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PubMed2000

Block of the lower interatrial connections: insight into the sources of electrocardiographic diversities in common type atrial flutter.

Whether the conduction disturbances of the interatrial connections play a role in the genesis of ECG variants of atrial flutter is almost completely unknown. We present a patient with typical counterclockwise atrial flutter in whom the ablation of the coronary sinus (CS) area during ongoing atrial flutter produced significant ECG changes without alterations in the activation sequence within the right atrium (RA). This case highlights the possible role of alterations of the interatrial connections in the genesis of atypical ECG manifestations of common type atrial flutter.

Aged↗
PubMed1987

Sotalol. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use.

Sotalol is a beta-adrenoceptor blocking agent devoid of intrinsic sympathomimetic activity, membrane stabilising actions and cardioselectivity. It lengthens repolarisation and the effective refractory period in all cardiac tissues independently of its antiadrenergic properties. Combining Class II and Class III antiarrhythmic properties, sotalol can be given either intravenously or orally and its pharmacokinetic properties permit long dosing (once or twice daily) intervals. Controlled and uncontrolled studies have established the efficacy of sotalol in mild-to-moderate essential hypertension and in angina of effort. Sotalol reduces anginal frequency and glyceryl trinitrate (nitroglycerin) consumption and increases exercise capacity during treadmill stress tests. In addition, although there is evidence that the drug reduces reinfarction rate in survivors of acute infarction, the data for reduction in sudden death rates in these patients are not as compelling as for other beta-blockers. However, comparative and additional long term studies are required before an accurate assessment of the use of sotalol in these disorders can be made. When used in the treatment of mild-to-moderate hypertension sotalol is more effective than placebo and comparable to other beta-blockers in reducing elevated blood pressures. In addition, a synergistic antihypertensive response is achieved when sotalol is combined with hydrochlorothiazide. Still, additional well-controlled comparative studies are required before the value of sotalol relative to other drug treatment regimens in the management of hypertension can be made. In preliminary studies sotalol appeared effective in most forms of supraventricular tachyarrhythmias with its effects being similar to those of other beta-blockers. However, preliminary data indicate that sotalol is likely to be more effective than than conventional beta-blockers in converting atrial flutter and fibrillation to sinus rhythm and maintaining stability post-conversion. Sotalol also appears to be a promising agent in the control of ventricular arrhythmias. In suppressing premature ventricular contractions it is at least as effective as procainamide. In ventricular tachycardia and fibrillation, intravenous sotalol (1.5 mg/kg), prevents reinduction by programmed electrical stimulation in 40 to 50% of cases if double stimuli are used. Both prevention of reinducible arrhythmia and the suppression of spontaneous arrhythmias on Holter recordings are predictive of a long term favourable clinical outcome. In patients with reduced ejection fractions, sotalol depresses ventricular function less than conventional beta-blockers.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1975

[Steinert's syndrome and the myocardium. Total gene expression by the myocardium].

As revealed by a very thorough cardiological study of Steinert's disease in 13 cases, it would appear that the incidence of cardiac involvement observed in this disease is not merely frequent; it is, in fact, usual, systematic, and forms an integral part of the pathological picture in the same way as peripheral muscular dystrophy. One is aware of the diagnostic interest of this fact in the juvenile or abortive forms of the disease. The cardiac involvement is an indication of the complete expression of the gene towards striated muscle tissue, whether skeletal or myocardial. Finally, it opens new perspectives on the prophylactic attitude to be adopted for such patients; regular and systematic cardiological checks, moderation in the prescription of digitalis and anti-arythmia drugs, implantation of a cardiac pacemaker before an auriculo-ventricular syncopal block occurs.

Adolescent↗
PubMed1993

[Stored intracardiac electrograms: accuracy of arrhythmia classification in patients with cardioverter/defibrillator system].

A cardioverter/defibrillator that is capable of storing endocardial electrograms before and after electrical device therapy was implanted in 29 patients presenting drug refractory ventricular arrhythmias. During a follow-up period of 7.5 +/- 4.6 months 15/29 patients (51%) experienced a total number of 112 pulse generator discharges. In 104 arrhythmia episodes the stored electrogram was analyzed. Morphological criterias of the stored electrogram as detectable P-waves and changes in the QRS-morphology during tachycardia compared to sinus rhythm served for classification of the documented arrhythmia. The analysis of the stored electrogram established a definitive diagnosis of the arrhythmia and allows to distinguish supraventricular arrhythmias from ventricular arrhythmias in every episode. 72/104 (69.2%) of the discharges were classified as appropriate, 32/104 (30.8%) of the device discharges were not appropriate and caused by atrial fibrillation and flutter, sinustachycardia and AV-nodal reentrant tachycardia. In two patients device discharges caused by a sensing malfunction ot the pulse generator was detected by the analysis of the stored electrogram. The new diagnostic feature of stored electrogram shows a high accuracy of rhythm classification and represents a major advance in the treatment with cardioverter/defibrillators.

Aged↗
PubMed2002

Cardiac arrhythmias: diagnosis and management. The tachycardias.

OBJECTIVE: To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts on tachycardias and bradycardias. SUMMARY OF REVIEW: Normal cardiac rhythm originates from impulses generated within the sinus node. These impulses are conducted to the atrioventricular node where they are delayed before they are distributed to the ventricular myocardium via the His-Purkinje system. Abnormalities in cardiac rhythm are caused by disorders of impulse generation, conduction or a combination of the two and may be life threatening due to a reduction in cardiac output or myocardial oxygenation. Cardiac arrhythmias are commonly classified as tachycardias (supraventricular or ventricular) or bradycardias. The differentiation between supraventricular and ventricular tachycardias usually requires an assessment of atrial and ventricular rhythms and their relationship to each other. In the critically ill patient the commonest tachycardia is sinus tachycardia and treatment generally consist of management of the underlying disorder. Other supraventricular tachycardias (SVTs) include, atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia (PSVT) all of which may require cardioversion, although to maintain sinus rhythm, antiarrhythmic therapy is often needed. Adenosine is useful in management and treatment many SVTs although its use in PSVT with Wolff-Parkinson-White syndrome is hazardous. Multifocal atrial tachycardia is a characteristic supraventricular tachycardia found in the critical ill patient. While it usually responds to intravenous magnesium sulphate, its management also requires removal of various precipitating factors. Ventricular tachycardia (VT) and ventricular fibrillation (VF) require urgent cardioversion and defibrillation respectively. Torsade de pointes should be differentiated from these ventricular arrhythmias as antiarrhythmic therapy may be contraindicated. CONCLUSIONS: Supraventricular and ventricular tachycardias in the critically ill patient often have underlying disorders that precipitate their development (e.g. hypokalaemia, hypomagnesaemia, anti-arrhythmic proarrhythmia, myocardial ischaemia, etc). While antiarrhythmic therapy and cardioversion or defibrillation may be required to achieve sinus rhythm, correction of the associated abnormalities is also required.

Journal Article↗
PubMed1977

Comparison of lidoflazine and quindine in prophylactic treatment of arrhythmias.

The efficacy of quinidine versus lidoflazine therapy was compared in the maintenance of sinus rhythm after electrical cardioversion for atrial flutter or fibrillation in a group of 35 patients. Both quinidine and lidoflazine were relatively ineffective in maintaining sinus rhythm after cardioversion. Lidoflazine was also used to prevent supraventricular and ventricular tachycardias in a miscellaneous group of patients; one of these with paroxysmal supraventricular tachycardia developed runs of venttricular tachycardia soon after starting lidoflazine. The trial was stopped after 4 patients died while receiving lidoflazine, on the suspicion that their deaths may have been related to drug-induced arrhythmias. The arrhythmogenic potential of lidoflazine when used in patients with supraventricular arrhythmias constrasts with reports of its apparent safety in large numbers of patients with angina pectoris.

Adult↗
PubMed1998

Use of adenosine in patients hospitalized in a university medical center.

PURPOSE: Adenosine is a useful agent for the diagnosis and termination of tachycardias. The purpose of this study was to identify the rhythms for which adenosine is prescribed in hospitalized adults and to identify the reasons for its misuse. PATIENTS AND METHODS: Data were collected from the medical records of 100 patients who received intravenous adenosine while hospitalized at a university medical center. The characteristics of the patients, rhythms treated with adenosine, and dosages of adenosine were analyzed. In addition, internal medicine house officers were administered a questionnaire referring to an electrocardiogram of atrial fibrillation with a rapid ventricular response. RESULTS: The arrhythmias for which adenosine was administered consisted of regular, narrow-QRS complex tachycardias in 33% of patients; atrial fibrillation in 32% of patients; regular, wide-QRS complex tachycardias in 23% of patients; atrial flutter in 10% of patients, and multifocal atrial tachycardia in 2% of patients. The mean (+/-SD) number of doses of adenosine given to each patient was 1.6+/-0.8, and the mean dose of adenosine was 7.8+/-2.8 mg. Internal medicine house officers prescribed 70% of the doses of adenosine and were as likely to use it for patients with atrial fibrillation as were surgical house officers. There was a 2% incidence of proarrhythmia, including asystole and polymorphic ventricular tachycardia. Thirty-one percent of the 100 house officers in our survey misdiagnosed a 12-lead electrocardiogram of rapid atrial fibrillation as paroxysmal supraventricular tachycardia, suggesting that adenosine may have been misused for atrial fibrillation because of errors in rhythm diagnosis. Only 5% of those who correctly diagnosed atrial fibrillation also answered that adenosine would be likely to terminate the arrhythmia, suggesting that a misunderstanding that adenosine terminates atrial fibrillation is not a common reason for its misuse. CONCLUSIONS: Approximately 40% of hospitalized adults who are treated with adenosine receive the medication unnecessarily for atrial fibrillation or atrial flutter, and this misuse results in unnecessary expenses and risks of adverse effects. The primary reason that adenosine is misused for atrial fibrillation is the inability to recognize that rhythm on an electrocardiogram. House officers need additional education on the electrocardiographic recognition of atrial fibrillation.

Adenosine↗
PubMed2005

Increased risk of sudden and non-sudden cardiovascular death in patients with atrial fibrillation/flutter following acute myocardial infarction.

AIMS: Atrial fibrillation (AF) is a common complication in patients with acute myocardial infarction and is associated with an increase in the risk of death. The excess mortality associated with AF complicating acute myocardial infarction has not been studied in detail. Observations indicate that AF facilitates induction of ventricular arrhythmias, which may increase the risk of sudden cardiovascular death (SCD). A close examination of the mode of death could potentially provide useful knowledge to guide further investigations and treatments. METHODS AND RESULTS: We analysed the relation between AF/atrial flutter (AFL) and modes of death in 5983 consecutive patients discharged alive after an acute myocardial infarction screened in the TRAndolapril Cardiac Evaluation registry. This cohort of patients with an enzyme-verified acute myocardial infarction was admitted to 27 centres in 1990-92. Survival status was obtained 2 years after screening of the last patient. An independent endpoint committee assessed the modes of death. Left ventricular ejection fraction was determined in all the screened patients and information about presence or absence of AF/AFL was prospectively collected. Sustained or paroxysmal AF/AFL was observed in 1149 patients (19%) during hospitalization. During follow-up, 1659 patients (34%) died: 482 (50%) patients with AF/AFL and 1177 (30%) patients without AF/AFL, P<0.001. SCD occurred in 536, non-SCD occurred in 725, and 398 died of non-cardiovascular causes (includes 142 unclassifiable cases). The adjusted risk ratio of AF/AFL for total mortality was 1.33 (95% CI: 1.19-1.49; P<0.0001) and the risk ratio for SCD was 1.31 (95% CI: 1.07-1.60; P<0.009). The adjusted risk ratio of AF/AFL for non-SCD was 1.43 (95% CI: 1.21-1.70; P<0.0001). CONCLUSION: The excess mortality observed in patients with AF/AFL following acute myocardial infarction is due to a significant increase in both SCD and non-SCD.

Adult↗