Cárdenas M

Language: Spanish
References: 11
Page: 35-38
PDF size: 50.71 Kb.

ABSTRACT

Arrhythmias result from alterations in the electrophysiological properties of the heart: excitability, automatism, conduction, refractary period, and repolarization. These properties depend on the cellular membrane voltage. This voltage is a consequence of macromolecular tunnels permitting the flow of electrical charged particles and the action of the electrogenic pumps against electro-chemical gradients. The voltage alterations in the membrane give rise to arryhthmogenic mechanisms resulting of automatism alterations or disorders in conduction, producing re-entry or circus movement. The medical treatment must be based on a correct integral diagnosis, knowledge of the trigger and maintenance mechanisms of the arrhythmia as well as on the pharmacology of the drug. The antiarrhythmic drug classifications are useful for didactic purposes but may be of little use in medical practice. In supraventricular arrhythmias, the mechanisms are known and can be identified; the re-entry pathways are also known and the electrophysiological mechanisms are normal, therefore the response to the drugs is predictable. In contrast, in ventricular arrhythmias, the mechanisms are variable, the circuits are very difficult to identify and involve healthy and sick tissues. The therapeutic indication is very difficult and incorrect in many occasions. It is possible that, in the future, the study of hereditary arrhythmias could be the basis for a better understanding of these problems.

REFERENCES

1. Zipes DP: A century of cardiac arrhytmias: in search of Jason’s golden fleece. J Am Coll Cardiol 1999; 34: 959-965.

2. Exaire S, Cárdenas M, Rotberg T: Intoxicación quinidínica. Arch Inst Cardiol Mex 1967; 37: 321-329.

3. The cardiac arrhytmicas suppression Trial (CAST) Investigators. Preliminary reports: effect of encainide and flecainide on mortality and a randomized trial of arrhytmias suppression after myocardial infarction. N Engl J Med 1989; 321: 406-412.

4. Vega HA, Felix R: Fisiopatología de los canales iónicos sensibles a voltaje. Avance y Perspectiva 2001; 20: 83-96.

5. Zipes DP, Wellens HJJ: What have we learned about cardiac arrhytmias? Circulation 2000; 102: IV52-IV57.

6. Voughan WSM: A classification of antiarrhytmic actions reassessed after a decade of new drugs. J Clin Pharmacol 1984; 24: 129-147.

7. The Sicilian Gambit: New approach to the classification of antiarrhytmic drugs based on their actions on arrhythmogenic mechanisms. Circulation 1991; 84: 1831-1850.

8. Coumel P, Wilde AAM: Learning from mistakes: The case of clinical electrophysiology. A perspective of evidence-based rhythmology. 9. Circulation 2001;104:845-847

9. Asensio EL, Alvarez MB, Lozano ED, Farías VA, Brugada RR, Brugada TP, Brugada JT: Elevación del ST, bloqueo de rama derecha y muerte súbita: Síndrome de Brugada. Arch Inst Cardiol Mex 2001; 70: 301-311.

10. Amiodarone trials meta-analysis investigators. Effect of prophylactic amiodarone on mortality after acute myocardial infarction and in congestive heart failure: meta-analysis of individual data from 6500 patients in randomized trials. Lancet 1997; 350: 1417-1424.

11. Roy D, Talajic M, Dorian P: Amiodarone to prevent recurrence of atrial fibrillation. Canadian trial of atrial fibrillation investigators. N Engl J Med 2000; 342: 913-920.