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Panminerva Medica 1999 December;41(4):295-306


lingua: Inglese

Na+ channel blockers vs class III antiarrhythmic drugs in treating sustained ventricular tachycardia: reversing and preventing as different electrophysiological mechanisms

Masotti C. S., Pierangeli A.

From the Division of Cardiovascular Surgery Department of Surgery University of Bologna, Bologna, Italy


Methods. 169 select­ed ­patients ­with pre­vi­ous AMI and indu­cible sus­tained ven­tric­u­lar tach­y­car­dia (sVT) at elec­tro­phys­io­log­i­cal ­study (EPS) ­were fol­lowed-up pros­pec­tive­ly for recur­rent sVT dur­ing a ­five ­year peri­od. At EPS, ven­tric­u­lar effec­tive refrac­to­ry peri­od (­VERP)/­action poten­tial dura­tion (APd) ­ratio, ven­tric­u­lar con­duc­tion veloc­ity, excit­able gap, ­cycle ­length and QRS dura­tion ­were meas­ured. The ­patients ­with indu­cible sVT at ­basic pro­grammed stim­u­la­tion or ­after iso­pro­ter­e­nol infu­sion (200 µg i.v.) under­went ­drug sup­pres­sion ­tests (ami­od­a­rone, pro­ca­mide, prop­a­nol­ol+pro­ca­mide, ami­od­a­rone+prop­a­phe­none). On ­this ­basis, ­they ­were lat­er ­assigned to 3 dif­fer­ent ­groups: the ami­od­a­rone-treat­ed ­group (n=112), the pro­ca­mide -treat­ed ­group (n=22) and the non­re­spond­er ­group (con­trol ­group, n=35).
Results. After pro­ca­mide infu­sion (100 mg/min for 10 min), at ­fast pac­ing ­drive the ­VERP/APd ­ratio was sig­nif­i­cant­ly ­increased ­from base­line lev­els (p<0.001), the con­duc­tion veloc­ity (Vmax) was sig­nif­i­cant­ly ­depressed (by 25%, p<0.005), the excit­able gap was sig­nif­i­cant­ly ­reduced (p<0.005, 23% of ­cycle ­length) and 71 ­patients ­were no long­er indu­cible; dur­ing ­sinus ­rhythm, Vmax was sig­nif­i­cant­ly ­reduced ­from base­line val­ues (by 14%, p<0.05) ,­VERP was ­only mod­er­ate­ly ­increased and the excit­able gap was slight­ly but sig­nif­i­cant­ly pro­longed (p<0.01, 53% of ­cycle ­length): 147 ­patients ­were ­still indu­cible, with­out sig­nif­i­cant dif­fer­ence ­from base­line val­ues. After ami­od­a­rone infu­sion (300mg/100ml i.v. ­over 10 min), Vmax was sig­nif­i­cant­ly ­reduced ­from base­line lev­els at ­fast pac­ing ­drive (by 21%, p<0.001), ­while the excit­able gap did not ­reduce sig­nif­i­cant­ly (34%) ­from base­line lev­els and 91 ­patients ­were ­still indu­cible; dur­ing ­sinus ­rhythm, con­duc­tion veloc­ity was mod­er­ate­ly ­depressed (by 7%, p<0.05), ­while ­VERP was sig­nif­i­cant­ly ­increased ­from base­line lev­els (p<0.002) and the excit­able gap was sig­nif­i­cant­ly ­reduced (p<0.001, 29% of ­cycle ­length); ­only 35 ­patients ­were ­still indu­cible. In the remain­ing 134 ­patients the ­reset ­curve ­showed excit­able ­gaps=24±3% of the ­cycle ­length. The abso­lute and rel­a­tive val­ues of the excit­able gap meas­ured in the 35 ­patients who ­were ­still indu­cible ­were sig­nif­i­cant­ly high­er ­than ­those meas­ured in ­patients no long­er indu­cible (p<0.05). At fol­low-up, the sVT recur­rence ­rate was: 28% in the ami­od­a­rone-treat­ed ­group, 43% in the pro­ca­mide-treat­ed ­group and 36% in the con­trol ­group: con­trol ­data ­were sig­nif­i­cant­ly dif­fer­ent ­from the for­mer (p<0.05) but not ­from the lat­ter ­group. Significant cor­re­la­tion was report­ed ­between the plas­mat­ic con­cen­tra­tion of pro­ca­mide and ami­od­a­rone and the per­cent­age of reduc­tion of Vmax at ­fast pac­ing ­drive (r=0.79, p<0.05; r=0.83, p<0.01). Resulting var­i­abil­ity ­checked by the anal­y­sis of var­i­ance ­showed no sig­nif­i­cant dif­fer­ence ­between the two ­series (p<0.12638). The devel­op­ment of con­duc­tion veloc­ity depres­sion was clear­ly ­dose-depen­dent. Drug sup­pres­sion ­test ­with pro­ca­mide+prop­a­nol­ol result­ed in non­in­du­cibil­ity of sVT in 115 ­patients, ­with ­strong sig­nif­i­cant dif­fer­ence ­from ­when the ­drug was ­used ­alone (p<0.0015). Better ­results at EPS ­were ­obtained by the com­bi­na­tion ami­od­a­rone+prop­a­phe­none, ­although no addi­tion­al ben­e­fit was report­ed ­when com­pared ­with ami­od­a­rone ­alone.
Conclusions. In con­clu­sion, anti­ar­rhyth­mic ­drugs ­with ­class I ­action may be high­ly effec­tive in ter­mi­nat­ing sVI (lid­o­caine, pro­ca­mide) but may be inef­fec­tive in pre­vent­ing it or ­even arrhyth­mo­gen­ic. According to our ­data, ­drugs ­with ­class III anti­ar­rhyth­mic ­action ­showed sig­nif­i­cant­ly dif­fer­ent behav­ior: ­they ­were ­more effec­tive in pro­long­ing refrac­tori­ness and reduc­ing the excit­able gap at long­er ­cycle ­lengths and, ­thus, ­capable of pre­vent­ing, rath­er ­than ter­mi­nat­ing. Although sta­tis­ti­cal dif­fer­ence was report­ed ­between the ami­od­a­rone-treat­ed ­group and the con­trol ­group, the inci­dence of recur­rent sVT ­remained too ­high to con­sid­er ­drug ther­a­py as a rad­i­cal treat­ment. Surgical abla­tion or implan­ta­tion of an ­ATPM-­AICD ­device is man­da­to­ry ­when pro­grammed stim­u­la­tion is pos­i­tive, ­despite an effec­tive ­drug sup­pres­sion ­test. The pro­phy­lac­tic use of anti­ar­rhyth­mic ­drugs ­with ­class III ­action, how­ev­er, is of ­great inter­est for ­those ­patients who ­have rel­a­tive or abso­lute coun­ter­in­di­ca­tion to ­heart sur­gery.

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