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.

[Antithrombotic therapy in atrial fibrillation]. / Terapéutica antitrombótica en la fibrilación auricular.

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.