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The Effect of Intracoronary Lidocaine on Ventricular Arrhythmia in the Infarcted Canine Heart
Author(s) -
Tordjman Therese,
Raeder Ernst,
Lampert Steven,
Lown Bernard
Publication year - 1988
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1988.tb04086.x
Subject(s) - lidocaine , medicine , anesthesia , bolus (digestion) , femoral vein , myocardial infarction , heart rate , cardiology , great cardiac vein , vein , fissipedia , ventricular fibrillation , antiarrhythmic agent , artery , blood pressure , heart disease
The efficacy of intracoronary administration of lidocaine was studied in three groups of dogs with experimental myocardial infarction induced by occlusion of the left anterior descending coronary artery (LAD). Group 1 included 14 anesthetized and group 2, 7 conscious animals to which lidocaine 1.4 μg/kg/minute was administered as an intracoronary infusion. Group 3 consisted of 17 anesthetized dogs that received an intracoronary bolus of lidocaine 40 μg/kg over 30 seconds. In group 1, lidocaine reduced ventricular arrhythmia by 59±30% (p 0.001), whereas systemic lidocaine achieved a reduction by 61±37% (p 0.06). In seven dogs, lidocaine blood levels were measured in the great cardiac and femoral veins. At the end of the infusion the drug concentration was 3.4 ± 2.2 μg/ml in the great cardiac and 1.3±1.1 μg/ml in the femoral vein (p<0.05). The reduction in ventricular arrhythmia correlated with the great cardiac vein lidocaine concentration (r = 0.70; p<0.05), but not with the drug level in the femoral vein (r = 0.06; NS). In group 2, lidocaine was ineffective by both routes of administration. This may have been related to higher sympathetic activity, as suggested by an elevated heart rate in conscious compared to anesthetized animals (186 ±6 vs 164 ± 21 bpm; p 0.0054). In group 3, bolus injections of lidocaine into the LAD reduced ventricular arrhythmia by 66% (p 0.001). We conclude that by perfusing the infarcted zone with lidocaine, a significant antiarrhythmic effect can be achieved with 2% of the systemic dose. This approach may permit abbreviated antiarrhythmic drug testing while avoiding the extracardiac side effects frequently observed with these agents.