Activated clotting times in acute coronary syndromes and percutaneous transluminal coronary angioplasty

Abstract A discrete fall in the ACT (activated coagulation time) has been observed in patients with known activation of the coagulation cascade. Injury to the coronary artery resulting in thrombin activation, whether spontaneous as in the case of acute myocardial infarction or planned as with percutaneous transluminal coronary angioplasty (PTCA), may there‐fore be reflected in a change in ACT values. We reviewed the records of patients under‐going PTCA at St. Luke's Episcopal Hospital/Texas Heart Institute from January 1990 through December 1992 for information regarding ACT values and clinical events. A total of 469 patients, whose record contained adequate information for study inclusion, were divided into four separate groups: acute myocardial infarction (group I, n = 62), unstable angina with heparin therapy that was withdrawn at least 4 hr prior to PTCA (group II, n = 102), unstable angina with heparin therapy continued until the time of PTCA (group III, n = 154), and stable angina undergoing elective PTCA (group IV, n = 151). Heparin was discontinued 12–15 hr after the procedure in all but group I where anticoagulation was often maintained up to 72 hr. ACT values were measured prior to the PTCA procedure (baseline), after the initial heparin bolus of 10,000 U (postheparin) and ∼ 12–18 hr after the procedure (heparin withdrawal). The “baseline” ACT was significantly lower in patients with unstable angina (93 ± 13 sec) or acute myocardial infarction (78 ± 9 sec) who had their baseline value obtained off of heparin therapy than in patients with stable angina (136 ± 21 sec) or 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, group III‐248 sec). Although groups I‐III were not significantly different 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 untreated with heparin in all but group I (whose heparin therapy was continued through the time of the 12–18‐hr postprocedure measurement time). Recurrent ischemic events were seen with increased frequency (16.6%) only in patients with unstable angina whose heparin therapy was interrupted prior to PTCA. In conclusion, low baseline ACT values and a blunted 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 evaluation.