How to manage patients with inappropriate sinus tachycardia.
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Publications and source records attributed to Win K Shen.
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BACKGROUND: Inappropriate sinus tachycardia (IAST) and postural orthostatic tachycardia syndrome (POTS) are syndrome complexes with some distinctive features, overlapping clinical manifestations, and potential common mechanisms. Pathogenesis of these overlapping syndromes is poorly understood. Diagnostic and therapeutic approaches have not been standardized. PURPOSE: This article provides an overview of the definition, clinical presentation, and proposed mechanisms of IAST and other overlapping syndromes. A stepwise diagnostic approach is suggested. A multidisciplinary management scheme is outlined. METHODS: A MEDLINE search for English-language articles on IAST, POTS, and chronic orthostatic intolerance published up to 2005 was performed. Published data incorporated with our clinical experience were synthesized and presented in this review. RESULTS: The population of IAST is heterogeneous and underlying mechanisms are complex and likely multifactorial. Evidence suggests that both cardiac and extracardiac causes are plausible. Regional and limited autonomic neuropathies, at least in part, can provide a mechanism-based explanation of the cardiovascular indices and clinical symptoms in a significant number of patients with IAST. The regional abnormalities can be detected by autonomic testing. Among patients with IAST and evidence of autonomic dysregulation, an integrated autonomic, cardiovascular, and psychiatric management approach appears to be logical and rational when appropriate. Sinus node ablation could be considered in patients with persistent IAST in the absence of autonomic neuropathy and multisystem symptoms. Data from long-term outcomes are lacking. CONCLUSION: The current understanding of IAST mechanisms is incomplete and management approach is not adequate. Significant effort needed in clinical research to improve therapeutic outcome.
BACKGROUND: The primary aim and central hypothesis of the study are that a designated syncope unit in the emergency department improves diagnostic yield and reduces hospital admission for patients with syncope who are at intermediate risk for an adverse cardiovascular outcome. METHODS AND RESULTS: In this prospective, randomized, single-center study, patients were randomly allocated to 2 treatment arms: syncope unit evaluation and standard care. The 2 groups were compared with chi2 test for independence of categorical variables. Wilcoxon rank sum test was used for continuous variables. Survival was estimated with the Kaplan-Meier method. One hundred three consecutive patients (53 women; mean age 64+/-17 years) entered the study. Fifty-one patients were randomized to the syncope unit. For the syncope unit and standard care patients, the presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P<0.001), respectively, hospital admission was required for 22 (43%) and 51 (98%) patients (P<0.001), and total patient-hospital days were reduced from 140 to 64. Actuarial survival was 97% and 90% (P=0.30), and survival free from recurrent syncope was 88% and 89% (P=0.72) at 2 years for the syncope unit and standard care groups, respectively. CONCLUSIONS: The novel syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope and all-cause mortality among intermediate-risk patients. Observations from the present study provide benchmark data for improving patient care and effectively utilizing healthcare resources.
BACKGROUND: We postulated that the variability of the phase shift between blood pressure and heart rate fluctuation near the frequency of 0.10 Hz might be useful in assessing autonomic circulatory control. METHODS AND RESULTS: We tested this hypothesis in 4 groups of subjects: 28 young, healthy individuals; 13 elderly healthy individuals; 25 patients with coronary heart disease; and 19 patients with a planned or implanted cardioverter-defibrillator (ICD recipients). Data from 5 minutes of free breathing and at 2 different, controlled breathing frequencies (0.10 and 0.33 Hz) were used. Clear differences (P<0.001) in variability of phase were evident between the ICD recipients and all other groups. Furthermore, at a breathing frequency of 0.10 Hz, differences in baroreflex sensitivity (P<0.01) also became evident, even though these differences were not apparent at the 0.33-Hz breathing frequency. CONCLUSIONS: The frequency of 0.10 Hz represents a useful and potentially important one for controlled breathing, at which differences in blood pressure-RR interactions become evident. These interactions, whether computed as a variability of phase to define stability of the blood pressure-heart rate interaction or defined as the baroreflex sensitivity to define the gain in heart rate response to blood pressure changes, are significantly different in patients at risk for sudden arrhythmic death. In young versus older healthy individuals, only baroreflex gain is different, with the variability of phase being similar in both groups. These measurements of short-term circulatory control might help in risk stratification for sudden cardiac death.
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We recently published data suggesting the presence of an intrinsic sinus node abnormality in a subgroup of patients with the postural tachycardia syndrome (POTS). Based on the hypothesis that more widespread abnormalities of cardiac electrophysiologic properties may be present in POTS, we undertook a study to compare cardiac conduction and repolarization at different heart rate levels in patients with POTS and healthy controls. Eleven healthy controls and fourteen patients with POTS participated in the study. Acquisition of 12-lead electrocardiogram recordings were made during supine rest and during gradual head-up tilt. The heart rate of controls was titrated by isoproterenol infusion to match the heart rate of patients. Indices for cardiac conduction (PR interval, QRS duration, and R wave axis) and repolarization (QT interval, QTc interval, and T wave axis) were then compared at different heart rate levels. The PR interval decreased with increasing heart rate in controls more than in patients, resulting in a significantly longer PR interval in patients at the fastest heart rate level. The QT and QTc intervals were significantly shorter in POTS over the entire analyzed heart rate range. The T wave axis decreased with increasing heart rate in patients only. This resulted in a significantly lower T wave axis in patients at the fastest heart rate level. Our data suggest abnormalities of atrioventricular conduction and ventricular repolarization in patients with POTS. These findings may reflect intrinsic cardiac electrophysiologic abnormalities or may be secondary due to abnormalities of cardiac autonomic innervation.
INTRODUCTION: Syncope and sudden death are associated with sympathetic stimulation in LQT1 while LQT2 patients are more susceptible to arrhythmias during nonexertional states. Abnormal spatial (QTd)- and transmural (TDR)-dispersion of repolarization may indicate increased arrhythmogenicity. This study compares the effect of phenylephrine on QTd and TDR in genotyped LQTS to control (C). METHODS AND RESULTS: Seventeen LQT1, 12 LQT2, and 18 age- and sex-matched normal controls received 2 mcg/kg of phenylephrine intravenously. At baseline and peak phenylephrine effect, BP, QT, RR, Bazett's QTc, precordial QTd (QTmax-QTmin), and T-peak to T-end (Tp-e) intervals were determined blinded to the patient's clinical and genotype status. Baseline QT intervals and QTc were significantly longer in LQT1 and LQT2 compared to C. Baseline QTd and Tp-e were greater in LQT2 than either LQT1 or C: QTd=79+/-29 ms (LQT2), 53+/-26 (LQT1), and 45+/-15 (C) and Tp-e=120+/-30 ms (LQT2), 99+/-20 (LQT1), and 90+/-11 (C). Overall, phenylephrine exerted no significant effect on either QTd or Tp-e except with subgroup analysis of symptomatic LQTS where LQT1 and LQT2 patients had a divergent response with TDR. CONCLUSIONS: Phenylephrine-induced bradycardia decreased TDR in symptomatic LQT1 but increased TDR in symptomatic LQT2. The observed effects of phenylephrine are consistent with the protective effect of beta-blocker in LQT1 and the increased arrhythmogenicity noted during nonexertional states in LQT2.
The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined. Dogs with (n = 6) and without (n = 6) rapid pacing-induced CHF underwent echocardiography (conscious) and electrophysiological (under anesthesia) studies. CHF dogs had more pronounced mitral regurgitation, higher atrial pressure, larger atrial area, and increased atrial fibrosis. An enhanced propensity to sustain AF was observed in CHF, despite significant increases in atrial effective refractory period and wavelength. Profound deficits in atrial bioenergetics were present with reduced activities of the phosphotransfer enzymes CK and AK, depletion of high-energy phosphates (ATP and creatine phosphate), and reduction of cellular energetic potential (ATP-to-ADP and creatine phosphate-to-Cr ratios). AF duration correlated with left atrial area (r = 0.73, P = 0.01) and inversely with atrial ATP concentration (r = -0.75, P = 0.005), CK activity (r = -0.57, P = 0.054), and AK activity (r = -0.64, P = 0.02). Atrial levels of malondialdehyde, a marker of oxidative stress, were significantly increased in CHF. Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF.
OBJECTIVES: [corrected] The aim of this study was to determine whether noncontact mapping is feasible in the right ventricle and assess its utility in guiding ablation of difficult-to-treat right ventricular outflow tract (RVOT) ventricular tachycardia (VT). BACKGROUND: In patients without inducible arrhythmia, RVOT VT may be difficult to ablate. Noncontact mapping permits ablation guided by a single tachycardia complex, which may facilitate ablation of difficult cases. However, the mapping system may be geometry-dependent, and it has not been validated in the unique geometry of the RVOT. METHODS: Ten patients with left bundle inferior axis VT, no history of myocardial infarction and normal left ventricular function underwent noncontact guided ablation; seven had failed previous ablation and three had received a defibrillator. All noncontact maps were analyzed by a blinded reviewer to determine whether the arrhythmia focus was epicardial and to predict on the basis of the map whether arrhythmia would recur. RESULTS: The procedure was acutely successful in 9 of 10 patients. During a mean follow-up of 11 months, 7 of 9 patients remained arrhythmia-free. Both patients in whom the blinded reviewer predicted failure had arrhythmia recurrence: one due to epicardial origin with multiple endocardial exit sites and one due to discordance between site of lesion placement and earliest activation on noncontact map. CONCLUSIONS: Mechanisms of ablation failure in RVOT VT include absence of sustained arrhythmia, difficulty with substrate localization and epicardial origin of arrhythmia. In this study, noncontact mapping was safely and effectively used to guide ablation of patients with difficult-to-treat RVOT VT.
Bidirectional isthmus block is associated with successful atrial flutter ablation, whereas creation of increased isthmus conduction delay without block can be proarrhythmic. Often, halo catheter electrodes fail to provide adequate sub-Eustachian isthmus recordings. The aim of this study was to determine if progressive isthmus conduction delay results in the false appearance of block during atrialflutter ablation. A 20-pole deflectable catheter was prospectively positioned across the sub-Eustachian isthmus (from the coronary sinus os [CSO] to 7:00 on the tricuspid valve annulus [TVA] clock face in the left anterior oblique [LAO] projection) in nine patients undergoing atrial flutter ablation. During sinus rhythm, conduction time was measured from the CSO to the 7:00 position while pacing the CSO. Measurements were repeated after each linear lesion and after conduction block was achieved. Transisthmus conduction time at baseline, just prior to success, and after the presence of complete block was 54 +/- 9, 123 +/- 39, and 155 +/- 30 ms, respectively (P < or = 0.01). The marked delay prior to complete block resulted in reversal of the activation sequence in electrodes at TVA 7:00, creating the false appearance of isthmus block; the isthmus electrodes clearly distinguished delay from block. Catheter ablation results in progressive isthmus conduction delay prior to the creation of complete block. Electrodes spanning the isthmus and line of block are critical for distinguishing conduction delay (and pseudoisthmus block) from block.
Half of all pacemakers implanted in the United States are for patients aged 75 years and older. The expectations and needs of an older group are different from patients who are younger, yet it is only recently that different pacing mode benefits for elderly persons have been tested in clinical trials. Some of the results have been surprising and suggest new algorithms for management. Other issues are still on the threshold of investigation. These include pacing for heart failure in elderly patients and pacing combined with cardioverter-defibrillator implantation.