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J Farré

Publications and source records attributed to J Farré.

At least 55 records · Page 3Linked to original sources
PubMed1996

Current role and future perspectives for radiofrequency catheter ablation of postmyocardial infarction ventricular tachycardia.

The most common substrate for ventricular tachycardia (VT) is a postmyocardial infarction (MI) scar. Radiofrequency catheter ablation (RFCA) in post-MI VT faces clinical, electrophysiologic, anatomic, and methodologic difficulties not found in many other human tachycardias. The pathophysiologic understanding of post-MI VT is incomplete; this influences the process of selecting RFCA target sites, which is time consuming, demands catheter stability, and has low sensitivity and predictive value for VT interruption by RF current. Improving and simplifying the methodology of RFCA in post-MI VT is badly needed. We review the pathophysiology of post-MI VT from the data reported on endocardial, epicardial, and intramural ventricular mapping obtained either intraoperatively or in a Langendorff perfused set-up in hearts from transplanted patients. From these studies we conclude that (1) some post-MI VT cases are not amenable to RFCA (reentry around the scar, VT having a subepicardial or deep intramural substrate, or a wide, extensive, subendocardial intrascar area of slow conduction); and (2) searching for the endocardial exit is advantageous for selecting the RFCA targets. We also comment on a new self-reference mapping catheter that allows the recording of high gain, noise-free, unfiltered and filtered unipolar signals as well as unipolar pacing. Among the unresolved issues in these patients is the meaning of fast nonclinical VT induced after successful RFCA of the clinical VT, which may explain why a substantial number of these patients still receive an implantable cardioverter-defibrillator.

Catheter Ablation↗
PubMed1996

[Antithrombotic therapy in atrial fibrillation].

The known risk of embolic events in patients with recurrent or chronic atrial fibrillation makes it mandatory to recommend oral anticoagulation in patients with rheumatic mitral valve disease, specially mitral stenosis to maintain an INR between 2.0 and 3.0. If despite this treatment recurrent embolism occurs, the dose of oral anticoagulants should be increased (INR between 2.5 and 3.5) or dipyridamole (200 to 400 mg/day) or aspirin (160 to 320 mg/day) should be added to dicoumarinic drugs. In patients that must be cardioverted either electrically or pharmacologically and who have been on atrial fibrillation for more than 2 days, oral anticoagulation should be maintained for 3-4 weeks before cardioversion and for 3-4 weeks after regaining sinus rhythm. Transesophageal echocardiography may enable us to identify the group of patients with low risk for an immediate cardioversion. In patients under 60 years of age with atrial fibrillation and no evidence of associated cardiovascular abnormality (lone atrial fibrillation) the embolic risk is very low and antithrombotic therapy is probably not needed. In subjects over 60 years of age with a low risk profile (absence of previous stroke, heart failure or systemic hypertension) aspirin (300-325 mg a day) seems to offer sufficient protection against embolic events. In patients at a higher embolic risk (history of previous cerebral ischemic attacks, heart failure of left ventricular dysfunction, systemic hypertension) oral anticoagulation unless contraindicated, should be recommended (INR 2.0-3.0). The role of other antithrombotic agents such as ticlopidine or triflusal to prevent embolic events in patients with atrial fibrillation is unknown.

Atrial Fibrillation↗
PubMed1991

Mechanical cardiac valve thrombosis. Is thrombectomy justified?

To determine the incidence and results of the treatment offered to acute thrombotic obstructions of mechanical valvular prostheses, we have reviewed a series of 3,637 consecutive hospital survivors who, between January 1970 and September 1990, underwent single mitral or aortic and double mitroaortic valve replacements (MVR, AVR, and DVR, respectively). The cumulative follow-up in these patients was 22,783 years (mean, 7.2 years; range, 0.6-19 years). Sixty-five patients (24 MVR, 13 AVR, and 28 DVR) experienced 72 thrombotic prosthetic obstructions (42 mitral and 41 aortic prostheses) at a mean interval of 3.4 years (range, 0.6-14 years) after the operation. The actuarial prosthetic thrombosis free estimates were 96 +/- 0.9% for MVR, 97 +/- 0.9% for AVR, and 96 +/- 0.8% for DVR (all NS). Mortality associated with prosthetic thrombosis was 25% (four in the MVR group, five in the AVR group, and seven in the DVR group). Fifty-seven patients (22 MVR, 12 AVR, and 23 DVR) underwent a total of 62 reoperations, with a hospital mortality of 17% (two MVR, four AVR, and four DVR). In 37 of the latter patients (20 MVR, three AVR, and 14 DVR), we performed valve replacement (31 mitral prostheses and 14 aortic prostheses), with a hospital mortality of 16% (six of 37) and only one case of subsequent rethrombosis (actuarial rethrombosis free estimate, 96 +/- 3.6%). Conversely, five of the 27 patients (actuarial rethrombosis free estimate, 41 +/- 20%) (two MVR, 11 AVR, and 14 DVR) (seven mitral prostheses and 21 aortic prostheses) whose prosthetic valves were debrided developed rethrombosis during follow-up (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1990

Mechanism of action of sotalol in supraventricular arrhythmias.

Sotalol has a virtually unique antiarrhythmic profile in that it combines the properties of the Class II beta-blocking agents with the Class III properties that prolong repolarization. The Class II action exerts a marked effect on atrioventricular nodal conduction and makes sotalol a suitable drug for the treatment of adrenergic-induced supraventricular tachycardias. Sotalol helps to prevent or slow supraventricular arrhythmias involving the atrioventricular node as part of a reentrant pathway and also helps to control the ventricular rate during supraventricular arrhythmias conducted to the ventricles over the normal atrioventricular pathway. The capacity of conduction of accessory pathways is diminished by sotalol, thereby decreasing the ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome. The effects of sotalol on conduction of the cardiac impulse (Class I effects) have been probably overlooked and those on true refractoriness (Class III effects) overestimated.

Heart Conduction System↗
PubMed1989

[Predictive value of neopterin in boutonneuse fever].

Neopterin is an intermediate purine metabolite which can be determined in serum and has been shown to be elevated in processes that stimulate cell mediated immunity. Neopterin serum levels have been measured in 37 patients diagnosed of boutonneuse mediterranean fever. Serum titers were higher during the acute phase than during the convalescence in 97.2% of patients. Neopterin levels normalized as the disease improved clinically. On the other hand, the highest levels were found in patients with a torpid evolution and appearance of complications.

Adult↗
PubMed1987

Arrhythmogenic effects of antiarrhythmic drugs in patients with an old myocardial infarction and asymptomatic ventricular ectopic activity as studied by programmed electrical stimulation.

In 22 patients with a previous myocardial infarction and documented Lown class II to IV asymptomatic ventricular arrhythmias, the arrhythmogenic effect of mexiletine (18 patients) and propafenone (10 patients) has been assessed by programmed electrical stimulation. Ventricular arrhythmias induced during the basal study were: repetitive ventricular responses (RVR) (11/22, 50%), nonsustained ventricular tachycardia (VT) (3/22, 14%), sustained VT (7/22, 32%) and ventricular fibrillation (VF) (1/22, 4%). The induction of sustained VT or VF increased to 50% after mexiletine and to 80% following propafenone. An arrhythmogenic effect was found in 7/11 patients (64%) without VT at the control study (P = 0.004). One patient of this group spontaneously developed sustained VT both after mexiletine and propafenone. Only 1/8 patients (13%) with sustained VT/VF at the basal study had RVR after drug administration. The R-R interval of sustained VT at the basal state tended to be faster than that after the drugs (260 +/- 60 ms vs 293 +/- 56 and 332 +/- 77 ms for mexiletine and propafenone, respectively) (P = 0.052). Statistical significance was only reached in the propafenone group (P = 0.03). Facilitation of VT induction after antiarrhythmic drugs is most likely due to a modest lengthening of refractoriness in contrast with a more evident reduction in conduction velocity within the reentry pathway. Our study illustrates that treating asymptomatic ventricular ectopic activity in patients with an old myocardial infarction may be dangerous and that antiarrhythmic drugs show a significant arrhythmogenic potential at least in the laboratory setting.

Adult↗
PubMed1981

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.

Adult↗
PubMed1980

Initiation and termination of ventricular tachycardia by supraventricular stimuli. Incidence and electrophysiologic determinants as observed during programmed stimulation of the heart.

In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longst ventricular premature stimulus interval resulting in tachycardia and th duration of the basic cycle length of the paced ventricular rhythm) above 54 percent. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54 percent or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

Adult↗
PubMed1980

Effect of drugs in the Wolff-Parkinson-White syndrome. Importance of initial length of effective refractory period of the accessory pathway.

The effect of procainamide, quinidine, ajmaline and amiodarone on the effective refractory period of the accessory pathway in the (A-V) anterograde and retrograde directions was studied in relation to the length of this period before drug administration. All patients had the Wolff-Parkinson-White syndrome and were studied with intracavitary recordings and programmed electrical stimulation of the heart using identical basic cycle lengths and test stimulus intervals before and after drug administration. The patients were separated into two groups, those in whom the effective refractory period of the accessory pathway was 270 ms or greater (Group 1) and those in whom it was less than 270 (Group 2). In the anterograde direction the magnitude of increase in the length of the effective refractory period of the accessory pathway after drug administration was related to its initial length. Only modest lengthening of this period could be accomplished in patients with an initially short period. In evaluating the effect of drugs in patients with the Wolff-Parkinson-White syndrome, the role of the initial length of the effective refractory period of the accessory pathway should be considered.

Accessory Nerve↗