Saphenous vein graft disease treated with the Wiktor Hepamed stent: procedural outcome, in-hospital complications and six-month angiographic follow-up.

OBJECTIVES: To evaluate the effectiveness of electively placed heparin-coated stents in the treatment of coronary saphenous vein bypass grafts with de novo lesions less than 15 mm in diameter in a prospective study with all eligible consecutive patients presenting to Middelheim Hospital, Antwerp, Belgium between September 1997 and August 1998. PATIENTS AND METHODS: Fifty patients with 53 lesions were studied. Anginal class, risk factors, quantitative coronary angiographic measurements pre- and postprocedure, procedural outcome, in-hospital events, clinical status on discharge, and six-month clinical and angiographic follow-up (in 48 patients) were recorded. All patients received acetylsalicylic acid and ticlopidine, unless known intolerance was present. RESULTS: On average, 1.1 stents/patient were placed in very old saphenous vein grafts (11. 7+/-3.9 years). Procedural success was 98%. Only two non-Q wave myocardial infarctions (MIs) occurred, with no Q-wave MIs and no deaths during hospital stay. Length of hospital stay was short (2. 4+/-1.7 days), and 96% of patients were free of angina on discharge. At six-months' follow-up, two patients had died, one of whom died of a noncardiac cause. One patient suffered a non-Q wave MI. At six months, 86% of patients were free from angina. Minimal luminal diameter decreased from 1.14 mm before to 3.33 mm after stenting and to 2.52 mm at six months. Restenosis was present in 22% of patients (21.6% of lesions). CONCLUSIONS: In a selected population with coronary saphenous vein bypass graft disease, Wiktor heparin-coated stents can be delivered with an excellent periprocedural outcome. Six-month outcome appears favourable with a low recurrence of angina (18%) and a low rate of angiographic restenosis (21.6%).

Is the atrial high rate episode diagnostic feature reliable in detecting paroxysmal episodes of atrial tachyarrhythmias?

The atrial high rate episode diagnostic in the Thera pacemaker reports frequency, duration, and date/time of atrial tachyarrhythmias according to programmed criteria. The aim of the study was to validate the atrial high rate episode diagnostic feature. Episodes of atrial fibrillation recorded by Holter monitoring were compared to episodes detected by the pacemaker. Forty five ambulatory (Holter) recordings were used for evaluation. Thirty of 45 ambulatory (Holter) recordings showed sinus rhythm. On 4 of these 30 ambulatory (Holter) recordings, the Thera detected 12 episodes of atrial tachyarrhythmias as false-positives (sinus rhythm was detected as atrial tachyarrhythmia). The main reason was far-field R and T was oversensing. On 15 of 45 ambulatory (Holter) recordings, 125 episodes of atrial tachyarrhythmias were recorded. Ninety-three of these events also were detected by the pacemaker, while for 32 events the Thera reported sinus rhythm. The main reason was that the episodes were of too short duration. Therefore, the Thera (programmed with detection rate 160 beats/min, detection beats 40, termination beats 10) was unable to detect atrial tachycardias. Software simulation of the diagnostic algorithm under several programming settings using the digitized Holter files demonstrated highly reliable detection of atrial tachyarrhythmias (sensitivity 98%, specificity 100%) when programmed as follows: detection rate 220 beats/min, detection beats 10, termination beats 20. It can be concluded that Thera's high rate episode monitor is a reliable tool for detection of atrial tachyarrhythmias, if programmed as recommended.

Safety of radiofrequency catheter ablation of accessory atrioventricular pathways.

The acute anatomic and valvular consequences of radiofrequency catheter ablation of accessory pathways were evaluated in 62 patients by means of serial echocardiographic examinations. Semiquantitative assessment of valvular incompetence and classification into one of four grades according to the width and the extension of the jet from the valvular orifice were carried out. Segmental wall motion abnormalities were evaluated semiquantitatively with four grades of severity (normal, hypokinesia, akinesia, or dyskinesia). New echocardiographic abnormalities were observed in five patients. One thrombus on the ventricular aspect of the mitral valve, three hemodynamically insignificant pericardial effusions, and one increase in severity of tricuspid incompetence were found 1 day after radiofrequency catheter ablation. We conclude that echocardiographic changes after radiofrequency ablation of accessory pathways are rare and of minor significance. These findings confirm the safety of the procedure.

Diagnostic value of R wave amplitude changes during exercise testing after myocardial infarction.

To determine the diagnostic value of R wave amplitude changes occurring during exercise testing after myocardial infarction, exercise ECG's and coronary angiograms were reviewed in 76 postinfarction patients and in 40 patients with normal coronary arteries. During exercise, an increase in R wave amplitude (mean: + 2.7 +/- 1.3 mm) was observed in the postinfarction patients, significantly different (P less than 0.001) from the decrease (mean: - 2.6 +/- 1.1 mm) observed in the group with normal coronary arteries. Although this change increased with the number of diseased coronary arteries, the difference between 1-vessel and multi- or 3-vessel disease was not significant. Extension of infarct size from one to more akinetic segments on the left ventricular angiogram was associated with a significant (P less than 0.001) increase of the R wave amplitude change during exercise (mean: + 1.6 +/- 1.1 vs 3.3 +/- 1.3 mm). It is concluded that the abnormal increase in R wave amplitude observed during exercise testing after myocardial infarction is more strongly related to infarct size then to the number of diseased coronary arteries. Furthermore exercise induced R wave amplitude changes have no diagnostic value in the prediction of multi- or 3-vessel disease in postinfarction patients.

Temporary AVI pacing by chest wall stimulation.

Temporary atrial pacing (coded AVI pacing) has recently been proposed to assess atrial capture in patients with unipolar dual chamber pacemakers. This pacing mode can usually be achieved by programming the ventricular output to a subthreshold value. In patients with noncommitted bifocal pacemakers, AVI pacing can also be obtained by prolonging the programmed AV delay allowing for spontaneous conduction after atrial capture. However, in patients with prolonged AV conduction and a low aventricular stimulation threshold, ventricular stimulation cannot be prevented using the forementioned procedures. Using chest wall stimulation, we developed and tested a new method of temporary AVI pacing in patients with noncommitted DDD or DVI pacemakers.

Adult Still's disease caused by Yersinia enterocolitica infection.

Clinical and biologic features of adult Still's disease developed in a patient who had high antibody titers against Yersinia enterocolitica during his illness. Immunocomplexes containing antibodies against Yersinia antigens were isolated at the beginning of the disease. Yersinia was not isolated from blood or stool specimens probably because we observed the patient during the secondary phase of the disease.

Temporary A-V sequential pacing using chest wall stimulation.

We describe the therapeutic application of chest wall stimulation enabling temporary A-V sequential pacing in patients with an implanted VVT pacemaker following the transvenous introduction of only one temporary electrode.

Cardiac involvement in juvenile ceroid lipofuscinosis of the Spielmeyer-Vogt-Sjögren type: prospective noninvasive findings in two siblings.

The results of prospective noninvasive cardiologic investigations, including echocardiography and Holter monitoring are described in 2 siblings with juvenile ceroid lipofuscinosis of the Spielmeyer-Vogt-Sjögren type. In the elder patient, echocardiography revealed ventricular hypertrophy with slowed ventricular relaxation. Holter monitoring showed not only bradycardia but also slow and fast ectopic atrial rhythms, sinus arrests and complex ventricular ectopic activity including ventricular tachycardia. In the younger patient the findings were less severe. These functional disturbances due to cardiac involvement, never reported before in this disease, are discussed.

Cardiac manifestations of Becker-type muscular dystrophy.

The electro-, phonomechano- and echocardiographic manifestations observed in a family with documented X-linked Becker-type muscular dystrophy (BMD) are described. Important myocardial dystrophic lesions may occur in young patients with BMD. They are associated with typical electrocardiological findings which were described as a distinctive pattern in Duchenne-type muscular dystrophy. Myocardial involvement is seldom observed in heterozygotes for BMD.

Delayed termination of re-entrant atrioventricular nodal tachycardia.

Termination of atrioventricular nodal (AVN) re-entrant tachycardia by one or two induced premature beats generally occurs within one tachycardia cycle from the last premature beat. Two cases are described in which programmed stimulation during sustained re-entrant AVN tachycardia caused delayed termination in the second or third tachycardia cycle following the extrastimuli. The site of block was the antegrade pathway in one case and the retrograde pathway in the other. The most likely mechanism was induced second degree block in one limb of the tachycardia circuit. Delayed termination provided evidence for concealed penetration of the tachycardia circuit in one case. We conclude that delayed termination of tachycardia is not an indicator of the underlying mechanism of tachycardia. Delayed termination may reveal concealed penetration of the tachycardia circuit. Lastly, in unusual cases programmed stimulation may fail to cause immediate termination of re-entrant tachycardia but may perturb the tachycardia circuit enough to cause termination in subsequent tachycardia cycles.

Cycle length alternation in circus movement tachycardia using an atrioventricular accessory pathway. A study of the role of the atrioventricular node using a computer model of tachycardia.

The possible role of the atrioventricular nodal (AVN) function curve during tachycardia as a cause of cycle length alternation was investigated using a computer model of circus movement tachycardia utilizing an atrioventricular accessory pathway. Two types of AVN function curves during tachycardia were entered into the computer: straight lines of various gradients and representative examples of patient-based AVN function curves obtained during clinical electrophysiologic studies. Perturbations of the tachycardia model were induced by introducing a short cycle, by suddenly prolonging a conduction interval, or by moving the AVN function curve relative to that in stable tachycardia. Using the straight line AVN function curves, stable, sustained cycle length alternation could be induced by perturbation of the tachycardia cycle if the gradient of the line was -1 (slope = 45 degrees). If the gradient was more than -1 (slope less than 45 degrees), the perturbation was damped. If the gradient was less than -1 (slope greater than 45 degrees), the perturbation was amplified, leading to termination of tachycardia by block in the AVN. Similar but more complex responses to perturbation of tachycardia were found using patient-based AVN function curves. Thus, sustained cycle length alternation and amplification or damping of perturbation could be produced. Using physiologic AVN function curves, the response to perturbation of tachycardia depended on the interrelationship of the shape of the AVN function curve, the location of the cycle length of tachycardia on the curve, the magnitude and direction of the perturbation, and the AVN effective refractory period. We conclude that cycle length alternation during tachycardia may be explained by the characteristics of a single antegrade AVN function curve without postulating the presence of additional AVN pathways. The stability of circus movement tachycardias depends on the interaction of several variables.

Medical treatment of ventricular tachycardia: considerations in the selection of patients for surgical treatment.

The decision of when and how to treat ventricular tachycardia is primarily determined by the type and severity of concomitant heart disease. After the ventricular origin of the tachycardia is established, extensive investigation into this problem is mandatory. Long-term medical treatment in patients with ventricular tachycardia in the setting of coronary artery disease is unsatisfactory. Although drug selection with the use of programmed cardiac stimulation seems logical and promising, the long-term value of this method remains to be demonstrated. The extensive myocardial damage present in most patients with coronary artery disease and ventricular tachycardia makes it unlikely that drug therapy will be the ultimate answer. These considerations justify careful evaluation of the long-term efficacy of surgical therapy of symptomatic ventricular tachycardia, especially in patients with arrhythmia in the subacute or chronic phase of myocardial infarction.

Observations in patients showing A-V junctional echoes with a shorter P-R than R-P interval.

Single test stimulation of the ventricle revealed initiation of echoes with a supraventricular QRS complex with a shorter P-R than R-P interval in 28 of 300 patients consecutively studied with programmed electrical stimulation of the heart because of documented or suspected tachycardias. In all 28 the initiation of echoes was related to a discontinuity in the retrograde conduction curve. In 10 patients a different atrial activation sequence in the endocavitary leads was present before and after the discontinuity in the retrograde conduction curve. In five of these a sustained tachycardia with a shorter P-R than R-P interval could be initiated, and in all five patients an accessory pathway with a long conduction time as the retrograde arm of the tachycardia circuit could be demonstrated. In these five patients spontaneous initiation of tachycardia was observed during sinus rhythm or after atrial premature beats. Tachycardia accelerated after the administration of atropine. In the remaining 23 patients the initiation of echoes showing a shorter P-R than R-P interval was nonsustained. In these patients spontaneous initiation of such echoes during sinus rhythm or initiation by atrial premature beats was not observed, and echoes with this relation of the P-R and R-P intervals systematically disappeared after administration of atropine. It is postulated that in these patients a slow atrioventricular (A-V) nodal pathway is used in the retrograde direction during echoes showing a shorter P-R than R-P interval. Sustained A-V junctional tachycardia showing this relation between P-R and R-P intervals favors incorporation of an accessory pathway with slow retrograde conduction in the tachycardia circuit.

Observations on mechanisms of circus movement tachycardia in the Wolff-Parkinson-White syndrome. Role of different tachycardia circuits and sites of block in maintenance of tachycardia.

Different mechanisms of block of impulse propagation in several re-entrant circuits resulted in a major discordance between the "echo-zone" and the "tachycardia-zone" in a patient with intermittent Wolff-Parkinson-White syndrome, dual atrioventricular nodal pathways, and bundle branch re-entry. This case illustrates the delicate balance in electrophysiological properties required between the tissues incorporated in a re-entrant circuit to initiate and sustain the arrhythmia. It also shows how the presence of several reentrant pathways can lead to refractoriness in the circuit responsible for the circus movement tachycardia.

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system. A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome.

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.

Spontaneous termination of circus movement tachycardia using an atrioventricular accessory pathway: incidence, site of block and mechanisms.

The incidence, mechanisms and sites of block of spontaneous termination of circus movement tachycardia (CMT) using an atrioventricular accessory pathway (AP) were analyzed in 24 consecutive patients (17 with Wolff-Parkinson-White syndrome and seven with a concealed AP) who were not receiving antiarrhythmic drugs. Spontaneous termination of tachycardia occurred in 10 patients (105 episodes). A reduced "safety margin" of tachycardia was the only factor that was significantly more common in the patients who manifested spontaneous termination (p less than 0.01). The site of spontaneous block was located in the AP in six patients (50 episodes), atrioventricular node (AVN) in six patients (37 episodes) and His-Purkinje system (HPS) in three patients (18 episodes). At least 14 mechanisms leading to block in the tachycardia circuit were identified. Labile conduction during tachycardia occurred at multiple sites (AVN, His bundle, bundle branches, and AP). Analysis of the duration of tachycardia before spontaneous termination showed a characteristic time pattern for block at each site, consistent with the autonomic and electrophysiologic changes that occur after induction of tachycardia. Spontaneous termination of CMT using an AP is a common phenomenon. Many mechanisms are involved, which are often complex and dependent on interplay of the electrophysiologic characteristics of the components of the tachycardia circuit.

Observations on spontaneous termination of atrioventricular nodal reentrant tachycardia.

Unusual mechanisms of spontaneous termination of atrioventricular (A-V) nodal reentrant tachycardia were observed in two patients during programmed electrical stimulation of the heart. In both patients the mechanism of termination was based on the use of another reentrant pathway than the use used during tachycardia. This pathway was located extranodally in one patient and intranodally in the other. The observations illustrate some of the complexities of reentry in the human heart and how they can play a role in spontaneous termination of A-V nodal tachycardia.

Electrophysiological effects of lorcainide, a new antiarrhythmic drug. Observations in patients with and without pre-excitation.

The electrophysiological effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 23 patients with atrioventricular conduction disturbances (four patients), ventricular tachycardia (five patients), and accessory atrioventricular pathway (14 patients). Lorcainide did not affect the refractory period of the atrium, ventricle, atrioventricular node, or the AH interval. It lengthened the duration of the HV interval, the refractory period of the accessory pathway, and the width of the QRS complex. The drug terminated ventricular tachycardia in four of five patients. It is concluded that the drug may be of potential benefit in patients with ventricular tachycardia or accessory atrioventricular pathways (especially those with a short refractory period). Lorcainide is contraindicated in patients with bundle-branch block and prolonged HV interval.