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PubMed1993

Lidocaine prophylaxis in coronary revascularization patients: a randomized, prospective trial.

Life-threatening ventricular ectopy can occur after cardiac operations. The actual incidence of ventricular ectopy and the ability to prevent it by the routine prophylactic use of lidocaine hydrochloride have not been established. We performed a double-blind, randomized, prospective trial involving 109 patients undergoing elective coronary artery revascularization. Patients received either lidocaine (n = 54) or a placebo (n = 55) after separation from bypass. A Holter monitor was affixed to each patient for subsequent review, and bedside intensive-care monitors with alarms were used for "real-time" surveillance. The code was broken when potentially malignant ventricular ectopy or side effects attributable to the study drug were noted. Three lidocaine patients and 2 placebo patients were dropped from the study because of hemodynamic instability or bleeding. Of the remaining 104 patients, the code was broken in 12 (24%) of the 51 in the lidocaine group (9 for ectopy and 3 for mental status changes) and 10 (19%) of the 53 in the placebo group (all for ectopy) (p = not significant). Twenty-four-hour Holter monitor evaluation demonstrated occasional ventricular ectopy in all patients and nonsustained ventricular tachycardia in 28% in the lidocaine group and 48% in the placebo group (p = not significant). The mean number of runs of ventricular tachycardia per patient was 0.53 in the lidocaine group and 1.6 in the placebo group (p = 0.035). There were no significant differences in terms of other ventricular ectopy, morbidity, or mortality. No ventricular fibrillation occurred in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

Differentiation of sinus rhythms from supraventricular tachydysrhythmias by activation sequence and timing.

Implantable device detection of tachydysrhythmias remains unreliable and inexact. False responses may occur because of misinterpretation of sinus tachycardia (ST) as a supraventricular tachydysrhythmia (SVTD). Timing of atrioventricular (AV) activation and ventricular dispersion identified and discriminated between ST and SVTDs in 11 dogs. Three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during normal sinus rhythm (NSR) (mean of 5 beats in 11/11 dogs), ST produced by phlebotomy (50 beats in 10 episodes in 6/11) or isoproterenol infusion (105 beats in 21 episodes in 10/11), sinus bradycardia (SB) produced by vagal stimulation (140 beats in 29 episodes in 10/11), and during atrial flutter (AFL) (15 beats in 3 episodes in 3/11) and atrial fibrillation (AF) (152 beats in 31 episodes in 9/11) induced by programmed electrical stimulation. During lidocaine infusion, NSR (55 beats in 11 episodes in 10/11 dogs), SB (84 beats in 17 episodes in 7/11), AFL (10 beats in 2 episodes in 1/11), and AF (103 beats in 21 episodes in 7/11) were recorded. During isoproterenol infusion, SB (45 beats in 9 episodes in 5/11), AFL (15 beats in 3 episodes in 2/11), and AF (64 beats in 13 episodes in 5/11) were recorded in addition to ST. The interval between the left atrial and left ventricular intrinsic deflections (A-V1) and between the left and right ventricular intrinsic deflections (V1-V2) of each beat was measured. The mean value (msec) of A-V1 and V1-V2 in each episode was compared to NSR in the same dogs. A difference of greater than or equal to 16 ms was used for differentiation. In all cases except SB with first-degree AV block, V1-V2 in each episode was insignificant (0-14 msec), categorizing the rhythms as supraventricular. During NSR, ST and SB without AV block, delta A-V1 was small (0-15 msec). In contrast delta A-V1 was greater than or equal to 16 ms in 6/8 episodes of AFL. The remaining two episodes could be differentiated by the greater number of atrial versus ventricular beats. AF could be detected by the variability of A-V1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Atrial sensing to augment ventricular tachycardia detection by the automatic implantable cardioverter defibrillator: a utility study.

The triggering of automatic implantable cardioverter defibrillator (AICD) discharges by supraventricular tachycardias, despite the presence of a probability density function algorithm, remains a limitation of an otherwise highly effective device. We systematically investigated the diagnostic utility which theroretically could derive form the addition of atrial sensing capability to the AICD in 25 patients with 30 inducible sustained monomorphic ventricular tachycardias (VTs) at clinically relevant rates (greater than or equal to 150 beats/min). Patients were included only if they were not taking medication capable of depressing ventriculoatrial (VA) conduction for at least 5 half-lives prior to electrophysiological testing. We tested the simple criterion for VT that ventricular cycle length (CL) be shorter than the atrial CL (not met in sinus or most other supraventricular tachycardias). Mean VT CL was 283 +/- 47 ms (range 210 to 370). In 25 (83%) VTs, the VT criterion was consistently satisfied. Of the five cases in which the criterion was not met, 1:1 VA conduction during VT was present in four, three of which initially manifested 2:1 VA conduction lasting from 14 to 28 s and therefore would have transiently fulfilled the VT criterion. The remaining patient who failed to satisfy the VT criterion had ongoing atrial flutter during a relatively slower sustained VT, but this circumstance could be recognized because of the varying AV interval. The absence of 1:1 VA conduction at CLS less than or equal to 400 ms during ventricular pacing accurately predicted the absence of 1:1 VA conduction during VT in 95% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Superiority of ibutilide (a new class III agent) over DL-sotalol in converting atrial flutter and atrial fibrillation. The Ibutilide/Sotalol Comparator Study Group.

OBJECTIVE: To compare the efficacy and safety of a single dose of ibutilide, a new class III antiarrhythmic drug, with that of DL-sotalol in terminating chronic atrial fibrillation or flutter in haemodynamically stable patients. DESIGN: Double blind, randomised study. SETTING: 43 European hospitals. PATIENTS: 308 patients (mean age 60 years, 70% men, 48% with heart disease) with sustained atrial fibrillation (n = 251) or atrial flutter (n = 57) (duration three hours to 45 days) were randomised to three groups to receive a 10 minute infusion of 1 mg ibutilide (n = 99), 2 mg ibutilide (n = 106), or 1.5 mg/kg DL-sotalol (n = 103). Infusion was discontinued at termination of the arrhythmia. MAIN OUTCOME MEASURE: Successful conversion of atrial fibrillation or flutter, defined as termination of arrhythmia within one hour of treatment. RESULTS: Both drugs were more effective against atrial flutter than against atrial fibrillation. Ibutilide was superior to DL-sotalol for treating atrial flutter (70% and 56% v 19%), while the high dose of ibutilide was more effective for treating atrial fibrillation than DL-sotalol (44% v 11%) and the lower dose of ibutilide (44% v 20%, p < 0.01). The mean (SD) time to arrhythmia termination was 13 (7) minutes with 2 mg ibutilide, 19 (15) minutes with 1 mg ibutilide, and 25 (17) minutes with DL-sotalol. In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was less obvious in the group that received 2 mg ibutilide. This dose converted almost 48% of atrial fibrillation that was present for more than 30 days. Concomitant use of digitalis or nifedipine and prolongation of the QTc interval were not predictive of arrhythmia termination. Bradycardia (6.5%) and hypotension (3.7%) were more common side effects with DL-sotalol. Of 211 patients given ibutilide, two (0.9%) who received the higher dose developed polymorphic ventricular tachycardia, one of whom required direct current cardioversion. CONCLUSION: Ibutilide (given in 1 or 2 mg doses over 10 minutes) is highly effective for rapidly terminating persistent atrial fibrillation or atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.

Adult↗
PubMed1985

Evaluation of transthoracic countershock with initial energy levels up to 200 J in a coronary care unit.

In a five year prospective study, transthoracic countershock of patients in the coronary care unit was evaluated with respect to efficacy, transthoracic resistance and arrhythmias. Those patients dying within 12 hours of the recorded event are referred to as agonal patients. Atrial arrhythmias were generally first treated with quinidine or disopyramide and/or a digitalis preparation. Patients with coronary heart disease were treated with lidocaine, disopyramide, or verapamil when there was time for appropriate diagnosis. The efficacy of the first shock with an energy level between 50 J and 200 J in non-agonal patients was: for atrial fibrillation, 44% (N = 34), and between 83% and 93% for tachycardias and ventricular fibrillation. The cumulative efficacy of two shocks with energy levels between 50 J and 200 J was: in atrial fibrillation 53% and others between 90% and 96%. In agonal patients with ventricular fibrillation and acute myocardial infarction the efficacy of one shock of 100-150 J was 39% and two shocks of 100-200 J, 69% (N = 13). No correlation was found between the transthoracic resistance and parameters such as body-weight, length or thorax-circumference, indicating that these should not be taken into account in the choice of the energy level for countershock. In non-agonal patients without coronary heart disease arrhythmias due to countershock increased in duration when the energy of the countershock increased (p less than 0.01, N = 39). It is concluded that the initial stored energy for defibrillation and cardioversion of nonagonal patients in a coronary care unit may be limited to 200 J (160 J delivered energy), even with atrial fibrillation after drug therapy in which case an initial energy level of 200 J seems more appropriate.

Arrhythmias, Cardiac↗
PubMed1983

Mitral valve E point-septal separation as an index of left ventricular function with valvular heart disease.

Echocardiographic mitral valve E point-septal separation (EPSS) has been found to be a useful hemodynamic index. Prior studies have shown a high negative correlation between EPSS and left ventricular ejection fraction (EF) in selected patients, but the utility of this index with valvular heart disease has not been examined in detail. Cardiac catheterization and M-mode echocardiographic data were retrospectively analyzed from 30 patients with aortic stenosis, 18 patients with chronic aortic regurgitation, and 25 patients with chronic mitral regurgitation. For aortic stenosis patients (including those with coronary artery disease), an excellent correlation (r = -0.89, p less than 0.001) was observed between EPSS and angiographic EF. More modest correlations were noted for patients with aortic regurgitation (r = -0.58, p less than 0.01) and mitral regurgitation (r = -0.63, p less than 0.001). For patients with aortic regurgitation, correlation improved to r = -0.83 by excluding subjects with marked (greater than 4 mm) fluttering of the anterior mitral valve leaflet. For patients with mitral regurgitation, the EPSS-EF correlation improved to r = -0.72 after excluding patients with atrial fibrillation. Compared with other echocardiographic indices of left ventricular function (percent shortening of the minor diameter or echo-derived EF), the EPSS demonstrated an equivalent or superior correlation with angiographic EF for each valvular lesion studied. We conclude that EPSS is a highly reliable index of left ventricular function with aortic stenosis, but its utility in unselected patients with chronic mitral or aortic regurgitation is limited.

Adult↗
PubMed1999

Dofetilide: a review of its use in atrial fibrillation and atrial flutter.

UNLABELLED: Dofetilide is a 'pure' class III antiarrhythmic agent which has demonstrated efficacy in the conversion of atrial fibrillation or flutter to sinus rhythm and the maintenance of sinus rhythm. By blocking the rapid component of the cardiac delayed rectifier potassium current (I(Kr)), dofetilide prolongs the cardiac action potential duration and the effective refractory period. This is thought to increase the likelihood of a re-entrant wavefront encountering refractory tissue and terminating the arrhythmia. Preliminary findings from the EMERALD (European and Australian Multicenter Evaluative Research on Atrial Fibrillation Dofetilide) and SAFIRE-D (Symptomatic Atrial Fibrillation Investigation and Randomized Evaluation of Dofetilide) studies suggest that oral dofetilide is effective in the conversion of atrial fibrillation or flutter to sinus rhythm. Both studies have yet to be published in full. In SAFIRE-D, dofetilide 500microg twice daily for 3 days achieved a conversion rate of 32% compared with a 1% rate for placebo. A similar conversion rate was achieved after 3 days in EMERALD with dofetilide 500microg twice daily (29%) which was significantly greater than that achieved with sotalol 80mg twice daily (6%; p < 0.05). Oral dofetilide also appears to be effective in the maintenance of sinus rhythm. An abstract report of EMERALD participants who had been converted to sinus rhythm showed that 71% of patients who received oral dofetilide remained in sinus rhythm after 6 months (compared with 26% of placebo and 59% of sotalol recipients: both p < 0.05). Restoration of sinus rhythm using intravenous dofetilide is more likely in patients with recent-onset versus prolonged-duration arrhythmia, and in those with atrial flutter rather than atrial fibrillation. Limitations of comparative data for intravenous dofetilide are such that few conclusions can be drawn. Although generally well tolerated in clinical trials, dofetilide has proarrhythmic potential. Torsade de pointes ventricular tachycardia was reported in up to 3.3% of patients who received oral dofetilide in the DIAMOND (Diamond Investigations of Arrhythmia and Mortality on Dofetilide) studies, although only a small proportion of patients in these studies had atrial fibrillation; most episodes occurred within the first 3 days. Whether the propensity of dofetilide for this life-threatening arrhythmia is similar to that of other class III antiarrhythmic agents has yet to be determined. Importantly, the long term use of oral dofetilide in patients at high risk for sudden cardiac death is not associated with an increased risk of mortality, although these DIAMOND findings cannot necessarily be extrapolated to patients with atrial fibrillation. CONCLUSIONS: Dofetilide offers an alternative to currently available antiarrhythmic agents for the pharmacological conversion of atrial fibrillation or atrial flutter to sinus rhythm and for the maintenance of sinus rhythm after cardioversion. However, further comparative data are necessary before its definitive place can be determined.

Animals↗
PubMed1993

[A case of primary systemic amyloidosis with skeletal muscle atrophy and congestive heart failure].

A 77-year-old male had been noticing progressive weakness of the legs for three years. By the age of 75 he had difficulty in climbing stairs. On admission, serum level of CPK was moderately high. There were weakness and atrophy of the proximal muscles. Deep tendon reflexes were depressed. Sensation was normal. The electromyogram and the biopsy of the femoral quadriceps muscles showed nonspecific changes. In 1989, he developed difficulty in walking and had congestive heart failure. On the second admission, moist rales were heard over the chest, and pitting edema was present in the lower extremities. The chest roentgenogram showed a cardiothoracic ratio of 63% and bilateral pleural effusion. The electrocardiogram showed atrial flutter with 2:1 conduction, QS in V1-3, rS in V4, and ST depression and T inversion in V5,6. The echocardiogram revealed a thick left ventricular wall and impaired left ventricular contraction (EF 22%). Macroglossia, hepatosplenomegaly and renal dysfunction were not noted. Congestive heart failure progressed and he suddenly died of ventricular tachycardia in December 1989. At autopsy, skeletal muscle fibers varied in size and showed fiber splitting. A cellular infiltration was observed in the stroma. Amyloid deposit was positively stained with Congo red. The heart weight was 570 g with marked left ventricular hypertrophy and moderate bilateral atrial dilatation. In both atria and ventricles, extensive amyloid deposition was found around myocardial fibers as well as in perivascular spaces. Amyloid was present also in the liver, the kidneys, the gastrointestinal tracts, and the other organs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2006

[Arrhythmia-induced dilated cardiomyopathies].

Arrhythmic cardiomyopathies are due to ventricular dysfunction following prolonged or chronic tachycardia; the clinical pictures one of congestive heart failure, which is totally reversible after the treatment of tachycardia and the restoration of sinus rhythm. Since Whipple's first description of this model of heart failure, several teams have shown that ventricular or atrial pacing at rates exceeding 220 beats per minute produces a profound and largely reversible depression of ventricular function, and a constellation of neuroendocrine abnormalities and metabolic, electrophysiological and anatomic alterations of the myocardium. The associated heart failure generally starts to improve within days of achieving ventricular rhythm control, but clinical recovery may take several weeks or months. All forms of chronic tachycardia may induce heart failure, but the onset of cardiomyopathy depends more on the heart rate and the duration of the arrhythmia than on its type. The pathophysiological mechanisms are multiple and complex, and include abnormalities in the structure and function of cardiomyocytes and disturbances in excitation-contraction coupling. Treatment consists of restoring and maintaining sinus rhythm, or at least of controlling the ventricular rate. Because of its curative effect, selective radiofrequency ablation is the treatment of choice when the arrhythmogenic substrate is localized. Control of the ventricular rate by radiofrequency modification of atrioventricular conduction is the treatment of choice for chronic atrial fibrillation.

Animals↗
PubMed1997

Ablation therapy for cardiac arrhythmias.

Ablation has become an important and, in some cases, the first-line therapy for a number of tachyarrhythmias. The feasibility of treating arrhythmias with ablation was initially demonstrated with surgical ablation techniques. Recently, catheter ablation techniques have replaced the surgical approach in nearly all cases. Catheter ablation is highly effective for the Wolff-Parkinson-White syndrome, atrioventricular nodal reentry, and atrial ectopic tachycardia. It is effective for atrial flutter, although approximately one quarter of patients treated with catheter ablation continue to require therapy for concomitant atrial fibrillation. The surgical maze procedure has proved to be feasible for preventing atrial fibrillation. The risks and long-term efficacy of catheter ablation maze procedures for atrial fibrillation need to be defined. The efficacy of ablation for ventricular tachycardia varies with the type of tachycardia. Catheter ablation is very effective for the rare idiopathic ventricular tachycardias that occur in structurally normal hearts and for bundle-branch reentry ventricular tachycardia, which occurs most frequently in patients with dilated cardiomyopathy. When performed at an experienced center, surgical ablation is an excellent option for selected patients with ventricular tachycardia due to prior myocardial infarction who have a discrete aneurysm but otherwise well-preserved ventricular function. Catheter ablation shows promise for this arrhythmia, but it can be offered only to those patients who have relatively slow tachycardias that allow catheter mapping. Substantial advances in mapping and ablation technology will continue to occur, allowing nonpharmacologic control of cardiac arrhythmias to be achieved in an ever greater number of patients.

Arrhythmias, Cardiac↗
PubMed2004

Identification and ablation of atypical atrial flutter. Entrainment pacing combined with electroanatomic mapping.

Differentiation between typical and atypical atrial flutter solely based upon surface ECG pattern may be limited. However, successful ablation of atrial flutter depends on the exact identification of the responsible re-entrant circuit and its critical isthmus. Between August 2001 and June 2003, we performed conventional entrainment pacing within the cavotricuspid isthmus in 71 patients with sustained atrial flutter. In patients with positive entrainment we considered the arrhythmia as typical flutter and treated them with conventional ablation of the cavotricuspid isthmus. As a consequence of negative entrainment we performed 3D-electroanatomic activation mapping (CARTO trade mark ). Conventional ablation of the right atrial isthmus was successful in all patients (n = 54) with positive entrainment. We performed electroanatomic mapping in the remaining 17 patients (14 male; age 60.9 +/- 16 years) resulting in the identification of 6 cases with typical and 11 cases with atypical flutter. Therefore, entrainment pacing was able to predict the true presence of typical atrial flutter in 91.5%. Atypical flutter was right sided in 4 patients and left sided in 7 cases. Electrically silent ("low voltage") areas probably demonstrating atrial myopathy were identified in all cases with left sided and in 2 patients with right sided flutter. In these patients targets for ablation lines were located between silent areas and anatomic barriers (inferior pulmonary veins, mitral respectively tricuspid annulus, or vena cava inferior). In 1 patient, the investigation was stopped due to variable ECG pattern and atrial cycle lengths. In the remaining cases, ablation was acutely successful. One patient, after surgical closure of a ventricular septal defect, demonstrated a dual-loop intra-atrial reentry tachycardia dependent on two different isthmuses. This arrhythmia required ablation of those distinct isthmuses to be interrupted. After a mean follow-up of 8.8 +/- 3.4 months, there was one patient with a recurrence of left-sided atrial flutter. Another patient developed permanent atrial fibrillation shortly after the procedure. Mean duration time of the procedure was 235.6 +/- 56.4 min (right atrium: 196 +/- 17.3 min; left atrium: 267.2 +/- 59.5 min), and average fluoroscopy time was 21.8 +/- 11.7 min (right atrium: 9.5 +/- 6 min; left atrium: 28.9 +/- 7 min). There was no incidence of serious complications associated with these procedures. In conclusion, conventional pacing in the cavotricuspid isthmus combined with electroanatomic mapping was an effective method to differentiate between typical and atypical atrial flutter. Electroanatomic mapping was a powerful tool both for identification of different atrial re-entrant circuits including their critical isthmuses as well as for effective application of individual ablation line strategies.

Adolescent↗
PubMed1994

Myocardial infarction 1979-1988 in Denmark: secular trends in age-related incidence, in-hospital mortality and complications.

All admissions to a coronary care unit (CCU) in Copenhagen County were prospectively registered over a 10-year period, from 1979 to 1988, i.e. after the introduction of CCUs but before the era of intervention with thrombolytic or prophylactic medical treatment. The catchment area remained nearly constant throughout the study period; all patients with MI were admitted to the CCU regardless of age and concomitant diseases, and treatment and discharge policy of the department was unchanged. A total of 4176 MI admissions were registered. During the study period, the age-specific incidence of MI decreased in males above 50 years of age, but was virtually unchanged in females, increasing the proportion of women in the MI population from 26 to 33%. In-hospital and 30-day mortality was unchanged. The occurrence of atrial fibrillation during the admission increased significantly (from 11 to 18%), while the incidence of ventricular fibrillation, heart failure and pulmonary oedema was unchanged.

Adult↗
PubMed1997

Frequency of disabling symptoms in supraventricular tachycardia.

The purposes of this study were to describe: clinical symptoms in a sample of consecutive patients with supraventricular tachycardia (SVT); incidence of sudden death, syncope, and other disabling symptoms; whether these symptoms differ by tachycardia mechanism; and to identify predictor variables of syncope in patients with SVT. Data were collected from chart reviews of 167 consecutive patients with SVT admitted for radiofrequency ablation. Three patients (2%) had nonlethal cardiac arrest, and a total of 16% (26 of 183) received at least 1 external direct-current shock for arrhythmia management. Twenty percent of subjects (33 of 167) reported at least 1 episode of syncope which was preceded by palpitations. The most frequent symptoms were: palpitations (96%), dizziness (75%), and shortness of breath (47%). We found atrioventricular nodal reentrant tachycardia (AVNRT) in 64 patients, atrioventricular-reciprocating tachycardia (AVRT) in 59, atrial tachycardia in 22, and atrial flutter in 22. The symptom profiles of patients with AVNRT, AVRT, and atrial tachycardia were very similar, but differed significantly (p <0.05) from those reported in the atrial flutter group. Multivariate analysis showed that heart rate > or = 170 beats/min was the only independent risk factor for syncope. Chi-square analysis demonstrated that SVT patients with heart rate > or = 170 beats/min had significantly more dizziness and syncope. Thus, despite a low incidence of associated heart disease, and good left ventricular function, there was a high frequency of disabling, potentially life-threatening symptoms associated with episodes of SVT in this sample. SVT can have potentially lethal consequences, and is more disruptive than previously thought.

Adult↗
PubMed2003

Impact of prophylactic i.v. magnesium on the efficacy of ibutilide for conversion of atrial fibrillation or flutter.

The impact of prophylactic i.v. magnesium on the efficacy of ibutilide for conversion of atrial fibrillation and flutter to normal sinus rhythm was studied. In this multicenter cohort study, all patients in three large, tertiary care centers who received ibutilide for acute chemical conversion of atrial fibrillation or flutter from August 1996 through December 2001 were identified through pharmacy or billing records. Patients who did not receive magnesium before or during ibutilide therapy served as the control group, while those who received magnesium less than two hours before or during ibutilide administration served as the study group. The rate of administration of direct-current cardioversion (DCC) and the occurrence of ventricular arrhythmia were compared between those who did and did not receive magnesium. The rates of successful cardioversion were also assessed. Categorical data were analyzed using chi-square analysis or Fisher's exact test. Demographic data were analyzed using Student's t test. The medical records of 321 patients were analyzed. Successful chemical cardioversion in the study group was approximately 19% higher than in those who did not receive magnesium (p = 0.040). The use of DCC in the group who received magnesium was reduced by approximately 34% (p = 0.045). The conversion rate of atrial fibrillation or flutter with ibutilide was enhanced by magnesium administration (p = 0.040), and the rate of administration of DCC was reduced (p = 0.045) in patients who received magnesium. There was a nonsignificant reduction in the occurrence of ventricular arrhythmias (p = 0.533). The efficacy of ibutilide was enhanced by concomitant administration with intravenous magnesium.

Aged↗
PubMed2004

Clinical experience with a new detection algorithm for differentiation of supraventricular from ventricular tachycardia in a dual-chamber defibrillator.

INTRODUCTION: Inadequate therapy for supraventricular tachyarrhythmias (SVT) is a frequent problem of implantable cardioverter defibrillators (ICD). Dual-chamber ICDs have been developed to improve discrimination of SVT from ventricular tachycardia (VT). We investigated the positive predictivity, sensitivity, and specificity of a new algorithm, the SMART detection trade mark algorithm, incorporated in the Phylax AV (Biotronik) dual-chamber ICD. METHODS AND RESULTS: Two hundred nine patients (185 men, age 64 +/- 11 years) received a Phylax AV ICD with SMART detection trade mark activated. In 138 of these patients, 1,245 sustained tachycardia episodes with a detailed electrogram were stored in the device during a follow-up period of 10 +/- 6 months. Episodes were correctly classified as ventricular fibrillation (VF, n = 178) in 52 patients, VT (n = 641) in 98 patients, and SVT (n = 385) in 48 patients by the algorithm. Forty-one true SVT episodes (3.3%) were misclassified as VT: atrial fibrillation (n = 7) and flutter (n = 1), sinus tachycardia (n = 12), and other SVT (n = 21). The positive predictivity for VF/VT was 94.5% (95% CI 92.7-95.8) uncorrected and 94.5% (95% CI 92.9-95.8%) corrected with the generalized equation estimation (GEE) method. The positive predictivity for SVT was 100%. The specificity was 88.9% (95% CI 85.6-91.6%) uncorrected and 89.0% (95% CI 85.6-91.6%) corrected with the GEE method with a sensitivity of 100%. CONCLUSION: The SMART detection trade mark algorithm was safe and reliable for the detection of all ventricular tachycardias. Although its specificity was high, it should be improved with regard to SVT to avoid inappropriate ICD therapies.

Adult↗
PubMed1996

[Conversion rate and prevention of recurrence of paroxysmal and sustained atrial fibrillation or atrial flutter with verapamil/quinidine].

BACKGROUND: Atrial fibrillation (AF) is the most common sustained arrhythmia, occurs in 0.4% of the adult population and in as many as 2% to 4% of those 60 years of age or older. PATIENTS AND METHODS: We studied retrospectively 102 patients, 76 males, 26 females, mean age 56 +/- 12 years, with paroxysmal or sustained atrial fibrillation or atrial flutter (AFlut) treated with verapamil/quinidine (Cordichin) (dosage 3 to 5 times 1 tablet/day). Coronary artery disease was present in 39 patients, dilated cardiomyopathy in 8 patients, valvular disease in 16 patients and various etiologies were present in 13 patients. Twenty-six patients had no discernable heart disease ("Jone atrial fibrillation"). Patients with long QT-syndrome (QT-duration > or = 500 msec; QTc > or = 440 ms) were excluded from this study. RESULTS: Using verapamil/quinidine conversion to sinus rhythm (SR) was possible in 64 patients (63%) within 2 +/- 1 day (range 1 to 6 days). The mean given dosage of quinidine was significantly higher in patients converted to sinus rhythm (762 +/- 129 mg) compared to those without successful conversion (638 +/- 161 mg) (p < 0.001). Diameter of left atrium and left ventricle as well as the degree of heart failure did not influence cardioversion rate significantly. During a mean follow-up of 34 +/- 32 months (range < 1 to 129 months), sinus rhythm remained constant in 28/64 patients (44%) with verapamil/quinidine in whom conversion to sinus rhythm was successful. During follow-up, side effects were present in 20/64 patients who were discharged with verapamil/quinidine: in 2 patients (2%) a torsade de pointes tachycardia was observed (1 patient died suddenly); gastrointestinal side effects were observed in 5 patients (5%); 4 patients had sinuatrial and 3 patients atrioventricular conduction disturbances. An increase in ventricular ectopic beats were present in 3 patients and allergic reactions occurred in 3 patients. CONCLUSIONS: The present data show that verapamil/quinidine is effective in conversion of atrial fibrillation and atrial flutter to sinus rhythm and is associated with an acceptable efficacy rate in preventing recurrences of atrial fibrillation or flutter. Final conclusions concerning side effects are only possible in prospective studies that are ongoing at the present time.

Adult↗