Dimensions of the triangle of Koch in humans.
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Biomedical subjects
Publications and source records attributed to D L Ross.
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Midazolam has several advantages over diazepam as a sedative agent in electrophysiologic studies, but its electrophysiologic effects in humans are unknown. Therefore, its effects were studied in 20 patients undergoing electrophysiologic studies. Electrophysiologic variables were measured before and after administration of intravenous midazolam (5 mg). There were no significant changes in the electrophysiologic variables, apart from a minor decrease in sinus cycle length (711 +/- 124 vs 647 +/- 91 ms; p = 0.005). Ease of inducibility of reentrant tachycardia was not significantly altered by midazolam, and tachycardia remained inducible in all patients. The drug was well-tolerated with no significant side effects, apart from a minor reduction (mean 18 mm Hg) in blood pressure (p less than 0.001). Good amnesic effect was achieved in 16 patients, and most patients preferred it to oral diazepam for sedation during the procedure. It is concluded that midazolam can be used safely in patients undergoing electrophysiologic studies without significantly interfering with electrophysiologic variables or the inducibility of reentrant tachycardias.
The coronary sinus (CS) orifice is an important reference point for determining electrode and, thereby, accessory pathway location at electrophysiologic study. The reliability of fluoroscopic landmarks used to identify the CS orifice is not known. This study compared the accuracy of several fluoroscopic landmarks for identifying the CS orifice with the location defined by radiopaque contrast injection of the CS. Forty patients were studied. Radiographic markers of the CS orifice that were examined included: (1) the point at which the CS catheter prolapsed during advancement, (2) the point of maximum convexity of the CS catheter when a superior vena caval approach was used, (3) the right side of the ventricular septum, and (4) the relation to the underlying vertebrae. The least-significant difference method of multiple comparisons was used for statistical analysis. The point at which the CS catheter prolapsed was the most accurate noncontrast method for determining the location of the CS orifice (p less than 0.05), but was possible without the use of excessive force in only 48% of patients. The point of catheter prolapse was a median of 1 mm (range 0 to 11) from the true location of the os. Errors with other examined landmarks ranged up to 3 cm. Identification of the CS orifice is best performed by radiopaque contrast injection. The point of prolapse during catheter advancement in the CS is an accurate alternative when contrast injection is not feasible. Other noncontrast fluoroscopic landmarks are less reliable and are best avoided.(ABSTRACT TRUNCATED AT 250 WORDS)
This study examined the role of electrophysiologic study in the evaluation of patients with unexplained syncope. The incidence of abnormalities (conduction disease, supraventricular tachycardia, ventricular tachycardia) was compared in patient groups with and without heart disease, and the effect of treatment of these abnormalities on recurrence of syncope was examined. Electrophysiologic study was performed in 111 consecutive patients with syncope, with antiarrhythmic medications being discontinued 1 week prior to study. There was no mortality associated with the procedure and only 9 patients (8%) had complications (groin haematoma, atrial fibrillation or brady-arrhythmias persisting after the procedure). Abnormalities were detected in 31 of 73 patients with heart disease (42%) but in only 6 of 38 patients with no heart disease (16%, P less than 0.01). During follow-up, syncope recurred in 2 of 37 patients (5%) treated because of abnormal findings, compared with a recurrence rate of 24% (18 of 74 patients) in the untreated group (P less than 0.05). Probability of remaining free from syncope at 2 years was 0.94 in the treated group and 0.72 in the untreated group (P less than 0.05). Mortality during follow-up was confined to the heart disease group with 5 of 30 treated patients in this group dying (17%) compared with 3 of 43 untreated patients (7%, P = not significant). Syncope patients with heart disease were thus more likely to have a diagnostically useful study than patients with normal hearts. Treatment directed at correction of abnormalities detected at electrophysiologic study reduced recurrence of syncope but did not significantly affect mortality. Syncope did not appear to be a prelude for sudden death in patients with normal hearts. Electrophysiologic study had no mortality and low morbidity.
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Accurate anatomic localization of accessory pathways during preoperative electrophysiologic study and during operative mapping depends on a knowledge of the dimensions of the posterior septal space and the left free wall. These dimensions were therefore studied in 48 human cadaver hearts. Mean distance from the coronary sinus orifice to the left margin of the posterior septal space was 2.3 +/- 0.4 cm and mean length of the left free wall was 5.0 +/- 1.0 cm. The posterior septal space at the level of the valve anuli extended a mean of 3.4 +/- 0.5 cm around the epicardium. The width of the posterior septum measured in the coronary sinus was related to heart weight and a combination of body weight and patient age (p less than 0.05). The probability of an accessory pathway being located in the left free wall or the posterior septum during catheter mapping was calculated for various distances from the coronary sinus orifice for adults of different ages and body weights. In adults, accessory pathways located in the proximal 1.5 cm of the coronary sinus are almost always in the posterior septum. Those located between 1.5 and 3 cm from the coronary sinus orifice may be in either the left free wall or the posterior septum, and those located greater than 3 cm from the coronary sinus orifice are almost invariably in the left free wall.
Of 3,286 consecutive patients treated for acute myocardial infarction, electrophysiologic testing was performed in 1,209 survivors (37%) free of significant complications at the time of hospital discharge to determine their risk of spontaneous ventricular tachyarrhythmias during follow-up. Sustained monomorphic ventricular tachycardia was inducible by programmed electrical stimulation in 75 (6.2%). Antiarrhythmic therapy was not routinely prescribed regardless of the test results. During the 1st year of follow-up, 14 infarct survivors (19%) with inducible ventricular tachycardia experienced spontaneous ventricular tachycardia or fibrillation in the absence of new ischemia compared with 34 (2.9%) of those without inducible ventricular tachycardia (p less than 0.0005). During the extended follow-up period (median 28 months) of those with inducible ventricular tachycardia, 19 (25%) had a spontaneous electrical event; 37% of these first events were fatal. These results suggest that the most cost-effective strategy for predicting arrhythmia will be obtained by restricting electrophysiologic testing to infarct survivors whose left ventricular ejection fraction is less than 40% and using a stimulation protocol containing four extrastimuli. Electrophysiologic testing is the single best predictor of spontaneous ventricular tachyarrhythmias during follow-up in infarct survivors. The majority (94%) with a negative test benefit from the more reliable reassurance that all is well, whereas the 25% risk of electrical events in those with inducible ventricular tachycardia justifies a prospective trial of effective prophylactic antiarrhythmic interventions.
In a nine-year-old female, cardiac failure was erroneously attributed to idiopathic cardiomyopathy and cardiac transplantation was planned. The actual cause of cardiac failure was permanent junctional reciprocating tachycardia (PJRT), a rare form of supraventricular tachycardia. The diagnostic error was discovered before transplantation was performed and the arrhythmia was treated surgically. This resulted in return of near normal cardiac function.
The success of surgery for supraventricular tachycardia (SVT) is evaluated by a variety of methods in different hospitals. Unfortunately, the predictive values of these methods are not known. We therefore compared the various methods in 261 patients undergoing surgery for SVT at Westmead Hospital since 1981. Surgical outcome was assessed by early tests during the first week after surgery (serial 12-lead electrocardiograms, telemetric monitoring of the electrocardiogram, and electrophysiological study performed using epicardial wires); later tests at 6 months after surgery (12-lead electrocardiograms and electrophysiological study); and symptomatic review done by telephone interview at a median of 34 months after surgery. Early tests were obtained in 97%, later tests were obtained in 76%, and symptomatic review was obtained in 98% of patients. All of the examined tests were inaccurate methods of surgical assessment compared with the late electrophysiological study. A large proportion of the patients proven to be surgical failures at the late electrophysiological study were not detected by early tests (83%), by later electrocardiograms (66%), or by symptomatic assessment (41%). Accurate assessment of surgical outcome requires a late electrophysiological study to permit comparison of surgical techniques. Late electrophysiological study also provides accurate information on the current risks and benefits of proposed surgery for communication to patients to enable them to make an informed decision on future treatment. Most patients are willing to have a late electrophysiological study and usually benefit from clarification of their true surgical outcome.
BACKGROUND: Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. METHODS AND RESULTS: Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. CONCLUSIONS: Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.
BACKGROUND: The site of the reentrant circuit in atrioventricular (AV) junctional reentrant tachycardia has not been defined; in particular, the existence of a common pathway of AV nodal tissue above the reentrant circuit is controversial. METHODS AND RESULTS: Two types of AV junctional reentrant tachycardia were induced in each of three patients at electrophysiological study. In one type of tachycardia (anterior), the onset of atrial activity occurred from 0 to 12 msec before the onset of ventricular activation, and earliest atrial activity was recorded near the His bundle. In the second type of tachycardia (posterior), the ventriculoatrial intervals were longer (76-168 msec), and earliest atrial activity was recorded near the mouth of the coronary sinus. In individual patients, the two types of tachycardia had different cycle lengths. Posterior AV junctional reentrant tachycardia was not a fast-slow form of AV junctional reentry in at least two of the three patients. Surgical cure was attempted in two patients. In one patient, anterior AV junctional reentrant tachycardia was abolished by dissection of the anterior perinodal atrium, but posterior AV junctional reentrant tachycardia could still be induced. At reoperation 4 months later, dissection of the posterior perinodal atrium abolished posterior AV junctional reentrant tachycardia while preserving AV conduction. CONCLUSION: Differences in ventriculoatrial intervals and cycle lengths and the results of selective surgery suggest that the two types of AV junctional reentrant tachycardia used different reentrant circuits. These observations imply that a common pathway of AV nodal tissue is not present above the reentrant circuit and suggest that perinodal atrium is part of these circuits.
Drugs that are described as antiarrhythmic drugs may actually aggravate arrhythmia in several ways and these are termed proarrhythmic effects. The most common type of proarrhythmia is a paradoxical increase in the frequency of episodes of the target arrhythmia. This type of effect had not been suspected until recently and has not been widely publicized. It is a phenomenon common to all antiarrhythmic drugs when they are used to treat arrhythmias based on a re-entrant mechanism (the most common mechanism of clinical arrhythmias). Different drugs vary in their tendency to produce this type of proarrhythmic response. These differences are explicable in terms of the relative effects of the drugs on refractoriness and conduction times in the re-entrant circuit. Proarrhythmic effects are most important in the treatment of ventricular tachycardias because recurrences are often fatal. Proarrhythmic effects on ventricular tachycardia can now be predicted at electrophysiological study before commencement of long-term therapy, and potentially dangerous treatment can be avoided. The key to proper treatment to proarrhythmia is to recognize that it is a drug-induced problem and to withdraw the offending drug.
The influence of isoproterenol on induction of ventricular arrhythmias was evaluated in 10 normal dogs and 17 dogs with experimentally induced myocardial infarction. Programmed stimulation (using up to 6 extrastimuli) was performed before and then during infusion of isoproterenol (2 micrograms/minute followed by 4 micrograms/minute). Isoproterenol facilitated induction of sustained monomorphic ventricular tachycardia (cycle length 163 +/- 26 msec) in 5 of the 10 animals with no inducible baseline arrhythmia (P less than 0.05). Isoproterenol did not affect cycle length or the number of extrastimuli required in animals with baseline ventricular tachycardia (cycle length 158 +/- 15 msec before versus 163 +/- 17 msec during isoproterenol, P = 0.3; extrastimuli 3.8 +/- 0.6 before versus 3.8 +/- 0.4 during isoproterenol infusion, P = 0.3). Isoproterenol did not significantly facilitate induction of ventricular fibrillation in either normal dogs or those studied after production of myocardial infarction. We conclude that infusion of isoproterenol increases the incidence of inducible ventricular tachycardia in the infarcted heart, but does not facilitate the induction of ventricular fibrillation in infarcted or normal hearts, despite the use of an aggressive protocol for programmed stimulation. Isoproterenol is, therefore, a safe and useful adjunct to programmed stimulation in this setting.
The contribution of left (versus right) ventricular stimulation to the induction of ventricular tachyarrhythmias was studied in 37 dogs with chronic experimental myocardial infarction, and 17 dogs with normal hearts. Programmed stimulation of the endocardium at both ventricular apices employed an aggressive protocol of up to 7 extrastimuli. The right ventricle was the most successful site for induction of ventricular tachycardia after myocardial infarction (74% of dogs with ventricular tachycardia). Ten of 11 animals with slow ventricular tachycardia (greater than or equal to 140 msec) were inducible from the right ventricle. In contrast, left ventricular stimulation was required to induce rapid ventricular tachycardia (cycle length less than 140 msec) in 5 of 10 dogs (P less than 0.05). No animal required more than five extrastimuli from any site for induction of ventricular tachycardia. In the normal heart, ventricular fibrillation was induced most often from the right ventricle (77% of dogs) when compared with the left ventricle (47%, P less than 0.05). Ventricular tachycardia was never induced in normal animals. These results show that the right ventricular apex is the most successful site for induction of "slow" ventricular tachycardia in this canine model when using five extrastimuli. Rapid ventricular tachycardia is frequently induced from the infarcted left ventricle, but this arrhythmia may not be clinically significant. The normal right ventricle is significantly more susceptible to ventricular fibrillation than is the left ventricle, but this does not interfere with induction of ventricular tachycardia in the infarcted heart.
Two infants with incessant tachycardia uncontrolled by multiple drug treatment were thought initially to have supraventricular tachycardia. Careful examination of the 12-lead electrocardiogram suggested ventricular tachycardia, which was confirmed by electrophysiological studies. Intra-operative mapping showed that the arrhythmia arose from the posterior left ventricular free wall in one infant and at the left ventricular apex in the other. Cryoablation of these foci led to cessation of ventricular tachycardia. Myocardial biopsy showed hamartomatous involvement in the first infant and normal tissue in the other. In the first infant the incessant arrhythmia was cured but in the other it recurred 4 months later. The origin of the recurrent tachycardia was adjacent to the previously cryoablated arrhythmogenic area. This area was also cryoablated, leading to disappearance of the ventricular tachycardia. Both patients are free of arrhythmia 10 months and 3 months after their surgery. Surgically ablatable lesions are common in infants with incessant ventricular tachycardia. Early diagnosis and prompt surgical treatment usually can effect 'cure' of this potentially fatal problem in childhood.
UNLABELLED: The influence of procainamide on inducible ventricular tachyarrhythmias was evaluated in 35 dogs with experimental myocardial infarction, and 9 normal dogs. Programmed stimulation was performed from the right ventricular apex via a percutaneously positioned electrode catheter, using up to five extrastimuli before and after intravenous administration of procainamide (15 mg/kg). Procainamide levels in postinfarct dogs were 8.5 +/- 0.7 micrograms/mL (range 5.3-13.6 micrograms/mL). Procainamide exerted its greatest effect in postinfarct dogs with reproducible baseline ventricular fibrillation. Six of nine dogs (P less than 0.05) with ventricular fibrillation had sustained monomorphic ventricular tachycardia (cycle length: 147 +/- 4 msec) induced after procainamide administration. This ventricular tachycardia required significantly more extrastimuli than baseline ventricular fibrillation (3 +/- 0.3 extrastimuli before vs 4 +/- 0.3 extrastimuli after procainamide). Procainamide never converted ventricular fibrillation to ventricular tachycardia in normal dogs. Procainamide had minimal effect on inducible ventricular tachycardia after myocardial infarction. Ventricular tachycardia induction was abolished in only 2 of 17 dogs despite significant prolongation of electrophysiological parameters. Ventricular tachycardia cycle length, and the number of extrastimuli required were unchanged by procainamide in this subgroup. CONCLUSION: Ventricular tachycardia is insensitive to the antiarrhythmic properties of procainamide in this model. In contrast, procainamide is able to convert postinfarction ventricular fibrillation to ventricular tachycardia, presumably by promoting sustained, organized reentry. This previously undescribed action is an unusual form of proarrhythmic effect, and suggests that this drug should be used cautiously in patients after myocardial infarction.
Supraventricular tachycardia is a common clinical problem. Although its primary mortality is usually low, it often causes significant life long symptoms. It can be life threatening when associated with rapidly conducting accessory atrioventricular connections or nodo-ventricular fibres. Electrophysiological study is now the "gold standard" investigation for diagnosis of this problem. It is also an essential tool for choosing therapeutic options. It is safe and cost effective and should be available in all major hospitals. Since surgical cure is currently feasible for almost all forms of supraventricular tachycardia with a high success rate and a low mortality, electrophysiological study and arrhythmia surgery should be offered to symptomatic patients early in the course of disease. Catheter ablation of supraventricular tachycardia is presently investigational but may in the future become the standard treatment for some forms of supraventricular tachycardia if the cure rate and risk of the procedure can be improved so that they are superior to surgery.
Eighteen adult patients with atrial tachycardia refractory to treatment with a mean of four drugs underwent attempted surgical cure. Atrial tachycardia originated in the right atrium in 17 patients and the left atrium in 1 patient. Tachycardia could be reproducibly induced and terminated by atrial extrastimuli or atrial pacing in 8 patients (44%). Resection of the arrhythmogenic area was performed in 16 patients (89%), and an isolation procedure was performed in 1 patient. In seven cases (39%), the area of isolation or excision included the sinoatrial node. One patient underwent His bundle section because the arrhythmogenic region was too close to the atrioventricular (AV) conduction system to enable resection. The mean duration of clinical follow-up was 56 +/- 34 months. Clinical tachycardia recurred in five patients (28%), but in two patients it did not recur until greater than 1 year after surgery. A permanent pacemaker was implanted in 3 (18%) of the 17 patients whose His-Purkinje system was left intact. One other patient had required permanent pacing before surgery. Only one of the seven patients undergoing sinoatrial node resection or isolation required permanent pacing for symptomatic bradycardia. Apart from the requirement for permanent pacing, no significant complications occurred. Surgical therapy for atrial tachycardia is a safe procedure, but the rate of cure appears to be less than that of supraventricular tachycardias associated with accessory AV connections. Excision or isolation of the sinoatrial node does not necessitate permanent pacing in most patients.