Byron J. Allen

Factors determining maintenance of sinus rhythm after chronic atrial fibrillation with left atrial dilatation

Successful therapy of atrial fibrillation (AF) has been reportedly influenced by a variety of factors including patient age, type of underlying heart disease, duration of arrhythmia, left ventricular function and left atrial (LA) size. To determine which of these factors are associated with maintenance of sinus rhythm after conversion, 43 patients with symptomatic chronic AF in the setting of a dilated left atrium (greater than or equal to 45 mm, range 45 to 78) were followed for at least 6 months after the return of sinus rhythm. Class IA drugs, IC drugs or amiodarone were used for therapy. Life table analysis showed sinus rhythm to be maintained in 81% for 6 months, 79% for 12 months and 60% for 24 months. Factors positively associated with success were conversion with drug therapy alone, duration of chronic AF less than or equal to 1 year, absence of mitral valve disease and LA dimension less than or equal to 60 mm (all p less than 0.05). Patient age, left ventricular function and presence of coronary disease were not associated with outcome. Thus, patients with moderate LA dilatation (45 to 60 mm) and a short duration of chronic AF can often be maintained in sinus rhythm, especially if they convert with pharmacologic intervention alone.

Amiodarone for maintenance of sinus rhythm after conversion of atrial fibrillation in the setting of a dilated left atrium

Previous reports suggest that the finding of left atrial (LA) dilatation (greater than 45 mm) by echocardiography identifies patients not likely to maintain sinus rhythm after conversion of atrial fibrillation (AF). However, these studies antedate the availability of amiodarone, an antiarrhythmic agent that reportedly is effective in patients with AF in whom other drug therapy has failed. To analyze the relation between LA size and the ability to maintain sinus rhythm with amiodarone therapy, 28 patients, aged 32 to 87 years (mean 61), with an LA dimension greater than 45 mm (range 46 to 78, mean 57) were studied. Thirteen patients (46%) had valvular heart disease, 10 (36%) dilated cardiomyopathy and 5 (18%) miscellaneous disorders. In 25 patients (89%) quinidine therapy had failed. After therapy with amiodarone, sinus rhythm returned in all patients and was maintained. Therapy was judged completely successful in 10 patients (alive and still in sinus rhythm with at least 1 year of follow-up), partially successful in 11 (maintaining sinus rhythm for at least 6 months before a change in status) and failed in 7. Completely successful therapy was accomplished in 9 of 18 patients with an LA dimension between 46 and 60 mm, but in only 1 of 10 patients with an LA dimension greater than 60 mm (p less than 0.05). Thus, patients with LA dimensions between 46 and 60 mm who are significantly compromised by AF can often be maintained in sinus rhythm with amiodarone therapy. However, in patients with larger LA dimensions. AF is likely to return despite aggressive antiarrhythmic therapy with amiodarone, a drug with potentially serious side effects.

New-onset ventricular tachycardia during pregnancy

During evaluation for palpitations, presyncope, or syncope, seven pregnant women had documented ventricular tachycardia. Before pregnancy none had a history of significant cardiac disease or symptomatic arrhythmia. The tachycardia rate ranged from 117 to 250 beats/min and lasted up to 65 seconds. Arrhythmia evaluation in five of the patients suggested catecholamine-sensitive ventricular tachycardia. This diagnosis was supported by either a positive relation to exercise or isoproterenol infusion, suppression of arrhythmia by beta-blockade or sleep, and lack of induction of arrhythmia by programmed electrical stimulation of the heart. The arrhythmias resolved in one patient soon after evaluation and in one other patient after 2 months of controlling therapy. Five other patients continued to receive therapy throughout pregnancy. Delivery was accomplished in all patients without significant maternal or neonatal complications.

Magnesium therapy in new-onset atrial fibrillation

Abstract In new-onset atrial fibrillation (AF), digoxin has a limited ability to control ventricular response, is no better than placebo for facilitating conversion to sinus rhythm, and has a slow onset of action with a narrow toxic-therapeutic ratio.1,2 Magnesium (Mg) has been shown to slow and sometimes normalize the heart rhythm in supraventricular tachyarrhythmias.3,4 A randomized trial found Mg prevents AF in patients after cardiac surgery.5 Because of these factors, we conducted a prospective, randomized, double-blind, placebo-controlled study addressing whether Mg and digoxin were superior to digoxin alone in controlling the ventricular response of AE.

Magnesium sulfate therapy for sustained monomorphic ventricular tachycardia

Abstract A variety of supraventricular and ventricular arrhythmias have responded favorably to therapy with intravenous magnesium sulfate (MgSO 4 ) regardless of the patients initial serum magnesium level. 1–9 The ventricular arrhythmia most commonly reported to be responsive to MgS 4 is torsades de pointes. 3,5–7,9 We report the responses of 11 patients with sustained monomorphic ventricular tachycardia (VT) to a bolus injection of MgSO 4 .

Ionic biology and ionic medicine in cardiac arrhythmias with particular reference to magnesium.

In this day and age, when so much advancement is being made in molecular biology, we tend to lose sight of the importance of basic ions in clinical medicine. This report deals with the concept of ionic biology involving Na+, K+, Ca++, and Mg++ ions with respect to the membrane and action potential of cardiac cells in the genesis of tachyarrhythmias. Various clinical disorders leading to arrhythmias will be examined as examples of ionic medicine, and treatment protocols will be recommended according to these concepts. Basic concepts. The cell membrane separates the various ions, and the concentrations of these ions vary considerably outside and inside the cell. Naf and K+ are fully ionized so that their concentrations represent their total ionic concentrations. Ca++ and Mg++, on the other hand, form complexes with proteins, organic acids, and phosphates so that their total extracellular and intracellular concentrations do not represent their ionic concentrations. The extracellular concentration of Na+ is as high as 140 mmol/L, whereas the intracellular concentration is only about 10 to 20 mmol/L. The reverse is true of K+. Extracellular K+ is approximately 4 mmol/L, whereas intracellular K+ is approximately 140 mmol/L. More than half of serum Ca++ is complexed so that its ionic strength is only about 1.3 mmol/L (5.2 mg/ dl). This extracellular Ca++ concentration, however, is still much greater than the micromolar (0.1 pmol/L) ionic concentration inside the cell. It is interesting to note that an ionic Mg++ concentration of 0.5 mmol/L (1.2 mg/dl) is approximately the same outside and

Effects of spontaneous respiration on diastolic left ventricular filling assessed by pulsed Doppler echocardiography

Abstract Left ventricular (LV) stroke volume decreases during spontaneous inspiration. 1–3 The explanations offered have been either decreased LV filling with a decrease in end-diastolic volume 2,3 or increased impedance to ejection by negative pleural pressure 4,5 resulting in an increased end-systolic volume. Meijboom et al 6 recently described variations in mitral mean temporal velocity during respiration. Because pulsed Doppler mitral flow velocity correlates with LV filling rate, 7 we used it to learn if, indeed, LV filling diminished during inspiration.

Antiarrhythmic efficacy of solitary beta-adrenergic blockade for patients with sustained ventricular tachyarrhythmias

To assess the efficacy and predictability of solitary beta-adrenergic blocker (BB) therapy for ventricular tachyarrhythmia (VT), 30 patients (16 men and 14 women) with a mean age of 55 years, who initially had sustained ventricular tachycardia (70%) or ventricular fibrillation (30%), were studied. Results of baseline arrhythmia tests showed VT on ECG monitoring in 57% of the patients, during exercise in 50%, induced by programmed stimulation in 69%, increasing to 86% during isoproterenol. BB therapy prevented inducible VT during programmed stimulation in 37% of the patients, prevented VT on ECG monitoring in 54%, and prevented VT during exercise in 83%. Long-term BB therapy was given to 24 of 30 patients, whereas six other patients with hemodynamically unstable VT during BB therapy received other long-term treatment. During a mean follow-up of 824 days, 6 of 24 patients had recurrent VT. BB therapy was discontinued in two patients because of side effects. Long-term success was predicted by left ventricular ejection fraction greater than 45%, absence of coronary disease, and age less than 60 years (all p less than 0.02). Neither suppression of arrhythmia during exercise testing, nor results of programmed stimulation or ECG monitoring were predictive of outcome. Thus beta-adrenergic blockers can be effective as solitary antiarrhythmic therapy in selected patients with VT.

Exercise testing in patients with life-threatening ventricular tachyarrhythmias: results and correlation with clinical and arrhythmia factors.

The results of exercise treadmill stress testing were analyzed in 64 consecutive patients presenting with either ventricular fibrillation (42%) or hemodynamically significant ventricular tachycardia (58%). Underlying diseases included coronary artery disease (55%), dilated cardiomyopathy (16%), and miscellaneous disorders (29%). Patients were additionally studied with ambulatory electrocardiographic monitoring and programmed stimulation. During exercise testing, 22 patients (34%) had nonsustained and five (8%) had sustained ventricular tachycardia. No patient experienced ventricular fibrillation or a major complication during exercise testing. Patients with a history of ventricular fibrillation were significantly less likely to have exercise-induced ventricular tachycardia than those with a history of ventricular tachycardia. Other clinical factors were not associated with the results of exercise testing. The results of programmed stimulation did not correlate with the results of exercise testing. Ventricular tachycardia was commonly documented during ambulatory monitoring (72%), but this was not predictive of ventricular tachycardia during exercise. However, patients who did not have ventricular tachycardia during ambulatory monitoring were predictably unlikely to have it during exercise testing (p less than 0.002). Thus exercise testing is safe and can provoke ventricular tachycardia in a significant proportion of patients with life-threatening arrhythmias.

Life-threatening alterations in heart rate after the use of adenosine in atrial flutter

Adenosine has become the preferred treatment for common types of supraventricular tachycardia because it is extremely effective and rarely associated with with serious side effects. It has also been advocated as an intervention for diagnostic use to assess uncommon types of tachycardia. Evidence is shown in this report that adenosine was associated with dangerous worsening of arrhythmia in patients with atrial flutter. In two patients, adenosine precipitated acceleration of ventricular response, in one case necessitating emergent cardioversion. Both patients had atrial flutter with 2 to 1 atrioventricular block that evolved into 1 to 1 atrioventricular conduction. In three other patients, adenosine was associated with prolonged bradyasystole and hypotension. In each of the five patients, adenosine was given in a standard fashion (6 or 12 mg). In summary, adenosine should be recognized as a potentially dangerous intervention in patients with atrial flutter. If it is used for diagnostic purposes, resuscitative equipment should be readily available.