Direct quantification of apparent binding indices from quinidine-induced in vivo conduction delay in canine myocardium.

To characterize quantitatively the quinidine (QUIN)-induced conduction delay (CD) in vivo, canine ventricular activation times were examined with an epicardial mapping technique. A high-resolution index of normalized (N) QUIN CD, derived from all 56 recording sites, was used to quantify QUIN effect. Repetitive stimulation elicited monoexponential increases in CD(N), the rates of which were a linear function of interpulse recovery interval, tr. Steady-state CD(N) was also linearly related to an exponential function of tr and drug uptake rates. The frequency-dependent properties of QUIN in 14 dogs were characterized by apparent binding and unbinding rates of ka = 7.1 +/- 3.5 x 10(6) M-1 s-1, la = 81 +/- 51 s-1 for activated, and kr = 12.6 +/- 11.3 x 10(3) M-1 s-1, lr = 0.51 +/- 0.26 s-1 for resting states. ka and la were similar to values previously derived in canine Purkinje fibers. Drug unbinding at resting potentials was faster in vivo than previously observed in vitro. The time constant of recovery from QUIN block extracted from the interpulse recovery rate was also identical to that determined from post-mature stimulus diastolic scanning. As predicted by the two-state model, similar binding rates were also derived from declining CD(N) elicited by step decreases in heart rate. These findings represent a complete quantitative description of use-dependent QUIN CD in vivo and provide a firm foundation for characterizing antiarrhythmic drug action under physiologic and pathologic conditions.

Characterization of concentration- and use-dependent effects of quinidine from conduction delay and declining conduction velocity in canine Purkinje fibers.

The dynamic response of squared conduction velocity, theta 2, to repetitive stimulation in canine Purkinje fibers with quinidine was studied using a double-microelectrode technique. With stimulation, a frequency-dependent monoexponential increase in conduction delay (CD) and a decline in theta 2 were observed. The exponential rates and changes in steady-state CD and theta 2 were frequency- and concentration-dependent. The overall drug uptake rates describing blockade and the interpulse recovery interval were linearly related and steady-state values of theta 2 were linearly related to an exponential function of the stimulus intervals. Based on first-order binding, the frequency- and concentration-dependent properties of quinidine were characterized by the apparent binding and unbinding rates of 14.2 +/- 5.7 X 10(6) mol-1.s-1 and 63 +/- 12 s-1 for activated and 14.8 +/- 1.0 X 10(2) mol-1.s-1 and 0.16 +/- 0.03 s-1 for resting states. The recovery time constant extracted from the pulse train interpulse interval was 5.8 +/- 1.5 s compared with 5.1 +/- 0.6 s determined from a posttrain test pulse protocol. This study demonstrates that the kinetics of drug action can be derived from measures of impulse propagation. This provides a basis for characterizing frequency-dependent properties of antiarrhythmic agents in vivo and suggests the plausibility of a quantitative assessment of drug binding and recovery rates in man.

An integrated system for real-time image guided cardiac catheter ablation.

Minimally invasive cardiac catheter ablation procedures require effective visualization of the relevant heart anatomy and electrophysiology (EP). In a typical ablation procedure, the visualization tools available to the cardiologist include bi-plane fluoroscopy, real-time ultrasound, and a coarse 3D model which gives a rough representation of cardiac anatomy and electrical activity. Recently, there has been increased interest in incorporating detailed, patient specific anatomical data into the cardiac ablation procedure. We are currently developing a prototype system which both integrates a patient specific, preoperative data model into the procedure as well as fuses the various visualization modalities (i.e. fluoroscopy, ultrasound, EP) into a single display. In this paper, we focus on two aspects of the prototype system. First, we describe the framework for integrating the various system components, including an efficient communication protocol. Second, using a simple two-chamber phantom of the heart, we demonstrate the ability to integrate preoperative data into the ablation procedure. This involves the registration and visualization of tracked catheter points within the cardiac chambers of the preoperative model.

Global right atrial mapping of human atrial flutter: the presence of posteromedial (sinus venosa region) functional block and double potentials : a study in biplane fluoroscopy and intracardiac echocardiography.

BACKGROUND: Previous studies of atrial flutter have found linear block at the crista terminalis; this was thought to predispose the patient to the arrhythmia. More recent observations, however, have demonstrated crista conduction. We sought to characterize the posterior boundary of atrial flutter. METHODS AND RESULTS: Patients with counterclockwise flutter (n=20), clockwise flutter (n=3), or both (n=5) were studied using two 20-pole catheters. Biplane fluoroscopy determined catheter positions. During counterclockwise flutter, craniocaudal activation occurred along the entire lateral and posterior right atrial walls. Septal activation proceeded caudocranially. In all patients, a line of block was seen in the posteromedial (sinus venosa) right atrium; this was manifested by the presence of double potentials where the upward and downward activations collided. Anatomic location was confirmed by intracardiac echocardiography in 9 patients. In patients with clockwise flutter, the line of block and double potentials were seen in the same location during counterclockwise flutter, but the activation sequence around the line of block was reversed. Pacing near the site of double potentials during sinus rhythm excluded a fixed line of block, and premature atrial complexes demonstrated functional block with manifest double potentials. In 2 patients, posterior ectopy organized to subsequently initiate isthmus-dependent atrial flutter. CONCLUSIONS: (1) A functional line of block is seen at the posteromedial (sinus venosa region) right atrium during counterclockwise and clockwise atrial flutter. (2) All lateral wall right atrial activation can be uniform during flutter, without linear block or double potentials in the region of the crista terminalis. (3) Activation at the site of posteromedial right atrial functional block can organize to subsequently initiate isthmus-dependent atrial flutter.

Impact of volume loading and load reduction on ventricular refractoriness and conduction properties in canine congestive heart failure.

OBJECTIVES: This investigations was undertaken to examine the alteration of electrophysiologic properties, including refractoriness, strength-interval relations and conduction, with the development of heart failure and to characterize the impact of volume loading on these indexes in the cardiomyopathic setting. METHODS: Electrophysiologic properties in eight dogs with pacing-induced dilated cardiomyopathy were compared with those in six control dogs before and after rapid infusion of 800 ml of intravenous saline. RESULTS: The right ventricular (RV) and left ventricular (LV) effective refractory period (ERP) and absolute refractory period (ARP) were significantly longer in dogs with pacing-induced cardiomyopathy than in control dogs: RV ERP 181 +/- 11 ms versus 138 +/- 7 ms (mean +/- SD) (p < 0.0001) and anterior LV ERP 177 +/- 13 ms versus 128 +/- 11 ms (p < 0.0001), respectively; ARP 159 +/- 14 ms versus 114 +/- 7 ms (p < 0.0001) at the RV site and 153 +/- 12 versus 117 +/- 5 ms (p < 0.0001) at the anterior LV site. After volume loading in cardiomyopathic animals, posterior and anterior LV ERPs became prolonged to 178 +/- 5 ms (p = 0.004) and 189 +/- 14 ms (p = 0.065), respectively, shifting the strength-interval relation in the direction of longer S1S2 coupling intervals. Anterior LV monophasic action potential durations at 90% repolarization also became prolonged from 192 +/- 10 ms to 222 +/- 23 ms (p < 0.012) with volume loading. These findings were not altered by subsequent sodium nitroprusside. Local conduction times parallel and perpendicular to fiber orientation were not altered by development of cardiomyopathy or volume alterations. CONCLUSIONS: The development of dilated cardiomyopathy results in significant prolongation of refractoriness and repolarization that is increased further by volume augmentation but is not reversed by pharmacologic load reduction. Although these abnormalities may contribute to the environment needed for a non-reentrant, triggered or stretch-mediated arrhythmogenic process in cardiomyopathic states, additional studies will be required to demonstrate such a focal mechanism conclusively.

Surface electrocardiographic clues suggesting presence of a nodofascicular Mahaim fiber.

Standard electrocardiograms from 87 consecutive patients with tachycardia of left bundle branch block configuration were analyzed retrospectively for features that might be characteristic of tachycardia utilizing a nodofascicular Mahaim fiber. The study group consisted of 13 patients with nodofascicular tachycardia, 34 with supraventricular tachycardia and aberrant conduction over the His-Purkinje system, 22 with ventricular tachycardia and 18 with antidromic tachycardia utilizing a right-sided accessory atrioventricular pathway. Six variables present during tachycardia of left bundle branch block configuration were predictive of a nodofascicular fiber: cycle length between 220 and 450 ms, QRS axis of 0 to -75 degrees, QRS duration 0.15 second or less, R wave in lead I, rS wave in precordial lead V1 and a precordial transition from a negative to a positive QRS complex after lead V4. All six criteria were present in 16 of the 87 patients. No patient with ventricular tachycardia satisfied these criteria, whereas 3 of 34 with supraventricular tachycardia, 1 of 18 with antidromic tachycardia and 12 of 13 with tachycardia using a nodofascicular fiber did. It is concluded that analysis of the surface electrocardiogram during tachycardia may suggest the presence of a nodofascicular fiber.

New observations on atrial fibrillation before and after surgical treatment in patients with the Wolff-Parkinson-White syndrome.

The records of 342 patients who received surgical treatment for the Wolff-Parkinson-White syndrome between 1968 and 1986 were reviewed to evaluate the characteristics of atrial fibrillation. The patients were classified into two groups according to the presence (n = 166) or absence (n = 176) of documented episodes of atrial fibrillation preoperatively. The mean follow-up duration was 6 years (range 2 to 20). As compared with reports based on smaller patient groups and shorter follow-up, the study revealed several new findings. 1) During follow-up, nine patients in the atrial fibrillation group developed recurrent atrial fibrillation after a successful operation; five of these nine patients did not have associated heart disease. 2) All three patients with a history of atrial fibrillation and an accessory pathway conducting in the anterograde direction only had a successful surgical procedure and no postoperative atrial fibrillation. 3) The cycle length of atrioventricular (AV) reciprocating tachycardia was significantly shorter in the atrial fibrillation group (304 +/- 42 ms, mean +/- SD) than in the no-atrial fibrillation group (321 +/- 54 ms, p less than 0.005), and the cycle length of AV reciprocating tachycardia that degenerated into atrial fibrillation (289 +/- 26 ms) was shorter than that for the AV reciprocating tachycardia without subsequent atrial fibrillation (316 +/- 51 ms, p less than 0.005). 4) Sustained atrial fibrillation was induced in 30% of patients without a history of atrial fibrillation. 5) Atrial fibrillation occurred in four patients with an accessory pathway that conducted only in the retrograde direction.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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

Rescue echocardiographically guided pericardiocentesis for cardiac perforation complicating catheter-based procedures. The Mayo Clinic experience.

OBJECTIVES: The purpose of this study was to determine the safety and efficacy of rescue echocardiographically guided pericardiocentesis as a primary strategy for the management of acute cardiac perforation and tamponade complicating catheter-based procedures. BACKGROUND: In this era of interventional catheterization, acute tamponade from cardiac perforation as a complication is encountered more frequently. The safety and efficacy of echocardiographically guided pericardiocentesis in this life-threatening situation and outcomes of patients managed by this technique are unknown. METHODS: Of the 960 consecutive echocardiographically guided pericardiocenteses performed at the Mayo Clinic (1979 to 1997), 92 (9.6%) were undertaken in 88 patients with acute tamponade that developed in association with a diagnostic or interventional catheter-based procedure. Most of the patients were hemodynamically unstable at the time of pericardiocentesis, with clinically overt tamponade in 40% and frank hemodynamic collapse (systolic blood pressure <60 mm Hg) in 57%. Clinical end points of interest were the success and complication rates of rescue pericardiocentesis and patient outcomes, including the need for other interventions, clinical and echocardiographic follow-up findings and survival. RESULTS: Rescue pericardiocentesis was successful in relieving tamponade in 91 cases (99%) and was the only and definitive therapy in 82% of the cases. Major complications (3%) included pneumothorax (n=1), right ventricular laceration (n=1) and intercostal vessel injury with right ventricular laceration (n=1); all were treated successfully. Minor complications (2%) included a small pneumothorax and an instance of transient nonsustained ventricular tachycardia; all were resolved spontaneously. Further surgical intervention was performed in 16 patients (18%). No deaths resulted from the rescue pericardiocentesis procedure itself. Early death (<30 days) in this series was due to injuries from cardiac catheter-based procedures (n=3), perioperative complications (n=2) and underlying cardiac diseases (n=2). Clinical or echocardiographic follow-up for a minimum of 3 months or until death (if <3 months) for recurrent effusion or development of pericardial constriction was achieved in 87 (99%) of the patients. CONCLUSIONS: Echocardiographically guided pericardiocentesis was safe and effective for rescuing patients from tamponade and reversing hemodynamic instability complicating invasive cardiac catheter-based procedures. For most patients, this was the definitive and only therapy necessary.

Adenosine: potential modulator for vasovagal syncope.

OBJECTIVES: This study examined the hypothesis that adenosine could provoke a vasovagal response in susceptible patients. Mechanisms of the vasovagal response were further explored by studying the adenosine-mediated reactions. BACKGROUND: Increased sympathetic activity is frequently observed before vasovagal syncope. Recent studies have demonstrated that adenosine, in addition to its direct bradycardiac and vasodilatory effects, can increase sympathetic discharge by activating cardiovascular afferent nerves. METHODS: The effects of adenosine and head-up tilt-table testing with or without isoproterenol were prospectively evaluated in 85 patients examined for syncope after negative results of electrophysiologic testing (51 men and 34 women, mean [+/- SD] age 61 +/- 17 years). Adenosine bolus injections of 6 mg and 12 mg were sequentially administered to patients in the upright position. The same protocol was implemented in 14 normal control subjects (7 men and 7 women, mean [+/- SD] age 38 +/- 10 years). RESULTS: Transient hypertension or tachycardia was observed in 57 (67%) and 20 (24%) patients after administration of 6 mg and 12 mg of adenosine, respectively, during the immediate phase (first 15 s), suggesting direct sympathetic activation. Hypotension and reflex tachycardia were observed in all patients during the delayed phase (15 to 60 s after adenosine injection), suggesting baroreceptor unloading. A vasovagal response was induced in 22 (26%) and 29 (34%) patients after adenosine administration and during tilt-table testing. Inducibility of a vasovagal response by these two methods was comparable (p = 0.12). Of the control subjects, one (7%) had a vasovagal response after adenosine administration and one (7%) had a positive response during tilt-table testing. CONCLUSIONS: These observations support the idea that adenosine is an endogenous modulator of the cardiac excitatory afferent nerves. Sympathetic activation by adenosine can be direct (i.e., cardiac excitatory afferent nerves) and indirect (i.e., vasodilation and reflex sympathetic activation). Adenosine could be an important modulator in triggering a vasovagal response in susceptible patients during examination for syncope.

Antiarrhythmic drug therapy in the Multicenter UnSustained Tachycardia Trial (MUSTT): drug testing and as-treated analysis.

OBJECTIVES: Using data from the Multicenter UnSustained Tachycardia Trial (MUSTT), we examined the factors used to select antiarrhythmic drug therapy and their impact on outcomes. BACKGROUND: The MUSTT examined the use of programmed ventricular stimulation (PVS) to guide antiarrhythmic therapy in patients with coronary arteriosclerosis, left ventricular dysfunction and asymptomatic, unsustained ventricular tachycardia (VT). Trial outcomes may reflect factors used to select antiarrhythmic drug therapy. METHODS: We compared subgroups of patients with inducible sustained VT randomized to PVS-guided antiarrhythmic therapy (n = 351), in particular those receiving PVS-guided antiarrhythmic drug therapy (n = 142) versus no antiarrhythmic therapy (controls, n = 353). RESULTS: "Effective" antiarrhythmic drug therapy (i.e., the term "effective" was used to denote therapy that resulted in noninducible VT or hemodynamically stable induced VT) was found for 142 of the 351 patients (43%), most often at the first or second PVS session (125/142, 88%). Mortality among the 142 patients did not differ from that among control patients. Of these 142 patients, the PVS end point was noninducibility in 91 patients and stable VT in 51 patients. Mortality did not differ between these two groups either, but arrhythmia was numerically more frequent in the PVS-induced stable VT group. Mortality was greatest in the few patients receiving propafenone (unadjusted p = 0.07, adjusted p = 0.14 vs. controls), but mortality with all agents did not differ from that of controls, even after adjustment. CONCLUSIONS: Even when presenting the results as favorably as possible, we found no benefit with PVS-guided drug therapy in patients with clinical unsustained VT who had inducible sustained VT. These findings are unaltered by using different end points for PVS or considering the response to individual drugs.

Altered response to ibutilide in a heart failure model.

OBJECTIVE: Despite the frequent use of anti-arrhythmic drugs in the general population, the electrophysiologic effects of these agents have not been elucidated in congestive heart failure (CHF). METHODS: To examine the impact of left ventricular dysfunction on actions of type III anti-arrhythmic drugs, we evaluated the actions of ibutilide in a canine model of pacing-induced dilated cardiomyopathy. Following ablation of the atrioventricular node, effects on action potential duration at 90% (APD(90)) were compared in vivo, between eight CHF animals and seven controls. Monophasic action potential recordings were obtained from right and left ventricular endocardium/epicardium during and after three doses of ibutilide (0. 01, 0.02 and 0.05 mg/kg), at pacing cycle lengths of 300-1000 ms. RESULTS: APD(90) prolongation with ibutilide (0.01 mg/kg) was significantly greater in CHF vs. controls (P=0.0026, ANOVA). However, plasma ibutilide levels at this dose, were not significantly different between the two groups. In CHF, maximal effects were observed at the lowest dose, whereas effects were gradual and dose-dependent in controls. With ibutilide administration (0.01 mg/kg), an increased dispersion of left-right ventricular APD(90) was observed in CHF, but not in controls (P=0.03). A trend was observed, for increased incidence of non-sustained polymorphic ventricular tachycardia in CHF. CONCLUSIONS: In the presence of CHF, the actions of ibutilide are altered significantly. These findings may reflect altered tissue effects, as a consequence of myocardial electrical remodeling in CHF.

Analysis of Left Atrial Respiratory and Cardiac Motion for Cardiac Ablation Therapy.

Cardiac ablation therapy is often guided by models built from preoperative computed tomography (CT) or magnetic resonance imaging (MRI) scans. One of the challenges in guiding a procedure from a preoperative model is properly synching the preoperative models with cardiac and respiratory motion through computational motion models. In this paper, we describe a methodology for evaluating cardiac and respiratory motion in the left atrium and pulmonary veins of a beating canine heart. Cardiac catheters were used to place metal clips within and near the pulmonary veins and left atrial appendage under fluoroscopic and ultrasound guidance and a contrast-enhanced, 64-slice multidetector CT scan was collected with the clips in place. Each clip was segmented from the CT scan at each of the five phases of the cardiac cycle at both end-inspiration and end-expiration. The centroid of each segmented clip was computed and used to evaluate both cardiac and respiratory motion of the left atrium. A total of three canine studies were completed, with 4 clips analyzed in the first study, 5 clips in the second study, and 2 clips in the third study. Mean respiratory displacement was 0.2±1.8 mm in the medial/lateral direction, 4.7±4.4 mm in the anterior/posterior direction (moving anterior on inspiration), and 9.0±5.0 mm superior/inferior (moving inferior with inspiration). At end inspiration, the mean left atrial cardiac motion at the clip locations was 1.5±1.3 mm in the medial/lateral direction, and 2.1±2.0 mm in the anterior/posterior and 1.3±1.2 mm superior/inferior directions. At end expiration, the mean left atrial cardiac motion at the clip locations was 2.0±1.5 mm in the medial/lateral direction, 3.0±1.8 mm in the anterior/posterior direction, and 1.5±1.5 mm in the superior/inferior directions.

Cardiac involvement in myotonic muscular dystrophy.

Cardiac illness in myotonic muscular dystrophy (MyD) is infrequent, but subclinical cardiac involvement in MyD is very common (found in 42 of 46 subjects) and may be responsible for sudden death. In this series, we found ECG abnormalities in 72%, left ventricular dysfunction in 70%, mitral valve prolapse in 37%, and sudden death in 4%. Four deaths during the study period were due to acute left ventricular failure, one to sepsis and respiratory insufficiency, and one was unexplained. We did not find ominous bradyarrhythmias or atrioventricular block, evidence of congestive heart failure, noninvasive evidence of coronary artery disease, or any correlation of type or amount of cardiac involvement with any clinical parameter such as age, sex, or severity of systemic dystrophy. We feel tachyarrhythmias may play as important a role in sudden death of myotonic muscular dystrophy subjects as bradyarrhythmias, and coronary artery disease in addition to cardiac dystrophy may produce arrhythmias and myocardial dysfunction in myotonic muscular dystrophy. In addition, some subjects have an unusual form of resting left ventricular dysfunction which improves with exercise. The most important problem in the clinical management of myotonic muscular dystrophy subjects is sudden death, and the solution does not appear to be empiric ventricular pacing. Our recommendations for prophylaxis of sudden death in myotonic muscular dystrophy are noninvasive investigation of coronary artery disease in subjects with significant risk factors, with angiography and surgery if indicated: detailed evaluation of syncopal and presyncopal events, including electrophysiologic testing, with pacemaker or antiarrhythmic drug therapy if indicated; and consideration of ventricular pacing of asymptomatic subjects if severe bradycardia or marked intraventricular conduction delay develops during follow-up, serial 12-lead ECGs. The documentation of tachyarrhythmias during sudden death and syncopal episodes in myotonic muscular dystrophy subjects makes ventricular pacing alone an uncertain modality for prevention of sudden death in subjects with only mildly lengthened PR or QRS intervals, and suggests a combination of pacemaker and antiarrhythmic drug therapy for the myotonic muscular dystrophy subject with syncope of no apparent cause.

Intracardiac Doppler hemodynamics and flow: new vector, phased-array ultrasound-tipped catheter.

Comprehensive intracardiac Doppler examination under simultaneous direct ultrasound visualization has not been previously possible. This human feasibility study demonstrates that a new 10Fr, 3.2-mm diameter, 5.5- to 10-MHz frequency agile, phased, vector array, ultrasound-tipped catheter with 4-way tip articulation provides diagnostic, high-quality, intracardiac Doppler signals using pulsed and continuous-wave, color flow, and tissue Doppler.

Beta-blocker therapy for the Wolff-Parkinson-White syndrome.

Two types of arrhythmias are associated with the Wolff-Parkinson-White syndrome: those in which the accessory pathway is a required part of the reentrant circuit, e.g., orthodromic atrioventricular reciprocating tachycardia, and those that conduct over the accessory pathway but do not require its activation for maintenance of tachycardia, e.g., atrial flutter/fibrillation. Increased sympathetic tone shortens the refractoriness of atrial and ventricular tissue; however, conduction in the atrium and ventricle is not considered the limiting factor for maintenance of atrioventricular reciprocating tachycardia or conduction over the accessory pathway in atrial arrhythmias. Intravenous beta-adrenergic blockers given to patients in the resting state have a minimal to moderate effect in depressing atrioventricular nodal conduction, but have little or no effect on accessory pathway refractoriness or conduction in most patients. In patients presenting with atrioventricular reentry, intravenous administration of beta-adrenergic blocking drugs often is not effective to terminate tachycardia. However, long-term oral therapy with these agents may be beneficial, especially in patients in whom enhanced sympathetic tone is responsible for the initiation or maintenance of tachycardia.

Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease.

Ten patients with an unusual form of ventricular tachycardia (VT) are described. All were young (mean age 21 years) at the onset of VT, symptoms were of long duration (mean 7 years), none had symptomatic organic heart disease, VT was induced by atrial and ventricular stimulation, VT had a characteristic QRS morphologic picture resembling right bundle branch block with left-axis deviation and 9 had early retrograde His deflections during VT. Supraventricular tachycardia (SVT) was excluded in every patient by electrophysiologic study, although QRS morphologic characteristics and clinical stability of these patients during tachycardia frequently led to the diagnosis of SVT before referral. Four patients received verapamil during electrophysiologic testing. Verapamil slowed and terminated VT in all. Three patients are being treated chronically with oral verapamil, 3 patients with conventional antiarrhythmic agents and 1 with a radiofrequency ventricular pacemaker.

Long-term survival after pacemaker implantation for heart block in patients > or = 65 years.

Permanent pacing can prevent recurrent symptoms and reduce mortality in elderly patients with symptomatic high-degree atrioventricular (AV) block. However, long-term survival with respect to comparable control subjects has not been well defined. In our study, relative long-term survival and prognostic predictors after permanent pacemaker implantation for symptomatic high-degree AV block were assessed among all residents of Olmsted County, Minnesota, who were > or = 65 years old. Of the 154 patients, 77 were men and 77 were women (mean age 80 +/- 7 years). Follow-up was 0.1 to 19.8 years (mean 4.2 +/- 2.8). Sixty-nine patients had isolated AV block and 85 had coexisting heart disease. Observed survival at 1, 3, 5, and 10 years was 85%, 68%, 52%, 21%, and 72%, 50%, 31%, 11% for patients with isolated AV block and patients with coexisting heart disease, respectively (p = 0.006). Observed survival in patients 65 to 79 years old with isolated AV block was comparable to age- and sex-matched cohorts (p = 0.53), but in patients aged > or = 80 years, it was less than that for control subjects (p = 0.014). In patients with coexisting heart disease, observed survival was less than that for control subjects in patients 65 to 79 years old (p < 0.001) and > or = 80 years (p < 0.001). Multivariate analysis identified congestive heart failure, chronic obstructive pulmonary disease, age, syncope, insulin-dependent diabetes mellitus, and male gender as independent predictors of increased mortality.

Value of the 12-lead electrocardiogram in discriminating atrioventricular nodal reciprocating tachycardia from circus movement atrioventricular tachycardia utilizing a retrograde accessory pathway.

The value of the 12-lead electrocardiogram for distinguishing atrioventricular (AV) nodal reciprocating tachycardia from circus movement AV tachycardia utilizing a retrograde accessory pathway was studied in 100 patients with narrow QRS complex tachycardia. Intracardiac electrograms showed AV nodal reciprocating tachycardia in 40 patients and circus movement AV tachycardia in 60. The 12-lead electrocardiograms recorded during tachycardia were randomly sorted and reviewed by 4 experienced cardiac electrophysiologists who were blinded to the diagnosis associated with each tracing, the relative proportion of each arrhythmia and the hypotheses to be tested. Each reviewer was asked to indicate the location of the P wave relative to the QRS complex, electrical axis of the P wave in the frontal and horizontal planes and presence or absence of QRS alternation, and to interpret the most likely mechanism. The performance of published electrocardiographic criteria to differentiate AV nodal reciprocating tachycardia from circus movement AV tachycardia was evaluated. The overall accuracy of the reviewers' interpretations was 75%, similar to the accuracy of the predefined criteria when applied by these observers (71% correct, difference not significant). Interobserver agreement of reviewer interpretations was 76% and the intraobserver agreement was 78%. Features associated with circus movement AV tachycardia by univariable analysis were P waves after the QRS complex, faster tachycardia rates and QRS alternation. Multivariable analysis showed that only the location of the P wave relative to the QRS complex was independently associated with the mechanism of tachycardia (p = 0.002). QRS alternation was found by multivariate analysis to be associated with the rate but not the mechanism of the tachycardia.

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways.

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebstein's anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p less than 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.