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Left ventricular function in patients with tachycardia induced cardiomypopathy can improve after cessation of the arrhythmia. We reported the intermediate results of 10 patients, 6 men and 4 women, with tachycardiomyopathy who successfully underwent radiofrequency catheter ablation (RFCA) for incessant tachycardia. Three had right atrial tachycardia, 5 ventricular tachycardia (2 and 3 from the right and left ventricles, respectively), 1 atrial flutter and 1 right accessory pathway. During the mean follow-up period of 19 months (range 11-38 months), one patient, right atrial tachycardia, had recurrence and reablation was successfully done without recurrence. Left ventricular ejection fraction, endsystolic and diastolic diameters from echocardiography gradually improved from 35 per cent, 51 and 61 mm to 58 per cent, 36 and 52 mm, respectively (p<0.001). The mean duration of reversibility was 7 months (range 1-15 months). There was no recurrence of tachycardiomyopathy after the return of left ventricular function. Conclusion, RFCA can terminate tachyarrhythmia and lead to significant improvement of left ventricular diameters and systolic function in patients with tachycardia induced cardiomyopathy.

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BACKGROUND: Electrical storm (ES), defined as recurrent multiple ventricular fibrillation (VF) episodes, often occurs in patients with recent myocardial infarction. Because treating ES according to the Advanced Cardiac Life Support (ACLS) guidelines yields a poor outcome, we evaluated the efficacy of sympathetic blockade in treating ES patients and compared their outcome with that of patients treated according to the ACLS guidelines. METHODS AND RESULTS: Forty-nine patients (36 men, 13 women, mean age 57+/-10 years) who had ES associated with a recent myocardial infarction were separated into 2 groups. Patients in group 1 (n=27) received sympathetic blockade treatment: 6 left stellate ganglionic blockade, 7 esmolol, and 14 propranolol. Patients in group 2 (n=22) received antiarrhythmic medication as recommended by the ACLS guidelines. Patient characteristics were similar in the 2 groups. The 1-week mortality rate was higher in group 2: 18 (82%) of the 22 patients died, all of refractory VF; 6 (22%) of the 27 group 1 patients died, 3 of refractory VF (P<0.0001). Patients who survived the initial ES event did well over the 1-year follow-up period: Overall survival in group 1 was 67%, compared with 5% in group 2 (P<0.0001). CONCLUSIONS: Sympathetic blockade is superior to the antiarrhythmic therapy recommended by the ACLS guidelines in treating ES patients. Our study emphasizes the role of increased sympathetic activity in the genesis of ES. Sympathetic blockade-not class 1 antiarrhythmic drugs-should be the treatment of choice for ES.

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INTRODUCTION: Conventional mapping and ablation rely on fluoroscopy, which can result in imprecise positioning of the ablation catheter and long fluoroscopic exposure times. We evaluated a nonfluoroscopic three-dimensional mapping system, termed CARTO, and compared the results of ablation using this technique with those of conventional mapping. METHODS AND RESULTS: We compared the results of 88 arrhythmia ablations (79 patients) using CARTO with 100 ablations (94 patients) using the conventional technique. The ablations were separated into four groups: (1) AV nodal reentrant tachycardia (AVNRT); (2) atrial tachycardia/flutter; (3) ventricular tachycardia (VT); and (4) bypass tract tachycardia. We compared the success rate, complications, and fluoroscopy and procedure times. The ablation outcomes were excellent and comparable in all four types of the arrhythmias between the two techniques. Major complications included one cardiac tamponade in each group and one second-degree AV block in the conventional group. Fluoroscopy time was shorter using the CARTO technique: 10+/-7 versus 27+/-15 minutes for AVNRT (P < 0.01), 18+/-17 versus 44+/-23 minutes for atrial tachycardia and flutter (P < 0.01), 15+/-12 versus 34+/-31 minutes for VT (P < 0.05), and 21+/-14 versus 53+/-32 minutes for bypass tract tachycardia (P < 0.01). Procedure times were similar except for the bypass tract patients, which was shorter in the CARTO group, 4+/-1.3 versus 5.5+/-2.5 hours (P < 0.01). CONCLUSION: The electroanatomic three-dimensional mapping technique reduced fluoroscopy time and resulted in excellent outcome without increasing the procedure time.

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Sudden unexplained death syndrome describes the death of apparently healthy individuals--usually young men--in whom postmortem examination does not reveal the cause of death. The victims are in apparently good health and usually die at night while sleeping. They die within minutes after the onset of agonal respiration. Patients who have been resuscitated were found to have ventricular fibrillation and inducible polymorphic ventricular tachycardia in the electrophysiologic laboratory. This syndrome has been most frequently described in young Southeast Asian men. In this review, the epidemiology, clinical and electrophysiologic manifestations, pathology and risk factors, prognosis, and treatments for sudden unexplained death syndrome are described.

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A nonfluoroscopic electroanatomical cardiac mapping system (CARTO) integrates anatomical and electrophysiological information to reconstruct a three-dimensional activation map. Information from the CARTO system helps to reveal the mechanism and perform successful ablation in scar re-entry ventricular tachycardia after cardiac surgery. Three-dimensional activation and propagation mapping was performed in a patient with ventricular tachycardia after surgical correction of a double outlet right ventricle. The ventricular tachycardia appeared in two morphologies and were refractory to antiarrhythmic medication including amiodarone. Both ventricular tachycardias were re-entered using the ventriculotomy scar but rotated in different directions. Successful radiofrequency ablation was performed by creating a line of conduction block from the pulmonic valve to the ventriculotomy scar using entrainment mapping and the ablation lesion tagging technique. The CARTO system is useful in mapping and guiding the ablation of complex ventricular tachycardia after surgical correction in congenital heart disease

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Using conventional technology, radiofrequency ablation of ventricular tachycardia in cardiomyopathy is frequently unsuccessful because of hemodynamic instability, multiple foci and recurrences. The Biosense CARTO nonfluoroscopic mapping and navigation system, when used to locate the area of the scar or reentry circuit, has the potential to improve the successful ablation, and reduce the rate of recurrence. We report 2 cases here of ventricular tachycardia in cardiomyopathy in which Biosense mapping was useful to identify the area of scar in 1 case, and the area of microreentry circuits in another. Radiofrequency ablation was possible and successful, while the use of conventional mapping was impossible or had recurrence.

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Sudden cardiac death due to ventricular tachyarrhythmia remains a significant problem in the in-hospital setting. Although the probability of survival is closely correlated with the rapidity of a response by qualified personnel, response times can be prolonged, even in specialized care units. In an effort to decrease response time, a fully automatic external cardioverter defibrillator was recently devised. This device was evaluated in the in-hospital setting to assess safety and efficacy. A total of 79 patients were studied in a multicenter trial. Patients were monitored with fully functional devices in the electrophysiology laboratory (51 patients) and in the cardiac care unit (28 patients). Performance of the device was assessed by comparing automatic responses to any sustained change in cardiac rhythm, either spontaneous or induced, to a retrospective review of stored ECG data and programmed parameters. During a total duration of 964 hours of monitoring, there were 99 episodes of sustained tachycardia. Therapy was appropriately delivered or advised in all episodes. Therapy was advised in one episode of supraventricular tachycardia. There were no episodes of inappropriate therapy delivery. There were no complications or adverse events. The device performed with a sensitivity of 100% and specificity of 98.8% with an average response time of 22 seconds. In conclusion, this automatic external defibrillator was safe, effective, and functioned as designed. Significant improvement in response time to life-threatening ventricular tachyarrhythmia in the in-hospital setting would be expected if this technology was widely adopted.

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Nonvalvular atrial fibrillation (AF) is the most common cardiac disorder causing stroke and systemic emboli. Recent clinical trials have clearly demonstrated the effects of antithrombotic treatment in preventing these devastating complications of AF. This review summarizes the salient findings of the first 5 published studies the Atrial Fibrillation, Aspirin, Anticoagulation Study (AFASAK) from Copenhagen, Denmark; the Boston Area Anticoagulation Trial for Atrial Fibrillation (BATAFF); the Canadian Atrial Fibrillation Anticoagulation study (CAFA); the Stroke Prevention in Non-rheumatic Atrial Fibrillation (SPINAF) study; and the Stroke Prevention in Atrial Fibrillation study (SPAF I) from the United States. These trials emphasize the unequivocal benefits of warfarin therapy compared with no treatment. SPAF II showed that aspirin is quite effective in younger patients (<75 years) who have no risk factors. The European Atrial Fibrillation Trial (EAFT) and SPAF III demonstrated that in older patients (>75 years) who had associated risk factors, warfarin therapy at the target international normalized ratio (INR) of 2-3, is the best treatment; however, a combination of low intensity fixed-dose warfarin and aspirin is ineffective. Thus, the guidelines recommended by the American College of Chest Physicians should be followed in treating patients with AF.

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The recent introduction of a nonfluoroscopic electroanatomical cardiac mapping system (CARTO) is an exciting development in catheter ablation treatment of cardiac arrhythmias. The system uses ultralow magnetic fields to locate a sensor positioned near the tip of a regular mapping and ablation catheter. The catheter location and electrograms are recorded and reconstructed in real-time and presented as a three-dimensional geometrical mapped color coded with the electrophysiological information. The CARTO represents an important tool to guide the ablation of patients who have focal tachycardia (e.g., right ventricular outflow tract [RVOT] tachycardia and idiopathic left ventricular [ILV] tachycardia). This study describes how the CARTO system is useful in mapping and ablating these arrhythmias. Two case illustrations, one patient with RVOT tachycardia and another with ILV tachycardia, are described in this article. The tachycardia was mapped and ablated using the new electromagnetic catheter technology creating an electroanatomical map of the arrhythmia focus for each tachycardia without fluoroscopy; both tachycardias were successfully ablated, terminated, and rendered noninducible. The CARTO system is useful in mapping and guiding the ablation of focal tachycardia and merits further study.

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BACKGROUND: Between 1981 and 1988, the Centers for Disease Control and Prevention reported a very high incidence of sudden death among young male Southeast Asians who died unexpectedly during sleep. The pattern of death has long been prevalent in Southeast Asia. We carried out a study to identify the clinical markers for patients at high risk of developing sudden unexplained death syndrome (SUDS) and long-term outcomes. METHODS AND RESULTS: We studied 27 Thai men (mean age, 39.7+/-11 years) referred because they had cardiac arrest due to ventricular fibrillation, usually occurring at night while asleep (n=17), or were suspected to have had symptoms similar to the clinical presentation of SUDS (n=10). We performed cardiac testing, including EPS and cardiac catheterization. The patients were then followed at approximately 3-month intervals; our primary end points were death, ventricular fibrillation, or cardiac arrest. A distinct ECG abnormality divided our patients who had no structural heart disease (except 3 patients with mild left ventricular hypertrophy) into two groups: group 1 (n=16) patients had right bundle-branch block and ST-segment elevation in V1 through V3, and group 2 (n=11) had a normal ECG. Group 1 patients had well-defined electrophysiological abnormalities: group 1 had an abnormally prolonged His-Purkinje conduction time (HV interval, 63+/-11 versus 49+/-6 ms; P=.007). Group 1 had a higher incidence of inducible ventricular fibrillation (93% for group 1 versus 11% for group 2; P=.0002) and a positive signal-averaged ECG (92% for group 1 versus 11% for group 2; P=.002), which was associated with a higher incidence of ventricular fibrillation or death (P=.047). The life-table analysis showed that the group 1 patients had a much greater risk of dying suddenly (P=.05). CONCLUSIONS: Right bundle-branch block and precordial injury pattern in V1 through V3 is common in SUDS patients and represents an arrhythmogenic marker that identifies patients who face an inordinate risk of ventricular fibrillation or sudden death.

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OBJECTIVES: This study sought to assess endothelium-dependent vasorelaxation in long-term users of cocaine. BACKGROUND: Cocaine use has been associated with myocardial infarction, stroke and intestinal infarction. Previously demonstrated effects of the drug, including increased heart rate and blood pressure and increased vascular tone, do not explain the sporadic nature of these vascular events or the occurrence of ischemia remote from acute administration. Abnormal endothelial function could contribute to focal vasospasm and thrombosis and predispose to premature atherosclerosis, all of which have been demonstrated in cocaine users with myocardial infarction. METHODS: Using plethysmography, we studied the change in forearm blood flow in response to intraarterial acetylcholine and nitroprusside in 10 long-term cocaine users and 13 control subjects of similar age who had not used cocaine; sample size was based on a 70% power to detect a 20% reduction in flow with acetylcholine between subjects and control subjects. Using graded doses of intracoronary acetylcholine (from 10(-9) to 10(-6) mol/liter), we studied a second group of 10 cocaine users with angiographically normal or near-normal arteries. RESULTS: Mean forearm blood flow during acetylcholine infusion was significantly lower in cocaine users than in control subjects (p = 0.02). During nitroprusside infusion, there was no difference (p = 0.2) between cocaine users and control subjects. Cigarette smoking did not explain the differences between cocaine users and control subjects. Acetylcholine elicited coronary vasoconstriction in 8 of 10 subjects. CONCLUSIONS: We conclude that endothelium-dependent vasorelaxation is impaired in long-term users of cocaine.

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Patient welfare requires routine follow-up procedures of implantable pacemakers. However, the assessment of atrial sensing and pacing functions in implantable pacemakers is often a challenge due to difficult identification of low amplitude P waves on surface electrocardiograms (ECGs). A previous body surface mapping study suggested that a novel P wave lead vector (P lead) had larger root mean square values than other standard leads. However, for pacemaker follow-up procedures, peak-to-peak amplitudes are more relevant than root mean square values. In this study, the peak-to-peak amplitudes of intrinsic and paced P waves recorded from surface ECG standard lead II and the P lead were compared. In addition, intrinsic and paced R waves were also compared. Data recorded from 15 patients undergoing electrophysiological studies indicated that peak-to-peak amplitudes of the P lead were significantly larger than standard lead II: 24% for intrinsic P waves, 30% for paced P waves, and 72% for intrinsic R waves. In addition, the P lead amplitude of paced R waves showed a nonsignificant increase of 24% compared with standard lead II. Therefore, the use of this new lead vector may improve the clinical ease-of-use and reduce the time required for follow-up procedures of implantable pacemakers for atrial sensing and pacing assessments.

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We successfully implanted transvenously the AICD in a case of sudden cardiac arrest survivor. Though the device is very expensive, it is useful in some selected cases. With its diagnostic capabilities, the device may be useful in elucidating the underlying mechanism of Lai Tai.

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BACKGROUND: The effects of sotalol on refractoriness in human ventricular and atrial muscles have been well established, but the drug's effect on the electrical properties of the His-Purkinje system in humans is not known, especially whether sotalol's effect is due solely to its action on prolonging repolarization or in combination with its beta-blocking properties. We studied the electrophysiologic effects of intravenous sotalol and propranolol in patients undergoing electrophysiologic studies of cardiac arrhythmias. METHODS AND RESULTS: We studied 22 patients (19 men, 3 women; mean age, 60 +/- 6 years) who had coronary artery disease and assessable anterograde, retrograde, or both, His-Purkinje system function. Fifteen patients underwent electrophysiologic studies before and after intravenous sotalol (1.5 mg/kg), and 7 patients underwent electrophysiologic studies before and after intravenous propranolol (0.15 mg/kg). Both sotalol and propranolol had no significant effect on the H-V interval, but sotalol significantly increased ventricular refractoriness and His-Purkinje refractoriness, both in anterograde and retrograde conduction, whereas propranolol did not, Sotalol's effect on His-Purkinge refractoriness also caused atrioventricular block distal to the His bundle during atrial pacing at a moderately fast rate. Sotalol was not effective in preventing bundle branch re-entry tachycardia, nevertheless, it increased cycle length of bundle branch re-entry tachycardia by increasing refractoriness. CONCLUSIONS: Sotalol increased His-Purkinje refractoriness in humans but had no effect on His-Purkinje conduction. The drug must be used judiciously in patients with a diseased His-Purkinje system because it may cause atrioventricular block distal to His at fast heart rates. Sotalol had no effect on macrore-entry utilizing bundle branches.

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Patients with supraventricular arrhythmias have been safely and effectively treated with flecainide. We conducted an open-label, 20-center trial to define further the safety and efficacy profile of oral flecainide in patients with supraventricular arrhythmias, including atrial tachycardias (ectopic or multifocal), atrial-ventricular tachycardias (reentrant), paroxysmal atrial fibrillation/flutter (PAF), and chronic atrial fibrillation (CAF). Our study population of 151 patients with documented supraventricular arrhythmias requiring treatment included 67 with paroxysmal supraventricular tachycardia (PSVT), 67 with PAF (symptoms < 15 days), and 17 with CAF (symptoms > of = 15 days)> The initial flecainide dose of 100 mg twice daily could be increased by 50 mg bid every 4 days to a maximum of 200 mg twice daily. Patients who were effectively treated could receive flecainide for 1 year. The study was terminated April 26, 1989, in response to interim results reported by the Cardiac Arrhythmia Suppression Trial (CAST). All patients were removed from the study by August 1989. At study termination 87% of PSVT, 73% of PAF, and 56% of CAF patients had improved symptomatically while on flecainide therapy. Eleven patients experienced cardiac adverse experiences: proarrhythmic events (3 patients), new or worsened congestive heart failure (7 patients), sinus pauses (1 patient). Cardiac side effects appeared to be more frequent in patients in the CAF group (5/17 patients), all of whom had structural heart disease. Overall, 45 (67%) PSVT, 43 (64%) PAF, and 9 (56%) CAF patients reported at least 1 noncardiac adverse experience; the most common were abnormal vision, dizziness, and headaches. One patient from the CAF group died; the death was considered to be unrelated to flecainide. Flecainide appears to be safe and effective treatment for patients with supraventricular arrhythmias of a variety of mechanisms and appears particularly effective for patients with PSVT. The efficacy is lowest and side effects most frequent in patients with CAF, as seen with other trials of antiarrhythmic medication in these patients. In the context of the CAST experience and other trials of antiarrhythmic drugs in patients with CAF, the balance of risk and benefit of therapy should be considered carefully before initiating treatment.

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The objective of this investigation was the assessment of the response rate of oral atenolol in patients with vasovagal syncope after 1 month of treatment. We randomized into two groups all patients referred to our unit who had had at least one episode of syncope or two episodes of presyncope 1 month before presentation and had a positive isuprel Tilt Table Test (TTT). Group 1 (Gr 1) received oral atenolol, and group 2 (Gr 2) received placebo medication. After a 1-month period patients were reassessed for degree of their symptoms and underwent repeated TTT. Forty-two patients were enrolled in the study. Gr 1 and Gr 2 were comparable in age (38 +/- 13 years vs 43 +/- 14 years, p = 0.216 and sex (male/female = 6:15 vs 10:11, p = 0.204). The severity of attack was similar in both groups. Eight patients in Gr 1 and six patients in Gr 2 had mitral valve prolapse (p = 0.5). No significant differences were seen in systolic blood pressure (122 +/- 17 vs 117 +/- 16 mmHg, p = 0.334), diastolic blood pressure (70 +/- 11 vs 72 +/- 11 mm Hg, p = 0.677), and heart rate (79 +/- 12 vs 79 +/- 13, p = 0.98) between the two groups. The response rates (negative TTT) after 1 month of treatment were 62% versus 5% (p = 0.0004) in the atenolol and control group, respectively. Moreover, patients who received atenolol reported feeling better compared with those who received placebo (71% vs 29%, p = 0.02). In conclusion, atenolol significantly improved symptoms of patients with vasovagal syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

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A double-blind, randomized, placebo-controlled study was conducted to test the peak and trough antianginal and antiischemic monotherapy efficacy and safety of a new extended-release formulation of nisoldipine (nisoldipine Coat Core [Bayer Corporation], 20 mg, 40 mg, and 60 mg once daily compared to placebo). Study patients had a history of chronic, stable angina pectoris, exercise-induced angina in association with ST segment depression, and exercise test reproducibility. Of the 483 patients enrolled in the study, results were valid for safety analysis for 312 and for efficacy analysis for 284. There was a statistically significant improvement in total exercise time at both peak and trough for patients taking 20 mg and 60 mg of nisoldipine compared with patients taking placebo, but the group taking 60 mg was not better than the group taking 20 mg (33.9 and 33.7 seconds, respectively, at trough). The results were similar for the secondary endpoints (time to onset of angina and time to 1 mm ST segment depression). No correlation was evident between plasma nisoldipine levels and total exercise duration. Headache and peripheral edema were the most frequently reported adverse events and were dose related. There were no discontinuations due to adverse events in patients randomized to the 20-mg nisoldipine group. No deaths occurred while patients were receiving active nisoldipine therapy. Therapy with this extended-release formulation of nisoldipine is an effective once-daily treatment for chronic stable angina pectoris. It represents one of the few dihydropyridine calcium channel antagonists that has shown efficacy when administered as monotherapy to patients with angina.

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The purpose of this study was to examine the efficacy and safety of amiodarone to maintain sinus rhythm in patients with refractory atrial fibrillation or flutter. One hundred ten patients with atrial fibrillation or flutter, refractory to > or = 1 class I antiarrhythmic agents (mean +/- SD 2.5 +/- 1.5, median 2), were given low-dose amiodarone (mean maintenance dose 268 +/- 100 mg/day) to determine its efficacy to maintain normal sinus rhythm after chemical or electrical cardioversion. Fifty-three patients had chronic and 57 patients had paroxysmal atrial fibrillation or flutter. Mean age of the study population was 60 +/- 13 years, and the mean follow-up was 36 +/- 38 months (range 31 days to 137 months). Actuarial rates for maintenance of sinus rhythm were 0.87, 0.70, and 0.55 at 1, 3, and 5 years, respectively. Twenty-one patients (19%) with arrhythmia recurrence had an increase in amiodarone dose, and after a mean additional follow-up of 2.5 years, 86% remained in normal sinus rhythm. The only observed predictor of atrial fibrillation or flutter recurrence was paroxysmal arrhythmia (40% recurrence vs 9% in patients with chronic atrial fibrillation or flutter; p < 0.001). Actuarial rates for withdrawal because of adverse effects were 0.08, 0.22, and 0.30 at 1, 3, and 5 years, respectively. The most frequent adverse effects necessitating withdrawal were skin discoloration (4.5%), pulmonary fibrosis (3.6%; none fatal), and thyroid toxicity (2.7%). No deaths occurred during the study period. In conclusion, amiodarone sinus rhythm in patients with atrial fibrillation or flutter, with a relatively low incidence of adverse effects necessitating withdrawal.

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