Clinical pharmacology of intravenous enoximone: pharmacodynamics and pharmacokinetics in patients with heart failure.

Twenty-one patients with heart failure (New York Heart Association [NYHA] class II to IV) received a 24-hour infusion of enoximone followed by a 12-hour washout period. Patients were randomly assigned to one of four treatment groups. Groups I to III received an 0.5 mg/kg bolus, followed by a maintenance infusion of 2.5, 5.0, or 10.0 micrograms/kg/min. Group IV patients received a maintenance infusion of 5.0 micrograms/kg/min without a loading dose. Serial assessment of hemodynamics, plasma levels of enoximone and enoximone sulfoxide, and ventricular ectopy were performed. Enoximone produced a clinically significant increase in cardiac index, and a decrease in mean pulmonary artery wedge pressure and systemic vascular resistance in all groups. Enoximone mildly increased heart rate, and had a minimal effect on mean arterial pressure. There was no statistically significant change in ventricular ectopy during the infusion. Significant hemodynamic improvement was noted at even the lowest infusion rate, and did not increase in linear fashion at higher infusion rates. In patients who did not receive an initial loading bolus of 0.5 mg/kg, the increase in cardiac index was delayed by approximately 1 hour. Plasma concentrations of both enoximone and its major metabolite continued to rise throughout the 24-hour infusion in group III (10.0 micrograms/kg/min), rather than reaching steady state as predicted by the terminal exponential half-lives of these compounds. This is suggestive of nonlinear pharmacokinetics and indicates a potential for excessive accumulation of enoximone and its metabolite during prolonged infusion. These findings may have important implications in guiding the intravenous administration of enoximone.(ABSTRACT TRUNCATED AT 250 WORDS)

Disposition kinetics of orally administered enoximone in patients with moderate to severe heart failure.

Enoximone is a phosphodiesterase inhibitor, which has been studied extensively for use in the management of patients with moderate-to-severe heart failure. The authors have studied the absorption and disposition kinetics of enoximone and its primary metabolite, enoximone sulfoxide, after both single oral doses of enoximone and at steady-state after short-term chronic oral therapy. A total of ten patients (two female, eight male) with moderate-to-severe heart failure (NYHA class II-IV) were enrolled into the study after giving written informed consent. The plasma levels of enoximone sulfoxide were greater than those of enoximone at all sampling times. The peak enoximone sulfoxide plasma concentrations ranged from 3.5 to 17.3 times the peak enoximone plasma levels for individual patients. The average steady-state plasma concentrations for enoximone were 115 +/- 40 ng/mL and 190 +/- 78 ng/mL for 50 mg every 8 hours and 100 mg every 8 hours dosage regimens, respectively. The absorption and disposition kinetics of enoximone were found to be significantly variable between patients. The authors also evaluated the relationship between dose administered and steady-state plasma levels as well as the relationship between the observed and predicted steady-state plasma levels. The authors found a linear relationship between the dose that was administered and the accrued plasma levels, as well as a good correlation between the predicted and observed steady-state levels. Although these data confirm previous reports that the sulfide metabolite of enoximone accumulates extensively in the plasma during oral therapy, reaching levels much higher than those of enoximone, these data do not support previous suggestions that the disposition of enoximone is nonlinear.

Comparison of pre- and postoperative conduction patterns in patients surgically cured of atrioventricular node reentrant tachycardia.

Patients with atrioventricular (AV) node reentrant tachycardia characteristically have short and constant retrograde His-atrium conduction times (H2A2 intervals) during the introduction of ventricular extrastimuli. It has therefore been suggested that the tachycardia circuit involves retrograde conduction up an accessory pathway located in perinodal tissue. If the mechanism of surgical cure of AV node reentrant tachycardia is interruption of this accessory pathway, postoperative changes in retrograde conduction would be expected. Thirteen patients with drug-refractory AV node reentrant tachycardia underwent surgery. Preoperatively, H2A2 intervals were short and constant. During AV node reentrant tachycardia, earliest atrial activation was seen near the His bundle and was 0 to 25 ms before ventricular activation in all patients except one. Surgery consisted of dissection of right atrial septal and anterior inputs to the AV node and central fibrous body. Postoperatively, the H2A2 interval remained short and constant compared with preoperative values although it was slightly prolonged (74 +/- 18 versus 61 +/- 21 ms, p less than 0.005). Twelve of the 13 patients are free of tachycardia after 28 +/- 13 months and no patient has had evidence of AV node block. Thus, surgical cure of AV node reentrant tachycardia is highly successful; however, there is no reason to postulate an accessory pathway or use of perinodal tissue as part of the tachycardia circuit and the mechanism of surgical success remains obscure.

Pharmacodynamics of enoximone during intravenous infusion.

Twenty-one patients with heart failure (NYHA class II-IV) received a 24-hour infusion of enoximone, followed by a 12-hour washout period. Patients were randomly assigned to one of four treatment groups. Groups I-III received a 0.5 mg/kg bolus, followed by a maintenance infusion of 2.5, 5.0 or 10.0 micrograms/kg/minute. Group IV patients received a maintenance infusion of 5.0 micrograms/kg/minute without the bolus. Serial assessments of haemodynamics, plasma levels of enoximone and enoximone sulphoxide, and ventricular ectopy were performed. Enoximone produced a significant increase in cardiac index (28.1-46.7%) and a decrease in mean pulmonary artery wedge pressure (6.4-35.7%) and systemic vascular resistance (34.7-78.9%). Enoximone had minimal effect on heart rate and blood pressure. In patients who did not receive an initial bolus of 0.5 mg/kg, haemodynamic changes were delayed by approximately 1 hour. Significant haemodynamic improvement was noted at even the lowest infusion rate and did not increase in linear fashion at higher infusion rates. During infusion of enoximone at 10.0 micrograms/kg/minute, both enoximone and its sulphoxide accumulated non-linearly and did not achieve a steady state. No significant adverse effects were noted in these patients. Enoximone infusion at rates greater than 5.0 micrograms/kg/minute may confer minimal additional haemodynamic benefit, while resulting in significant accumulation of enoximone and enoximone sulphoxide. Ventricular ectopy did not increase significantly in most patients.

Effect of duration of ventricular fibrillation on defibrillation efficacy in humans.

The currently available automatic implantable cardioverter-defibrillator has proven highly successful for termination of ventricular tachycardia and fibrillation. Newer devices, however, permit lower energy shocks to be delivered initially and longer episodes of arrhythmia to occur before shocks are delivered. These changes may result in longer durations of arrhythmia before successful termination. Little is known about the effects of the duration of ventricular fibrillation on the efficacy of defibrillating shocks. In this study, we examined the efficacy of defibrillating shocks in 22 patients undergoing automatic implantable cardioverter-defibrillator implantation or generator change. Defibrillating shocks ranging from 300 to 600 V (5.9-24.2 J) were delivered in matched pairs after 5 and 15 seconds of ventricular fibrillation. For the 300-V shocks (5.9 J), defibrillation was accomplished in 82% of patients when the shocks were given after 5 seconds of ventricular fibrillation and in only 45% of patients when the shocks were delivered after 15 seconds (p less than 0.01). At higher energies, there was no difference in the efficacy of defibrillation shocks delivered after 5 compared with 15 seconds of ventricular fibrillation. The postshock aortic, systolic, and diastolic blood pressures were significantly lower when the shocks were given after 15 seconds of ventricular fibrillation than after only 5 seconds. We conclude that the duration of ventricular fibrillation affects defibrillation efficacy especially at energies that are relatively low compared with maximal device outputs and that longer episodes of ventricular fibrillation cause more postshock hemodynamic depression. These observations have implications for defibrillation threshold testing at the time of device implantation and for the design and programming of future automatic implantable antitachycardia devices.

Long-term outcome with the automatic implantable cardioverter-defibrillator.

The automatic implantable cardioverter-defibrillator was implanted in 270 patients because of life-threatening arrhythmias over a 7 year period. There was a history of sustained ventricular tachycardia or fibrillation, or both, in 96% of these patients, 80% had one or more prior cardiac arrests and 78% had coronary artery disease as their underlying diagnosis. The average ejection fraction was 34%, and 96% of these patients had had an average of 3.4 antiarrhythmic drug failures per patient before defibrillator implantation. There were four perioperative deaths and eight patients had generator infection or generator erosion, or both, during the perioperative period or during long-term follow-up. Concomitant antiarrhythmic drug therapy was given to 69% of patients. Shocks from the device were given to 58% of patients. and 20% received "problematic" shocks. The device was removed from 16 patients during long-term follow-up for a variety of reasons. There were 7 sudden cardiac deaths and 30 nonsudden cardiac deaths, 18 of which were secondary to congestive heart failure. The actuarial incidence of sudden death, total cardiac death and total mortality from all causes was 1%, 7% and 8%, respectively, at 1 year, and 4%, 24% and 26% at 5 years. The automatic implantable cardioverter-defibrillator nearly eliminates sudden death over a long-term follow-up period in a high risk group of patients. It has an acceptable rate of complications or problems, or both, and most late deaths in these patients are nonsudden and of cardiovascular origin.

Improved low energy defibrillation efficacy in man with the use of a biphasic truncated exponential waveform.

The standard implantable defibrillator waveform is a truncated exponential of approximately 6 msec duration. This study compares the defibrillation efficacy of a standard monophasic truncated exponential to a biphasic 12 msec truncated exponential waveform in 21 patients undergoing automatic implantable cardioverter defibrillator (AICD) surgery. For the biphasic waveform, the polarity was reversed and remaining capacitor voltage was attenuated by 75% after 6 msec. Two hundred thirty episodes of VF were induced with 115 "matched pairs" of monophasic and biphasic waveforms of identical initial capacitor voltages given over a range from 70 to 600 V (0.35 to 25.7 joules). The biphasic waveform was superior to the monophasic waveform (p less than 0.006), especially for "low energy" defibrillation. For initial voltages less than 200 V, the percent successful defibrillation was 28% for the monophasic waveform versus 64% for the biphasic waveform and from 200 to 290 V (energies less than 6.4 joules) it was 45% versus 69%. There was no difference in the two waveforms in time to the first QRS complex or in the blood pressure following defibrillation. This study shows that a 12 msec biphasic truncated exponential is superior to a 6 msec monophasic waveform for defibrillation in man, especially at energies less than 6.4 joules. The waveform can be achieved in an implanted device without any increase in capacitor size or in battery energy consumption.

Clinical experience with sotalol in patients with drug-refractory ventricular arrhythmias.

Sixty-five patients with symptomatic, drug-refractory, sustained ventricular tachycardia or fibrillation were treated with oral sotalol (80 to 480 mg twice daily). Sotalol was withdrawn in 11 patients because of continued inducibility of ventricular tachycardia at the time of follow-up electrophysiologic study. Therefore, the clinical effectiveness of sotalol could be evaluated in 54 patients followed up for 11.5 +/- 6 months (range 0.2 to 25). The actuarial incidence of successful sotalol therapy was 54 +/- 13% at 6 months and 47 +/- 13% at 12 months. In 39 patients who underwent electrophysiologic testing while receiving oral sotalol, the drug prevented the reinduction of ventricular tachycardia/fibrillation in 8 (20%). During follow-up study, arrhythmia recurred in 1 (17%) of 6 patients whose ventricular tachycardia was noninducible with oral sotalol and in 8 (44%) of 18 with inducible tachycardia but who were continued on oral sotalol therapy. Adverse effects were noted in 28 patients (42%), requiring drug withdrawal in 13 (22%) and dose reduction after hospital discharge in 10 (15%). Exacerbation of ventricular arrhythmia occurred in six patients (9%), one of whom had associated hypokalemia. Sotalol is frequently useful in the control of intractable, life-threatening ventricular arrhythmias, and its efficacy appears to be predicted by programmed stimulation. However, there is a high rate of limiting side effects, which precludes its use in a large number of patients, and a substantial risk of arrhythmia exacerbation.

Transvenous catheter ablation of extranodal accessory pathways.

Twelve patients with an accessory pathway and recurrent symptomatic reciprocating tachycardia or atrial fibrillation, or both, underwent attempted transvenous catheter ablation of the accessory pathway. In one patient with a small right coronary artery, the pathway was along the right free wall. In 11 patients, the pathway was located at or within 15 mm of the coronary sinus os. For these patients, a quadripolar electrode catheter was placed in the coronary sinus and positioned, if possible, so that the proximal pair of electrodes straddled the pathway. For those patients with a pathway greater than 5 mm within the coronary sinus, the most proximal electrode was placed at the os. This proximal pair of electrodes was connected to the cathodal output of a defibrillator with an anterior chest wall patch serving as the current sink. Two shocks were then delivered for a cumulative energy of 500 to 600 J (stored energy). Among the eight patients with a pathway at or within 5 mm of the coronary sinus os, conduction over the pathway was abolished in five and modified in one. Among the four patients with a pathway farther from the os (10 to 15 mm) and along the right free wall, pathway conduction was modified only in two. Rupture of the coronary sinus did not occur in any patient. There were no serious complications. Minor damage surrounding the area of ablation was seen at the time of surgical division of the accessory pathway in two of five patients with unsuccessful ablation who subsequently underwent surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of catheter-delivered electrical discharges near the tricuspid anulus in dogs.

The possibility of using electrical discharges to ablate right free wall accessory pathways by delivering a series of catheter shocks near the tricuspid anulus was assessed in a canine model. Before the shock, the amplitudes of the atrial and ventricular electrograms recorded from the distal electrodes were compared (A/V ratio), and the atrial pacing threshold was determined. To assess effects on function and arrhythmogenicity, right heart pressures were measured and programmed ventricular stimulation was performed before the shock and prior to sacrifice 7 to 10 days after the shock. Nine dogs received a total of 24 discharges at varying energies (50 to 400 J). Nonsustained ventricular tachycardia occurred with 13 shocks (62%) and transient atrioventricular block with 9 shocks (43%). There was no worsening in cardiac or valvular function as determined by right heart pressure measurements or right ventriculography. Programmed ventricular stimulation performed before the shocks and repeated before sacrifice failed to induce ventricular arrhythmias. The endocardial lesion produced by the shock was roughly circular and its area correlated with both the magnitude of the shock as well as the atrial pacing threshold. Transmural necrosis always occurred at the anulus when the A/V ratio was between 1.00 and 1.50 and preshock atrial pacing threshold suggested adequate wall contact (less than 1.5 mA). There was mild inflammation of the adventitia of the right coronary artery near two discharge sites (both 200 J) and inflammation of the media near one discharge site (400 J); no intimal involvement was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Coexistent Mahaim and Kent accessory connections: diagnostic and therapeutic implications.

Six patients with coexistent Mahaim and Kent accessory connections are described. Two had left nodoventricular Mahaim connections, the first reported cases demonstrating these findings. In neither were the left-sided Mahaim connections components of a tachycardia and their presence was incidental. In two of four with nodoventricular connections, associated atrioventricular (AV) node conduction and coexistent posteroseptal accessory pathways were found. One of these had the unusual finding of a right-sided Mahaim connection arising from a "fast" AV node pathway. In only one patient did the tachycardia incorporate the Mahaim connection. In this patient, anterograde conduction during tachycardia occurred over a right nodoventricular connection whereas retrograde conduction occurred through a concealed right free wall Kent connection. Two patients had fasciculoventricular connections that were associated with either septal (one patient) or left free wall (one patient) Kent connections. The latter also had evidence of enhanced AV node conduction. This report is unique in that it describes in detail two patients with left nodoventricular connections (Mahaim) inserting in or near the left posterior fascicle. Combined Kent and Mahaim connections, present in the six patients, appear to occur in approximately 5% of patients with the Wolff-Parkinson-White syndrome. Precise identification of bypass connections critical for reentrant circuits is essential for intelligent application of treatment options.

Catheter atrioventricular junctional ablation in patients with accessory pathways.

Seven patients with accessory pathway and symptomatic atrioventricular reciprocating tachycardia underwent catheter ablation of the atrioventricular junction (AVJ). Four patients had the Wolff-Parkinson-White syndrome, two had concealed left free-wall accessory pathways, and one patient had a nodoventricular connection. All patients failed multiple antiarrhythmic drugs and one failed attempted surgical ablation of a posteroseptal accessory pathway. Chronic interruption of atrioventricular node-His conduction was achieved in all patients. Over a mean follow-up period of 21 +/- 14 months, four patients remained asymptomatic without antiarrhythmic therapy. One patient developed atrial fibrillation after magnet application to her VVI pacemaker, another developed atrial flutter, and a third had nonparoxysmal sinus or atrial tachycardia. Two patients required chronic quinidine therapy. Two patients with concealed accessory pathways had pacemaker-mediated tachycardia which was controlled by pacemaker reprogramming. Atrioventricular junctional ablation in patients with accessory pathways proved effective in that all are currently controlled without need for surgical intervention. On follow-up, a relatively high incidence of atrial arrhythmias requiring antiarrhythmic therapy was found.

Ablation of cardiac tissues by an electrode catheter technique for treatment of ectopic supraventricular tachycardia in adults.

Five patients with chronic or recurrent ectopic supraventricular tachycardias unresponsive to drugs underwent programmed stimulation, endocardial mapping, and attempted catheter ablation of the arrhythmia focus. For attempted ablation, an intracardiac electrode catheter was positioned near the exit point of the tachycardia and served as the cathode while a chest wall patch served as the anode. In two patients with tachycardia originating near the coronary sinus, discharges of 200 or 400 J each were delivered to two electrodes at the earliest area of endocardial activation. These two patients with incessant tachycardia remain free of tachycardia for 17 and 11 months, respectively. In one patient with tachycardia originating from the right atrial appendage, both catheter and surgical ablation proved unsuccessful in that a new focus of atrial tachycardia supervened. This patient subsequently underwent successful catheter ablation of the atrioventricular junction. Two patients with junctional tachycardia underwent catheter ablation of the atrioventricular junction. Complete atrioventricular block followed atrioventricular junctional ablation and these patients required permanent cardiac pacing. The junctional tachycardia was replaced by sinus rhythm with episodes of unsustained atrial tachycardia. However, after 13 +/- 5 months follow-up, neither of the patients require antiarrhythmic drugs. Catheter ablation can be effective for atrial foci near the coronary sinus os, and can be performed with preservation of atrioventricular conduction. Arrhythmia ablation is possible in those with atrioventricular junctional tachycardia but requires the sacrifice of atrioventricular conduction. After ablation, other automatic atrial foci may become operative and complicate use of dual-chamber pacemakers.

Procainamide-induced incessant supraventricular tachycardia in the Wolff-Parkinson-White syndrome.

A patient with the Wolff-Parkinson-White syndrome presented with incessant orthodromic atrioventricular tachycardia following initiation of procainamide therapy. This finding was repeatedly documented both clinically as well as during electrophysiologic testing. Escape atrial complexes, which occurred following junctional premature complexes, failed to initiate tachycardia in the control state but tachycardia was always reinitiated by an identical escape sequence after procainamide. In addition, the tachycardia persisted and was repeatedly spontaneously reinitiated for prolonged periods after procainamide. The pro-arrhythmic effects of procainamide may be explained on the basis of both its vagolytic action on the atrioventricular node as well as by prolongation of refractoriness in the accessory pathway. These observations add to the literature on pro-arrhythmic effects of commonly used antiarrhythmic drugs.

Histologic changes and arrhythmogenicity after discharge through transseptal catheter electrode.

Ventricular tachycardia commonly arises within the intraventricular septum and successful catheter ablation of septal tachycardia might be enhanced by transseptal electrode placement. We have evaluated the safety of a transseptal ablation procedure. Arrhythmogenicity and histology were examined after high-energy capacitor discharges were delivered to an intracavitary cathode-anode pair placed on opposite sides of the interventricular septum in pentobarbital-anesthetized dogs. After two discharges of 200 or 100 J proved lethal, paired discharges of 30 or 50 J (10 dogs) or a single discharge of 100 J (four dogs) was used to induce 28 lesions. Acute rhythm changes and risk of induction of ventricular tachycardia by programmed stimulation were measures of arrhythmogenicity. Gross and histologic examination of the hearts after 20 min to 28 days allowed characterization of the evolution of lesions. The conduction system in nearby and remote locations was extensively examined in four dogs. Refractory ventricular fibrillation developed with paired shocks at 200 or 100 J. At lower energy levels, acute ventricular fibrillation occurred with 12 of 20 shocks (60%), but defibrillation was consistently achieved. After ablation, no dog had ventricular tachycardia or fibrillation induced with programmed stimulation. Matching anodal and cathodal lesions spanned the septum without perforation in 10 of 16 dogs, and the lesions were of similar histology. Each contained central areas of hemorrhage surrounded by a region of coagulation necrosis merging with normal myocytes peripherally. There was necrosis and edema without inflammation at 20 min, acute inflammatory cell infiltration at 1 to 2 days, and myocyte replacement by granulation tissue after 6 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Observer variation in the echocardiographic diagnosis of mitral valve prolapse.

To assess inter- and intraobserver variation in the echocardiographic diagnosis of mitral valve prolapse, three independent observers analyzed M-mode echocardiograms (n = 80) and two-dimensional echocardiograms (n = 65) of patients with a mobile midsystolic click with or without a late or holosystolic murmur. In addition, a control group of 100 normal echocardiograms were interspersed among the echocardiograms of patients with mitral valve prolapse and were then interpreted. Each of the three observers analyzed all M-mode and two-dimensional echocardiograms initially and then 2 weeks later for the presence or absence of mitral valve prolapse. M-mode echocardiographic criteria for mitral valve prolapse consisted of late systolic posterior motion (greater than or equal to 3 mm) of one or both mitral leaflets or holosystolic hammocking (greater than or equal to 3 mm) of one or both mitral leaflets. Two-dimensional echocardiographic criteria for mitral valve prolapse consisted of: posterior systolic arching of one or both mitral leaflets in the parasternal long-axis view, and/or posterior systolic bowing of one or both mitral leaflets in the apical four-chamber view posterior to the plane of the mitral anulus, and/or excessive posterior coaptation of the mitral leaflets in either view flush with or posterior to the plane of the mitral anulus. There was insignificant observer variation both in the M-mode and two-dimensional echo groups, as determined using Cochran's Q test.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and electrophysiologic characterization of automatic junctional tachycardia in adults.

Junctional ectopic tachycardia has been described in infants but not in adults. Five adults with rapid symptomatic paroxysmal junctional tachycardia, distinct from the more common slower nonparoxysmal junctional tachycardia, were recently evaluated. The tachycardia was irregular (rate 120 to 250) and accompanied by periods of atrioventricular dissociation and narrow QRS complexes. A junctional origin was documented during electrophysiologic study in four of the five patients. Analysis of Holter recordings; the response to exercise, isoproterenol, and propranolol; and the effects of atrial and ventricular stimulation appeared to implicate abnormal automaticity of a high junctional focus that was catecholamine sensitive or dependent as the tachycardia mechanism. All patients responded somewhat to beta-blockers, although a combination of procainamide and propranolol proved to be the most effective therapy in one patient and another chose electrode catheter ablation of the atrioventricular junction rather than continued drug therapy. Thus, junctional ectopic tachycardia may occur in adults and its mechanism appears to be related to abnormal automaticity that is catecholamine sensitive or dependent. Initial therapy should include beta-blockers but selected patients may require more aggressive management.

Comparative cardiac effects of hemodialysis and continuous ambulatory peritoneal dialysis.

To assess the comparative cardiac effects of hemodialysis and continuous ambulatory peritoneal dialysis (CAPD), we performed M-mode echocardiography prior to and immediately following hemodialysis on 56 patients and during the dwell phase of CAPD on 39 patients. Hemodialysis produced a significant increase in the mean velocity of circumferential fiber shortening (VCF, an index of left ventricular systolic function) in patients with low VCF prior to dialysis, but resulted in no significant change in VCF in patients with normal predialysis VCF. Hemodialysis produced a significant increase in VCF in patients with a normal predialysis left ventricular end-diastolic volume index (LVEDVI), but resulted in no significant change in VCF in patients with left ventricular dilatation prior to dialysis. Hemodialysis produced a significant decrease in mean LVEDVI and mean stroke index, but resulted in no significant change in mean cardiac index due to a reflex increase in heart rate. Mean LVEDVI, mean stroke index, and VCF values in patients on CAPD were not significantly different from those observed immediately following hemodialysis. Mean cardiac index and mean heart rate were significantly lower in CAPD patients than in posthemodialysis patients. Pericardial effusion was observed in 25% of hemodialysis patients and 5% of CAPD patients (p less than 0.05). We conclude (1) the effects of hemodialysis on left ventricular performance are variable and depend in part on predialysis left ventricular volume and left ventricular systolic function, (2) except for a lower cardiac index, left ventricular hemodynamics for CAPD patients resemble those of posthemodialysis patients, and (3) pericardial effusion occurs with significantly higher frequency in patients on hemodialysis than in those on CAPD.