COLLATERAL CHANNELS THAT DEVELOP AFTER AN ACUTE MYOCARDIAL-INFARCTIONPREVENT SUBSEQUENT LEFT-VENTRICULAR DILATION

Objectives. We sought to evaluate the effect of collateral chan nels t hat develop late after a first anterior myocardial infarction on left ventricular dilation and function. Background. Collateral channels in an infarct-related artery may develop long after occlusion of the arte ry. Well visualized collateral channels that appear immediately after a myocardial infarction reduce infarct size and preserve left ventricu lar function. However, the functional significance of collateral chann els that develop late after myocardial infarction has not been evaluat ed in terms of left ventricular function. Methods. We studied 21 patie nts with a first anterior myocardial infarction and an infarct-related artery that remained totally occluded after reperfusion therapy and d id not reopen within 1 month of infarction. No collateral channels wer e observed during the acute period. Patients were classified into two groups according to the extent of collateral formation 1 month after i nfarction: group C, patients with well developed collateral channels ( n = 11), and group NC, patients with absent or poorly developed collat eral channels (n = 10). Infarct size was determined by peak creatine k inase activity and thallium-201 single-photon emission computed tomogr aphy. Global and regional left ventricular function and left ventricul ar volumes were assessed by left ventriculography. These measurements were identical in both groups 1 month after infarction. Left ventricul ar function was reevaluated after 2.12 +/- 0.79 years (mean +/- SD). R esults. There were no significant changes in global and regional left ventricular function between the two groups during the long term follo w-up period, However, the end-diastolic volume index of group NC incre ased from 71 +/- 14 to 85 +/- 19 ml/m(2), whereas that of group C decr eased from 64 +/- 18 to 59 +/- 12 ml/m(2). This important change durin g the long term follow-up period resulted in a significant difference (p = 0.006) in the end-diastolic volume index between the groups 2 yea rs after onset (p = 0.002), whereas 1 month after infarction the diffe rence was not significant (p = 0.36). A similar pattern was observed f or the end-systolic volume index (group C: 38 +/- 16 to 35 +/- 14 ml/m (2); group NC: 45 +/- 12 to 58 +/- 18 ml/m(2), p = 0.018). The power o f the tests to detect the observed differences showing nonsignificant results ranged from 0.05 to 0.38, whereas the power of the tests indic ating a significant difference in end diastolic and end-systolic volum e indexes was >0.88. Conclusions. Collateral channels that develop aft er a myocardial infarction do not reduce the infarct size or prevent l eft ventricular dilation within 1 month of infarction. In contrast, su ch collateral channels prevent subsequent ventricular dilation and the deterioration of left ventricular function over 2 years. How ever, ou r results may have been biased because of the small number of patients .