Presence and extent of cardiac magnetic resonance microvascular obstruction in reperfused non-ST-elevated myocardial infarction and correlation with infarct size and myocardial enzyme release.

OBJECTIVE: Microvascular obstruction (MO) is a factor of adverse outcome in patients with ST-elevated myocardial infarction (STEMI). We assessed the presence and extent of MO and its relationship with infarct size and left ventricular (LV) functional parameters after acute non-ST-elevated myocardial infarction (NSTEMI). METHODS: Twenty-five patients with first acute NSTEMI underwent a cine and first-pass perfusion cardiac magnetic resonance (CMR) study, with late gadolinium enhancement imaging 72 h after myocardial infarction. RESULTS: MO was detected in 32% of patients, and its extent comprised 0.5-3.1% of the total LV mass (mean 1.9 +/- 1.2%). Patients with MO had a significantly larger infarct size than patients without (14.1 +/- 5.9 vs. 5.3 +/- 4.1% LV mass; p < 0.001). There was no significant difference between both groups for the LV functional parameters and LV ejection fraction (58.5 +/- 6.8 vs. 62.6 +/- 9.6%; p = 0.29). Patients with MO showed a higher troponin I release (570 +/- 364 vs. 148 +/- 103 IU; p = 0.003) and a higher creatine kinase release (29,887 +/- 18,263 vs. 10,287 +/- 5,283 IU; p = 0.007). CONCLUSIONS: In patients with acute NSTEMI, MO has a frequency similar to that observed in patients with STEMI and also correlates with the infarct extent. The prognostic significance on clinical outcome remains to be shown in this specific population.

[Ictero-haemorrhagic leptospirosis with a cardiac presentation in a patient returning from an endemic zone]. / Leptospirose ictéro-hémorragique de presentation cardiaque chez une patiente de retour de zone d'endémie.

On returning from a tropical area, the occurrence of rapidly evolving cardiogenic shock in an infectious context should quickly suggest the diagnosis, for which specific treatment can affect the outcome. The dramatic case of a young female presenting with ictero-haemorrhagic leptospirosis diagnosed post-mortem, demonstrated this pathology with the unusual association of complete atrio-ventricular block and myocarditis in a haemorrhagic context.

Bundle branch reentrant tachycardia treated by electrical ablation of the right bundle branch.

A 66 year old man presented with multiple episodes of tachycardia. Some had QRS complexes with a right bundle branch block configuration identical to those of sinus beats. The onset of the tachycardia was preceded by premature His bundle depolarizations. There was a His potential before each QRS complex of the tachycardia. Atrial activity was dissociated. Occasionally the appearance of sinus beats with a left bundle branch block pattern announced a tachycardia with an identical configuration and atrioventricular dissociation. His bundle activity occurred before the QRS complex and was followed by a right bundle branch deflection. A reentrant mechanism within the bundle branch system was invoked. One 200 J shock was delivered through an electrode catheter to the site of the right bundle branch. The postprocedure course was uneventful (follow-up 10 months).

Gated blood-pool SPECT evaluation of changes after radiofrequency catheter ablation of accessory pathways: evidence for persistent ventricular preexcitation despite successful therapy.

OBJECTIVES: This study was designed to prospectively evaluate the effects of radiofrequency ablation in Wolff-Parkinson-White (WPW) syndrome by scintigraphic analysis. BACKGROUND: The functional changes triggered by radiofrequency current ablation of atrioventricular accessory pathways are not fully known. METHODS: Forty-four patients with WPW syndrome were consecutively investigated before and 48 h after radiofrequency therapy. Fourteen patients had right sided atrioventricular pathways and 30 patients had left sided bypass-tracts. Planar gated imaging and gated blood pool tomography were performed in all of these patients. RESULTS: A significant increase in the left ventricular ejection fraction (LVEF) was demonstrated in patients with left preexcitation (62.2+/-7.9% before ablation against 64.4+/-6.3% after ablation, p = 0.02) but not for those with right sided anomalous pathway. Phase analysis only gave significant differences following ablation of right sided pathways (left-to-right phase difference = 14.4+/-13.8 degrees before ablation versus 7.5+/-7.2 degrees after ablation, p<0.05). Early abnormal ventricular contraction persisted in 12 patients with right accessory pathways and in 8 patients with left accessory pathways despite the complete disappearance of any abnormal conduction as proven electrophysiologically. CONCLUSIONS: Following catheter ablation of atrioventricular accessory pathways: 1) an improvement of left ventricular function may be seen, particularly in patients with left sided accessory pathways, and 2) unexpected persistence of local ventricular preexcitation at the site of successful ablation may be detected.

Arrhythmic cardiac arrest due to isolated coronary artery spasm: long-term outcome of seven resuscitated patients.

OBJECTIVES: Our aim was to look at the clinical features and long-term follow-up of seven patients without coronary artery disease, who had a history of life-threatening ventricular arrhythmias due to coronary spasm. BACKGROUND: Arrhythmic cardiac arrest due to isolated coronary spasm is rare, and there is limited information on the patients affected by this entity alone. METHODS: The seven patients were recruited retrospectively from a cohort of survivors of cardiac arrest. None had a history of angina pectoris, structural heart disease or significantly narrowed coronary segments. All had a positive ergonovine provocation test result. RESULTS: The patients' mean age was 44 years; three were male and four female. All were habitual cigarette smokers. No arrhythmias were induced on programmed ventricular stimulation; corrected QT interval (QTc) and corrected JT interval (JTc) dispersion were within normal ranges. After the ergonovine provocation test, treatment with calcium channel blocking agents (diltiazem, verapamil, nifedipine or amlodipine) was initiated at a dose determined by titration until a negative test result was obtained. At a mean follow-up interval of 58 months for the total group, six patients remained free of symptoms, whereas the one patient who did not stop smoking had a new cardiac arrest despite treatment for coronary spasm. CONCLUSIONS: A favorable long-term outcome may be expected in survivors of cardiac arrest due to coronary spasm, in the absence of significant coronary artery disease. Calcium channel blockers are the most appropriate therapy in these patients. These observations provide further evidence for the role of silent ischemia in cardiovascular death.

Non-invasive testing of acquired long QT syndrome: evidence for multiple arrhythmogenic substrates.

BACKGROUND: Although well-defined clinically and electrocardiographically, Acquired Long QT Syndrome (LQTS) remains elusive from a pathophysiologic point of view. An increasingly accepted hypothesis is that it represents an attenuated form of Congenital Long QT Syndrome. To test this hypothesis further, we investigated patients with Acquired LQTS, using various investigations that are known to give information in patients with Congenital LQTS. METHODS: All the investigations were performed in patients with a history of Acquired Long QT Syndrome, defined by marked transient QT lengthening (QT>600 ms) and/or torsades de pointes. Measurement of the QT interval dispersion, the interlead difference for the QT interval on a 12-lead ECG, was performed in 18 patients and compared with 18 controls, matched for age and sex. To assess sympathetic myocardial innervation, I-123 Meta-iodobenzylguanidine (I-123-MIBG) scintigraphy was performed in 12 patients, together with Thallium scintigraphy, to rule out abnormal myocardial perfusion. Time-frequency analysis of a high-resolution ECG using a wavelet technique, was made for nine patients and compared with 38 healthy controls. Finally, genetic studies were performed prospectively in 16 consecutive patients, to look for HERG, KCNE1, KCNE2 and KCNQ1 mutations. The functional profile of a mutated HERG protein was performed using the patch-clamp technique. RESULTS: Compared with the control group, a significant increase in QT dispersion was observed in the patients with a history of Acquired LQTS (55+/-15 vs. 33+/-9 ms, P<0.001). In another group of patients with Acquired LQTS, 123 I-MIBG tomoscintigraphy demonstrated a decrease in the sympathetic myocardial innervation. Time--frequency analysis using wavelet transform, demonstrated an abnormal frequency content within the QRS complexes, in the patients with Acquired LQTS, similar to that found in Congenital LQTS patients. Molecular screening in 16 consecutive patients, identified one patient with a missense mutation on HERG, one of the LQTS genes. Expression of the mutated HERG protein led to altered K(+) channel function. CONCLUSION: Our results suggest that Acquired and Congenital Long QT Syndromes have some common features. They allow the mechanism of the clinical heterogeneity, found in both syndromes, to be understood. Further multi-facet approaches are needed to decipher the complex interplay between the main determinants of these arrhythmogenic diseases.

Electrophysiologic effects of propranolol in intraventricular conduction disturbance.

Sixteen patients underwent electrophysiologic studies before and after intravenous infusion of propranolol, 0.1 mg/kg. All of them had intraventricular conduction disturbances. A significant (p less than 0.01) increase occurred after propranolol in the mean spontaneous cycle length (mean change 122 ms) and the AH interval (mean 28 ms). The HV interval did not change significantly. The effective refractory period of the His-Purkinje system increased in 4 of 5 patients (mean net change 44 ms, p greater than 0.10). In 7 patients with phase 3 infranodal block, the longest cycle length for producing block increased after propranolol in 5 and remained unchanged in 2 (mean increase 40 ms, p less than 0.02). Two patients showed phase 4 atrioventricular block. Propranolol increased the critical cycle length by an average of 120 ms. Propranolol-induced bradycardia restored stable atrioventricular conduction in 2 patients with intermittent 2:1 block but facilitated the occurrence of high grade infranodal block in 1 patient. Thus, propranolol can impair His-Purkinje conduction in patients with preexisting infranodal abnormalities.

Electrophysiologic basis of catheter ablation in atrial flutter.

A reentrant mechanism is believed to be responsible for atrial flutter. The recent development of the entrainment criteria further supports this theory, and there is a general consensus that circus movement is the underlying abnormality that supports this arrhythmia. In most clinical studies, abnormal fragmented (or double spike) electrograms, suggesting the presence of areas of localized slowing of conduction or block, have been reported. They are almost always recorded in the lower and posterior portion of the right interatrial septum, but also frequently in the high lateral portion of the right atrium. The determination of their involvement in the reentry pathway is important for designing curative procedures such as surgery or ablation. The low atrial septal area surrounding the mouth of the coronary sinus was suspected as being the critical area of slow conduction in atrial flutter. Rapid pacing at that site can yield a surface electrocardiographic pattern similar to the clinically occurring arrhythmias. Additionally, the flutter circuit can be accelerated during atrial pacing at fixed and slightly faster rates than the intrinsic tachycardia rate--the so-called entrainment phenomenon. When entrainment criteria are fulfilled, tachycardia termination being by definition ruled out, any concomitant recorded local type II block identifies an area that must be outside the circuit. Such local block may be recorded either spontaneously or during entrainment and therefore helps in identifying atrial slow conduction areas that do not belong to the reentrant path. This approach was applied to identify the optimal ablation site in 8 patients with long-standing drug resistant atrial flutter. In 7 of 8 patients, we were able to identify a fragmented potential in the low posteroseptal area during sustained atrial flutter.(ABSTRACT TRUNCATED AT 250 WORDS)

Premature atrial stimulation during regular atrial pacing: a new approach to the study of the sinus node.

Using an induced premature atrial depolarization after atrial pacing for 8 beats to scan the postpacing cycle, sinus node (SN) response was studied in 23 patients and the results were compared with those obtained using the Strauss method. Late extrastimuli resulted in compensatory return cycles (zone I), increasing prematurity gave rise to less-than-compensatory return cycles (zone II or "plateau") and interpolation or echo responses occurred at shorter coupling intervals (zone III). The sinoatrial (SA) conduction time was defined as the difference between return cycle and postreturn cycle lengths that fell in the latter portion of zone II. The SA conduction time was similar to those derived from the Strauss method (r = 0.91, n = 17, p less than 0.01) and remained similar at the 2 pacing cycles, 172 +/- 52 ms (mean +/- standard deviation) at 739 +/- 71 ms (cycle 1) and 170 +/- 60 ms at 596 +/- 57 ms (cycle 2). In 4 patients, the atrial pacing method could unmask zone II. The SN refractory period was defined as the longest coupling interval at which zone III was apparent. It was compared at cycles 1 and 2 in 14 patients. There was a significant increase in the SN refractory period with faster pacing rates, from 406 +/- 104 ms (cycle 1) to 462 +/- 112 ms (cycle 2) (p less than 0.05). The atrial pacing method provides an alternative evaluation of SA conduction and may permit the study of drug effects at identical basic rates.

Cardiac troponin I does not increase after cardioversion.

BACKGROUND: Serum total creatine kinase (total CK) level increases in the patients following electrical cardioversion. The same has been observed with CK-MB, an isoenzyme of the total CK with some cardiospecificity. Cardiac troponin I (cTnI), a new specific cardiac biological marker, is highly effective to discriminate myocardial and muscular injuries after noncardiac surgery. METHODS: To assess cardiac damage after cardioversion, we measured serum cTnI, myoglobin, total CK, CK-MB mass, 1, 2, 3, 4, 8, 12, and 24 h after elective cardioversion of supraventricular tachycardia in 28 patients (eight women, 20 men; mean age, 64 +/- 10 years). Cumulative energy was below 370 J in 17 patients, between 370 and 900 J in eight patients, and 1,020 J in three patients. Serum cTnI was measured using a sandwich immunoenzymologic assay. The detection limit of the assay was 0.35 microgram/L and normal values range from 0.35 to 1.3 micrograms/L. RESULTS: In all but three patients, cTnI remained below 0.35 microgram/L. In these three patients, cTnI ranged between 0.35 and 0.9 microgram/L. There was no correlation between cTnI and the number or the energy of cardioversion. Myoglobin and total CK increased to abnormal concentrations in 11 patients (myoglobin, 630 +/- 190 micrograms/L, and total CK, 2,584 +/- 780 U/L) and reached myocardial infarction-like values in five patients. Modest increases of CK-MB were then also observed. A strong correlation was observed between the total energy of direct current cardioversion and the increase of either myoglobin (r = 0.87; p < 001) or total CK (r = 0.81; p < 001). CONCLUSION: Cardioversion in a clinical setting does not induce elevation of cTnI. Increase in total CK, CK-MB, and myoglobin may be due solely to muscular lesions and is closely related to the cumulative energy delivered.

Troponin I, troponin T, or creatine kinase-MB to detect perioperative myocardial damage after coronary artery bypass surgery.

STUDY OBJECTIVES: To compare cardiac troponin I (cTnI), cardiac troponin T (cTnT), and creatine kinase MB (CKMB mass) in patients with and without new Q wave on the ECG following coronary artery bypass graft (CABG) surgery. PATIENTS: After ethic committee's approval and informed consent, 82 patients, mean age 63+/-10 years, scheduled for CABG were included. INTERVENTIONS: Arterial blood samples were drawn during cardiopulmonary bypass, before, and 6, 12, 24, and 48 h after aortic cross-clamp release. cTnI, cTnT, and CKMB mass were measured. The appearance of new Q wave on the ECG performed preoperatively and 24 h postoperatively was used to assess myocardial lesion independently of biological markers. RESULTS: There were 69 patients without new Q wave on the ECG (group 1) and 13 with (group 2). In group 1, cTnI reached a peak of 2.1 microg/L (median, interquartile range [IQ]=2.4) at 12 h, cTnT increased progressively with a peak of 0.22 microg/L (IQ=0.2) at 48 h, and CKMB presented an earlier peak of 10 microg/L (IQ=6.2) at 6 h. Starting with the same median value, group 2 patients presented significantly higher peaks: cTnI: 17 microg/L (IQ=16) at 12 h; cTnT: 1.4 microg/L (IQ=2.3) at 12 h; and CKMB mass: 74 microg/L (IQ=61) at 6 h. Receiver operating characteristic (ROC) curves were constructed. The area under the curve was 0.90 for cTnI, 0.84 for CKMB, and 0.81 for cTnT (not significant). The best cutoff values to discriminate between group 1 and group 2 patients were determined with the ROC curves: cTnI=5 microg/L; CKMB mass=20 microg/L; cTnT=0.3 microg/L. Sensitivity, specificity, and positive and negative values for cTnI (5 microg/L) were 91%, 82%, 53%, and 98%, respectively. CONCLUSIONS: There was little differences among cTnI, cTnT, and CKMB after CABG to diagnose myocardial damage as assessed by new Q wave on the ECG. There was a trend of cTnI to be a better discriminator than cTnT, but it did not reach statistical significance.

Retrospective risk analysis for early heart-related death after cardiomyoplasty. The Worldwide Cardiomyoplasty Group.

BACKGROUND: Dynamic cardiomyoplasty is an evolving treatment for heart failure that uses an electrically stimulated latissimus dorsi muscle wrapped around the heart to improve cardiac function. Preoperative patient characteristics and deaths after cardiomyoplasty have been recorded during the past 5 years in a cumulative database representing worldwide experience of 42 medical centers. METHODS: Statistical models of hazards (monthly death rates) were used to identify risk factors for transiently increased risk of cardiovascular mortality within 2 months after cardiomyoplasty. RESULTS: Actuarial survival (n = 261) was 88%, 80%, and 76% at 1, 3, and 6 months after cardiomyoplasty, respectively. The peak hazard of 6% dying per month occurred during the first month after the surgical procedure. Lower ejection fraction, increased number of major coronary arteries with > or = 70% stenotic lesions, and lower chronotropic responses during exercise were independent risk factors for the transient increase in early cardiovascular mortality. Early risk of cardiovascular mortality was significantly reduced as centers gained experience with more than 3 patients. CONCLUSION: Early survival after cardiomyoplasty has improved with experience and might be reduced further by preoperative assessments that identify patients at highest risk.

Subdiaphragmatic implantation of implantable cardioverter defibrillator generator.

Despite several improvements in the surgical technique and in the technologic design of cardioverter defibrillators made over the past years, abdominal placement of the generator device, done as Mirowski did it in his first implantation performed in 1980, remains the widely used method. Although smaller defibrillators are available, they remain bulky and are a source of local complications. To prevent such complications and to enhance patient comfort, we performed a subdiaphragmatic implantation in 31 patients.

Electrophysiological properties in man of L 9394, a substance chemically related to amiodarone.

The effects of L 9394, a new compound closely related to amiodarone, were investigated in 44 patients by electrophysiological studies. Thirty two patients were given an intravenous injection of one of the following doses: 0.5, 1, 1.5 or 2 mg/kg. Conduction times of the A-V node (A-H interval) and of the His-Purkinje system (H-V interval) were measured by recording the His bundle potential. Refractory periods were determined by the extrastimulus technique. In the remaining 12 subjects, the action of L 9394 on sinus node was assessed. Sinus node recovery time was measured by rapid atrial stimulation and estimated atrial-sinoatrial conduction time deduced from the effects of atrial premature stimulation on sinus node activity. Results were as follows: (1) A-V nodal conduction was depressed after L9394. The A-H interval increased in direct proportion to the dose. Similarly, the effective and functional refractory periods of the A-V node were prolonged, more markedly after higher doses. (2) No change was shown in the His-Purkinje system. The H-V interval was unaltered. (3) L 9394 had no significant effects on the atrial or ventricular muscle. (4) Sinus cycle length as well as sinus node recovery time did not change significantly. In 7/12 patients, results of premature atrial stimulation suggested the formation of a sinoatrial block.

Safety and tolerability of intravenous cibenzoline for acute termination of spontaneous sustained ventricular tachycardia. Cibenzoline and spontaneous VT.

STUDY OBJECTIVES: To evaluate prospectively, the tolerability and safety of intravenous cibenzoline therapy, for the cardioversion of spontaneous monomorphic ventricular tachycardia (VT). SETTING AND PATIENTS: Between February 1990 and December 1996, fifty-eight patients aged 59+/-10 years old (fifty-three males, five females), with spontaneous VT not causing cardiac arrest, received intravenous cibenzoline. Their underlying heart conditions were: ischemic heart disease [35], dilated cardiomyopathy [14], right ventricular dysplasia [3], hypertrophic cardiomyopathy [1], valvulopathy [2], Fallot's Tetralogy [1] and primary arrhythmogenic disease [2]. The left ventricular ejection fraction was 42+/-13% (range 20%-76%). RESULTS: The mean dose of cibenzoline was 70+/-12 mg. The tachycardia stopped within 6+/-3 min in 47 (81%) patients. Side effects from cibenzoline occurred in two patients. The hemodynamic complications were limited to hypotension, that required vasopressor therapy in one patient. The only apparent proarrhythmic effect consisted of an isolated change in the morphology of the VT, that resolved spontaneously on withdrawal of the drug. No mortality occurred at the hospital. CONCLUSION: With appropriate rules for its administration, intravenous cibenzoline has the potential to become one of the first-line antiarrhythmic drugs, to be used for cardioversion of patients with spontaneous VT.

Mechanical cardiac valve thrombosis in patients in critical hemodynamic compromise.

BACKGROUND: Valve obstruction is a life threatening complication of mechanical valve prosthesis. METHODS: From 1985 to 1993, 29 consecutive patients were hospitalized in our intensive care unit for mechanical prosthetic valve thrombosis (PVT). There were 12 men and 17 women aged 25-75 years (57 +/- 12). Prosthetic valve location was mitral in 14 patients, aortic in 6, aortic and mitral in 9. PVT occurred from 15 days to 174 months (67 +/- 52 months) after surgery. Delay from first symptoms to hospitalization ranged from 1 to 45 days (11 +/- 11). RESULTS: First clinical symptoms were progressive left heart failure in 17 patients, stroke in 6, and chest pain in 6. Furthermore, acute myocardial infarction was later documented in 3. Left heart failure NYHA III-IV was present in 26 patients (90%) on admission and 10 of those were in cardiogenic shock. Anticoagulation regimen was inadequate in 13 cases (45%). It has been recently stopped in 8 patients and incorrectly conducted in 5. Total hospital mortality was 41.3% (12). It was independent of type and position of the valve prosthesis. Diagnosis of PVT was only made at autopsy in 3 patients who died of recurrent myocardial infarction (2) or cardiogenic shock (1). Five further patients died before any surgery could be attempted (cardiac arrest: 2, cardiogenic shock: 3). Valve replacement could be done in 21 cases, 7 of whom were in cardiogenic shock and 9 had severe pulmonary edema. Four patients died after surgery, the operative mortality was 19%. CONCLUSION: PVT remains a serious complication of mechanical heart valve prostheses. Overall mortality rate is high, related to difficulty to diagnosis, delay to hospitalization and severe clinical condition at admission. In our study, operative risk remained acceptable even when the clinical presentation was severe.

Hypertrophic cardiomyopathy and pregnancy.

The case of a young primiparous woman with defibrillator-assisted familial hypertrophic cardiomyopathy (HCM) has led us to review the literature on this pathology, which is exceptional because of its scarcity and the originality of the problems encountered. To our knowledge, this is the first observation ever reported of defibrillator-assisted activation during pregnancy in a woman with HCM. Several questions raised from this particular case, e.g. what are the risks caused by pregnancy in these patients, what is the impact of therapeutics, does the activation of an internal defibrillator involve particular risks, what is the best disposition for delivery and what are the risks for fetuses? We have tried to ask all of these questions, using as exhaustive a literature review as possible.

Defibrillation threshold and electrode configurations: an experimental study testing three configurations in twelve pigs.

OBJECTIVE: The choice between epicardial or subcutaneous patches remains unclear and depends essentially on the team's habits. This study tested how much an additional patch can decrease defibrillation threshold (DFT), and compared a Subcutaneous Array and an epicardial patch. Today most implantable automatic defibrillators have a transvenous endocardial configuration alone but when the DFT remains high an additional patch is necessary. EXPERIMENTAL DESIGN: Three different configurations were tested with biphasic shocks in 12 pigs: Endovenous lead (Endo), Endovenous lead + subcutaneous patch (Endo + SQ) and Endovenous lead + epicardial patch (Endo + Epi). For each animal DFTs were determined in a balanced random order for the 3 configurations. Ventricular fibrillation was induced by pacing (30 Hz, 8 V, for 5 seconds). DFT was accurately measured with the up/down procedure until 3 reversal of defibrillation success or failure occurred. DFTs (mean +/- SD) were extracted and compared using paired t test and analysis of variance. RESULTS: DFTs were 14.6 +/- 11.0 J for Endo and significantly decreased (p < 0.01) when an additional SQ (9.4 +/- 7.2 J) or epicardial patch (8.9 +/- 6.5 J) was added to endovenous lead, without significant difference between Endo + SC and Endo + Epi configurations. CONCLUSIONS: Regarding this important decrease of DFT (respectively -35% for Endo + SC and -39% for Endo + Epi), additional patches should be more often recommended in patients with low safety margin of DFT. In those cases subcutaneous patches should be preferred instead of epicardial patches. Moreover, an additional reason to recommend this attitude could be the possible generator batteries saving.

[Non-pharmacological treatment of atrial fibrillation]. / Traitement non pharmacologique de la fibrillation auriculaire.

Although often denigrated in recent years, antiarrhythmic drugs frequently enable control of atrial fibrillation in patients who are symptomatic or at high risk of complications. In patients resistant to therapy, a number of non-pharmacological options have become available. The choice is no longer limited to his bundle ablation, a method previously at the point of progress but which has gradually given way to more sophisticated and less definitively destructive techniques. Modulation of atrioventricular conduction is currently under development, the feasibility of which has not yet been completely evaluated, but whichmay provide a less radical alternative in selected patients. Restoration of sinus rhythm by electrical cardioversion has benefitted from the advances of cardiac defibrillation in general. The theoretical information which its use implies has improved its efficacy, especially in the case of endocavitary electrical shock. This method can also be employed with automatic implantable defibrillators but using specific algorithms. Atrial pacing is credited with a preventive efficacy but this has never been definitely demonstrated. Research is under way in this domain. Future hopes are also centered on atrial surgery, especially the operation described by Cox which is generally accepted to be effective and which may be adapted medically using endocavitary radiofrequency current. Most of these methods are insufficiently experimented but they should be considered reasonably in particularly symptomatic patients duely informed of the nature of the treatments which are proposed.

[Role of accessory atrioventricular pathways in the genesis of permanent junctional tachycardia. Apropos of 2 cases]. / Le rôle des voies accessoires auriculo-ventriculaires dans la genèse des tachycardies jonctionnelles permanentes. A propos de 2 cas.

Electrophysiological studies were performed in two patients with permanent junctional tachycardias. In both cases, the heart rate was 160/mn and standard ECG showed negative P waves in leads D2, D3 and AVF, isobiphasic or negative P waves in the left precordial leads and a PR interval of 0.12 and 0.13 secs. respectively. The tachycardia started without lengthening of the PR interval or preceding extrasystoles. Shortening of the sinus cycle before the tachycardia was inconstant. The reciprocating mechanism was shown by stimulation studies. Premature ventricular depolarisations not conducted to the atria were capable of terminating the attacks. Proof of His bundle bypass was obtained by the recording of the early atrial activity after ventricular stimulation at the time of His bundle depolarisation. The emergence of retrograde excitation in the left atrium in one of the cases was strongly suggestive of an accessory AV pathway. Atrial participation in the reentry loop was shown in both patients by premature atrial stimulation during tachycardia. This resulted in an earlier appearance of the His potential and QRS complex without affecting the reentrant excitation of the opposite atrium. The present study shows that accessory AV pathway with long retrograde conduction times may play a role in the initiation of permanent reciprocating junctional tachycardia. The functional characteristics of such pathways are suggestive of the presence of tissue with properties similar to that of the AV node. This data adds to our present knowledge of the mechanism of supraventricular tachycardia.