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PubMed1993

Ventricular fibrillation following adenosine administration. A case report.

An 86-year-old woman was treated for atrial fibrillation. A total of 1.00 mg of digoxin and 12.5 mg of verapamil hydrochloride were administered intravenously during an 8-hour period with no slowing of her heart rate, but the rhythm became regular. Subsequently, 15 mg of verapamil hydrochloride was administered intravenously during a 40-minute period with no reduction in heart rate. Adenosine (6 mg) was then administered intravenously. Approximately 20 seconds after adenosine infusion into a vein in the patient's right arm, a 2.2-second pause developed, followed by ventricular flutter and then fibrillation. The patient required resuscitation and defibrillation.

Adenosine↗
PubMed2006

Cardiac safety of formoterol 12 microg twice daily in patients with chronic obstructive pulmonary disease.

BACKGROUND: Some evidence suggests an increased risk of myocardial infarction and dysrhythmia events associated with beta(2)-agonist use in patients with chronic obstructive pulmonary disease (COPD). This prospective, multicenter, randomized, double-blind, placebo-controlled study compared the cardiac safety of formoterol and placebo in patients with COPD. METHODS: After a 3-14-day run-in, 204 patients were randomized to receive formoterol 12 microg dry powder inhalation or matching placebo twice daily for 8 weeks. Twenty four-hour continuous electrocardiography (Holter monitoring) was performed at screening and after 2 and 8 weeks of treatment. RESULTS: Only a small number of patients met the predefined criteria for a proarrhythmic event (4 formoterol and 2 placebo patients). No patients had sustained postbaseline ventricular tachycardia events, postbaseline run of ventricular ectopic beats associated with relevant symptoms (e.g. hypotension, syncope), or an episode of ventricular flutter or fibrillation. Holter monitoring data were variable but showed no clinically meaningful differences between the formoterol and placebo groups, respectively, for variables such as (mean+/-SD at end of treatment): heart rate (80+/-8.6 vs. 80+/-10.6 bpm), number and rate of ventricular premature beats (total 732+/-2685.4 vs. 650+/-2090.6; rate 35+/-131.0 vs. 30+/-101.3 per h), ventricular tachycardia events (total 0.4+/-1.70 vs. 1.0+/-9.23; rate 0.02+/-0.082 vs. 0.05+/-0.479 per h), and supraventricular premature beats (total 504+/-1844.1 vs. 823+/-2961.8; rate 22+/-80.6 vs. 37+/-129.6 per h). Vital signs and electrocardiogram data, including corrected QT intervals (Bazett and Fridericia), were similar across treatment groups. The overall adverse event experience was similar in the formoterol (n=26 [27%]) and placebo (n=33 [31%]) groups. The most common adverse events, infections and respiratory events, were expected for this patient population. The incidence of cardiac adverse events was low (1 formoterol and 4 placebo patients). CONCLUSIONS: The results of this study confirm the good cardiovascular safety profile of formoterol in patients with COPD.

Administration, Inhalation↗
PubMed1986

[Therapy of refractory ventricular tachycardia by transvenous electrical ablation].

In 6 patients (mean age 49 +/- 11 years) with chronic recurrent ventricular tachycardia which were relatively slow during antiarrhythmic therapy and had been proven to be resistant to various antiarrhythmic drugs, catheter ablation of the site of origin of ventricular tachycardia was performed after endocardial activation and/or pace-mapping. According to the results of catheter mapping, the sites of origin of ventricular tachycardia were in the region of the infero-lateral wall (n = 3), in the anterolateral wall (n = 1) and in the right ventricle (n = 2). In 3 cases, two ablative procedures were performed as the first was only transiently successful. A total of 51 shocks was delivered (200 J 45 times, 100 J 5 times and 400 J once). The following complications were observed: multiple episodes of spontaneous, partly polymorphous ventricular tachycardia which degenerated into ventricular flutter on several episodes (n = 1); transient third degree AV-block and intermittent complete right bundle branch block (n = 1); transient ST-elevation (n = 3); and self-terminating atrial tachycardia lasting for several minutes (n = 1). Immediately after the first ablative procedure, either no ventricular tachycardia could be induced any longer (n = 2) or non-clinical ventricular tachycardia was induced (n = 2). In the remaining 2 patients, programmed ventricular stimulation was not repeated immediately at the end of the ablative procedure. During a follow-up study at the end of the first week, the clinical ventricular tachycardia could be induced again in 3 of 4 cases. In 3 cases, a second ablative procedure was performed because of recurrences of ventricular tachycardia (n = 2) or syncope (n = 1). During final follow-up (mean 4.3 +/- 3.4 months), no recurrences of ventricular tachycardia were observed in 5 cases. In one case, recurrences occurred. Therefore, an automatic cardioverter was implanted. In conclusion, these preliminary results show that catheter ablation of drug-resistant ventricular tachycardia is feasible and may be an alternative to surgical procedures.

Adult↗
PubMed2005

Arrhythmias and conduction abnormalities in children after repair of tetralogy of Fallot.

AIM: To find out types and frequency of cardiac arrhythmias and conduction abnormalities in the group of children who underwent surgery for tetralogy of Fallot (TOF). METHODS: Forty-six pedicatric patients who underwent a complete repair of TOF at the age of 1 to 13 (mean 2.89+/-2.36) were studied Thirty-eight (82.60%) had total correction and 8 (17.40%) had palliative operation first, and total correction afterwards. Twenty-four-hour Holter ECG monitoring was performed in all 46 pediatric patients aged from 1 to 16 yrs (mean 6.48+/-4.04) after surgery as follows: in 1 patient (2.17%) after a year, in 20 patients (43.477%) after 2 to 5 years and in 25 patients (54.34%) after 5 years. Mean age of patients on Holter monitoring was 9.25+/-4.39 (range 4-19). Twenty of them (43.47%) were girls and 28 (56.53%) were boys. All the patients were evaluated by standard methods (clinical signs, clinical findings, ECG before surgery, ECG before Holter monitoring and 2D Doppler echocardiography. RESULTS: Types of heart rhythm found out by Holter monitoring were: sinus nodus dysfunction in 1 child (2.17%), significant premature atrial contraction (PAC) in 8 (17.39%), supraventricular paroxysmal tachycardia in 3 (6.535), transient nodal rhythm in 2 (4.34%), premature ventricular contraction (PVC) Lown grade 1-III in 9 (19.56%) and Lown grade IV in 2 (4.34), atrioventricular (AV) block grade I in 2, right bundle branch block (RBBB) in all 46 (100%) and RBBB + left anterior hemiblock (LAH) in 4 (8.96%). There was no presence of atrial flutter, ventricular tachycardia or complete A V block. None of them experienced sudden death. Using cross procedure statistical methods, it was found that all the patients with PVC had right ventricular dilatation. There was no relation of other types of arrhythmia found on Holter monitoring to the other parameters from echocardiography, neither to the other standard methods. Children did not need the pace-maker, but 36.95% of the them required antiarrhythmic drugs. CONCLUSION: Twenty-four hour Holter ECG is a noninvasive and very sensitive method for discovering heart rhythm disturbances in children after the repair of tetralogy of Fallot, especially in asymptomatic patients. The patients after the repair of this congenital heart disease needed a long-term follow-up for early recognition of serious heart rhythm disturbances and their treatment.

Adolescent↗
PubMed2006

Radiofrequency ablation of arrhythmias guided by non-fluoroscopic catheter location: a prospective randomized trial.

AIMS: To compare the utility of non-fluoroscopic mapping systems (Carto and Ensite NavX) with that of conventional mapping in patients referred for catheter ablation of a wide variety of arrhythmias. METHODS AND RESULTS: Patients referred for catheter ablation (excluding atrial fibrillation, atypical atrial flutter, ventricular tachycardia in structural heart disease, and complete AV nodal ablation) were randomized equally to a procedure guided by Carto, Ensite NavX, or conventional mapping. A total of 145 patients were recruited (82 men, aged 49+/-16, range 18-85). In 19 patients, no ablation was performed, and in the remaining, typical atrial flutter, atrioventricular nodal re-entrant tachycardia, and atrioventricular re-entrant tachycardias [including Wolff-Parkinson-White (WPW)] accounted for 93% of ablations. Overall procedure time, immediate and short-term success, complication rate, and freedom from symptoms at follow-up were identical for all groups. NavX led to the least X-ray exposure: Navx vs. conventional, median (range): 4 (0-50) vs. 13 (2-46) min (P<0.001); NavX vs. Carto, median (range): 4 (0-50) vs. 6 (1-55) min (P=0.008). Both Carto and NavX increased disposable costs by 50% when compared with conventional (P<0.001). For typical atrial flutter, Carto and NavX reduced screening times without increasing procedure cost. If ablation was not performed, NavX was twice as expensive as Carto or conventional. CONCLUSION: Ensite NavX and Carto procedures have similar effectiveness and safety to a conventional approach; however, they both reduce X-ray exposure, with NavX producing a significantly greater effect than Carto. Although this benefit is achieved at a greater financial cost, there may be long-term benefits to catheter laboratory staff.

Arrhythmias, Cardiac↗
PubMed1987

Holter detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage.

To determine the frequency and severity of cardiac arrhythmias in intracranial subarachnoid hemorrhage, 120 nonselected patients were prospectively studied by 24-hour Holter monitoring. Arrhythmias were found in 96 of 107 patients (90%) with adequate Holter recording: ventricular premature complexes in 49, nonsustained ventricular tachycardia in 5, supraventricular premature complexes in 29, paroxysmal supraventricular tachycardia or atrial fibrillation in 9, sinoatrial block and arrest in 29, second-degree atrioventricular block in 1, atrioventricular dissociation in 4 and idioventricular rhythm in 2. Life-threatening ventricular arrhythmias (torsades de pointes-type ventricular tachycardia) occurred in 4 patients, degenerating into either ventricular flutter or fibrillation in 2. ST-segment changes suggestive of acute transitory myocardial ischemia were found in 8 patients (1.5 mm or more of ST depression in 7 patients and 1.5 mm or more of ST elevation in 1 patient). The frequency and severity of arrhythmias were significantly higher in patients studied within 48 hours of subarachnoid hemorrhage; serious ventricular arrhythmias were associated with QTc prolongation more than 550 ms and with hypokalemia less than 3.5 mEq/liter. No correlation was found between age, clinical condition, site and extent of subarachnoid hemorrhage and either the occurrence or severity of arrhythmias. The results of our study indicate an extremely high incidence of arrhythmias, sometimes serious, in subarachnoid hemorrhage, especially in the first 48 hours after hemorrhage. Continuous electrocardiographic monitoring is therefore mandatory.

Adolescent↗
PubMed1990

[Signal averaged ECG and mechanisms of sudden death].

The aim of signal averaged electrocardiography is to detect late potentials (LP) which are markers of ventricular tachycardia. As sudden death is often due to ventricular fibrillation which can complicate ventricular tachycardia, some workers have suggested that the presence of LP may increase the risk of sudden death. We analysed the results of signal averaged ECG in 17 subjects who died suddenly and compared them with 8 patients who died from ventricular tachycardia. These two groups of patients were part of a general population of 450 subjects who underwent programmed ventricular stimulation and signal averaged ECG by Simson's method (25 Hz filter). Three parameters of this ECG were analysed: total QRS duration (Dur QRS), amplitude of the signal 40 ms before its termination (V 40), and the duration of the terminal activity less than 40 microV (Dur LP). The criteria of diagnosis of Lp were: Dur QRS greater than or equal to 120 ms, V 40 less than or equal to 20 microV, Dur LP greater than or equal to 40 ms. The results of signal averaged ECG of patients who died suddenly were different to those of patients who died from VT: Dur QRS 116 +/- 40 vs 140 +/- 25 ms, V 40 27 +/- 24 vs 7 +/- 8 microV, Dur LP 39 +/- 27 vs 59 +/- 14 ms. Only 8 patients who died suddenly had LP (47%) whereas all patients who died of VT had LP. A correlation was observed between the presence of LP and 2 factors: the LV ejection fraction which was significantly lower in patients with LP (28 +/- 8 vs 46 +/- 19%) and the results of programmed ventricular stimulation: patients with induced sustained VT less than 270/mn usually had LP (15/16). LP were usually absent (4/6) in cases of ventricular flutter (VT greater than or equal to 270/mn) or induced VF. The presence of LP in 2 patients could signify a risk of developing VT later on. In conclusion, 9/17 patients who died suddenly did not have LP. The risk of sudden death due to primary VF or V flutter cannot be predicted. Other causes of VF are even harder to identify.

Adult↗
PubMed1987

[Prognostic value of ventricular tachycardia induced by stimulation in patients without documented tachycardia].

In order to determine the cause of syncopes or disorders of conduction, 584 programmed stimulations using 2 ventricular extrastimuli delivered during an imposed rhythm were performed, between 1981 and 1985, in patients without ventricular tachycardia (VT) proven by Holter recordings. Eighty-seven non-sustained VT (NSVT) (15%), 8 ventricular fibrillations (VF) (1%), 16 ventricular flutters (VF1) (3%) and 23 sustained VT (SVT) (4%) were induced. To appraise the significance of these responses the patients were followed up for a mean period of 2 +/- 1 years. Among the NSVT patients the first 47 were followed up until 1984 and the others, less numerous, until 1985. Patients who responded to stimulation with NSVT had (4.4%) or did not have an underlying cardiopathy; their mean left ventricular ejection fraction (LVEF) was 53.5 +/- 17% (n = 10); 17% died of heart disease, but the disease was related to VT in only one case; 36% of these patients had cardiac symptoms, but only one presented with episodes of NSVT. Patients who responded with VF had a normal (50%) or abnormal heart; their mean LVEF was 52 +/- 19%; one died of heart failure, the others were asymptomatic. All but one of the patients who responded with VF1 had an underlying cardiopathy and a mean LVEF of 38 +/- 19%; 3 died, 2 of heart failure and 1 of sudden death; 13 were asymptomatic. All patients who responded with SVT had an underlying cardiopathy and a mean LVEF of 37 +/- 13%; 7 (30%) died, including 2 sudden deaths; 2 had episodes of VT and 12 were asymptomatic. In summary, an underlying cardiopathy was present in one-half of the patients who responded with NSVT or VF and in all patients who responded with VF1 or SVT. The risk of VT was low (5%) in patients who responded with NSVT, VF or VF1 and was higher (17%) in those who responded with SVT.

Adolescent↗
PubMed1985

Activation mapping in patients with coronary artery disease with multiple ventricular tachycardia configurations: occurrence and therapeutic implications of widely separate apparent sites of origin.

Catheter or intraoperative activation mapping studies, or both, were performed in 17 patients with coronary artery disease with two to four distinct configurations of ventricular tachycardia, resistant to a mean of 12.1 +/- 6.0 antiarrhythmic drug trials per patient. Mapping studies were performed to guide anticipated surgical ablation of arrhythmias. Activation map data were adequate to determine sites of origin of 30 (64%) of 47 observed tachycardia configurations. These 30 ventricular tachycardias (26 observed clinically) were mapped to 22 separate endocardial sites of origin. Sites of origin of distinct tachycardias were identical or closely adjacent (within 3 cm) in six patients and widely separate (greater than or equal to 4 cm) in eight patients (47% of the group). Activation maps were not adequate to determine sites of origin of 17 (36%) of the 47 tachycardias, including all configurations in three patients. Fifteen patients underwent surgery for control of ventricular tachycardia: aggressive, map-guided endocardial resection (mean 26.5 +/- 14.2 cm2) in 12 patients with identified sites of tachycardia origin and extensive resection of visible endocardial scar (2 patients) or encircling endocardial ventriculotomy (1 patient) in those in whom the sites of origin of all clinical tachycardias remained undetermined. Two inoperable patients were treated with amiodarone. During postoperative electrophysiologic tests (11 of 13 surgical survivors), ventricular tachyarrhythmias were initially uninducible in only 4 of 11 patients. However, in two patients only nonclinical arrhythmias (ventricular flutter) were induced. Six (21%) of 29 clinical tachycardias whose sites of origin were either not determined or not resected (right septum or papillary muscle) remained inducible in five patients. Using previously ineffective antiarrhythmic drugs, initially inducible arrhythmias became uninducible (two patients), or harder to induce than preoperatively (five patients). As a result of surgical resections alone or in combination with previously ineffective drugs (and amiodarone in two inoperable patients), there were no recurrences of ventricular tachycardia in 14 (93%) of 15 patients discharged during 19.0 +/- 14.3 months of follow-up study. Thus, activation mapping may commonly reveal separate apparent sites of origin for clinically observed, morphologically distinct, highly drug-refractory ventricular tachycardias in patients with coronary artery disease with multiple tachycardia configurations. Extensive surgical resection of identified sites of origin may be required to ablate arrhythmias in these patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2004

[Causes and prognosis of syncope in patients with primary dilated cardiomyopathy].

The causes of adverse prognosis of patients with primary dilated cardiomyopathy remain controversial. Classically, it is thought that syncope is associated with an increased risk of mortality. The aim of this study was to try and identify the causes and prognostic significance of syncope in patients with primary dilated cardiomyopathy. Sixty-five patients aged 31 to 80 with primary dilated cardiomyopathy were admitted for investigation of syncope. The average ejection fraction was 27 +/- 10%. Invasive and non-invasive investigations including complete electrophysiological investigations, were performed. Sustained monomorphic ventricular tachycardia was induced in 14 patients (21.5%), ventricular flutter or fibrillation was induced in 9 patients (14%), a supraventricular arrhythmia in 17 patients (26%), and a conduction defect alone or associated with another arrhythmia in 7 patients (11%). A pathological result of tilt testing was observed in 5 patients (8%). No cause of syncope could be demonstrated in 15 patients (23%). During follow-up (4 +/- 2 years) there was a mortality of 15% which was only correlated with the reduction in left ventricular ejection fraction. The authors conclude that there are many causes of syncope in primary dilated cardiomyopathy: ventricular arrhythmias represent only 35% of cases and do not impact on the prognosis; above all, left ventricular ejection fraction is the most important prognostic factor.

Adult↗
PubMed1997

[Clinico-electrophysiologic effects of magnesium, especially in supraventricular tachycardia].

Clinical electrophysiological effects of magnesium (Mg2+) are known for more than 60 years. Mg2+ is a cation to be found ubiquitously in the human body and is involved in more than 300 different enzymatic reactions. However, so far this ion has not been established as a standard therapeutic tool for the treatment of supraventricular tachyarrhythmia. This may be explained by the inconsistent efficacy of Mg2+, partly in relationship to a given plasma Mg(2+)-concentration, partly caused by the uncertainty regarding the dosage and injection rate or the unawareness of the clinical effects of the cation. Mg2+ influences myocardial metabolism by its effects on contractility and electrical activity. Both effects are closely linked. About 12% of cardiac Mg2+ is found in the mitochondria and 2 to 3% in the myofibrils. A large portion is incorporated in adenosin mono-, di- and triphosphate. Mg2+ affects intracellular calcium by inhibiting the influx of calcium into the myocyte through sarcolemmal channels, by modulation of cyclic AMP and by competing with calcium for binding to a single high affinity site on actin. Mg2+ has been linked to a naturally occurring calcium channel blocker. Furthermore Mg2+ blocks the outward current through some potassium channels resulting in an inward rectification of these channels. This suggests that internal magnesium functions as a potassium channel-blocking agent. Early afterdepolarizations are oscillations in the membrane potential and lead to triggered activity and therefore are the electrophysiological substrate of "torsade de pointes" type of ventricular flutter. Mg2+ is able to inhibit both early afterdepolarizations and tachyarrhythmias. Additionally Mg2+ interferes with the sodium-potassium-ATPase system by stabilizing the transmembrane gradient of both cations. Mg2+ deficiency alters this balance and leads to increased neuromuscular excitability. Digitalis is able to block the sodium-potassium-ATPase system, which can be cancelled by Mg2+. Thus the first clinical reports of the therapeutic use of Mg2+ refer to digitalis-induced atrial arrhythmia and ventricular ectopy which could be converted to sinus-rhythm or suppressed by the intravenous application of Mg2+ in 1935. Some years later, the first successful termination of paroxysmal supraventricular and ventricular tachycardia following application of 1.5 to 3 g of Mg2+ was published. But only in the late eighties, systematic studies of the electrophysiological effects of Mg2+ were performed and clinical use was first tested in random fashion in the nineties. Summarizing studies in older patients with different heart diseases and young healthy volunteers the most pronounced and clinically important effect seems to be related to the modulation of the AV node function. The prolongation of the PR interval by 7 to 12% without changing significantly heart rate, QRS duration and QT duration, can be considered a consistent and reproducible effect of Mg2+. In electrophysiological studies a prolongation of the AH interval by 8 to 18%, of the Wenckebach cycle length by up to 20% and of the refractory period of the AV node by 6 to 20% is usually observed, but no change of the retrograde conduction, or the HV interval can be found. Furthermore sinus node recovery time increases by 10% and sinuatrial conduction time by up to 25%. There is no significant effect on intraventricular conduction and atrial and ventricular refractory period. Additionally no significant effect on the anterograde and retrograde refractory period of accessory pathways could be measured; however in some cases (up to 40%) an anterograde block in the accessory pathway may be observed after intravenous Mg(2+)-injection. For the treatment of paroxysmal atrioventricular tachycardia like AV-nodal reentrant tachycardia or orthodromic atrioventricular reentrant tachycardia in WPW syndrome, Mg2+ has been applied in a limited number of recent prospective but uncontrolled studies. Recently, an

Adult↗
PubMed1975

[Effect of ajmaline and its therapeutically used derivatives N-propylajmaline and di-monochloracetylajmaline on the functional refractory period and contractility of guinea pig atrium and aconitine arrhythmia in the rat].

1. In the isolated left atrium of the guinea pig ajmaline and di-monochloracetylajmaline (DCAA) show almost the same activity concerning prolongation of the functional refractory period. 2. In contrast to this N-propylajmaline (NPA) is much more effective than ajmaline. 3. NPA as compared to ajmaline and DCAA, however, shows a considerably smaller difference between the concentrations prolonging refractory period (I) and those decreasing contractility (II) in the guinea pig atrium (EC25). The quotient from I and II is 0.4 with NPA, 1.2 with ajmaline and 1.6 with DCAA. 4. Differences in efficacy similar to those observed in the guinea pig atrium are also found in experimental cardiac arrhythmias in the intact animal. NPA is much more effective than ajmaline regarding inhibition of extrasystoles, ventricular tachycardia and ventricular flutter due to aconitine infusion in the rat. In this experimental model DCAA shows slightly less activity than ajmaline; this difference is statistically significant.

Aconitine↗
PubMed2002

Implantable cardioverter defibrillator utilization based on discharge diagnoses from Medicare and managed care patients.

INTRODUCTION: Implantable cardioverter defibrillators (ICDs) have become an accepted therapy for patients at high risk of sudden cardiac death. To assess the current utilization of this therapy, we estimated the number of patients at risk of sudden death using an historical claims-based study and compared these results to current ICD usage volumes. METHODS AND RESULTS: Managed care and Medicare databases (claims related to 4.6 million covered U.S. lives during a 12-month period) were analyzed to identify patients who had either a primary or secondary diagnosis of ventricular tachycardia, ventricular fibrillation, ventricular flutter, or cardiac arrest. These patients were further required to have a diagnosis code indicating a previous myocardial infarction or congestive heart failure. Patients who died during the study period or did not have medical insurance were excluded. In the base case scenario, 1,226 patients per million population were identified as potential ICD candidates. Sensitivity analyses reduced that value to a range from 736 to 1,140 ICD candidates per million population. Sensitivity factors considered included acute myocardial infarction, comorbidities, age, secondary ventricular tachycardia/ventricular fibrillation diagnosis, and varying degrees of left ventricular dysfunction. These results contrast with an ICD usage rate of 416 per million population in the United States and lower rates in other countries. CONCLUSION: This study suggests that, based on discharge diagnoses, many patients who could benefit from ICDs are not receiving this therapy. Diverse reasons for this underutilization should be addressed to improve access to, and appropriate use of, this therapy.

Adolescent↗
PubMed1988

Assessment of a device for trans-telephonic control of defibrillation.

The safety and efficacy of a device allowing the trans-telephonic control of defibrillation have been assessed in 32 attempted defibrillations performed in 29 patients. The initial rhythm was atrial fibrillation in 27; ventricular tachycardia in 4; and ventricular flutter in 1. Satisfactory voice and ECG transmission were established in all cases. The mean time taken by the patient unit to dial and activate the base station was 20.3 seconds. The mean defibrillator charge time was 5.5 seconds to 50 joules and 9.3 seconds to 360 joules. A total of 84 synchronised and 5 unsynchronised shocks were delivered satisfactorily. Lay persons were trained to use the patient unit, and were able to operate the device at home. This device has the potential for rapid defibrillation of patients who develop ventricular fibrillation outside hospital.

Adult↗
PubMed1993

[Results of high amplification electrocardiogram in primary dilated cardiomyopathy].

Idiopathic dilated cardiomyopathy carries a high risk of sudden death. It is also associated with sustained ventricular tachycardia. A complex ventricular arrhythmia is recorded in 3/4 of cases on Holter monitoring which has a low specificity. The aim of the study was to determine whether signal-averaged electrocardiography could provide a better evaluation of the prognosis of this condition. The results of signal-averaged electrocardiography were compared with those of 24 hour Holter monitoring and of systematic programmed ventricular stimulation in 58 patients with idiopathic dilated cardiomyopathy. Late ventricular potentials were recorded in 13 of the 14 subjects with inducible and usually spontaneous sustained ventricular tachycardia. The sensitivity of the technique for evaluating the risk of sustained VT was therefore good (93%). Late potentials were also recorded in 9 patients with induced ventricular flutter or fibrillation, these patients being symptomatic (dizzy spells). Late potentials were also demonstrated in 14 of the 35 asymptomatic patients without inducible VT, indicating that this non-invasive investigation had a limited specificity (60%). In addition, during follow-up of the patients, the risk of sudden death was difficult to demonstrate. Late potentials were only found in subjects with inducible sustained VT but no in the other cases. In conclusion, signal-averaged electrocardiography seems to be valuable for evaluating the risk of sustained VT in subjects with idiopathic dilated cardiomyopathy and complex ventricular arrhythmias. The detection of the risk of sudden death is probably impossible by this technique.

Adult↗
PubMed2004

Arrhythmias of a sudden traumatic death.

A 73-year-old man was treated because of his paroxysmal palpitations became persistent. At the time of hospital admission atrial flutter was found. Antiarrhythmic drug treatment was unsuccessful therefore electrical cardioversion was indicated which restored his sinus rhythm. After one year of uneventful follow up Holter monitoring was indicated again. When the machine was hooked up sinus rhythm was observed. After 53 minutes a tram knocked down the patient, and he died immediately. During autopsy brain laceration, multiple cranial fractions, mediastinal hemorrhage were found. The Holter recording time was 66 minutes. Before the accident sinus rhythm was recorded. At the time of accident an electrical noise was found, followed by long sinus arrest, atrial fibrillation, nodal escape rhythm, sinus bradycardia, ventricular flutter, tachycardia, fibrillation and "dying heart" rhythm. According to our knowledge this is the first Holter monitoring observation during a sudden traumatic death.

Accidents, Traffic↗
PubMed1977

Pulmonary valve fluttering in subpulmonic ventricular septal defect.

Three patients with subpulmonic ventricular septal defect and pulmonary valve fluttering by echocardiography are presented. The echographic changes appear identical to that reported with infundibular pulmonic stenosis and the mechanism causing this fluttering is probably similar.

Adolescent↗
PubMed2005

Fatal ventricular arrhythmia as a complication of transesophageal echocardiography.

AIM: To report a case of serious ventricular arrhythmia during transesophageal echocardiography. METHODS AND RESULTS: A 58-year-old woman with previous mitral and tricuspid valve replacement and permanent pacemaker implantation suffered from recurrent fever and Staphylococcus aureus bacteremia. Transesophageal echocardiography was performed as part of the assessment for infective endocarditis. During this procedure the patient developed sustained ventricular tachycardia and subsequently ventricular flutter. She was successfully resuscitated. Subsequently the procedure was undertaken under general anesthesia with no complications. CONCLUSION: The increasing use of TEE in a wider spectrum of patients, many of whom are seriously ill, may result in serious side-effects.

Anesthesia, General↗