Stokes-Adams Attacks Research Articles

Stokes-Adams attack

Stokes-Adams attack

Obstructive sleep apnoea and driving.

This article describes the risks to patients with obstructive sleep apnoea of falling asleep while driving. Patients with this disease often report loss of concentration while driving, particularly on motorways in the dark. Many long distance lorry drivers have the disease, as they commonly have the major risk factor, obesity. In a survey of fatal truck accidents, the American National Transportation Safety Board is now asking relatives routinely about features of obstructive sleep apnoea, as three recent reports have shown that the road traffic accident rate of patients with this condition is up to seven times greater than that of normal drivers. The proportion of crashes in which the driver was at fault and the number of traffic violations were both appreciably higher in patients with obstructive sleep apnoea than in other drivers. About one third of the patients had had car crashes in the previous 5 years. It is suggested that as regards fitness to drive, obstructive sleep apnoea should be classified with epilepsy, hypoglycaemia and adams-stokes attacks, and that further research should be done in order to ascertain its contribution to deaths on British roads. (TRRL)

Clinical characteristics of chronic recurrent ventricular tachycardia

The clinical characteristics of chronic recurrent ventricular tachycardia were studied in 47 patients. In 28 patients out of them, no underlying heart diseases were found (NHD group). The remaining 19 patients were diagnosed as having cardiomyopathy, old myocardial infarction, or other underlying heart diseases (HD group). NHD group showed a lower mean age and higher female proportion than the HD group. Nine patients (32%) in NHD group and 13 patients (68%) in HD group showed sustained ventricular tachycardia. Adams-Stokes attack was observed in 70% of this patient series, and was highly related to the tachycardia rate and sustainability. Ventricular tachycardia in the NHD group showed a faster heart rate and narrower QRS duration than in the HD group. Characteristic QRS configurations during ventricular tachycardia ("CRBBB + LAD" pattern or "CLBBB + inferior axis" pattern) were demonstrated in the NHD group, while no consistent QRS pattern was observed in the HD group. Electrical induction of ventricular tachycardia was only successful in patients with sustained ventricular tachycardia, mainly in the HD group. On the other hand, treadmill testing was more likely to provoke ventricular tachycardia in the NHD group than in the HD group. Poor prognosis was noted in patients in the HD group (7 deaths in the 4-month to 10-year follow up period), while there were no cardiac deaths in the NHD group. These results suggest that the QRS pattern during ventricular tachycardia and the response to electrical induction and treadmill testing may play an important role in predicting the prognosis of patients with chronic recurrent ventricular tachycardia.

Subsidiary pacemaker function in complete heart block after His-bundle ablation.

To investigate the electrophysiological properties of ventricular impulse formation after His-bundle ablation in 11 patients, incremental ventricular overdrive stimulation studies were performed. The studies, which were spread over a follow-up period of up to 601 days, were carried out invasively with temporary leads as well as noninvasively with the implanted pacemakers and chest wall inhibition. The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 2 minutes at each level. Ten out of 11 patients had a reliable ventricular escape rhythm; in the remaining patient, consistently no subsidiary pacemaker function was observed up to 10 seconds. In 83% of the studies, incremental ventricular overdrive stimulation caused progressive suppression of ventricular impulse formation with exponential increase in ventricular recovery time and progressive postrecovery subsidiary pacemaker depression. In the remaining 17%, ventricular recovery time showed a heterogeneous response to overdrive stimulation--as possible cause alterations in the sympathetic tone and limitations attributable to the method used are discussed. The results of this study demonstrate a rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue. This can be of clinical importance in patients with complete heart block and rate-adaptive pacemakers because sudden pacemaker failure or temporary pacemaker inhibition at high stimulation rates may cause Stokes-Adams attacks not reproducible at lower pacing rates.

Survival rate and causes of death in patients with pacemakers: dependence on symptoms leading to pacemaker implantation.

The survival rate of 2256 patients with pacemakers was analyzed. Patients paced for Adams-Stokes equivalents (e.g. dizziness) showed a significantly better survival rate than did patients with pacemakers implanted for Adam-Stokes attacks or heart failure (P less than 0.0001). The estimated survival of the latter two groups did not differ significantly. Of the deceased patients who had received a pacemaker for the treatment of heart failure, 54% died due to this condition despite pacemaker implantation. The relative percentage of cases of sudden death after pacemaker implantation was high in the groups with Adams-Stokes attacks (12%) and Adams-Stokes equivalents (13%). In patients paced for Adams-Stokes attacks, sudden death occurred more frequently in the first year after pacemaker implantation (P less than 0.015) than during the following years. Therefore, increased efforts should be made to monitor patients carefully after pacemaker implantation to enable prompt detection of malignant tachyarrhythmias, probably the cause of sudden death in a substantial number of patients with pacemakers.

Recovery from congenital complete atrioventricular block

Congenital complete atrioventricular block without any other intracardiac anomaly reverted to sinus rhythm at the age of 7 years. The girl had had heart failure and Adams-Stokes attacks when aged 1 year, requiring pacemaker implantation. Electrocardiography confirmed sinus rhythm for the first time at the age of 7 years. At the same time, a treadmill test yielded a normal tracing without any arrhythmias.

Atropine, isoproterenol induced Adams-Stokes syndrome in patient with tachycardia-dependent paroxysmal A-V block

Atropine, isoproterenol induced Adams-Stokes syndrome in patient with tachycardia-dependent paroxysmal A-V block

Study on congenital complete heart block in children by 24-hour ambulatory electrocardiographic monitoring.

Ambulatory electrocardiographic monitoring was performed in 18 children with a congenital complete heart block (CCHB). They had no cardiac structural anomalies. These patients could be divided into 3 groups according to the pattern of fluctuations in beat-to-beat ventricular rates. Type 1 patients showed rapid and transient fluctuations and demonstrated a high correlation between atrial and ventricular rates. Type 3 patients showed a constant ventricular rate and little variation through the 24 hour period and there was no appreciable correlation between atrial and ventricular rates. Twelve of 18 patients had additional arrhythmias. A few sporadic ventricular premature contractions (VPCs) were found in 9 patients, and bigeminy of VPCs or ventricular tachycardias were seen in 2 patients during exercise. Frequent and sudden prolongation of RR intervals was found during sleep in 3 patients. The longest intervals of ventricular asystoles were 7.2, 3.2 and 3.2 sec, respectively. The mechanism of this phenomenon appeared to be not only an exit block, but also arrest or a lack of automaticity of a subsidiary pacemaker. One of these patients developed frequent Stokes-Adams attacks. Type 3 patients with sudden prolongation of RR intervals and/or frequent ventricular arrhythmias should be under careful observation. Ambulatory electrocardiographic monitoring is recommended for children with CCHB for evaluation of potential risk factors for Stokes-Adams attacks.

QT Prolongation and Torsade de Pointes Ventricular Tachycardia Produced by Ketanserin

A 65-year-old man with arterial hypertension received oral treatment with Ketanserin, a new drug, during a period of five months. He developed marked QT interval prolongation and have several Stokes-Adams attacks. A Holter recording obtained during one of these episodes showed torsade de pointes ventricular tachycardia. The arrhythmias occurred during maximum QT interval prolongation. The correlation between Ketanserin and QT interval prolongation was evaluated by using several Holter studies during administration and withdrawal of the drug. The effect of Ketanserin on the QTc interval was analyzed retrospectively in six patients who had been taking the drug orally. Following a period of four to eight months, the QTc interval was prolonged by the drug (5 to 31%, mean 17%) in five patients. We conclude that torsade de pointes is a potential hazard of long-term treatment with Ketanserin.

Competence, persistence and motivation: Relationships in structured and unstructured assessments of high social risk 13 month olos

A case of a 29 year old female patient with sinoatrial block, first degree A-V heart block and Adams-Stokes seizures since the age of 11 is reported. The mechanism of the syncopal attacks was established by continuous radioelectrocardiographic monitoring as episodes of sinoatrial heart block or arrest, or both. There was no evidence of inflammatory, degenerative or congenital heart disease, and the patient had never received drugs assocated with the production of Adams-Stokes seizures. From the etiologic standpoint exaggerated vagal effects undoubtedly played a role; the existence of a congenital abnormality of the conduction system must, however, be taken into consideration. Treatment with artificial pacemaker stimulation proved effective and prevented further Adams-Stokes attacks.

Effect of Carbamazepine on the Ouabain-Induced Arrhythmia in Rabbits

Carbamazepine is a derivative of iminostilbene with carbamyl group and related chemically to the tricyclic antidepressants. Carbamazepine has been introduced for treatment of trigeminal neuralgia. Recently it is used as an antiepileptic agent such as diphenylhydantoin. Antiepileptic drugs are known to affect experimentally induced cardiac arrhythmia and are now widely used clinically for treatment of ventricular tachyarrhythmias, particularly those produced by digitalis intoxication. Steiner et al.(1970) reported that carbamazepine was found to be very effective in converting ventricular tachycardia due to digitalis toxicity to normal sinus rhythm. Clinically bradycardia, complete heart block, ventricular standstill and Adams-stokes attack were reported in the course of carbamazepine treatment. The purpose of this study was to investigate the effects of carbamazepine on the ouabain-induced arrhythmia in vivo. The rabbits of either sex, weighing from 1.6 to 3.2kg were anesthesized by urethane. After the trachea was cannulated, the rabbits were ventilated with room air using a respirator. Drugs were given into polyethylene cannula in the femoral vein. Blood pressure were recorded by physiograph via pressure tranducer connected with the cannula in the femoral artery. EKG were recorded by Physiograph via electrode implanted in both fore leg and left hind leg. The results are summarized as follows; 1. Arrhythmia was induced by continuous infusion of ouabain.() 2. Single administration of ouabain() induced arrhythmia which was persisted for 7-8 min. 3. Ouabain induced arrhythmia was restored to normal sinus rhythm by administration of carbamazepine.(The more dosage, the less frequent and the longer duration) 4. Severe bradycardia, A-V block, atrial fibrillation were seen on the EKG after injection of carbamazepine alone. By the above results, it may be concluded that carbamazepine inhibits the ouabain-induced arrhythmia by dose-dependent.

Pacemaker management for acute onset of heart block in childhood

Four children aged 2 to 15 years are described who had Stokes-Adams syndrome as the primary cardiac manifestation of complete heart block. All had mild, nonspecific antecedent symptoms without signs of congestive heart failure. Viral neutralizing antibody titers (coxsackievirus B1 and B2) rose significantly in two patients. Electrocardiography demonstrated complete heart block associated with one or more of the following: right bundle branch block, left anterior hemiblock, left bundle branch block, intraventricular conduction delay, and ventricular standstill. In addition, second-degree heart block was seen during the initial or resolving phases of illness. To prevent further life-threatening episodes of Stokes-Adams syndrome, temporary transvenous pacemakers were placed. Two patients with persisting complete heart block required permanent pacemakers. At last examination, the remaining two patients had sinus rhythm and normal conduction. Nonsurgical acquired complete heart block is unusual in childhood, and may be the only manifestation of myocarditis. Extreme bradycardia, which causes syncope, requires immediate temporary cardiac pacing; if the bradycardia persists, a permanent pacemaker should be implanted.

Emergency differentiation of vasovagal syncope from Stokes-Adams attack: Craig IH Am J Cardiol 54:1155 Nov 1984

Emergency differentiation of vasovagal syncope from Stokes-Adams attack: Craig IH Am J Cardiol 54:1155 Nov 1984

Emergency differentiation of vasovagal syncope from stokes-adams attack

Emergency differentiation of vasovagal syncope from stokes-adams attack

A new pacemaker for monitoring asystole and prevention of Adams-Stokes syndrome and sudden cardiac death.

Patients with suspected Adams-Stokes syndrome are examined by Holter monitoring. During the monitoring, there is the danger of syncopes occurring and there are even reports of sudden cardiac death. We therefore developed a pacemaker for cardiac arrest monitoring and the prevention of Adams-Stokes syndrome and sudden cardiac death, which has the following functions: (1) the longest escape interval of the pacemaker not exceeding the value at which syncope is induced is determined by the decline of the mean heart rate including the asystole to a certain threshold rate; (2) once the pacemaker escapes from the interval it continues pacing for a while at a physiological rate to allow recover from ischemias in organs or tissues; and (3) to prevent overdrive suppression to the heart, the pacing rate gradually declines and stops pacing until the next asystole. This pacemaker is useful not only in the diagnosis of Adams-Stokes syndrome but also in pharmacological and pathophysiological studies and in determining when pacing should cease.

BRADYCARDIA, VENTRICULAR PAUSES, SYNCOPE, AND SPORTS

16 athletic patients were examined because of syncope, Stokes-Adams attacks, or both. The life-threatening condition required pacemaker implantation in 7 patients. 8 of the 9 other subjects became symptom-free after stopping heavy physical training. 37 topranking athletes underwent 24 h Holter monitoring. Pauses longer than 2 s occurred in 19% and resulted from sinus arrest. The longest pause lasted 2·5 s. Second-degree atrioventricular block was noted in 13%.

Developments in transcutaneous and transthoracic pacing during bradyasystolic arrest

Transthoracic cardiac pacing historically has been relegated to the role of the technique of last resort in treating cardiac arrest. Recent studies have shown that this technique has a high rate of successful electrical capture, but often without mechanical activity. Survival rates have been shown to be dismal when the technique is used late in cardiac arrest. Results of several recent studies of patients paced by the transcutaneous technique have suggested that electrical capture can often be rapidly obtained in asystolic or pulseless bradycardic patients. Even though electrical capture can occur late in a cardiac arrest, the development of mechanical activity with survival is rare. Survivors generally have been treated early in their arrest and have had hemodynamically ineffective bradycardias. These findings suggest that rapid initiation of transcutaneous pacing in patients with Stokes-Adams attacks, increasing heart block associated with myocardial ischemia, postdefibrillation asystole, or pulseless bradycardia may improve survival. However, victims of a prolonged cardiac arrest whose myocardium has irreversibly ceased to function mechanically are unlikely to benefit from any pacing technique.

Cardiac pacing in retrospect

As precursors of permanent pacemakers, Lidwill (1929) and Hyman (1932) introduced temporary pacemakers for resuscitation. Callaghan (1950) intravenously paced the sinus nodal region for bradycardia in hypothermic dogs. Zoll (1952) used external electrodes to treat Adams-Stokes attacks, and Lillehei (1957) fixed stainless steel electrodes to the myocardium, successfuly treating iatrogenic total atrioventricular block with a percutaneous pacemaker. Since 1951, by experimental and clinical use of ventricular fibrillation to obtain a functional cardiac standstill during open heart surgery, we used all known methods of stimulation to treat asystole or bradycardia after defibrillation. Since 1957, percutaneous stimulation by Adam-Stokes attacks has been performed. The most serious complication is infections along the electrodes causing death from sepsis. The solution of the problem was the implantation of the pacemaker and its energy supply. Percutaneous leads were used to study the different parameters for electric stimulation and to find the lowest frequency (to spare energy) with the best variation of cardiac output. In October 1958 in Stockholm a fixed rate pacemaker was implanted by thoracotomy. At present, the patient is living with his 23rd pacemaker. Four additional patients had pacemaker implantations until 1960. In 1961, Chardack and Greatbach successfully implanted pacemakers with mercury batteries. Johanson and Lagergren connected the pacemaker to an intravenous electrode to avoid thoracotomy. The enormous development in the electronic field made more elaborate pacemakers possible, and eliminated the risk of the fixed rate (interference, repetitive firing, and ventricular fibrillation).

The underlying heart rhythm in patients with an artificial cardiac pacemaker.

One-hundred forty-two patients with atrioventricular block (AVB) and 61 patients with sick sinus syndrome (SSS) were followed for an average of 50 months after permanent pacemaker insertion. Their underlying heart rhythms (UHR) were evaluated repeatedly by chest wall stimulation (CWS). A deficient UHR was defined as ventricular asystole lasting 4 seconds or longer. The underlying conduction disturbance increased in 14% of AVB patients, decreased in 14%, and remained constant in 68%. The occurrence of Adams-Stokes attacks before pacemaker implantation was associated with a higher incidence of deficient UHR both in AVB and SSS; a deficient UHR was seen more frequently in AVB than in SSS. Among AVB patients (1) atrial fibrillation, flutter or tachycardia and (2) sinus rhythm with incomplete AVB, especially Mobitz 1, when present before pacemaker implantation, were associated with a significantly lower incidence of deficient UHR during subsequent pacing in comparison with other AVB patients. CWS is a non-invasive method which allows the evaluation of UHR and which can contribute to the early recognition of pacemaker-dependent patients.

Predictive use of routine 24-hour electrocardiography in suspected Adams-Stokes syndrome. Comparison with cardiac rhythm during symptoms.

Using strictly defined criteria of significant arrhythmias, long term electrocardiographic recording has been evaluated for confirmation of arrhythmias as the cause of cerebral symptoms in 81 patients with suspected Adams-Stokes syndrome. Extension of long term electrocardiographic recording for more than 24 hours gives marginal additional information at a high cost. Among 43 patients monitored until symptoms appeared, non cardiogenic causes were confirmed in 20 of 22 patients because the recording showed normal rhythm during symptoms. Fifteen of 21 patients with a significant arrhythmia during an asymptomatic 24 hour recording later had the same arrhythmia during symptoms. Of 38 patients who failed to develop symptoms, 21 had a significant arrhythmia detectable within 24 hours and 23 when 48 hours of recording were analysed.