Biomedical subjects

F Paganelli

Publications and source records attributed to F Paganelli.

At least 73 records · Page 4Linked to original sources

PubMed1994

The use of HPLC to evaluate the variations of blood coronary adenosine levels during percutaneous transluminal angioplasty.

Although it is well established that adenosine is released during acute ischemia, little is known of the behaviour of adenosine levels following treatment of coronary lesion by percutaneous transluminal coronary angioplasty (PTCA). Using high performance liquid chromatography, we measured intracoronary adenosine levels before and 5 min after PTCA in ten patients with one-vessel disease and a significant (> 70%) coronary stenosis. Adenosine levels decrease in all patients after PTCA. Nevertheless, more studies are now necessary to evaluate the possible predictive value (with regard to restenosis) of coronary adenosine levels after PTCA.

Adenosine↗

PubMed1994

Intrapulmonary artery coiling of a permanent pacing lead.

Intrapulmonary artery displacement of a permanent ventricular lead is reported to be a severe form of lead coiling and is attributed to the failure of the fixation procedure. The lead instability indicated a need for surgical correction.

Equipment Failure↗

PubMed1994

[Percutaneous venoplasty for the implantation of a dual-chamber cardiac pacemaker].

During reoperation for pacemaker implantation, venous catheterisation of the homolateral subclavian vein encountered obstruction at the brachiocephalic vein. Balloon angioplasty of the severe brachiocephalic stenosis was performed via the femoral vein. After repeat subclavian venous catheterisation two new pacing wires could be introduced without difficulty followed by active fixation in the atrium and passive fixation in the ventricular apex. The initial ventricular pacing wire was isolated and respected. The femoral vein approach gave simple and direct access to the site of dilatation at a distance to the operative field which was shielded from an infectious risk. The technique and results of percutaneous venous recanalisation have not been extensively analysed during reoperation for cardiac pacing. In chronic cardiac pacing, the success of homolateral operation despite venous occlusion or stenosis, ensures preservation of the venous capital.

Aged↗

PubMed1993

[Comparison of the efficacy of 2 delayed-action preparations of hydroquinidine and quinidine in the prevention of pacing induced ventricular tachycardia].

The effects of two antiarrhythmic agents, hydroquinidine and quinidine on the prevention of pacing induced sustained ventricular tachycardia (VT) were studied in 14 patients. The underlying cardiac disease was old myocardial infarction (12 patients) or dilated cardiomyopathy (2 patients). Sustained monomorphic VT was induced in 14 patients during the initial electrophysiological study performed at least 48 hours after withdrawal of all antiarrhythmic therapy. The same stimulation protocol including 3 extrastimuli (S2 S3 S4) and 2 paced cycles (600 ms and 400 ms) was repeated at least 48 hours after the administration of 600 mg (2 gelules) per 24 hours of hydroquinidine or 1100 mg of quinidine arabogalactane sulphate, 3 to 4 hours after the last dose. This was an open, randomised, crossed over trial. Irrespective of the result observed with the first antiarrhythmic, used in an order attributed by a randomised table, the other antiarrhythmic was tested. Plasma concentrations were measured during the programmed stimulation test for both drugs. Induced VT was prevented by the two antiarrhythmics in 4 patients (28%). In one patient, VT was prevented by hydroquinidine but not by the quinidine compound, resulting in a prevention rate of 35% for the hydroquinidine. On the other hand, the quinidine compound was a total success in one patient in whom only a partial success was observed with hydroquinidine. VT remained inducible with both antiarrhythmics in 9 patients (64%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

[Pharmacological treatment of ventricular tachycardia].

Pharmacological antiarrhythmic therapy is the treatment of first intention for the prevention of ventricular tachycardia (VT). In sustained VT, electrophysiological investigations without treatment enable the induction of VT, the demonstration of its reproducibility, the confirmation of diagnosis (if necessary), the determination of its mechanism and the choice of treatment. In an effort to standardise the technique, a minimum acceptable protocol of stimulations was agreed upon: at least 2 cycles (600 milliseconds and 400 milliseconds) and 3 extrastimuli (S2, S3, S4). The percentage of inducibility (sensitivity) depends on the underlying heart disease and is of the order of 90-95% in coronary artery disease with a history of infarction. Serial electrophysiological studies show non-inducibility of VT with treatment in 20-60% of cases. This result is influenced by the ejection fraction, the type of ventricular arrhythmia (fibrillation or tachycardia) and the antiarrhythmic agent tested. A Class IA, then a Class IC antiarrhythmics or sotalol (if the ejection fraction is over 40%) are evaluated by this technique. Empiric therapy has no place in the management of malignant poorly tolerated arrhythmias. In recurrent, well tolerated arrhythmias which are non-inducible, treatment may be guided by the results of Holter monitoring, providing the patient has a sufficient number of extrasystoles. Exercise stress tests may be useful in effort or catecholamine-induced tachycardias. There is no consensus about the management of non-sustained VT. When these arrhythmias are associated with syncope or cardiac arrest, programmed ventricular stimulation seems indicated. The choice of antiarrhythmic drugs and their results are reviewed.

Anti-Arrhythmia Agents↗

PubMed1993

[Acute effects of nicardipine on the vascular reactivity of oxygen in patients with respiratory insufficiency and pulmonary hypertension].

Pulmonary vascular response to the inhalation of various concentrations of oxygen (FIO2) was studied under basal conditions and after nicardipine in 10 patients with pulmonary hypertension secondary to chronic bronchitis. Hemodynamic data and blood gases were measured during inhalation of 3 gas mixtures: hypoxia (FIO2 = 0.15), normoxia (FIO2 = 0.21) and hyperoxia (FIO2 = 0.30). Each gas mixture was administered for 20 minutes, initially during an infusion of placebo and then of nicardipine giving a steady plasma concentration of 29 +/- 4 ng/ml. This was obtained by continuous I.V. infusion of 0.06 mg/kg/hour. Under basal conditions with placebo, the heart rate, cardiac output and pulmonary hypertension increased with decreasing concentrations of inhaled oxygen. The systemic blood pressure was unchanged with hypoxia but decreased during hyperoxia. Nicardipine increased the heart rate and the cardiac output but reduced the blood pressure with every inhaled oxygen mixture. The blood pressure was independent of FIO2 and the reduction observed during hyperoxia with placebo no longer occurred with nicardipine. However, the pulmonary hypertension was unaffected. At the dosage used in this study, nicardipine modified the systemic vascular response to oxygen but not the pulmonary vascular response. The vasodilation induced was much greater in the systemic than in the pulmonary circulation. In relation to the absence of significant pulmonary vasodilation, no changes in blood gases, due to a possible pulmonary shunting effect, were observed. At this dosage, nicardipine is ineffective in reducing pulmonary hypertension. However, its systemic hypotensive action may be used in patients with respiratory failure due to chronic bronchitis without deleterious effects on blood gases.

Blood Gas Analysis↗

PubMed1993

[Intravenous and oral propafenone in the treatment and prevention of paroxysmal atrial fibrillation].

The efficacy of propafenone in the treatment of paroxysmal atrial fibrillation was investigated in 16 patients presenting with frequent and/or poorly tolerated paroxysmal atrial fibrillation despite prophylactic treatment in 13 patients. Prolonged atrial fibrillation (> 10 minutes) was triggered in 16 patients following a standard atrial stimulation protocol. Intravenous injection of propafenone (2 mg/kg over 5 minutes) restored sinus rhythm in 12 patients (75%) within 15 minutes after the end of the injection. In five of the 10 patients in whom this was possible, propafenone prevented the induction of atrial fibrillation in response to programmed stimulation by the same protocol. Oral propafenone (900 mg/24 hours) was indicated in 11 patients. The treatment was discontinued in 1 patient due to severe dizziness. Atrial fibrillation recurred in 4 patients 10 to 91 days after treatment began. With a mean follow-up time of 8 months, 4 patients had been brought under control and 2 had relapsed despite a generally beneficial effect. Three patients suffered side effects which did not make it necessary to stop treatment. This study suggests that intravenous propafenone is effective against persistent atrial fibrillation induced by stimulation. Oral propafenone may be useful for the prevention of attacks of recalcitrant paroxysmal atrial fibrillation.

Administration, Oral↗

PubMed1992

[Parkinson syndrome, a possible adverse effect of calcium inhibitors].

The effects of calcium inhibitors are not limited to the muscles and may affect other systems and cause varied side effects. Two cases of Parkinsonian syndrome occurring after starting therapy with calcium inhibitors (verapamil in one case and diltiazem in the other) are reported. Complete regression of the symptoms after withdrawing the drugs was strongly in favour of a causal relationship. The condition could be due to inhibition of the calcium channels in the central nervous system disturbing neurotransmission. This seems to be a rare side effect as there have only been three other reported cases of secondary extrapyramidal syndromes in the literature. However, a Parkinsonian syndrome is very invalidating and clinicians using this family of drugs should be aware of this possible complication.

Aged↗

PubMed1992

[Atrioventricular block at nodal and infrahissian level during atrial tachycardia. Apropos of a case].

The authors report the case of a patient with atrial tachycardia and surface electrocardiographic signs of left anterior hemiblock and complete right bundle branch block with 10/3 atrioventricular block. The regularity of the RR intervals which were an exact multiple of the atrial cycle suggested the absence of a Wenckebach phenomenon. The sequence of atrioventricular conduction cannot be explained by classical models of intranodal conduction. Endocavitary recordings confirmed this hypothesis. They showed block at 2 levels: supra- and infrahisian. The suprahisian block functioned in the 2/1 mode and the infrahisian block in the 5/3 mode without incremental conduction distal to the His potential before the apparition of block. A double zone of intrahisian block could explain the observed sequence of atrioventricular conduction. The absence of Wenckebach phenomenon on the surface ECG during tachycardia could be a sign of infrahisian block. The authors suggest that the association of this sequence of atrioventricular conduction with intraventricular conduction defects is a formal indication for electrophysiological studies.

Aged↗

PubMed1992

[Value and limits of the tilt-test in the etiological diagnosis of transient malaise].

This study was undertaken to assess the usefulness of the head-up tilt test in the diagnosis of vasovagal syncope and to evaluate the indications of this investigation. The test consists in a 30 minute period in the horizontal decubitus position followed by a 60 degrees head-up tilt position for 30 minutes. In the 26 subjects in whom the diagnosis of repeated vasovagal syncope had been made on the basis of typical prodromic symptoms after exclusion of all other causes, the test induced a vasodepressive or vagal reaction in 10 cases (38%) 20 +/- 4 minutes after tilting. In 8 patients in whom the test was performed within 48 hours of their syncopal episode, a similar malaise was induced in 7 cases. Twenty patients with repeated malaise without loss of consciousness had no symptoms during the test which was also negative in 10 normal control subjects. In a group of 27 subjects with unexplained syncope after clinical and paraclinical investigations, the test was accompanied by a malaise on five occasions (19%). Using this protocol, the tilt test had good specificity but moderate sensitivity in the diagnosis of vasovagal syncope. Its sensitivity increased when performed within 48 hours of syncope. It is of no value in the diagnosis of recurrent malaise without loss of consciousness.

Blood Pressure↗

PubMed1976