) from secondary (extracardiac) mechanisms of inappropriate sinus tachycardia is limited. It has been reported that ablative therapy of sinus node is effective in treating patients with symptomatic inappropriate sinus tachycardia. Acute success of sinus node modification/ablation can be accomplished in 70%-100% of the various study populations. Although long-term successful outcome may be accomplished in a few patients, symptoms of palpitations and autonomic characteristics frequently persist. Identification and differentiation of patients who are suitable for ablative therapy versus medical therapy should be one of the central clinical research issues in this patient population. This brief review first considers the clinical and electrophysiologic diagnosis of inappropriate tachycardia and then summarizes the mechanisms of inappropriate sinus tachycardia and related syndromes such as postural orthostatic tachycardia syndrome. Techniques of mapping and ablation of sinus node are discussed briefly. A critical review of the acute and long-term clinical outcomes following sinus node ablation and modification is updated. In conclusion, the precise role of sinus node modification in patients with inappropriate sinus tachycardia remains to be determined. Sinus node modification could be considered in patients with inappropriate sinus tachycardia with persistently increased heart rate in the absence of any autonomic abnormalities. Autonomic laboratory testing should be performed to exclude any evidence of autonomic dysregulation. Clinical research on the pathophysiology of inappropriate sinus tachycardia should be pursued vigorously.

Body Surface Potential Mapping↗

PubMed2002

Evidence of an intrinsic sinus node abnormality in patients with postural tachycardia syndrome.

OBJECTIVE: To determine whether an intrinsic sinus node abnormality is involved in the pathophysiology of the postural tachycardia syndrome (POTS). SUBJECTS, PATIENTS, AND METHODS: In this prospective study, we compared the relationship between P-wave axis (PWA) and heart rate (HR) in 11 healthy controls and 14 patients with POTS by obtaining 12-lead electrocardiographic recordings during supine rest and during gradual head-up tilt. The HR of controls was titrated with isoproterenol infusion to match the HR of patients. The PWA was compared at different HR levels, and the relationship between HR and PWA was assessed for patients and controls. Primary end points were the PWA-HR relationship in healthy controls, comparison of these data with data from patients with POTS as a group, and identification of a possible subgroup of patients with POTS with irregular PWA-HR relationship. RESULTS: The PWA increased with increasing HR following a similar logarithmic trendline in both groups. The PWA of patients was significantly lower at the lowest comparable HR level but not different at faster HR levels. Three patients (21%) had a clearly abnormal HR-PWA relationship with substantial shift toward lower PWA. CONCLUSIONS: Our data support the hypothesis of a primary sinus node abnormality in a subset of patients with POTS. The ability to identify patients with primary sinus node abnormality may have important therapeutic implications.

Adult↗

PubMed2002

Epinephrine-induced QT interval prolongation: a gene-specific paradoxical response in congenital long QT syndrome.

OBJECTIVE: To determine the effect of epinephrine on the QT interval in patients with genotyped long QT syndrome (LQTS). PATIENTS AND METHODS: Between May 1999 and April 2001, 37 patients (24 females) with genotyped LQTS (19 LQT1, 15 LQT2, 3 LQT3, mean age, 27 years; range, 10-53 years) from 21 different kindreds and 27 (16 females) controls (mean age, 31 years; range, 13-45 years) were studied at baseline and during gradually increasing doses of intravenous epinephrine infusion (0.05, 0.1, 0.2, and 0.3 microg x k(-1) x min(-1)). The 12-lead electrocardiogram was monitored continuously, and heart rate, QT, and corrected QT interval (QTc) were measured during each study stage. RESULTS: There was no significant difference in resting heart rate or chronotropic response to epinephrine between LQTS patients and controls. The mean +/- SD baseline QTc was greater in LQTS patients (500+/-68 ms) than in controls (436+/-19 ms, P<.001). However, 9 (47%) of 19 KVLQT1-genotyped LQT1 patients had a nondiagnostic resting QTc (<460 milliseconds), whereas 11 (41%) of 27 controls had a resting QTc higher than 440 milliseconds. During epinephrine infusion, every LQT1 patient manifested prolongation of the QT interval (paradoxical response), whereas healthy controls and patients with either LQT2 or LQT3 tended to have shortened QT intervals (P<.001). The maximum mean +/- SD change in QT (AQT [epinephrine QT minus baseline QT]) was -5+/-47 ms (controls), +94+/-31 ms (LQT1), and -87+/-67 ms (LQT2 and LQT3 patients). Of 27 controls, 6 had lengthening of their QT intervals (AQT >30 milliseconds) during high-dose epinephrine. Low-dose epinephrine (0.05 microg x kg(-1) x min(-1)) completely discriminated LQT1 patients (AQT, +82+/-34 ms) from controls (AQT, -7+/-13 ms; P<.001). Epinephrine-triggered nonsustained ventricular tachycardia occurred in 2 patients with LQTS and in 1 control. CONCLUSIONS: Epinephrine-induced prolongation of the QT interval appears pathognomonic for LQT1. Low-dose epinephrine infusion distinguishes controls from patients with concealed LQT1 manifesting an equivocal QTc at rest. Thus, epinephrine provocation may help unmask some patients with concealed LQTS and strategically direct molecular genetic testing.

Adolescent↗

PubMed2002

Safety of electrical cardioversion in patients with atrial fibrillation.

OBJECTIVES: To determine the incidence of thromboembolic complications after electively performed electrical cardioversion in patients with atrial fibrillation and to assess the clinical variables associated with an increased risk of thromboembolism after cardioversion. PATIENTS AND METHODS: This is a retrospective analysis of 834 successful electrical cardioversions performed in 717 patients from 1990 through 1994. Outcome measures included embolic complications at 1-month follow-up after cardioversion and logistic regression models to measure the associations among clinical, anticoagulation, and thromboembolic events and to identify independent predictors of these events. RESULTS: The rate of embolic events after cardioversion was low (0.9%; 95% confidence interval, 0.4%-1.8%). Patients with a therapeutic international normalized ratio had no embolic events. Adequate anticoagulation was independently associated with reduced risk of thromboembolism. Hypertension and diabetes mellitus were independently associated with increased risk of embolization. CONCLUSION: Adequate anticoagulation reduced the risk of embolization after cardioversion. Diabetes mellitus and hypertension are independently associated with increased risk of embolization early after cardioversion.

Aged↗