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PubMed1998

[Serum noradrenaline and ventricular tachycardia].

Sudden cardiac death is in the majority of cases due to ventricular tachycardia (VT) developing into ventricular flutter or ventricular fibrillation. It is therefore very important to detect patients with the risk of sudden cardiac death because their mortality depends on the treatment selected. The authors tried to shift the problem of sudden cardiac death into the sphere of cardioendocrinology. They examined the serum levels of norepinephrine (NE) in 17 patients. They collected simultaneously blood samples from the left cubital vein and right atrium after 5 minutes stimulation of the apex of the right ventricle, the frequency of stimulation being 100/min. In ten patients during electrophysiological examination VT was induced (four patients had persisting VT). The authors found a declining NE serum value in the periphery and rising intracardial NE serum level after ventricular stimulation. These differences were statistically significant in patients with VT but not in patients without VT.

Aged↗
PubMed2001

[Cardiac arrhythmias in pregnancy].

Atrial premature beats are frequently diagnosed during pregnancy (PR), supraventricular tachycardia (SVT; atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50-100 J is indicated in all unstable patients (pts). In stable SVT the initial therapy includes the vagal maneuver to terminate breakthrough tachycardias. For short-term management, when the vagal maneuver fails, intravenous adenosine is the first-choice drug and may safely terminate the arrhythmia. For long-term therapy, beta-blocking agents with beta 1 selectivity are first-line drugs; class Ic agents or the class III drug sotalol (sot) are effective and therapeutic alternatives. Ventricular premature beats are also frequently present during PR and benign in most pts; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia [VT], ventricular flutter [VFlut], ventricular fibrillation [VF]) were observed less frequently. Electrical cardioversion is necessary in all pts with a hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable pts, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, beta-blocking agents with beta 1 selectivity are considered as first-choice drugs. If this therapy is ineffective, class Ic agents or sot can be considered. In pts with syncopal VT, VF, VFlut or aborted sudden death an implantable cardioverter-defibrillator is indicated. In pts with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of PR. The treatment of the pregnant patient with cardiac arrhythmias requires important modification of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.

Anti-Arrhythmia Agents↗
PubMed1981

[Use of CO2 euthanasia cabinet for experimental animals (author's transl)].

The process of CO2 euthanasia on mouse, rat, guinea pig and rabbit was observed using a CO2 euthanasia cabinet. The cabinet was filled with CO2 gas and the caged animal was placed into the cabinet. These animals quietly collapsed and their respiratory movement ceased within 25--225 seconds. A-V block was the first arrhythmia recognized on ECG in all cases. The arrhythmia recorded on ECG included complete A-V block, A-V dissociation, ventricular escape rhythm, atrial fibrillation, ventricular flutter and ventricular fibrillation. It could be concluded that euthanasia was satisfactorily performed on these species by means of the CO2 euthanasia cabinet.

Animals↗
PubMed1980

Survival following spontaneous ventricular flutter-fibrillation associated with QT syndrome. Documentation during ambulatory monitoring.

A 56-year-old woman complaining of recurrent syncope was admitted to the coronary care unit after a fainting episode. Three days of continuous monitoring indicated prolongation of the QT interval and occasional premature ventricular beats. After transfer to another hospital wing, the patient was given ambulatory status. On the fifth day, while wearing a Holter monitor recorder, the patient lost consciousness. Review of the ambulatory ECG demonstrated multiple premature ventricular beats and an episode of paroxysmal ventricular flutter-fibrillation. The ventricular arrhythmias were correlated with telephone calls. It is concluded that (1) prolonged monitoring be performed in such subjects, and (2) the absence of ventricular tachyarrhythmias on repeated ECG recording should not preclude pharmacologic intervention in patients with the prolonged QT interval syndrome, ventricular ectopy, and a history of recurrent syncope.

Arrhythmias, Cardiac↗
PubMed1993

Clinical significance of rapid ventricular tachycardia (> 270 beats per minute) provoked at programmed stimulation in patients without confirmed rapid ventricular arrhythmias.

Rapid uniform ventricular tachycardia (VT) (> 270 beats/min) or ventricular flutter induced during electrophysiological studies is thought not to be clinically significant in patients without cardiac arrest or documented rapid VT. The purpose of the study was to follow up 73 patients with inducible ventricular flutter but without confirmed rapid spontaneous VT. A long follow up (mean 3.5 years) identified two groups of patients. The first group had an excellent outcome and was characterised by a normal 24 hour Holter monitoring. In the second group, however, the risk of cardiac mortality was high (35%) and spontaneous VT was < 270 beats/min (26%) and was characterised by couplets or salvos of extrasystoles on Holter monitoring. In this group the history of syncope and decreased left ejection fraction increased the risk of mortality and VT. The presence of late potentials increased the risk of spontaneous VT. Electrophysiologically guided antiarrhythmic therapy reduced the risk of VT. Ventricular flutter was a non-specific finding in patients with normal Holter monitoring. In contrast, in patients with salvos of extrasystoles, ventricular flutter was associated with a high risk of cardiac mortality and VT.

Adult↗
PubMed2003

[Risk factors for cardiac mortality in cases of syncope with previous history of myocardial infarction].

Syncope is considered to be a clinical sign predictive of sudden death in patients with a previous history of myocardial infarction. The aim of this study was to determine the prognostic factors in this population. The study population included 228 patients with myocardial infarction over one month old and who had no documented ventricular tachycardia. The patients were referred for investigation of syncope. The left ventricular ejection fraction (LVEF) was measured by echocardiography or radionucleide technique. Complete electrophysiological study including programmed atrial and ventricular stimulation was performed in all cases. The patients were followed up for 6 months to 5 years or until cardiac transplantation (average 3+/-1 years). One hundred and nineteen patients had a LVEF <40% (Group I) and 109 patients had a LVEF >40% (Group II). Sustained monomorphic ventricular tachycardia (VT) with a rate inferior to 280/min was induced in 44 patients in Group I (37%) and in 18 patients in Group II (16.5%), p<0.05. Ventricular flutter or fibrillation was induced in 24 patients in Group I (19%) and in 19 patients in Group II (17%) (NS). Different causes of syncope (conduction disturbances, supraventricular tachycardia, increased vagal tone, severe coronary ischaemia) were found in 23 patients in Group I (19%) and 32 patients in Group II (29%) (NS). Syncope was unexplained in 43 patients in Group I (36%) and 40 patients in Group II (37%) (NS). The prognosis was very different. In Group I, the cardiac mortality was 49% in patients with inducible monomorphic VT <280/min, 35% in those with inducible ventricular flutter or fibrillation but only 9% in patients without inducible ventricular arrhythmias. In Group II, the prognosis was independent of the results of programmed stimulation and much better: cardiac mortality was 5.5% in patients with inducible VT, 5% in those with inducible ventricular flutter or fibrillation and 4% in patients without inducible ventricular arrhyhtmias. The authors conclude that LVEF is the most powerful predictor of cardiac mortality and sudden death in cases of syncope with a past history of myocardial infarction. The prognosis also depends on the results of programmed ventricular stimulation when the LVEF is inferior to 40%. Sustained monomorphic VT is the most frequently induced arrhythmia in this case and the prognosis of these patients is particularly poor. On the other hand, syncope does not appear to be a poor prognostic factor in the group with normal LVEF, even when it is possible to induce VT.

Adult↗
PubMed2003

Comparative follow up of patients with implanted cardioverter-defibrillators after induction of sustained monomorphic ventricular tachycardias or ventricular fibrillation by programmed stimulation.

OBJECTIVE: To investigate the prognostic value of induced monomorphic ventricular tachycardia (VT) and ventricular flutter or fibrillation (VF) during programmed electrical stimulation in patients with a high risk for sudden arrhythmogenic cardiac death. DESIGN: Prospective cohort study. PATIENTS: 102 patients at high risk for arrhythmogenic sudden cardiac death who received an automated implantable cardioverter-defibrillator (AICD) were evaluated. 56 patients received the AICD for primary prevention and 46 for secondary prevention. 58 patients had induction of a monomorphic VT (VT group) and 44 had induction of a polymorphic VT, ventricular flutter, or ventricular fibrillation (VF group) during programmed electrical stimulation. Average follow up was 20 months in both groups. MAIN OUTCOME MEASURES: Appropriate AICD protocol. RESULTS: In patients who received the AICD for primary prevention, 16 of 32 patients in the VT group, compared with only four of 24 patients in the VF group, received an appropriate AICD protocol (p = 0.02). In the entire study population, 479 appropriate AICD protocols were recorded in 28 (48%) patients in the VT group and 28 appropriate protocols in 11 (25%) patients in the VF group. Cumulative Kaplan-Meier event-free survival curves were significantly different (p = 0.02). CONCLUSION: Induction of VF during programmed electrical stimulation is of no prognostic value even in high risk patients without previously documented ventricular fibrillation.

Aged↗
PubMed1990

[Terminating ventricular tachycardias by mechanical heart stimulation with precordial thumps].

To determine value and limitations of mechanical cardiac stimulation by precordial thumps for termination of ventricular arrhythmias, we systematically treated 47 consecutive cases of ventricular tachycardias (resp. ventricular flutter or fibrillation) by this method. In 20 of 37 cases of ventricular tachycardias the arrhythmia was terminated by manual stimulation. The mean tachycardia rate amounted to 145/min (range from 102 to 222/min) in successfully treated patients. Bursts of rapid precordial thumps were more effective than single precordial thumps. In 17 of the 37 cases of ventricular tachycardia. The mean tachycardia rate was significantly higher (176/min, range from 120 to 250/min) than in successfully treated cases. Altogether, ventricular tachycardias with heart rate less than or equal to 160/min were terminated by mechanical stimulation in 17 of 22 cases, and ventricular tachycardias with heart rate greater than 160/min only in 3 of 15 cases. Ventricular fibrillation (n = 3) or ventricular flutter (n = 7) was not interrupted in any case by precordial thumps. In patients with ventricular tachycardia, mechanical stimulation extends the therapeutic possibilities. The rate of success is higher, the lower the tachycardia rate. The tachycardia rate is the only predictive parameter for therapeutic success.

Adult↗
PubMed1983

Sudden death in hospitalized patients: cardiac rhythm disturbances detected by ambulatory electrocardiographic monitoring.

To determine the cardiac rhythm disturbances underlying sudden death, 15 patients (14 inpatients and 1 outpatient) who had cardiac arrest unexpectedly while undergoing ambulatory electrocardiographic monitoring were identified. Heart disease was present in 11 patients and 7 patients were admitted to the hospital with chest pain before sudden cardiac death occurred. The terminal event at the time of cardiac arrest in 3 (20%) of the 15 patients was a bradyarrhythmia expressed as complete heart block; none survived. A ventricular tachyarrhythmia was the precursor of sudden cardiac death in the remaining 12 patients (80%). Two of these 12 had slow ventricular tachycardia and both died. Five had polymorphous ventricular tachycardia associated with prolonged QT interval (torsade de pointes) and three were receiving a class I antiarrhythmic agent. This rhythm degenerated into ventricular fibrillation in one patient; four of the five patients survived after electrical cardioversion. One patient had ventricular tachycardia followed by asystole. Four patients had ventricular flutter (rate greater than 250/min) that degenerated into ventricular fibrillation in each case; only one of these four patients survived after cardioversion. Frequent (greater than 30/h) premature ventricular complexes were present in 9 of 10 patients with ventricular tachycardia or flutter and R on T phenomenon was seen in only 1 patient. In conclusion, a ventricular tachyarrhythmia is usually found on Holter monitoring during sudden cardiac death in hospitalized patients; torsade de pointes (polymorphous ventricular tachycardia) is a frequent cause of sudden death in these patients. Ventricular fibrillation is always preceded by ventricular tachycardia or ventricular flutter.

Aged↗
PubMed1989

Algorithmic sequential decision-making in the frequency domain for life threatening ventricular arrhythmias and imitative artefacts: a diagnostic system.

A preliminary study to approach the problem of reliably detecting life threatening ventricular arrhythmias in real time is described. An algorithm (DIAGNOSIS) has been developed in order to classify ECG signal records on the basis of the computation of four simple parameters calculated from a representation in the frequency domain. This algorithm uses a set of rules constituting an operative classification scheme based on the comparison of the parameters with a set of pre-established thresholds. This allows us to differentiate four general categories: ventricular fibrillation-flutter, ventricular rhythms, imitative artefacts and predominant sinus rhythm.

Algorithms↗
PubMed1995

Programmed ventricular stimulation in survivors of acute myocardial infarction: long-term follow-up.

The prognostic significance of ventricular tachyarrhythmias induced by programmed ventricular stimulation was evaluated in 492 consecutive survivors of acute myocardial infarction (AMI). Holter monitoring, signal-averaged electrocardiogram (ECG) and measurement of left ventricular ejection fraction (EF) were also performed. The protocol used up to 3 extrastimuli. Sustained monomorphic ventricular tachycardia (VT) < 270 beats/min, > 270 beats/min (ventricular flutter) (VFI), and ventricular fibrillation (VF) were induced in 99, 66 and 52 patients, respectively. Long term follow-up (mean 3.7 +/- 2.2 years) showed that most episodes of VT occurred during the first months following AMI (n = 14), but some patients (n = 6) could develop VT as late as 4 years after AMI. Sudden death (SD) (n = 22) always occurred during the first year following AMI. Multivariate analysis demonstrated that EF < 30% and induction of a VT < 270 beats/min were the only predictors for total cardiac death (P < 0.001). EF < 30%, induction of a VT < 270 beats/min and also of VFI (P < 0.05) were predictors for VT and SD: the risk was 4% in patients without inducible VT, 12% in those with inducible VF1, and 21% in those with inducible VT < 270 beats/min. In conclusion, induction of a sustained monomorphic VT < 270 beats/min or > 270 beats/min is a predictor of arrhythmic events during the first year as well as 4 years after myocardial infarction. However the risk of arrhythmic sudden death decreases after the first year, while the risk of VT persists. Because of the low positive predictive value of programmed stimulation (respectively 21% and 12% for the induction of a sustained VT and VFI), we recommended the indication of programmed stimulation in only the patients with one abnormal non-invasive investigation.

Actuarial Analysis↗
PubMed1976

Attacks of ventricular fibrillation and unconsciousness in a patient with prolonged QT interval. A family study.

A syndrome previously recognized by Romano and Ward is characterized by prolonged QT interval on the ECG, and spells of unconsciousness. The case of a patient is reported with successive ECG recordings during the attacks; ventricular flutter and multifocal ventricular tachycardia were noted, with rapid spontaneous recovery and relapse. Cases of stillbirth and sudden death in infancy among the siblings, together with QT interval tachycardia were noted, with rapid spontaneous recovery and relapse. Cases of stillbirth and sudden death ininfancy among the siblings, together with QT interval prolongation in the relatives point to an autosomal dominant transmission, with the propositus being apparently homozygous. The chromosomes of the patient are normal. The attacks were controlled by the association of propranolol and digitalis which seems to be the optimal long-term therapy in such cases. In view of the poor prognosis in untreated cases, and the good results of a correct therapy, an ECG should be recorded at rest and after exercise in all children suffering from spells of unconsciousness.

Adolescent↗
PubMed1991

Alpha- but not beta-receptor blocking agents inhibit the antiarrhythmic effect of iloprost on ouabain-induced arrhythmia in guinea-pigs.

The effects of iloprost, prazosin and propranolol were tested on ouabain-induced arrhythmia in guinea-pigs. Each drug used alone showed an antiarrhythmic effect. In a second step, iloprost was given in combination with drugs blocking alpha- and beta-adrenergic receptors. Propranolol and iloprost caused a statistically significant and comparable increase of the threshold dose of ouabain for the onset of arrhythmia (OA), the occurrence of premature ventricular beats (PVB), ventricular flutter (VF) and ventricular fibrillation (FIB). The effect of a combination of iloprost and propranolol was comparable to the effect of each drug administered alone. Prazosin enhanced the threshold dose of ouabain for OA and PVB in a statistically significant manner. The effect of a combination of iloprost and prazosin was nearly the same for OA and PVB compared to the single effect of these drugs. The threshold dose of ouabain was decreased for VF and FIB when a combination of iloprost and prazosin was given, compared to iloprost used alone. These results support the assumption that the adrenergic nervous system is involved in the antiarrhythmic effect of iloprost.

Adrenergic alpha-Antagonists↗
PubMed1993

[Correlation between parameters measured by high amplification ECG and results of programmed ventricular stimulation after myocardial infarct].

The presence of late ventricular potentials and the induction of sustained ventricular tachycardia (SVT) by programmed ventricular stimulation (PVS) after myocardial infarction are markers of the risk of serious ventricular arrhythmias. The authors studied the value of signal averaged electrocardiography (SAECG) compared with induction of SVT by PVS in 118 consecutive patients 4 to 8 weeks after myocardial infarction. In addition to this study population, a control group of 22 patients with spontaneous SVT after myocardial infarction was also considered. Three parameters were measured after averaging 200 QRS complexes: the duration of the filtered QRS complex (QRSd), the duration of signals not exceeding 40 microV (LAS) and the root mean square of the voltage of the last 40 milliseconds (RMS). Abnormal values were defined as: QRSd > or = 120 ms, LAS > or = 39 ms, RMS < or = 20 microV. Patients in the study population were subdivided into 3 groups: Group I (n = 17) inducible SVT; Group II (n = 72) no inducible arrhythmias; Group III (n = 29) induction of sustained ventricular flutter or primary ventricular fibrillation requiring immediate cardioversion. The results showed a good correlation between SAECG and induction of SVT. The sensitivity (Se), specificity (Sp), positive predictive value (PPV) and negative predictive value (NPV) were as follows: 1) QRSd > 120 ms: Se = 82%, Sp = 80%, PPV = 41%, NPV = 96%; 2) LAS > 39 ms: Se = 59%, Sp = 85%, PPV = 38%, NPV = 92%; 3) RMS < 20 V: Se = 59%, Sp = 88%, PPV = 43%, NPV = 93%.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗