ACTIVATED CLOTTING TIMES IN ACUTE CORONARY SYNDROMES AND PERCUTANEOUSTRANSLUMINAL CORONARY ANGIOPLASTY

A discrete fall in the ACT (activated coagulation time) has been obser ved in patients with known activation of the coagulation cascade. Inju ry to the coronary artery resulting in thrombin activation, whether sp ontaneous as in the case of acute myocardial infarction or planned as with percutaneous transluminal coronary angioplasty (PTCA), may theref ore be reflected in a change in ACT values. We reviewed the records of patients undergoing PTCA at St, Luke's Episcopal Hospital/Texas Heart Institute from January 1990 through December 1992 for information reg arding ACT values and clinical events. A total of 469 patients, whose record contained adequate information for study inclusion, were divide d into four separate groups: acute myocardial infarction (group I, n = 62), unstable angina with heparin therapy that was withdrawn at least 4 hr prior to PTCA (group II, n = 102), unstable angina with heparin therapy continued until the time of PTCA (group III, n = 154), and sta ble angina undergoing elective PTCA (group IV, n = 151), Heparin was d iscontinued 12-15 hr after the procedure in all but group I where anti coagulation was often maintained up to 72 hr, ACT values were measured prior to the PTCA procedure (baseline), after the initial heparin bol us of 10,000 U (postheparin) and similar to 12-18 hr after the procedu re (heparin withdrawal). The ''baseline'' ACT was significantly lower in patients with unstable angina (93 +/- 13 sec) or acute myocardial i nfarction (78 +/- 9 sec) who had their baseline value obtained off of heparin therapy than in patients with stable angina (136 +/- 21 sec) o r those receiving heparin at the time of baseline measurement (135 +/- 14 sec, P < 0.001). All patients with unstable coronary syndromes had a blunted response to heparin (group 1-189 sec, group II-221 sec, gro up III-248 sec), Although groups I-III were not significantly differen t compared to one another, each was significantly lower than group IV whose past heparin ACT was 279 sec. Heparin withdrawal ACT values fell within the ranges seen in patients with unstable coronary syndromes u ntreated with heparin in all but group I (whose heparin therapy was co ntinued through the time of the 12-18-hr postprocedure measurement tim e), Recurrent ischemic events were seen with increased frequency (16.6 %) only in patients with unstable angina whose heparin therapy was int errupted prior to PTCA. In conclusion, low baseline ACT values and a b lunted ACT response to heparin are associated with clinical syndromes known to result from thrombus formation, The possibility that the ACT may be of value in reflecting thrombus activity requires prospective e valuation, (C) 1995 Wiley-Liss, Inc.