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In atrial tachycardias, catheter ablation using conventional mapping system is associated with high immediate success and low recurrence. Three-dimensional electroanatomical mapping system combined to catheter ablation of atrial tachycardias has reached, in small uncontroled series, success rates of 100%. However, limited data are available about rates of recurrence or complication using this approach. In order to compare both mapping systems, we have conducted a study of 65 consecutive patients (36 women and 29 men) that underwent both electrophysiologic study and catheter ablation for suspected atrial tachycardias. Pre-existing heart disease was noted in 43%, hypertension in 32% and a history of atrial fibrillation of flutter in 52%. Catheter ablation guided by conventional mapping was undertaken in 44 patients and by three-dimensional electroanatomical mapping in 21. Successful ablation was performed in 68% of patients with conventional mapping and in 90% with three-dimensional electroanatomical mapping. No complication and recurrence were observed with the latter approach, while 5 patients had a recurrence and 2 had immediate complication with conventional mapping. Catheter ablation of atrial tachycardias combined with three-dimensional electroanatomical mapping appeared to be effective and safe, however, conventional mapping system still remains a reliable approach that must be considered as the first choice for atrial tachycardias ablation.

Background An abnormal signal-averaged ECG (SAECG) is a noninvasive marker of the substrate of sustained ventricular tachycardia after myocardial infarction. We assessed its prognostic ability in patients with asymptomatic unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction. Methods and Results A blinded core laboratory analyzed SAECG tracings from 1925 patients in a multicenter trial. Cox proportional hazards modeling was used to examine individual and joint relations between SAECG variables and arrhythmic death or cardiac arrest (primary end point), cardiac death, and total mortality. We also assessed the prognostic utility of SAECG at different levels of ejection fraction (EF). A filtered QRS duration >114 ms (abnormal SAECG) independently predicted the primary end point and cardiac death, independent of clinical variables, cardioverter-defibrillator implantation, and antiarrhythmic drug therapy. With an abnormal SAECG, the 5-year rates of the primary end point (28% versus 17%, P =0.0001), cardiac death (37% versus 25%, P =0.0001), and total mortality (43% versus 35%, P =0.0001) were significantly higher. The combination of EF Conclusions SAECG is a powerful predictor of poor outcomes in this population. The noninvasive combination of an abnormal SAECG and reduced EF may have utility in selecting high-risk patients for intervention.

Empirical antiarrhythmic therapy has not reduced mortality among patients with coronary artery disease and asymptomatic ventricular arrhythmias. Previous studies have suggested that antiarrhythmic therapy guided by electrophysiologic testing might reduce the risk of sudden death.We conducted a randomized, controlled trial to test the hypothesis that electrophysiologically guided antiarrhythmic therapy would reduce the risk of sudden death among patients with coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia. Patients in whom sustained ventricular tachyarrhythmias were induced by programmed stimulation were randomly assigned to receive either antiarrhythmic therapy, including drugs and implantable defibrillators, as indicated by the results of electrophysiologic testing, or no antiarrhythmic therapy. Angiotensin-converting-enzyme inhibitors and beta-adrenergic-blocking agents were administered if the patients could tolerate them.A total of 704 patients with inducible, sustained ventricular tachyarrhythmias were randomly assigned to treatment groups. Five-year Kaplan-Meier estimates of the incidence of the primary end point of cardiac arrest or death from arrhythmia were 25 percent among those receiving electrophysiologically guided therapy and 32 percent among the patients assigned to no antiarrhythmic therapy (relative risk, 0.73; 95 percent confidence interval, 0.53 to 0.99), representing a reduction in risk of 27 percent). The five-year estimates of overall mortality were 42 percent and 48 percent, respectively (relative risk, 0.80; 95 percent confidence interval, 0.64 to 1.01). The risk of cardiac arrest or death from arrhythmia among the patients who received treatment with defibrillators was significantly lower than that among the patients discharged without receiving defibrillator treatment (relative risk, 0.24; 95 percent confidence interval, 0.13 to 0.45; P0.001). Neither the rate of cardiac arrest or death from arrhythmia nor the overall mortality rate was lower among the patients assigned to electrophysiologically guided therapy and treated with antiarrhythmic drugs than among the patients assigned to no antiarrhythmic therapy.Electrophysiologically guided antiarrhythmic therapy with implantable defibrillators, but not with antiarrhythmic drugs, reduces the risk of sudden death in high-risk patients with coronary disease.

In contrast to the high success rates for catheter ablation of focal ventricular tachycardia, radiofrequency ablation for ventricular tachycardia due to coronary artery disease has met with limited to variable success. In performing catheter ablation for ventricular tachycardia due to coronary disease, mapping techniques used to locate the isthmus of the reentrant circuit are crucial. Appropriate use of mapping techniques determines the success rate of the procedure. We classify different methods of mapping into indirect and direct. The indirect methods include analysis of the 12-lead electrocardiogram, endocardial pace-mapping, and analysis of electrograms recorded from different parts of the heart during sinus rhythm. The direct methods include activation sequence mapping and entrainment mapping. The direct methods are more important in evaluating ventricular tachycardia due to coronary disease. While using the technique of entrainment mapping, three criteria are important: a) entrainment with concealed fusion; b) post pacing interval within or less than 10 ms of tachycardia cycle length; c) stimulus-to-QRS interval should equal electrogram-to-QRS interval. A high success rate in terminating the tachycardia is seen if these criteria are met.

Atrial fibrillation (AF) is a re-entrant rhythm, and patients with AF have intra-atrial conduction abnormalities as evidenced by prolonged P-wave duration, abnormal SAECG of P wave, fragmented atrial electrograms and greater intra-atrial conduction delays in response to APDs. Our previous work has proposed that intra-atrial conduction delays and dispersion of refractoriness during extrastimulus testing are site dependent; high right atrial (HRA) stimulation results in marked prolongation of intra-atrial conduction times and AF, whereas distal coronary sinus (CS) stimulation is associated with minimal conduction delays and absence of AF inducibility. Patients with AF induction during HRA stimulation also manifest non-uniform anisotropic conduction in the region of the posterior triangle of Koch. We postulated that if the posterior triangle of Koch is a critical area for re-entry that initiates AF, then prevention of early activation of the posterior triangle may prohibit AF induction by HRA APDs. Distal CS pacing pre-excites the posterior triangle in relation to HRA activation, therefore a subsequent HRA APD will activate the posterior triangle with a longer coupling interval. AF induction by HRA APDs following HRA pacing is prevented when same HRA APDs follow distal CS pacing. We propose that distal CS pacing eliminates the propensity of HRA extrasystoles to induce AF. This observation may have further clinical applicability in AF prevention.

Although FK 506 has been shown to effectively reverse refractory renal allograft rejection, its ability to reverse accelerated renal allograft rejection as a primary agent has not been specifically addressed. Herein evidence of the ability of FK 506 to reverse accelerated renal allograft rejection is presented. A 16-yr-old highly sensitized (PRA 75%) male underwent a second cadaveric renal transplant procedure. Despite induction immunosuppression with ATGAM, cyclosporine, azathioprine, and corticosteroids, a marked elevation in serum creatinine (1.6--2.1 ng/dl) and reduction in urine output (4000 ml/d--1000 ml/d) were observed on the sixth post-transplant day. Renal allograft biopsy performed at that time revealed typical features of accelerated rejection including neutrophil margination in glomerular and interstitial capillaries, and C3, IgG, and fibrin deposition in glomerular and interstitial capillaries (by immunofluorescence). FK 506 therapy was promptly instituted and ATGAM therapy discontinued. Serum creatinine peaked within 3 d of FK 506 therapy (2.5 mg/dl) and subsequently progressively dropped to 1.2 mg/dl. Repeat biopsy on FK 506 treatment day 12 revealed marked histologic improvement. Renal function remains excellent (1.3 mg/dl) 18 months after initiation of FK 506 therapy, and recurrent rejection has not been observed. This experience provides evidence that FK 506 therapy may effectively reverse accelerated renal allograft rejection, and that it provides a means for treating antibody-mediated mechanisms of allograft rejection.

Sustained uniform monomorphic ventricular tachycardia is usually due to abnormalities of conduction, including coronary artery disease and right ventricular dysplasia. These conduction abnormalities are due to non-uniform anisotropy which is characterized by fragmented electrograms. Less is known about the pathophysiologic substrate of sustained ventricular tachycardia in the absence of coronary artery disease or cardiomyopathy.

Many physicians believe that electrocardiographic characteristics of nonsustained ventricular tachycardia correlate with the risk for sudden death in survivors of myocardial infarction. Sustained ventricular tachycardia induced by programmed electrical stimulation has also been shown to predict sudden death.To determine whether electrocardiographic characteristics of spontaneous nonsustained ventricular tachycardia can predict the inducibility of sustained ventricular tachycardia by programmed electrical stimulation in patients with coronary artery disease having abnormal ventricular function.Observational cohort study.70 clinical electrophysiology laboratories in the United States and Canada.1480 consecutive patients with coronary artery disease, left ventricular ejection fraction of 0.40 or less, and asymptomatic nonsustained ventricular tachycardia.Electrophysiologic study attempting to induce sustained monomorphic ventricular tachycardia.Daily frequency, duration, and cycle length of spontaneous episodes of nonsustained ventricular tachycardia, measured by standard electrocardiographic recordings.No statistically significant difference in the frequency or duration of spontaneous nonsustained ventricular tachycardia was seen between patients with and those without inducible sustained ventricular tachycardia. Rates of spontaneous tachycardia were slightly slower in patients with inducible ventricular tachycardia than in patients without inducible ventricular tachycardia (P = 0.047), but the difference was not clinically significant.Electrocardiographic characteristics of spontaneous nonsustained ventricular tachycardia do not predict which patients with coronary artery disease will have inducible sustained ventricular tachycardia.

Despite substantial gains in our understanding of the electrophysiologic effects of antiarrhythmic drugs, the mechanism(s) responsible for their clinical efficacy remains elusive. The purpose of this discussion is to examine what is known about the mechanism of antiarrhythmic drug action in the treatment of clinical reentrant arrhythmias. Ventricular tachycardia in the setting of healed myocardial infarction will serve as the focus for the discussion as: (a) the reentrant mechanism of this arrhythmia is well established [1, 2], and (b) the effect of antiarrhythmic drugs on the individual components of the circuit is more difficult to determine than in macroreentrant arrhythmias such as AV reentry or AV nodal reentry. In this sense, the determination of antiarrhythmic mechanisms for VT is more difficult, but also more fundamental, than for macroreentrant rhythms because the vulnerable parameter [3] is not as evident.

Sudden cardiac death (SCD) is responsible for 300,000-400,000 deaths per year with a recurrence rate of up to 40% in survivors within the first 2 years. SCD often occurs in patients with chronic coronary artery disease, which is manifested by myocardial infarction and left ventricular dysfunction but is infrequently associated with acute infarction. SCD may be the initial symptom of coronary artery disease. Primary or rapid ventricular tachycardia are the most common arrhythmic causes of SCD. Endocardial mapping studies during electrophysiological study have shown areas of slowed conduction with abnormal endocardial electrograms in SCD patients with moderately damaged ventricles. SCD increases with age and occurs more frequently in men with coronary artery disease as a significant risk factor. Complex ventricular ectopy, once thought of as an independent risk factor, is not as good a predictor as poor left ventricular function for recurrence of SCD. While signal-averaged electrocardiograms can identify patients with slowed conduction, their positive predictive value for SCD is poor. Initial evaluation should be aimed at the identification of ischemia, since those patients with SCD and acute myocardial infarction do well when treated for their ischemia. The arrhythmias that are inducible during electrophysiological study are rapid and poorly tolerated. Patients with inducible ventricular tachycardia who are rendered noninducible pharmacologically have a good prognosis, whereas those who are still inducible or have no inducible arrhythmias have a high recurrence rate of SCD and should be considered for subendocardial resection when appropriate or for placement of an implantable defibrillator.

Training in clinical cardiac electrophysiology should take place in an Accreditation Council for Graduate Medical Education accredited cardiology program, and the electrophysiology training program itself should be accredited by the Council. Each trainee must be eligible for board certification in Internal Medicine and either eligible for certification in Cardiovascular Diseases or in a program leading to eligibility. Training faculty should be certified in clinical cardiac electrophysiology or demonstrate equivalent credentials. At least two training faculty members are preferred. The faculty must be dedicated to teaching, active in performing or promoting research and must spend a substantial portion of their time in research, teaching and practice of clinical electrophysiology. A curriculum of training should be established. Faculty experts in the related basic sciences should be available and involved in teaching. The institution should have a fully equipped clinical electrophysiology laboratory and complete noninvasive capabilities. A close working relation with a cardiac surgery faculty member skilled in surgical treatment of arrhythmias is required. Training in application of pharmacologic and all current nonpharmacologic therapies, in the outpatient and inpatient setting, is necessary. The clinical exposure must include all facets of arrhythmia diagnosis and treatment and must be quantitatively sufficient to allow the trainee to develop proficiency. The period of training should not be less than one year in addition to the period of cardiology fellowship required by the ABIM for board eligibility. A continuous period of training is preferred.

Sustained ventricular tachycardia with left ventricular aneurysm formation is a rare complication following penetrating cardiac trauma. We present an unusual case of serious ventricular tachycardia which developed 35 years after a World War II injury and was successfully treated with aneurysmectomy, map-guided subendocardial resection, and cryoablation.

We firmly believe that a systematic approach to the 12-lead ECG can provide information that can diagnose the difference between ventricular and supraventricular tachycardia, and in many instances diagnose the mechanism and site of origin of the supraventricular tachycardia. The mechanism of supraventricular tachycardia is able to be diagnosed in more than 80% of narrow complex tachycardias, and one should be able to distinguish supraventricular from ventricular tachycardia in more than 90% of tachycardias. In the presence of aberration, the mechanism of supraventricular tachycardias is more difficult to define unless retrograde P waves are seen. In such instances the morphology of the P wave (if seen), the effect of oscillation of cycle length on the RP interval, and response to vagal maneuvers may be useful in distinguishing mechanisms for ventricular tachycardia.

Electrocardiographic signal averaging techniques have demonstrated a low-amplitude late potential and a long filtered QRS complex in patients with ventricular tachycardia (VT) after myocardial infarction. Complex ventricular ectopy and left ventricular aneurysms have also been associated with VT. The purposes of this study were (1) to determine whether the findings from the signal-averaged electrocardiogram (ECG) were independent of those from Holter monitoring and cardiac catheterization and (2) to determine the combination of findings from the signal-averaged ECG, cardiac catheterization, and Holter monitoring that best characterize patients with VT after myocardial infarction. We studied 174 patients after myocardial infarction, 98 of whom had recurrent sustained VT. By multivariate logistic regression only three parameters were found to be independently significant, listed in order of power: positive signal-averaged ECG (presence of a late potential or a long filtered QRS duration), peak premature ventricular contraction greater than 100/hr, and presence of a left ventricular aneurysm (p less than .001). The signal-averaged ECG provides independent information in identifying patients with VT after myocardial infarction.

Seventy-eight patients with ventricular tachycardia associated with coronary artery disease underwent intraoperative mapping while in sinus rhythm to evaluate the frequency and significant of late potentials. In 30 of these patients, the surface ECG was subjected to signal averaging to correlate the incidence and duration of low-amplitude, delayed electrograms with the presence of late potentials recorded during epicardial mapping. One to four epicardial late potentials were observed in nine patients (11.5%). These nine patients did not differ hemodynamically from patients without late potentials. In four patients, the site of epicardial breakthrough during ventricular tachycardia bore no relationship (i.e., greater than 3 cm away) to the late potential or the site of origin of the tachycardia. In the five other patients with late potentials, epicardial breakthrough and site of origin of ventricular tachycardia were closely related to the free wall of an apical aneurysm. However, three of these patients had additional tachycardias from disparate sites. Twenty-seven of 30 patients in whom signal averaging was used had a low-amplitude signal in the terminal 40 msec of the amplified QRS complex. In 24 of these 27 patients (89%), the low-amplitude tail was demonstrated in the absence of epicardial late potentials. We conclude that epicardial late potentials are found infrequently in patients with ventricular tachycardia associated with coronary artery disease; epicardial late potentials cannot be used to localize ventricular tachycardia; and the specific low-amplitude tail on the signal-averaged electrogram is unrelated to epicardial events.

The pattern of retrograde His-Purkinje conduction was evaluated in 28 patients using ventricular extrastimuli. In each patient progressive prolongations of His-Purkinje conduction (S2H2) which appeared as ventricular extrastimuli were induced at closer coupling intervals (S1S2). There was an inverse linear relationship of S2H2 to S1S2 which was cycle length-dependent: i.e., at any S1S2 interval the resultant S2H2 was less at shorter drive cycle lengths. The degree of S2H2 delay varied widely (from 30 to 340 ms) and was unrelated to the presence of bundle branch block, H-V intervals, or capability of ventriculoatrial conduction. Prolongation of S2H2 was independent of intraventricular (muscle) conduction delay; such delay was usually absent at most, and occasionally all, S1S2 coupling intervals during which S2H2 was lengthening. Furthermore, in two patients both left and right ventricles were activated before the timed depolarization of the His bundle occurred, demonstrating that under the stress of extrastimuli, the impulse conducts through ventricular muscle with less delay than through the His-Purkinje system. We conclude that the His-Purkinje system typically displays slow conduction response to ventricular stress. The site of this conduction delay is probably at the distal "gate".

We analyzed the resetting response (a noncompensatory pause after electrical stimulation) during 37 hemodynamically tolerated ventricular tachycardias (VTs) induced by programmed electrical stimulation in 32 patients with chronic coronary artery disease. The mean cycle length of VT was 369 +/- 59 msec. Single extrastimuli were delivered at the right ventricular apex during all 37 VTs, and double extrastimuli were delivered at the same site during 23 VTs. The resetting response pattern was considered increasing, decreasing, or flat if the return cycle increased, decreased, or remained constant in response to progressively shorter coupling intervals of the extrastimuli. Ten VTs had an increasing pattern and nine a flat pattern. In 11 VTs the pattern was mixed (flat at longer coupling intervals and increasing at shorter ones), and in the remaining seven the pattern could not be defined. No VT had a decreasing pattern. The mean duration of the resetting interval (range of coupling intervals resulting in resetting) was 66 +/- 45 msec, or 17% of the cycle length of VT. VT with a mixed pattern had longer resetting intervals than VT with an increasing pattern (102 +/- 34 vs 64 +/- 40 msec; p less than .035); however, cycle lengths of VT were similar (370 +/- 58 vs 386 +/- 86, p = NS). An excellent correlation was observed between the shortest return cycles in response to single and double extrastimuli (r = .99), with a mean difference of 5 msec. The cycle length of VT exceeded the return cycle (measured to the QRS onset) during 15 VTs (41%).(ABSTRACT TRUNCATED AT 250 WORDS)

Mapping-guided endocardial resection has proved to be an effective therapy for recurrent sustained ventricular tachycardia. However, some patients cannot be mapped during ventricular tachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. We examined the frequency, timing, and duration of several abnormal types of electrograms recorded endocardially during sinus rhythm and related these findings to activation mapping during sustained ventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recurrent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and induced ventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface. Fractionated electrograms (multicomponent with amplitude less than 1 mV and duration greater than 50 msec) were recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Split electrograms (two components separated by isoelectric period) were also frequently seen but involved only a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex) were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of these electrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activation recorded during ventricular tachycardia. The longest fractionated electrogram was closely related to nine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of 16 morphologies, and late electrograms to two of four morphologies. We have concluded that extremely abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients with extensive myocardial infarction complicated by ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Whether or not the atrium plays an essential role in initiating and/or sustaining atrioventricular (A-V) nodal re-entrant tachycardia was evaluated in eight patients. In all eight patients, the atrium could be rendered refractory to retrograde atrial echoes during the tachycardia without interrupting the arrhythmia. This was accomplished by introducing atrial premature depolarizations prior to the time the atrium would normally be retrogradely depolarized by atrial echoes. In one patient, two atrial premature depolarizations could be introduced, producing A-V dissociation, without terminating the tachycardia. In another patient, the tachycardia could be initiated without an atrial echo. Our data suggest that most, if not all of the atrium is unnecessary for the initiation and maintenance of A-V nodal re-entrant supraventricular tachycardia.

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (less than or equal to 2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTs]) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 11 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (greater than 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.

The properties of the binding of [125I]iodopindolol ([125I]IPIN) to beta adrenergic receptors on plasma membranes prepared from right atrial tissue removed during cardiac bypass surgery were investigated. Some of the patients from whom the tissue was removed had been treated before surgery with either a beta adrenergic receptor antagonist or a calcium entry blocker or both. The specific binding of [125I]IPIN to beta adrenergic receptors was saturable, stereoselective and rapidly reversible. Studies of the inhibition of the specific binding of [125I]IPIN by drugs selective for beta-1 or beta-2 adrenergic receptors suggested that both beta-1 and beta-2 adrenergic receptors are present in the tissue, with approximately 55% of the receptors having the properties of beta-2 adrenergic receptors. The density of receptors in patients not treated with beta adrenergic receptor antagonists or calcium entry blockers was approximately 80 fmol/mg of protein, whereas the density of beta adrenergic receptors in treated patients was increased by approximately 50%. The relative proportion of beta-1 to beta-2 adrenergic receptors in subjects treated with beta adrenergic receptor antagonists and/or calcium entry blockers was not significantly different from that in untreated subjects. Studies were also carried out with a limited number of samples of human ventricular muscle obtained from untreated subjects at the time of surgery. The density of receptors was lower than that observed in studies with atrial tissue. However, as with atrial tissue, approximately half of the receptors appeared to be beta-2 adrenergic receptors.

The QRS configuration is a representation of the pattern of ventricular activation. Normally both ventricles are activated relatively synchronously and symmetrically giving rise to a narrow QRS complex. Ventricular activation is initiated along the left side of the interventricular septum and shortly thereafter (approximately 10 ms) at the anterior papillary muscle of the right ventricle [1]. An intact proximal His-Purkinje system, that is, the bundle branches, is required for the early and nearly simultaneous activation of both ventricles. While the ventricular muscle is activated at these regions, the impulse continues through the more distal His-Purkinje system to initiate activation at other ventricular sites. As the impulse continues through the distal His-Purkinje system, ventricular muscle is activated from endocardium to epicardium at each point of endocardial excitation [1]. Thus, it is apparent that a normal QRS morphology is dependent upon the functional and/or anatomic integrity of both the proximal and distal His-Purkinje system as well as factors influencing intramyocardial conduction.

The cardiac catheterization laboratory at this VA facility provides a wide variety of services, using state-of-the-art technology, to a large population of veterans with cardiac problems.

The effects of maternal diabetes upon fetal lung surfactant phospholipid metabolism were studied using 19-day gestational age fetal rats from mothers with streptozotocin-induced diabetes mellitus. In this experimental animal model, maternal glucose intolerance significantly impaired fetal body and lung development. However, incorporation of [14C]palmitate and [3H]choline into lung total and disaturated phosphatidylcholine was unimpaired in offspring of diabetic mothers. Dexamethasone, which is known to promote fetal lung maturation in normal pregnancies, was administered to diabetic and control mothers during late gestation. Prenatal dexamethasone inhibited lung growth in both diabetic and control pregnancies. While this agent slightly stimulated [14C]palmitate incorporation into total phosphatidylcholine and markedly enhanced [3H]choline incorporation into both disaturated and total phosphatidylcholine in control pregnancies, it failed to stimulate incorporation of either precursor into fetal lung from diabetic pregnancies.

The refinement of the techniques of programmed stimulation and intracardiac recording has provided an understanding of the mechanism of ventricular tachycardia which can be applied clinically to the development of therapeutic regimens. The efficacy of drug therapy can be assessed by sequential studies evaluating the ability of drugs to prevent the initiation of the arrhythmia. The efficacy of pacemaker therapy can be evaluated by the effects of stimulation during the tachycardia. The recent development of endocardial mapping provides the surgeon with a tool to guide therapeutic surgical ablation. We believe that such an electrophysiologic approach to recurrent ventricular tachycardia can lead to the rapid development of successful therapy under controlled conditions.

We measured 11 amino acids in untimed urine samples, to determine whether such samples are suited for use in diagnosis of aminoacidurias. Results for untimed samples varied by as much as 25% more than for 24-h collections when amino acid excretions were expressed in terms of urinary creatinine. Values decreased with increasing age for either type of specimen. Urinary amino acid excretions were also determined with untimed or 24-h samples from patients with cystinuria. Lowe's syndrome, nonketotic hyperglycinemia, or phenylketonuria. In all cases studied, the amino acids diagnostic of the diseases significantly exceeded the reference interval obtained for 260 control subjects in six age categories. We conclude that untimed urine samples can be used for diagnosis of these inborn errors of amino acid metabolism, but further studies are needed to evaluate their usefulness for other metabolic disorders.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Temporary epicardial pacing leads are routinely placed in patients after cardiac surgery, but the positioning of ventricular leads and the use of atrial leads is not uniform. We examined the effect of the epicardial pacing site on ventricular function in 18 patients undergoing coronary surgery. Pacing wires were sutured in the right atrium, left ventricular apex, right ventricular apex, and right ventricular outflow tract before cardiopulmonary bypass. After atrial pacing, eight patients were ventricularly paced (group I) and 10 were atrioventricular (AV) sequentially (PR = 0.12 sec) paced (group II) at 100/minute from the three ventricular sites. Comparison of the groups showed that the addition of atrial activation during ventricular pacing resulted in higher cardiac indexes (2.54 +/- 0.61 vs 1.67 +/- 0.45 liters/min/m2;p less than .00005), higher systolic blood pressures (121 +/- 24 vs 89 +/- 26 mm Hg; p = .006), lower central venous pressures (5.5 +/- 3.2 vs 10.2 +/- 2.2 mm Hg; p = .048), and similar pulmonary arterial pressures (19.5 +/- 7.6/10.8 +/- 6.7 vs 24.7 +/- 3.5/15.4 +/- 3.4 mm Hg; p = NS). Cardiac index did not differ among group I patients during pacing from the different ventricular sites. In group II, cardiac index during pacing from the right ventricular apex was higher than during pacing from the right ventricular outflow tract or the left ventricular apex (2.62 +/- 0.57 vs 2.49 +/- 0.54 and 2.51 +/- 0.76 liters/min/m2, respectively; p = .03). Right ventricular outflow tract pacing resulted in higher cardiac indexes than left ventricular apical pacing in patients with stenosis of the left anterior descending coronary artery of 90% or more, while left ventricular apical pacing produced higher cardiac indexes in the absence of such lesions (p = .006).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular tachycardia associated with inferior wall myocardial infarction has had a lower surgical cure rate with localized subendocardial resection than ventricular tachycardia related to anterior infarction. Some investigators have advocated visually directed extensive subendocardial resection, including resection of the papillary muscles and mitral valve replacement, even without documenting the origin of ventricular tachycardia at these sites. We have operated on 46 patients (43 men and three women) for ventricular tachycardia associated with inferior wall myocardial infarction. Thirty-one consecutive patients (Group I) had standard localized subendocardial resection. Two patients in this group had mitral valve replacement for mitral insufficiency. Fifteen consecutive recent patients (Group II) underwent subendocardial resection plus focal endocardial cryoablation (3 minutes at -70 degrees C) of the annular isthmus. The annular isthmus is defined as the ventricular muscle between the basal end of the ventriculotomy and the mitral valve anulus. In Group I there were four operative deaths (13%). Ventricular tachycardia was noninducible in 15 of 27 operative survivors (56%) at postoperative electrophysiologic studies. In Group II there was one operative death (7%) and 13 of 14 survivors (93%) had no inducible ventricular tachycardia at postoperative electrophysiologic studies (p less than 0.01 versus Group I). No Group II patient required mitral valve replacement. Six operative survivors in Group II had intraoperative activation maps consistent with macroreentry incorporating the annular isthmus. Group I and Group II were indistinguishable in terms of preoperative hemodynamics, number of coronary arteries diseased, or the presence of left ventricular aneurysm. These results suggest that subendocardial resection with additional cryoablation of the annular isthmus results in improved control of ventricular tachycardia in patients with ventricular tachycardia associated with inferior wall myocardial infarction. Mitral valve replacement is not required unless intrinsic mitral valve disease is present. These data also suggest that the annular isthmus is a critical component of the reentrant circuit in these tachycardias.