Treatment of atrioventricular node reentrant tachycardia with encainide: reversal of drug effect with isoproterenol.

To determine the efficacy of encainide in the treatment of atrioventricular (AV) node reentrant tachycardia, Holter electrocardiographic (ECG) monitoring, exercise treadmill testing and programmed electrical stimulation were performed in 16 patients while they were taking no medication and after steady state levels were reached during treatment with encainide (75 to 200 mg/day; mean 117 +/- 47). In addition, to study the possible reversal of drug effects by sympathetic stimulation, AV node conduction and tachycardia induction were reassessed during isoproterenol infusion (1 to 3 micrograms/min), a dose calculated to increase the rest heart rate by 25 +/- 10%. Sustained AV node reentrant tachycardia could be initiated in all 16 patients in the control state, in 2 patients after encainide and in 10 patients during isoproterenol infusion. The shortest mean atrial paced cycle length sustaining 1:1 AV conduction was 358 +/- 57 ms during the control study, which increased to 409 +/- 59 ms with encainide (p less than 0.01 versus control) and decreased to 313 +/- 31 ms during isoproterenol infusion (p less than 0.01 versus control and encainide). The shortest mean ventricular paced cycle length with 1:1 ventriculoatrial conduction was 337 +/- 56 ms in the control study, 551 + 124 ms with encainide infusion (p less than 0.01 versus control) and 354 +/- 72 ms during isoproterenol infusion in the encainide-loaded state (p less than 0.01 versus both control and encainide). During a mean follow-up period of 19 +/- 10 months, significant clinical recurrences occurred in 4 of the 10 patients in whom tachycardia could still be initiated with encainide (with or without isoproterenol).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone: risk factors for recurrence of symptomatic ventricular tachycardia identified at electrophysiologic study.

Ventricular tachycardia induced by programmed electrical stimulation during amiodarone therapy often does not preclude a good clinical response. The purpose of this study was to determine whether use of discriminant analysis could distinguish patients who remained asymptomatic from those who subsequently developed symptomatic ventricular tachycardia or cardiac arrest. Studies were performed in 37 patients with sustained ventricular tachycardia who still had ventricular tachycardia induced during programmed electrical stimulation during amiodarone therapy. The mean follow-up time was 14.1 +/- 1.3 months (+/- SEM). Twenty-three patients remained asymptomatic, whereas 14 patients had symptomatic recurrence of their ventricular tachycardia. In patients with recurrence of arrhythmia compared with asymptomatic patients, administration of amiodarone caused a longer ventricular effective refractory period (296 +/- 8 versus 271 +/- 7 ms, p less than 0.05) and a greater change in corrected QT [QTc] interval (90 +/- 18 versus 44 +/- 9 ms, p less than 0.02), but no difference in the decrease in premature ventricular complexes after treatment with amiodarone. During amiodarone therapy, nonbundle branch reentrant repetitive ventricular responses were induced by a single ventricular extrastimulus during sinus rhythm in 9 of 14 patients with recurrent arrhythmias compared with 2 of 21 asymptomatic patients (p = 0.001). Also, less aggressive pacing techniques were required to induce ventricular tachycardia in 9 of 14 symptomatic patients compared with 4 of 23 asymptomatic patients (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of oral propafenone on defibrillation and pacing thresholds in patients receiving implantable cardioverter-defibrillators. Propafenone Defibrillation Threshold Investigators.

OBJECTIVES: The effects of propafenone, a predominantly class IC antiarrhythmic drug, on defibrillation and pacing thresholds were evaluated in patients undergoing cardioverter-defibrillator implantation. BACKGROUND: Previous studies have shown that the class IC agents encainide and flecainide may increase the energy requirements for pacing and defibrillation. Animal studies with propafenone have shown inconsistent results regarding its effect on defibrillation energy requirements. This report investigated the effects of propafenone on defibrillation and pacing thresholds in humans. METHODS: After cardioverter-defibrillator implantation, 47 patients were enrolled in a double-blind, three-way parallel, randomized trial of 450 mg/day (Group 1) or 675 mg/day (Group 2) of oral propafenone or placebo (Group 3) for 3 to 7 days. Predischarge defibrillation and pacing thresholds after treatment were compared with baseline thresholds obtained at implantation. RESULTS: There was no statistically significant difference between implantation and predischarge defibrillation thresholds in the three groups (Group 1: [mean +/- SE] 11.0 +/- 1.3 vs. 12.1 +/- 1.5 J; Group 2: 11.5 +/- 1.1 vs. 13.6 +/- 1.3 J; Group 3: 12.5 +/- 1.2 vs. 13.3 +/- 1.6 J), and no significant difference between treatment groups was found with a 0.86 power to detect a 5-J difference between groups. Paired pulse width pacing thresholds at 2.8 V were compared in 14 patients. A small increase of 0.02 ms was noted at predischarge testing in patients treated with propafenone and placebo. CONCLUSIONS: Short-term oral propafenone (450 and 675 mg/day) does not significantly affect defibrillation or pacing thresholds. Concomitant use of propafenone in patients with implantable cardioverter-defibrillators with recurrent ventricular or atrial tachyarrhythmias should not interfere with proper device function.

Practical guidelines for clinicians who treat patients with amiodarone. Practice Guidelines Subcommittee, North American Society of Pacing and Electrophysiology.

Amiodarone has become an important drug for the treatment of supraventricular and ventricular arrhythmias, in short-term inpatient and outpatient settings. It may also have a role in affecting outcome in patients at high risk for arrhythmic events and sudden death; its place among available therapies is being established in clinical trials.

The Brugada syndrome: clinical, genetic, cellular, and molecular abnormalities.

The Brugada syndrome is an arrhythmic syndrome characterized by a right bundle branch block pattern and ST segment elevation in the right precordial leads of the electrocardiogram in conjunction with a high incidence of sudden death secondary to ventricular tachyarrhythmias. No evidence of structural heart disease is noted during diagnostic evaluation of these patients. In 25% of families, there appears to be an autosomal dominant mode of transmission with variable expression of the abnormal gene. Mutations have been identified in the gene that encodes the alpha subunit of the sodium channel (SCN5A) on chromosome 3. This genetic defect causes a reduction in the density of the sodium current and explains the worsening of the above electrocardiographic abnormalities when patients are treated with sodium channel blocking antiarrhythmic agents, which further diminish the already reduced sodium current. The prognosis is poor with up to a 10% per year mortality. Antiarrhythmic drugs including beta-blockers and amiodarone have no benefit in prolonging survival. The treatment of choice is the insertion of an implantable cardioverter-defibrillator.

Value and limitations of clinical electrophysiologic study in assessment of patients with unexplained syncope.

We assessed the value of clinical electrophysiologic study using intracardiac recording and programed electrical stimulation in 34 patients who had unexplained syncope and/or presyncope. All patients had normal electrocardiograms, and no abnormality was detected by clinical examination, ambulatory electrocardiographic recording, or treadmill testing. The electrophysiologic results were diagnostic in four patients (11.8 percent) and led to appropriate therapy that totally relieved symptoms. The results were abnormal but not diagnostic in two patients (5.8 percent) and normal in the remaining 28 patients (82.4 percent). The patients were followed for a mean period of 15 months (range two to 44) after electrophysiologic testing. Sixteen patients (47 percent) had no further episodes in the absence of any intervention. In four patients (11.8 percent), a definitive diagnosis was made during follow-up. In seven patients, permanent pacing was instituted empirically with relief of syncope. Two patients continued to have syncopal spells. We conclude that the diagnostic yield of electrophysiologic testing is low in a patient population that has no electrocardiographic abnormality or clinical evidence of cardiac disease. Empirical permanent pacing in patients with symptoms continuing after our study appeared to be beneficial, but this result is difficult to evaluate because of the high incidence of spontaneous remission in this group. Persistent attempts to document electrocardiographic abnormalities during a typical episode of symptoms appears to be the only definitive way to confirm or exclude an arrhythmic cause of the symptoms.

Electrophysiology of phosphodiesterase inhibitors.

Phosphodiesterase inhibitors appear to uniformly enhance atrioventricular node conduction, although milrinone seems to have the least effect. Except for digoxin, this effect on atrioventricular node conduction is similar to that noted with other inotropic agents. Other electrophysiologic effects vary among patients, with enoximone being more theophylline-like in response. Because none of these drugs do not have an adverse effect on His-Purkinje conduction, they are safe to use in patients with intraventricular conduction disturbances. Significant proarrhythmia is uncommon, but can occur. The mechanisms causing these electrophysiologic changes are not well defined, but the changes may occur because of increased concentrations of cytosol cyclic adenosine monophosphate secondary to phosphodiesterase inhibition, increased cytosol calcium levels secondary to increased cyclic adenosine monophosphate, or reflex adrenergic stimulation secondary to the peripheral vasodilating effects of these drugs.

Efficacy and safety of class IC antiarrhythmic agents for the treatment of coexisting supraventricular and ventricular tachycardia.

Thirty-three patients with concurrent supraventricular (SVT) and ventricular tachycardia (VT) were treated with class IC antiarrhythmic agents. Twenty-two patients had atrial fibrillation (17 with paroxysmal and 5 with chronic fibrillation), 1 patient had ectopic atrial tachycardia and 11 patients had reentrant paroxysmal SVT (8 with atrioventricular node reentrant tachycardia, 3 with atrioventricular reentrant tachycardia). Of 5 patients with Wolff-Parkinson-White syndrome, 2 had only atrial fibrillation. Six patients had sustained VT and 27 had nonsustained VT. Twenty-nine patients had organic heart disease (16 with coronary artery disease, 8 with cardiomyopathy and 5 with valvular heart disease) and 4 had primary electrical disease. The mean ejection fraction was 40 +/- 14% (range 15 to 66%). The study population's arrhythmias were not controlled despite having received 2 to 5 (mean 3.1) previous drug trials. Eighteen patients were referred for treatment of SVT and 15 were referred for treatment of VT (mean symptom duration 107 months). Efficacy was determined in 13 of 33 patients with sustained SVT or VT by programmed electrical stimulation and in 20 of 33 by telemetry and 24-hour Holter response. Twenty-two flecainide and 15 encainide trials were conducted in the 33 patients. Four patients underwent trials with both drugs. Of 33 patients with coexisting SVT and VT, 15 (45%) were controlled with an IC agent alone and 3 continued therapy with an IC agent plus additional therapy (2 drugs, 1 antitachycardia pacing). During the follow-up period (mean 10.4 months), flecainide produced a complete response in 9 patients and encainide in 9 patients. SVT was not controlled in 7 patients and VT was not controlled in 7 patients. One patient had neither arrhythmia controlled. Atrial or ventricular proarrhythmia was seen in 9 of 33 patients (27%) (5 with ventricular and 4 with atrial arrhythmia). Noncardiac side effects were uncommon. Oral class IC agents may be effective therapy for some patients with coexisting VT and SVT of different mechanisms. Patients with such complex arrhythmias should be evaluated carefully because there is a potential for both atrial and ventricular proarrhythmia.

Assessment of antiarrhythmic drug efficacy in the treatment of supraventricular arrhythmias.

Few guidelines exist for judging the efficacy of antiarrhythmic drugs in patients with supraventricular arrhythmias. Useful definitions concerning the frequency and duration of supraventricular arrhythmias are offered, and complete and partial efficacy criteria are outlined for noninvasive electrocardiographic and invasive electrophysiologic techniques. Several open label, double-blind, parallel and crossover study designs are suggested for efficacy studies concerning the termination and prevention of supraventricular tachycardia. These recommendations are useful for designing new drug trials needed to evaluate properly the efficacy of antiarrhythmic agents in the treatment of various supraventricular arrhythmias.

Effect of pharmacologic autonomic blockade on ventriculoatrial conduction.

To determine the influence of autonomic tone on retrograde ventriculoatrial (VA) conduction, incremental atrial and ventricular pacing was performed before and after pharmacologic autonomic blockade in 28 patients. VA conduction during ventricular pacing was demonstrated, with highest frequency in patients capable of 1:1 atrioventricular (AV) conduction at atrial paced cycle lengths of 300 ms or less (7 of 7, 100%). In subjects with 1:1 AV conduction at minimum cycle lengths of 300 to 500 ms, 14 of 21 (67%) demonstrated VA conduction in the control state; however, only 12 of 21 (57%) did so after autonomic blockade. The lowest frequency was observed in those capable of 1:1 AV conduction at minimum cycle lengths of 505 ms or more before and after autonomic blockade (2 of 7, [29%], p less than or equal to 0.02 compared with values in the first group). No change in the mean minimum ventricular paced cycle length at which 1:1 VA conduction could be maintained was demonstrated after autonomic blockade. In individual subjects, incremental change in this cycle length after autonomic blockade correlated positively with the corresponding change in minimum atrial cycle length at which 1:1 AV conduction could be maintained (r = 0.62, p less than 0.005), and was concordant in direction in 18 of 21. In conclusion, the sympathetic and parasympathetic modulation of VA conduction is balanced and concordant in direction to the effect on AV nodal conduction.

Electrophysiology and pharmacology of ibutilide.

Ibutilide fumarate is a new class III intravenous antiarrhythmic agent indicated for the acute termination of atrial fibrillation and flutter. Ibutilide prolongs repolarization in the atria and ventricle by enhancing the inward depolarizing, slow sodium current, a unique mechanism of action for a class III agent. Atrial refractoriness is prolonged with no evidence of reverse use dependence. Ibutilide may also block the delayed rectifier current, but this does not appear to be clinically relevant. In vitro and at high doses, ibutilide may shorten action potential duration, although this effect has not been noted clinically. Ibutilide can cause torsades de pointes in a rabbit model of proarrhythmia dependent on the formation of early afterdepolarizations. However, it causes less proarrhythmia than sotalol, dofetilide, or sematilide in this model. The pharmacokinetics of ibutilide are linear, its extravascular distribution is rapid and extensive, while its systemic clearance is high (elimination half-life 3-6 hours). Eight metabolites are formed by the liver, only one of which is slightly active. QT prolongation is dose dependent, is maximal at the end of the infusion, and returns to baseline within 2-4 hours following infusion. The pharmacokinetic and electrophysiologic characteristics of ibutilide are complementary in that any risk of proarrhythmia is made manageable by a short half-life. Almost all reported cases of drug-induced torsades de pointes ventricular tachycardia associated with ibutilide have occurred within 40 minutes of starting the infusion. Nevertheless, clinicians using ibutilide can further reduce the chance of torsades de pointes by being very familiar with the criteria for patient selection, and by being prepared to treat it should it occur. When used with full knowledge of its potential risks, ibutilide is a very effective intravenous agent for the acute termination of atrial fibrillation and flutter and is likely to become a significant treatment option for these arrhythmias.

Prospective comparison of flecainide versus quinidine for the treatment of paroxysmal atrial fibrillation/flutter. The Flecainide Multicenter Atrial Fibrillation Study Group.

In order to compare the efficacy and long-term tolerability of flecainide acetate versus quinidine, 239 patients with paroxysmal atrial fibrillation were prospectively treated with flecainide (n = 122) or quinidine (n = 117) in an open-label, randomized trial. All patients were followed for 1 year after initiation of therapy unless their antiarrhythmic drug was discontinued due to an inadequate therapeutic response or intolerable side effects. Although both drugs were equally effective in adequately controlling recurrences of atrial fibrillation (difference, p = 0.282; not significant), fewer flecainide patients had to have their therapy discontinued due to adverse experiences (p = 0.012). Based on both endpoints (efficacy and tolerability), an estimated 70.5% of flecainide versus 55.4% of quinidine patients would remain effectively treated at the end of 1 year on therapy (p < or = 0.007). The findings of this prospective study suggest that in the treatment of paroxysmal atrial fibrillation (1) flecainide and quinidine are equally effective in the acceptable suppression of symptomatic paroxysmal atrial fibrillation; (2) flecainide is better tolerated than quinidine and is less likely to be discontinued due to adverse effects; and (3) given the overall endpoint of efficacy and tolerability, more patients are likely to continue long-term therapy with flecainide than with quinidine.

Role of adrenergic stimulation by isoproterenol in reversal of effects of encainide in supraventricular tachycardia.

Reversal of the electrophysiologic effects of oral encainide with isoproterenol was evaluated in 16 patients with atrioventricular (AV) nodal reentry (group A) and in another 16 patients with Wolff-Parkinson-White syndrome (group B). Sustained AV nodal reentry was induced in all group A cases before administration of encainide, in 2 cases after oral encainide, and in 12 patients during infusion of isoproterenol. Among group B cases, 14 of 16 had sustained AV reentry during control, 6 of 16 after receiving encainide, and 8 of 16 with addition of isoproterenol. During a mean follow-up of 19 +/- 10 months in group A and 17 +/- 9 months in group B, clinical tachycardia recurred in 8 patients (4 from each group). These 8 patients were among the 20 patients who demonstrated (1) isoproterenol-induced reversibility of encainide-suppressed tachycardia, or (2) acceleration of tachycardia rate slowed by encainide. No recurrences were seen among any of the 12 cases in which isoproterenol failed to reverse the encainide-induced tachycardia suppression. Patients with clinical recurrences were controlled with a variety of means, which included beta blockers in 3 and nonpharmacologic methods in the remaining 5. In patients with AV junctional tachycardia treated with oral encainide, our findings suggest that lack of tachycardia inducibility with isoproterenol predicts freedom from clinical recurrences. Furthermore, addition of a beta blocker to oral encainide may prevent clinical recurrence in some who demonstrate adrenergic reversal of encainide effect.

Electrophysiologic effects of amrinone.

Patients with congestive heart failure (CHF) have a high prevalence of complex ventricular arrhythmias. Accordingly, the electrophysiologic effects of new drugs for the treatment of CHF should be studied to determine whether they are safe in this population of patients. Fifteen patients with New York Heart Association functional classes II to IV CHF underwent hemodynamic and electrophysiologic testing during control conditions, and after 10 to 20 micrograms/kg/min of intravenous amrinone (dosages that increased cardiac output and decreased left ventricular filling pressures). All cardioactive drugs were stopped for at least 5 half-lives before entry into the study. Amrinone decreased the atrial effective refractory period from 256 to 240 ms (p = 0.015) and the AV nodal functional refractory period from 374 to 356 ms (p less than 0.05), and enhanced maximal 1:1 AV nodal conduction from 371 to 334 ms (p = 0.006). Prolonged HV intervals were present in 9 of 15 patients and were not affected by amrinone. Holter monitoring was performed in 10 patients during acute oral administration of amrinone. There were no significant changes in the frequency of ventricular extrasystoles or ventricular tachycardia, although the frequency of ventricular couples tended to increase slightly. Amrinone therefore enhances AV conduction and does not appear to have significant arrhythmogenic potential during acute administration.

Acute conversion of paroxysmal supraventricular tachycardia with intravenous diltiazem. IV Diltiazem Study Group.

Diltiazem has electrophysiologic effects similar to those of verapamil. Its efficacy and safety in 4 doses for treatment of induced supraventricular tachycardia (SVT) were examined and compared with those of placebo in 87 patients (25 with atrioventricular [AV] nodal reentry tachycardia, 60 with AV reentry associated with an accessory AV connection, and 2 with atrial tachycardia). Conversion to sinus rhythm occurred in 4 of 14 patients (29%) with 0.05 mg/kg of diltiazem, 16 of 19 (84%) with 0.15 mg/kg, 13 of 13 (100%) with 0.25 mg/kg, and 14 of 17 (82%) with 0.45 mg/kg compared with 6 of 24 (25%) treated with placebo. Conversion rates in groups receiving doses of 0.15 to 0.45 mg/kg of diltiazem were superior to that in the placebo group (p less than 0.001). Time to conversion was 3.0 +/- 2.6 minutes in responding diltiazem patients compared with 5.9 +/- 6.1 minutes in responding control patients. Diltiazem administration resulted in significant lengthening of SVT cycle length, AH interval, and AV nodal effective refractory period and block cycle length. The most frequent adverse response to diltiazem was hypotension (7 of 63 patients); however, only 4 patients had symptoms related to hypotension. Thus, intravenous diltiazem in doses of 0.15, 0.25 and 0.45 mg/kg is an effective and safe treatment for the acute management of SVT.

Efficacy and safety of flecainide acetate for atrial tachycardia or fibrillation.

Thirty-nine patients with symptomatic ectopic atrial tachycardia (9 paroxysmal, of which 5 were incessant) and atrial fibrillation (AF) (25 paroxysmal, 5 chronic) were treated with oral flecainide acetate (100 to 400 mg/day). Thirty-two patients had organic heart disease (16 coronary artery disease, 6 valvular, 10 cardiomyopathy, 7 primary electrical abnormality). Previous antiarrhythmic trials consisted of 0 to 5 drugs (mean 2.2). Of 39 patients with atrial tachycardia or AF, a complete response (no recurrent symptomatic atrial arrhythmia) was achieved in 22 (56%), a partial response (more than 95% reduction in arrhythmia occurrence) in 3 (8%) and no response in 14 (36%). Left atrial size, ejection fraction, underlying heart disease, duration of symptoms before treatment and drug levels were not useful for predicting clinical response. Therefore, during the follow-up period of 5.4 +/- 6.7 months (range 4 weeks to 2.5 years), flecainide had a complete or partial effect in 25 patients (64%). Complete or partial responses were noted in 8 of 9 patients (90%) with ectopic atrial tachycardia and 17 of 30 (57%) with AF. In 14 patients with concurrent ventricular arrhythmias, a significant reduction in episodes of nonsustained ventricular tachycardia was also achieved. Treatment was discontinued in 8 patients (20%) because of cardiac adverse reactions, including pulmonary edema and ventricular or atrial proarrhythmic response. Thus, oral flecainide acetate is effective therapy for some patients with ectopic atrial tachycardia or AF.

Cost-effective management of acute atrial fibrillation: role of rate control, spontaneous conversion, medical and direct current cardioversion, transesophageal echocardiography, and antiembolic therapy.

Management strategies for the acute treatment of atrial fibrillation (AF) include: (1) the use of intravenous drugs for rate control, (2) drug termination, or (3) direct current (DC) cardioversion. Delays in cardioversion can promote atrial remodeling and add thromboembolic risk. Rate control awaiting spontaneous or pharmacologic conversion may be a cost-effective strategy in patients presenting with recent onset of symptoms. Early DC cardioversion can be cost-effective and minimize antiembolic therapy issues in the acute setting. In patients presenting with AF of unknown or >48 hours' duration, rate control and therapeutic warfarin for 3-4 weeks followed by medical or DC cardioversion is standard practice. However, delays in conversion promote atrial remodeling that makes restoration of sinus rhythm more difficult and increases the likelihood of postcardioversion AF recurrence. Transesophageal echocardiography can identify patients at low risk for a cardioversion-related embolic event and allows cardioversion to be performed earlier, thereby minimizing atrial remodeling.

A randomized comparison of flecainide versus verapamil in paroxysmal supraventricular tachycardia. The Flecainide Multicenter Investigators Group.

Reentrant paroxysmal supraventricular tachycardia (PSVT) are frequently encountered in clinical practice. Verapamil and flecainide have both been successfully used as chronic oral therapy to prevent PSVT recurrences. This open-label, randomized, multicenter study was designed to compare the efficacy and adverse effects of verapamil (median dose, 240 mg/day) versus flecainide (median dose, 200 mg/day) in patients with frequent and symptomatic attacks of PSVT (other than atrial fibrillation or flutter). A total of 121 patients receiving flecainide (n = 63) or verapamil (n = 58) were followed for 8.1 +/- 5.1 and 7.5 +/- 5.4 months, respectively. Response was judged clinically as effective or not by the treating physician. By life table analysis, 11% discontinued flecainide and 19% discontinued verapamil for inefficacy at 1 year (difference not significant). Both groups showed a marked reduction in the frequency of attacks of PSVT. Before therapy, 71% of flecainide patients and 73% of verapamil patients had > or = 2 attacks per month. During therapy, 86% of all flecainide patient-months and 73% of all verapamil patient-months occurred with 0 or 1 attack; 19 (30%) patients on flecainide completed the trial ( > 270 days) without symptomatic attacks versus 7 (13%) of the patients on verapamil (p = 0.026). Both drugs were well tolerated; 19% of the flecainide group discontinued primarily because of adverse effects, compared with 24% discontinuing verapamil for this reason (difference not significant). Both flecainide and verapamil are effective and well tolerated for the prevention of recurrences of PSVT. For patients in whom radiofrequency ablation procedures cannot be performed or are not indicated, either therapy is a reasonable choice for long-term prophylaxis.

Acute treatment of atrial fibrillation: spontaneous conversion rates and cost of care.

Acute treatment of atrial fibrillation is costly although spontaneous conversion rates are high. We reviewed 114 patients admitted to our inpatient service via the emergency department with a principal diagnosis of atrial fibrillation and found the spontaneous conversion rate was 50% in 48 hours, the average length of stay was 3.9 +/- 5.2 days, and the average cost was $6,692 +/- $4,928.

Congestive heart failure with normal systolic function.

Although there have been isolated reports of congestive heart failure (CHF) with normal systolic function, the prevalence and characteristics of this condition have not previously been described. Accordingly, 188 patients with CHF undergoing radionuclide ventriculography were prospectively evaluated. Sixty-seven (36%) had a normal ejection fraction (EF) of 0.45 or greater, and 121, an abnormal EF of less than 0.45. Of these, 72 (55 with an abnormal EF [group I] and 17 with a normal EF [group II]) were also reviewed for clinical characteristics. There was no demographic difference between groups, except that systemic hypertension appeared to be a contributing factor in 65% of the patients in group II, compared with 23% of the patients in group I (p less than 0.002). Echocardiographic left atrial emptying index, reflecting left ventricular compliance, was determined in 72 patients and 14 normal subjects. Left atrial emptying index in normal control subjects was 0.93 +/- 0.11 (+/- standard deviation), compared with 0.41 +/- 0.18 in group I and 0.44 +/- 0.19 in group II patients (p less than 0.001 vs control in both groups). Thus, normal systolic function is common among patients with CHF. Diastolic dysfunction, consistent with a noncompliant left ventricle, was found in both CHF groups.