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Biomedical subjects

N Saoudi

Publications and source records attributed to N Saoudi.

At least 73 records · Page 4Linked to original sources
PubMed1990

Catheter ablation of the atrial myocardium in human type I atrial flutter.

To avoid atrioventricular node-His bundle ablation, catheter ablation of the atrial myocardium was attempted in eight patients with drug refractory type I atrial flutter. In seven of eight patients, a zone of prolongation and fragmentation of the endocardial electrogram was found in the low posterior part of the right atrium. Entrainment of the atrial flutter by high right atrial pacing was accompanied by local recording of second-degree regional block in several atrial sectors but never in the low septal area. We, therefore, hypothesized that the latter represented the critical slow conduction zone of the reentrant flutter circuit. One or two cathodal DC shocks were locally delivered without immediate or late complications. One single ablation attempt was performed in five patients, whereas three patients underwent a second attempt because of early flutter recurrence. Patients were initially discharged without (and after a second session with) antiarrhythmic drugs. After a mean follow-up of 15.5 months (range, 10-23 months), five patients are free of arrhythmias without antiarrhythmic drug therapy. Two patients did not experience atrial arrhythmias while on a drug regimen that was previously found to be ineffective, and a third patient had flutter recurrences. This study suggests that patients with type I atrial flutter referred for atrioventricular node-His bundle ablation may be successfully managed by delivering the ablative shock directly on the atrial arrhythmia substrate.

Adult↗
PubMed1989

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)

Atrial Flutter↗
PubMed1989

Closed-chest ablation of retrograde conduction in patients with atrioventricular nodal reentrant tachycardia.

We applied a new technique of catheter ablation to treat atrioventricular nodal reentrant tachycardia and preserve anterograde conduction, performing this procedure in 21 patients with repetitive episodes of tachycardia refractory to antiarrhythmic drugs. Using atrial activation in the His-bundle lead as a reference, we selected the optimal site of ablation by positioning an electrode catheter so that atrial activation occurred simultaneously with or earlier than the reference activation during tachycardia. At this site, the His-bundle deflection was completely absent or was present only at a low amplitude (less than 0.1 mV). In the majority of patients, these criteria could be met by withdrawing the catheter 5 to 10 mm from the site of the His-bundle recording (adjacent to the reference catheter). Shocks of 160 or 240 J were delivered at this site (cumulative energy [mean +/- SD], 689 +/- 442 J). Treatment resulted in preferential abolition or impairment of retrograde nodal conduction. Anterograde conduction, although modified, was preserved in 19 patients; complete heart block persisted in 2 patients. Sixteen patients remained free of arrhythmia, without medication or implantation of a pacemaker, for a mean follow-up period of 14 +/- 8 months (range, 7 to 42). Tachycardia was not inducible in 14 patients in a follow-up electrophysiologic study performed 3.6 +/- 6 months after the procedure. We conclude that catheter ablation is an effective alternative for the treatment of atrioventricular nodal tachycardia in patients with drug-resistant tachycardia.

Adult↗
PubMed1989

[Autoregulation of ventricular parasystole. The triphasic phase response curve].

In the previously published examples where parasystolic rhythms were modulated and entrained, the electrotonic events came from the action potentials arising from the surrounding myocardium. In the two present cases, a ventricular parasystolic focus was entrained by the electrotonic image of the action potentials resulting from its own discharges. The electronic transmission across the protection zone being delayed, the resulting ventricular action potentials were able to automodulate, and entrain, the parasystolic focus according to a triphasic phase response curve. The development of the theory of parasystolic modulation may explain certain bizarre EKG recordings.

Action Potentials↗
PubMed1988

Ventricular tachycardia with alternating cycle lengths: self-entrainment of parasystolic rhythm?

A patient had ventricular tachycardia with cycle lengths consistently varying between 400 and 490 ms. Arrhythmias with a similar electrocardiographic pattern had been thought to result from the regular activity of an automatic pacemaker with either 3:2 exit block of the Wenckebach type or alternation in exit conduction times. However, the findings in our patient could also be explained by postulating the existence of modulated ventricular parasystole having 3:2 exit block or with alternating (short-long) exit conduction times. In either case, the action potentials elicited by the parasystole must have reached (with variable delays) the ventricular tissue beyond the zone of protection to produce electrotonic depolarizations which, in turn, were reflected back to the ectopic focus itself. This resulted in runs of 2:3 or 2:2 "self-entrainment" of the parasystolic pacemaker. Similar phenomena have been produced in biologic and mathematical models of modulated parasystole.

Action Potentials↗
PubMed1988

[Bundle branch reentry tachycardia: a possible mechanism of flecainide proarrhythmia effect].

A 42-year old man with non-obstructive myocardiopathy complicated by paroxysmal atrial fibrillation treated with amiodarone (200 mg per day) received flecainide in daily doses of 400 mg for undocumented palpitations. Ten syncopes and numerous malaises occurred during the following two months. Electrophysiological testing was performed, showing prolongation of HV to 80 ms and discreet widening of QRS to 100 ms. Programmed atrial stimulation failed to demonstrate a second degree subnodal block and to induce tachycardia. In contrast, ventricular stimulation elicited a critical SH delay (260 ms), always followed by a left delay-type complex preceded by His bundle deflection which suggested reentry within the His-Purkinje system. Three extrasystoles on imposed rhythm started sustained ventricular tachycardia with the same 270 ms cycle morphology and reproducing the symptoms. Each V wave was preceded by an H potential, with HV varying from 100 to 300 ms. Three weeks after flecainide was discontinued, HV was 60 ms, and no ventricular tachycardia could be triggered by programmed stimulation. The patient remained symptom-free throughout the 5-month follow-up. This case illustrates the proarrhythmic effect of the flecainide-amiodarone combination. The mechanism of provoked tachycardia probably involves ventricular reentry through the His bundle branches, induced by a critical depression of conduction below the His bundle.

Amiodarone↗
PubMed1987

Percutaneous transluminal balloon valvuloplasty of adult aortic stenosis: report of 92 cases.

Percutaneous transluminal balloon valvuloplasty was attempted in 92 adult patients with severe calcific aortic stenosis. The mean age was 75 +/- 11 years (range 38 to 91) and 35 patients were more than 80 years old. Most of the patients were severely disabled; 66 were in New York Heart Association functional class III or IV, 27 had syncopal attacks and 21 had severe angina pectoris. Because of unacceptably high surgical risk or contraindication to thoracic surgery, 42 patients could not be considered for valve replacement. Other patients either were in a category of high operative risk or refused the surgical intervention. Valvuloplasty was performed by way of the femoral route (82 patients) or the brachial route (10 patients). Catheters of size 15, 18 and 20 mm were successively placed across the aortic valve and three inflations were usually done with each of them, lasting 80 seconds on average, until a decrease in peak to peak systolic pressure gradient to 40 mm Hg or less was attained, a result considered satisfactory. The inflated balloons were not totally occlusive in most cases and clinical tolerance of inflation was good. Valvuloplasty resulted in a reduction of mean systolic gradient from 75 +/- 26 to 30 +/- 13 mm Hg (p less than 0.001); the final gradient was less than 40 mm Hg in 78 patients. Mean calculated aortic valve area increased from 0.49 +/- 0.17 to 0.93 +/- 0.36 cm2 (p less than 0.001). Immediately after the procedure, ejection fraction increased from 48 +/- 16 to 51 +/- 16% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Unusual electrocardiographic patterns of modulated parasystole.

Modulation of a parasystolic rhythm implies that the latter is affected by nonparasystolic beats in predictable ways. When modulation occurs the diagnosis of ventricular parasystole cannot be made by applying the well-known 'classical' criteria. This report deals with clinical tracings from three cases having modulated parasystole with unusual characteristics. Case 1 showed a 24-hour diurnal variability of parasystolic modulation characterized by its occurrence during only part of the period of sleep (from 1 to 5 am). In case 2, modulated ventricular parasystole produced episodes of intermittent ventricular bigeminy with fixed coupling resembling those attributed to a reentry mechanism. The proper diagnosis was made when the sinus cycle length changed abruptly. Finally, in case 3, the idionodal rhythm from a patient with complete AV block was shown to be not only parasystolic, but also modulated. In addition, the idionodal rhythm was entrained (captured) in a concealed fashion by paced beats so that the post-pacing events did not conform with those occurring during overdrive pacing of parasystolic nonmodulated, or nonparasystolic, idionodal rhythms. These findings constitute the clinical counterpart of experimental studies performed with microelectrode techniques.

Adult↗
PubMed1987

[Circadian variations and modification of ventricular parasystole].

As shown by Jalife and Moe, brief subliminar depolarizations induced upstreams of the protection zone may predictably modify the discharge from a parasystolic focus. In the biological and mathematical models of parasystole, numerous arrhythmias which do not fulfil the classical criteria of parasystole have been identified, some of them even mimicking a re-entry mechanism. In this paper we report the electrocardiograms of three patients in whom an electrotonic modulation mechanism may be involved. In the first patient the classical pattern of continuous parasystole without exit block was observed throughout daytime. However, between 1 and 5 a.m. non parasystolic beats lengthened or shortened the parasystolic rhythm, depending on their time-related position in the cycle. Later, the usual continuous parasystole pattern reappeared. In the second patient the patent 1:1 entrainment of parasystole by sinus beats resulted in long episodes of ventricular bigeminy with fixed coupling. A sudden slowing down of the cardiac rate disrupting the harmony of the two rhythms and, consequently, the regular entrainment of the ectopic focus, shortened the parasystolic cycle and suppressed bigeminy. In the third patient ventricular stimulation produced a hisian parasystolic rhythm resembling intermittent parasystole on surface ECG. It is concluded that, as suggested by experimental models, many disorders of cardiac rhythm which do not fulfil the criteria of parasystole can be explained in terms of modulated parasystole.

Adolescent↗
PubMed1987

[Pharmacological bases of the treatment of cardiac insufficiency].

Congestive heart failure is a complex physiopathological state where both myocardial hypo-contraction and excessive peripheral vasoconstriction lead to lower cardiac output. The increase in cytosolic calcium concentration triggers the contractile processus. Digitalis inhibits the Na+/K+ ATPase enzyme and indirectly increases intracellular calcium concentration. beta 1 agonists increase the synthesis of cAMP-dependent protein kinase and hence the recruitment of new receptor-operated calcium channels which increase the calcium influx and the mobilization from its intracellular storage sites. Vascular smooth muscle contraction occurs with calcium influx into the cell resulting from various receptor activation. In congestive heart failure, activation of the sympathetic nervous system and of the renin-angiotensin system leads to neurohumoral-induced peripheral vasoconstriction. Renal effects of angiotensin II and aldosterone are responsible for sodium and water retention. alpha 1-blocking agents are drugs that block competitively the catecholamines effects on vascular receptors. Angiotensin I-converting-enzyme inhibitors block the formation of the key-element of the system: angiotensin II. Both alpha 1-blocking agents and converting-enzyme inhibitors show vasodilatator effects and acutely improve hemodynamic status of patients with congestive heart failure. Converting-enzyme inhibitors exhibit specific improvement of intrarenal hemodynamics and do not induced sodium and water retention in longterm therapy.

Calcium↗
PubMed1987

[Gap, phase III and IV block and supernormal conduction of the right bundle branch].

A recent review of the literature corroborated that several factors explained why supraventricular impulses falling gradually earlier in the cycle could traverse the His-Purkinje system while other impulses occurring later could fail to do so. The present report deals with the coexistence (in the same patient) of three distinct mechanisms whereby progressively more premature impulses could be "unexpectedly" conducted. Phase III left bundle branch block coexisted with the following conduction disturbances in the right bundle branch; late "pseudosupernormal" conduction sandwiched in between periods of phase III and phase IV block; intermediate "pseudosupernormal" conduction resulting from the so-called type 2 gap, during which propagation occurred, but with H-V intervals longer than later in the cycle; early "true" supernormal conduction (related temporarily to the end of the T wave) exposed when a premature ventricular beat reached the affected zone in a concealed retrograde fashion. These findings show how, with block late in the cycle, conduction in earlier part of the cycle was not always due to "true" supernormal conduction.

Aged↗
PubMed1987

[Systemic and coronary hemodynamic effects of intravenous nicardipine at rest and in ischemia induced by rapid atrial stimulation].

The systemic and coronary haemodynamic effects of intravenous nicardipine were investigated in 10 patients with a more than 70 p. 100 stenosis of the left coronary artery. Two brief atrial pacing tests (ST1 and ST2) were performed. ST2 was performed 30 minutes after an intravenous injection of nicardipine 2.5 mg over 5 minutes. Nicardipine produced a 25 p. 100 decrease in ventricular systolic pressure and a substantial increase in cardiac index (from 2.74 +/- 0.48 to 3.46 +/- 0.35 l/min/m2, p less than 0.001). Measurement of the coronary flow rate by the thermodilution method showed a 40 p. 100 increase in sinus blood flow while coronary resistance decreased not only in territories with normal supply but also in myocardial territories distal to the coronary stenosis (from 2.76 +/- 2.3 to 1.83 +/- 1.5 mmHg/ml, p less than 0.02). With the same paced heart rate the ventricular function parameters were significantly improved during ST2 (cardiac index ST2 3.56 +/- 0.65 vs ST1 2.8 +/- 0.48, p less than 0.001; dp/dt max ST2 2143 +/- 369 vs ST1 1874 +/- 301 mmHg/sec, p less than 0.05), reflecting a lower degree of myocardial ischaemia. This was confirmed by the lower amplitude of electrocardiographic depression and by a higher lactate extraction coefficient (LE ST1 6 +/- 7 p. 100 vs LE ST2 12 +/- 12 p. 100, p less than 0.05). Mean arterial blood pressure and coronary sinus blood flow rate values were identical during the two atrial pacing tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Comparison of the effects of ajmaline and procainamide in the diagnosis of paroxysmal atrioventricular block].

14 suspected of having a paroxystic atrio-ventricular block underwent a complete electrophysiological exploration including an ajmaline test. It was administered at the standard dose of 1 mg/kg at the rate of 1 mg/s. In order to evaluate a replacement test, an equivalent dose of procainamide was injected at the same rate (10 mg/kg, 10 mg/s) a few hours later. In 4 out of 14 cases the ajmaline test was positive. In only one patient, procainamide was able to demonstrate a sub-nodal block. The maximal lengthening of HV occurred at an earlier time after ajmaline than after procainamide (2.2 +/- 0.75 min. versus 4.1 +/- 1.59 min, p less than 0.02) and certainly more clear-cut (MaxHV = 73.5 +/- 12.9 ms versus 59.5 +/- 12.1 ms, p less than 0.01). The lengthening of HV after administration of these two products was significantly correlated but always markedly lesser with procainamide. In conclusion, the procainamide is less sensitive than the ajmaline test in the positive diagnosis of paroxystic atrio-ventricular blocks concerning absolute criteria in the positive diagnosis as well as relative criteria such as a definite lengthening of HV with ajmaline.

Aged↗
PubMed1986

Percutaneous transluminal valvuloplasty of acquired aortic stenosis in elderly patients: an alternative to valve replacement?

Percutaneous transluminal balloon catheter aortic valvuloplasty (PTAV) was carried out in three elderly patients with acquired severe aortic valve stenosis. Transvalvular systolic pressure gradient was considerably decreased at the end of the procedure, during which there were no complications. Increased valve opening was confirmed by angiography and echocardiography. Subsequent clinical course showed a pronounced functional improvement. PTAV is recommended as a simple alternative to aortic valve replacement in elderly and/or high-risk patients.

Aged↗