The Surgical Anatomy of Tetralogy of Fallot with Pulmonary Atresia Rather than Pulmonary Stenosis

We examined the pertinent surgical features of the anatomy of 56 hearts having tetralogy of Fallot with pulmonary atresia instead of stenosis, or malformations with pulmonary atresia closely related to tetralogy. We took particular cognizance of the pulmonary arterial supply in 15 hearts in which this was derived through systemic-to-pulmonary collateral arteries, dissecting, as far as possible, the bronchopulmonary segmental distribution of the collateral arteries compared to the intrapericardial pulmonary arteries in 11 of these hearts. Two of the hearts had absence of intrapericardial pulmonary arteries, so that a solitary arterial trunk left the base of the heart. Evidence of an atretic subpulmonary infundibulum was found in 40 of the hearts, while such an infundibulum was lacking in the remainder. The pulmonary atresia was muscular in 43 hearts, valvar in 11, while the pulmonary trunk was absent in the other two hearts. In the hearts with collateral arteries, on average 2.6 collaterals were found in each case, varying from two to five per case. Only one of these arose from a brachiocephalic artery, the others all arising from the descending aorta. The distribution of collateral arteries in two cases was remarkably reminiscent of the arrangement of bronchial arteries. As far as could be judged, 16.5 bronchopulmonary segments on average were supplied in each heart, 5.1 exclusively by collateral arteries, 11.8 by intrapericardial pulmonary arteries and an average of 0.64 segments per case having a shared supply.     

Hemodynamic Deterioration Following Radiofrequency Ablation of the Atrioventricular Conduction System

Radiofrequeucy ablation of the atrioventricular conduction system (ACS) has become an estoblished theTapy for patients with drug refroctory atrial fibrillation. We observed eight patients with hemodynamic deterioration ofteT radiofrequency oblotion of the otTioventTicular conduction system. As we found hemodynamic deterioration related to worsening mitral regurgitation, we compared the clinical history, eiectrophysiologicai, ond echocardiographic dato from the patients with hemodynamic deteriorotion and worsening mitral regurgitation (group 1) to those without hemodynamic deterioration and stable mitral regurgitation after the procedure (group 2). Eight out of 108 patients (7.4%) undergoing ablation of the ACS deteriorated hemodynamically with acute pulmonary edema in three and congestive heart failure in five patients occurring at a mean of 3 and 8 weeks, respectively, after the procedure. Three of these patients were referred for mitral valve surgery. Two patients underwent ablation using a left-sided approach. A right-sided approach was used in five patients. In one patient, a left- and right-sided approach was used. Compared to group 2 patients, group 1 patients had significantly higher left ventricular end-diastolic diameters (64 ± 6 mm vs 56 ± 9 mm) at baseline despite similar fractional shortening (32%± Il% vs 34%± 13%), left ventricular end-systolic diameters (43 ± 9 mm vs36 ± 7 mm) and degree of mitral regurgitation (1.4 ± 1.1 vs 1.4 ±0.7) on echocardiographic analysis. Thus, hemodynamic deterioration together with progression of mitral regurgitation is a potential complication of ablation of the ACS (up to 7.4%). Patients with high left ventricular end-diastolic diameters ond moderate mitral regurgitation at baseline seem prone to this complication.     

Unipolar Waveforms and Monophasic Action Potentials in the Characterization of Slow Conduction in Human Atrial Flutter

Anisotropic propagation may be involved in the development of areas of slow conduction in atrial flutter. We evaluated monophasic action potentials (MAPs) and simultaneous unipolar (0.2–400 Hz) and bipolar electrograms from multiple atrial sites of patients undergoing RF ablation of idiopathic atrial flutter. Nine patients (mean age 46 ± 20 years) with typical atrial flutter (one with both types) were studied. Unipolar electrograms with triphasic complexes of small amplitude and with a slow, negative deviation of the baseline preceding the rS deflection indicated transversal conduction in relation to the orientation of cardiac fibers; smooth rS complexes longitudinal conduction; QS complexes onset of activation; and R complexes end of activation or collision. In all patients with typical atrial flutter, slow conduction occurred in the corridor between the inferior vena cava, the tricuspid annulus, and the coronary sinus. Transversal conduction was observed in this area, whereas the remaining sites showed longitudinal conduction. Anatomically guided RF ablation was successful in five patients. Transversal conduction was recorded in all successful sites. In the patient with atypical atrial flutter, slow conduction was noted in the high lateral right atrium, also exhibiting transversal conduction. Ablation at this area terminated the arrhythmia. All the areas of transversal conduction during flutter displayed longitudinal conduction after restoration of sinus rhythm. MAPs were normal in all patients during atrial flutter and sinus rhythm, even at the areas where transversal conduction was recorded. These findings suggest that anisotropic propagation is involved in the genesis of functionally determined areas of slow conduction during typical atrial flutter.     

Standard Diagnostic Programmed Electrical Stimulation Protocols in Patients with Paroxysmal Recurrent Tachycardias

La Stimulation programée manque une certaine standardisation en ce qui concerne son rôle diagnostique et thérapeutique en matière d'arythmies. Si la sensibilityé et la spécificité de ces tests doivent être considérées comme valables, l'evaluation de divers protocoles de stimulation est obligatoire. Les variables sont nombreuses et peuvent influencer les résultats de ces études.     

Pacemaker Syndrome with AAI Rate Variable Pacing: Importance of Atrioventricular Conduction Properties, Medication, and Pacemaker Programmability

A patient who received an AAI Activitrax rate variable pacemaker for treatment of symptomatic sinus bradycardia is described. disopyramide prolonged the anterograde effective refractory period of the fast conducting atrioventricular (AV) nodal pathway to such an extent, that conduction switched to the slow AV nodal pathway at low atrial pacing rates. This gave rise to symptoms of the pacemaker syndrome during moderate exercise because the paced atrial event was conducted with a long, spike to Q interval with occurrence of the paced atrial event just after the preceding QRS complex. A change of medication solved this problem. Programming a bipolar electrode configuration avoided sensing of far-field QRS signals with the associated problems of resetting the basic pacing interval as well as the upper rate interval. AAI rate variable pacing requires careful evaluation of AV conduction properties, AV conduction intervals as well as the influence of medication to be given. The use of multiprogrammable pacemakers with marker channel capability will significantly facilitate the understanding and resolution of anomalous behavior.     

The Value of DDD Pacing in Patients with an Implantable Cardioverter Defibrillator

Although the beneficial effects of DDD pacing are well known, currently available ICDs provide only fixed rate ventricular antibradycardia pacing. In a consecutive series of 139 patients with ICDs, we have analyzed the need for antibradycardia pacing and the indications for DDD pacing. We also report our initial experience with the Defender 9001 (ELA Medical, France) DDD-ICD. Out of 139 patients, 25 (18%) were in need of antibradycardia pacing. Ten patients already had a pacemaker at the time of ICD implantation and ten other patients had a conventional pacemaker indication at that time. Five patients became pacemaker dependent during a follow-up of 20 ± 8 months. The disorders necessitating pacemaker therapy were high degree AV conduction disturbances in 72%, sick sinus syndrome in 12%, and AF with a slow ventricular response in 16% of patients. Based upon current indications, DDD pacing was indicated in 20 (80%) of 25 patients. The Defender 9001 DDD-ICD (ELA Medical) was used in two patients with ischemic cardiomyopathy and pacemaker syndrome with VVI pacing. Cardiac output during DDD pacing increased by 36% in one patient with an increase in VO₂ max during exercise of 29%. The other patient showed an increase in cardiac output of 50% with DDD pacing, and, while unable to exercise with VVI pacing, had a VO_2max of 24 mL/kg per minute during DDD pacing. Up to 18% of our ICD patients are in need of antibradycardia pacing. Of these pacemaker dependent patients, 80% have an indication for DDD pacing. Our first clinical experience with a DDD-ICD confirms the hemodynamic benefit of AV synchronous pacing in ICD patients with pacemaker syndrome.     

Complete Epicardial Resynchronization Device Implantation in a Patient Who Underwent a Replacement of Mitral and Tricuspid Valve

A 71‐year‐old woman with severe nonischemic dilated cardiomyopathy and low ejection fraction with severe mitral regurgitation and tricuspid regurgitation and pulmonary hypertension underwent multiple valve repairs and cardiac resynchronization therapy implantation with epicardial shock leads. (PACE 2013; 36:e56–e58)     

Cortical correlates of semantic classical conditioning

Event-related potentials to visually displayed pseudowords were registered from 13 individuals. In a differential conditioning paradigm, half of the pseudowords had previously been paired with a painful electric shock (shock words) and the other half had been presented without shock (nonshock words). Participants were asked to decide if the words had been presented during the conditioning phase or not. Larger N100 amplitudes and a more negativegoing slow wave 400–800 ms after word presentation were found for shock as compared with nonshock words. This effect was stronger over the left than over the right hemisphere. This left-lateralized negativity might reflect the activation of a cell assembly representing the memory of the learned word-shock contingency. Furthermore, the increased N100 amplitude elicited by shock as compared with nonshock words may be interpreted as an increased attentive facilitation for aversive pain-related information as a consequence of conditioning.     

Effect of calcium antagonists on acetylcholine-induced contractions in longitudinal smooth muscle strips from sheep duodenum

The effect of several calcium antagonists on acetylcholine-induced contractions has been examined in longitudinal smooth muscle strips from sheep duodenum. Contractions induced by 10^?5 M acetylcholine were inhibited up to 65% in Ca²⁺-free solution and were blocked in the absence of extracellular Ca²⁺ plus 1 mM EGTA; 10 mM lanthanum reduced acetylcholine-induced contractions by 97%: 10⁵m verapamil and W^?4m nifedipine reduced contractions by 58 and 42%, respectively, but sodium nitroprusside did not modify these responses: 10^?4m trifluoperazine inhibited acetylcholine-induced responses by 75%: 10^?2m caffeine produced a contraction; 2 mm procaine antagonized acetylcholine responses by 85%. We suggest that acetylcholine-induced contractions were mediated by extracellular Ca²⁺ that enters through a potential-dependent Ca²⁺ channel by intracellular Ca²⁺ release, probably from sarcoplasmatic reticulum because procaine inhibits the response.     

Analysis of Rabbit Vascular Responses to DBI,an Ingol Derivative Isolated from Euphorbia canariensis

We have analysed the effects of 7,12-O-diacetyl-8-O-benzoil-2,3-diepiingol (DBI), an ingol derivative isolated from E. canariensis, on isometric tension developed by isolated rabbit basilar and carotid arteries. Concentration-response curves to DBI (10^?8 - 3 × 10^?5 m) were obtained cumulatively in both arteries at resting tension and active tone (KC1, 50 mm). At resting tension, DBI induced a concentration-dependent contraction, which was not inhibited in Ca²⁺-free medium. H7 (1-(5-isoquinoline sulphonyl)-2-methylpiperazine dichloride) (10^?4 m) inhibited the DBI-induced contraction both in basilar and in carotid arteries. Calmidazolium (10^?4 m) inhibited the maximum contraction of the carotid artery to DBI, and completely abolished the response in the basilar artery. In pre-contracted basilar arteries DBI induced a concentration-dependent relaxation that was not modified by incubation with N^G-nitro-l-arginine (l-NOARG; 10^?5 m) or indomethacin (10^?5 m). In the carotid artery with active tone DBI induced further contractions, which were not significantly modified by l-NOARG (10^?5 m) and were potentiated by indomethacin (10^?5 m). These results suggest that DBI contracts rabbit basilar and carotid arteries by a mechanism that is independent of extracellular Ca²⁺ and involves the participation both of protein kinase C and of calmodulin. DBI relaxes basilar but not carotid arteries by a mechanism independent of the liberation of nitric oxide and prostacyclin. In the carotid artery prostacyclin but not nitric oxide partially counteracts the contractile action of DBI.