The implantable defibrillator: an electronic bridge to cardiac transplantation.

BACKGROUND: Sudden cardiac death (SCD) is common among patients awaiting heart transplantation. Medical management of SCD may fail due to lack of efficacy or adverse side effects. The implantable cardioverter-defibrillator (ICD) may extend patient survival until a donor heart is available. METHODS AND RESULTS: We reviewed 16 patients listed for transplantation between November 1988 and October 1991 who underwent ICD implantation for ventricular arrhythmias refractory to medical management. Mean age was 51.4 +/- 11.4 years (range, 19-66 years), mean ejection fraction was 15.4 +/- 3.0% (range, 10-21%), and underlying cardiomyopathy was ischemic (12 patients), valvular (one patient), or dilated (three patients). There was no mortality from ICD insertion. Fourteen patients were discharged before transplantation, and two patients remained in the hospital until transplantation. Twelve patients underwent transplantation after a mean of 155.7 +/- 113.7 days (range, 3-319) on the transplant list. The ICD delivered shocks for tachyarrhythmia associated with near syncope in 15 of 16 patients. ICD shocks numbered > 10 in five patients, 5-9 in three patients, and 1-4 in seven patients. There was no morbidity or mortality attributed to patch electrode removal. CONCLUSIONS: We conclude that the ICD can be implanted with minimal morbidity in transplant candidates, allowing the patients to be ambulatory and to leave the hospital while awaiting heart transplantation. In patients at risk of SCD, the ICD is an effective electronic bridge to transplantation.

Methods of implantable cardioverter-defibrillator-pacemaker insertion to avoid interactions.

Experience with combined transvenous pacemaker and implantable cardioverter-defibrillator insertion in 21 patients is described. Special techniques are needed to avoid potentially lethal pacemaker-implantable cardioverter-defibrillator interaction. Separation between leads for the two devices should be maximized. The electrophysiologic criteria for successful device function can be met, even when some leads for both devices must be placed by a transvenous approach.

Effect of electrophysiological testing on ejection fraction during cardioverter/defibrillator implantation.

To evaluate the effect of repeated induction of ventricular tachycardia or ventricular fibrillation, or both, in patients with poor left ventricular function, we performed intraoperative two-dimensional echocardiography in 6 patients undergoing implantation of the automatic implantable cardioverter/defibrillator. Changes in left ventricular ejection fraction in sinus rhythm were assessed before the first inducible ventricular arrhythmia and after a mean of 6 +/- 1.9 (SD) episodes of ventricular tachycardia or ventricular fibrillation. During the procedure no significant change in mean ejection fraction was observed (28 +/- 14 versus 27 +/- 17%). Only 1 of the 6 patients studied had a change in ejection fraction greater than 3% (a decrease from 20 to 11%). In an overall clinical series of 38 primary implants or generator changes (including electrophysiological testing) in 29 patients, 1 patient recovered after postoperative inotropic support and 1 died of acute postoperative ischemic heart failure. We conclude that ventricular arrhythmias induced during automatic implantable cardioverter/defibrillator implantation have no immediate deleterious effects on ejection fraction in most patients with compromised left ventricular function and without ongoing ischemia.

Electrophysiologic testing in patients with recurrent syncope: are results predicted by prior ambulatory monitoring?

Syncope is a common medical problem which can result from many etiologies, including cardiac dysrhythmias. Because ambulatory monitoring usually fails to capture a syncopal episode, electrophysiologic testing has been used to elucidate dysrhythmic mechanisms in patients with recurrent syncope. To assess whether findings on ambulatory monitoring not obtained during syncope can be used to indicate the results which are found on electrophysiologic testing in patients with recurrent syncope, we reviewed the ambulatory monitoring records of 59 such patients referred for electrophysiologic testing. Although 29 patients had abnormalities on electrophysiologic testing, 13 of which were severe, in only six were the findings suggested by the abnormalities recorded during ambulatory monitoring. Twenty-one patients actually had concordance between electrophysiologic testing and ambulatory monitoring results, but in 15 of the 21 results of both tests were normal. Severe abnormalities were more frequently detected in our patient population by electrophysiologic testing than by ambulatory monitoring, especially if patients had organic heart disease.

Sinus node echoes and concealed concealed conduction: additional sinus node phenomena confirmed in man by direct sinus node electrography.

Direct sinus node electrography has been previously used to assess several aspects of sinus node physiology: sinus node pauses, overdrive suppression, sinoatrial entrance block. This report presents data in which sinus node electrograms confirm two additional physiologic phenomena in man: concealed conduction in the sinoatrial junction and sinus node reentry. These findings verify the presence of previously suspected phenomena by careful deductive analysis of electrocardiographic and electrographic tracings.

Indirectly estimated sinoatrial conduction time by the atrial premature stimulus technique: patterns of error and the degree of associated inaccuracy as assessed by direct sinus node electrography.

The atrial premature stimulus method for estimating sinoatrial conduction time (SACT) is commonly used. When the stimulated atrial premature depolarization (APD) does not appear to affect sinus node automaticity or conduction, the indirectly estimated SACT (SACT1) is quite accurate. That is, SACT1 correlates quite highly with SACT measured directly (SACTD) on sinus node electrograms (SNE). In this study we used direct SNE recordings in 17 patients to assess SACT1 when factors thought to produce inaccuracy in SACT1 were present. Three patients had sinoatrial entrance block, which might make some expect sinoatrial exit delay to be present. However, SACTD was normal in two (60 and 70 msec) and prolonged (130 msec) only in the one who had other evidence of sinus node dysfunction. Therefore, sinoatrial entrance block does not necessarily indicate sinoatrial exit delay. Thirteen patients had apparent depression of sinus node automaticity by the induced APD (A3A4 greater than A1A1). In all 13, SACT1 overestimated SACTD. One patient had apparent sinoatrial conduction delay induced by the APD and/or vagal transmitter release induced by the APD. In this patient, too, SACT1 exceeded SACTD. Thus when sinoatrial automaticity or conduction are depressed by the stimulated APD, SACT1 will overestimate SACTD. If SACT1 is normal, SACTD will be normal; however, if SACT1 is prolonged, SACTD may or may not be prolonged.

Sinus node recovery times following the spontaneous termination of supraventricular tachycardia and following atrial overdrive pacing: a comparison.

We compared the pauses that followed the spontaneous termination of supraventricular tachyarrhythmias with the pauses that followed the cessation of atrial overdrive pacing in 21 patients. In 10 patients with abnormal sinus node function and in 11 patients with normal sinus node function we recorded the spontaneous termination of supraventricular tachyarrhythmia in the clinical electrophysiology laboratory; a strong correlation (r = 0.94) was found between the maximal spontaneous sinus node recovery time and the maximal paced sinus node recovery time. A weaker correlation was found between the paced and spontaneous sinus node recovery times (r = 0.57) when the spontaneous termination of supraventricular tachyarrhythmia was recorded during ambulatory electrocardiographic recording in seven patients. Spontaneous sinus node recovery times were significantly shorter than maximal paced sinus node recovery times (p less than 0.001). However, no significant difference was detected between the paced and spontaneous sinus node recovery times when atrial pacing was performed at the rate of the tachycardia. We conclude that spontaneous and postpacing sinus node recovery times are closely correlated. The paced sinus node recovery time is, however, frequently more prolonged than spontaneous sinus node recovery time because of probable atriosinus entrance block during rapid supraventricular tachycardia.

Sinus node recovery time related to paced cycle length in normals and patients with sinoatrial dysfunction.

Depressed conduction in the sinoatrial junction, common in the sick sinus syndrome (SSS), should decrease the maximum pacing rate at which 1:1 capture of the SA node occurs. This may result in shorter than expected sinus recovery times (SRT) and maximal prolongation of SRT at relatively slow pacing rates. To test this hypothesis we evaluated the range of pacing rates necessary to demonstrate maximal SRT in 34 patients with and 20 patients without sinus node dysfunction. Atrial pacing was performed at multiple paced cycle lengths (PCL) between 400 and greater than or equal to 1000 msec, four times at each. A mean corrected SRT (CSRT) was determined at each PCL, and the PCL of the longest CSRT was determined (PCLp). PCLp varied linearly with sinus cycle length, was dependent on sinoatrial conduction time, and was longer in patients with SSS than in normal persons. Only 2 of 20 normal persons, but 21 of 34 patients with SSS, had a PCLp greater than 600 msec. A long PCLp (greater than 600 msec) suggests the possibility of recovery times that have been limited by A-S entrance block and appears to be indicative of sinus node dysfunction.

Response to programmed ventricular stimulation: sensitivity, specificity and relation to heart disease.

This prospective study of 100 patients evaluated the sensitivity and specificity of the repetitive ventricular response and ventricular tachycardia induced by programmed electrical stimulation for identifying patients with spontaneous ventricular tachyarrhythmias. The influence of underlying heart disease on such sensitivity and specificity was also evaluated. The repetitive ventricular response was sensitive (92 percent) for detecting patients with prior spontaneous ventricular tachyarrhythmias, but lacked specificity (57 percent); the rate of false positive responses was 43 percent. Inducible ventricular tachycardia was less sensitive (65 percent) but more specific (98 percent); the rate of false positive responses was only 3 percent. Among the 100 patients, 71 had heart disease, 29 did not. The presence of underlying heart disease had no significant effect on the sensitivity and specificity of repetitive ventricular responses or ventricular tachycardia induced by programmed stimulation; it did not increase the rate of false positive responses. It is concluded that (1) ventricular tachycardia induced with programmed ventricular stimulation is an excellent basis for guiding the management of clinically significant ventricular tachyarrhythmias, regardless of underlying heart disease; and (2) the repetitive ventricular response is not useful for this purpose because of its high rate of false positive responses among patients with or without significant heart disease.

A model of chronic ischemic arrhythmias: the relation between electrically inducible ventricular tachycardia, ventricular fibrillation threshold and myocardial infarct size.

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a "clinical" stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction. Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean +/- standard deviation 29 +/- 11 to 10 +/- 5 mA, p less than 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct. It is concluded that: (1) inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.

Electrophysiologic effects of procainamide on sinus function in patients with and without sinus node disease.

To compare the effects of procainamide on sinus node (SN) function in the presence (seven patients) and absence (nine patients) of SN dysfunction, sinus cycle length (SCL), maximal corrected sinus recovery time (maximal CRST), paced cycle length yielding peak SN suppression (PCLp), and indirect sinoatrial conduction time (SACT) were determined before and after intravenous administration of 10 to 15 mg/kg procainamide in each patient. Plasma procainamide concentration was in the therapeutic range in all patients. The mean SCL did not change significantly in either group (-24 +/- 58 and -73 +/- 171 msec for patients with normal and abnormal SN function, respectively). The maximal CSRT shortened 136 +/- 112 msec (p less than 0.01) in the group with normal SN function (nine of nine patients)( but tended to lengthen 85 +/- 95 msec (p less than 0.10) in the group with SN dysfunction (six of seven patients). PCLp shortened in only two of nine of the normal group but tended (NS) to shorten in five of seven patients with SN dysfunction. We conclude that in the absence of SN disease, procainamide does not adversely affect SN function. In apparent contrast in patients with SN dysfunction, procainamide tended (NS) to prolong CSRT and seemed (NS) to enhance conduction in the sinoatrial junction (PCLp and SACT both declined). The occasional lengthening of CSRT implies that procainamide might prolong post-tachycardia pauses and thus could worsen symptoms in certain patients with the bradycardia-tachycardia syndrome.

Clinical and electrophysiologic characteristics of sinoatrial entrance block evaluated by direct sinus node electrography: prevalence, relation to antegrade sinoatrial conduction time, and relevance to sinus node disease.

When AV conduction is normal, the absence of VA conduction is not abnormal. Analogous information about retrograde sinoatrial conduction is not available. Although the premature atrial stimulas (PAS) technique can demonstrate the presence of sinoatrial entrance block (SAEB), both its prevalence and its relationship to antegrade SA conduction are unknown. Using PAS, we determined the incidence of SAEB in 59 patients with known or suspected dysrrhythmias or conduction defects to be 6.8%. Using catheter recorded sinus node electrograms (SNE), we then directly measured sinoatrial conduction time (SACT) in three patients with SAEB. Antegrade SACT was normal in two and prolonged in one. Only the latter had sinus node dysfunction recognized by ECG and/or conventional sinus node testing. We conclude that SAEB occurs infrequently, may occur when antegrade SACT is normal, is probably analogous to behavior at the AV node, and should not be used as an indicator of sick sinus syndrome.

Unexplained in-hospital fever following cardiac surgery. Natural history, relationship to postpericardiotomy syndrome, and a prospective study of therapy with indomethacin versus placebo.

In Part I of this study, the in-hospital course of 219 patients who had undergone a cardiac operation is analyzed. Fever (greater than or equal to 37.8 degrees C, rectal) was present after postoperative day 6 in 159 patients (73%) and was of unexplained cause in 118. Fever decay in the population of unexplained fever patients was exponential. All patients with unexplained postoperative fever were afebrile by postoperative day 19. In-hospital pericardial rub and pleuritic chest pain, widening of the mediastinum on chest film, and pleural effusion were not specifically associated with unexplained postoperative fever. In Part II, 67 patients with unexplained postoperative fever were given indomethacin (100 mg per day) or placebo for 7 days by a randomized, double-blind protocol. Indomethacin resulted in a shorter duration of fever (2.4 vs 3.5 days, P is less than 0.01) and in a shorter duration of chest pain, malaise, and myalgias compared to placebo. Sixty-seven percent of the patients in Part I and all of the patients in Part II were contacted 2-8 months following hospital discharge. Five percent had experienced an illness that we considered to be acute pericarditis, but its occurrence was unrelated to whether the patient had had in-hospital unexplained postoperative fever, in-hospital rub or chest pain, or in-hospital administration of indomethacin.