Catheterization and Cardiovascular Diagnosis 34:6-7 (1995)

Editorial Comment

THE ACTS OF CORONARY ANGIOPLASTY

Roger S. Blumenthal, MD and Jeffrey A. Brinker, MD Johns Hopkins Medical Institutions Baltimore, Maryland

Interventional procedures directed at the coronary ar- tery result in a disruption of endothelial integrity, pre- disposing the vessel to acute thrombosis. Systemic anti- coagulation with heparin is generally considered a necessary adjunct to angioplasty and traditionally has been administered in empiric dosages with the caveat that too much predisposes to bleeding, while too little increases the risk of acute ischemic complications [ l ] . While the ideal degree of heparin anticoagulation for interventional procedures has not been established, based on observational experiences with manually determined activated clotting times (ACT) during cardiopulmonary bypass, an ACT of 300 sec has been proposed [2].

The introduction of automated bedside devices facili- tates measurements of ACT and provides a means of titrating heparin therapy during angioplasty . Some con- fusion accompanies the fact that the two principal devices available employ different measurement techniques and yield different ACT values for any level of heparin anti- coagulation. The Hemochron (International Technidyne Corp.) unit is more frequently used and reports values 25-75 sec greater than the HemoTec (Medtronic Hemo- Tec) [3]. Suggested “thresholds” for procedural antico- agulation as measured with both devices have been rising with increasing experience to 350 sec with the former and to 275-300 sec with the latter technique [4,5].

There can be little doubt that measurements of ACT have influenced the way heparin is used for intervention. We have shown that procedural heparin requirements are not reduced when patients come to the laboratory on a heparin infusion, despite partial thromboplastin time (PTT) levels indicative of an “anticoagulated state” [6]. We, and others, have also noted that a significant number of patients do not reach threshold ACT levels after the usual 10,000 units heparin bolus [1,6]. Similarly, the ACT falls below threshold in about one-fourth of patients prior to termination of the procedure, thus requiring ad- ditional heparin [6].

The paper by Wilson et al. [7] suggests that baseline

ACTs may provide information about the thrombotic po- tential of patients. These investigators observed lower ACTs in patients with acute coronary syndromes com- pared to those with stable angina. Furthermore, in pa- tients with unstable angina, there appeared to be a higher incidence of ischemic events if anticoagulation was stopped 4 hr or more prior to angioplasty. It is not clear, however, as to whether a lower baseline ACT predicts underlying hypercoaguability of patients with unstable physiology or whether it is related to prior heparin ther- apy and the depletion of antithrombin 111. A number of physiologic states have been associated with heparin re- sistance in the coronary bypass literature [8]. The impor- tance of routine baseline ACT measurements, which re- mains to be determined, will presumably be based on the ability to risk-stratify patients or predict their procedural heparin requirement.

A third potential role for ACT is in the post-procedural management of interventional patients. Such measure- ments have been used to guide removal of intravascular sheaths and to titrate heparin dosage during the early stages of conversion to oral anticoagulants (e.g., stent patients). There are relatively few data relating the risk of bleeding subsequent to sheath removal (e.g., retro- peritoneal or superficial hematoma formation, pseudo- aneurysm) to ACT [9,10]. In part, this may be due to the lack of correlation between ACT and heparin levels within subtherapeutic and therapeutic ranges [ 1 11. It has been shown that the hospital laboratory APTT and the rapid bedside determined whole blood APTT more closely reflect the degree of anticoagulation at these lev- els [ 1 1,121. Thus, in these situations, the primary advan- tage of the ACT, i.e., its “quick and easy” determina- tion, may be achieved by using the more accurate whole blood APTT or other bedside measurements of APTT post-procedure [12,13].

Thus, while ACT determination seems to have an es- tablished niche in monitoring the “super” anticoagula- tion currently deemed necessary during interventional procedures, its import before and after intervention re- mains to be determined. Other bedside techniques may offer considerable advantage at baseline or at standard therapeutic levels of heparin anticoagulation. Similar in- novations to provide guidance for antiplatelet and non- heparin anticoagulants (e.g., hirudin) therapy in the in- terventional setting would be welcomed.

0 1995 Wiley-Liss, Inc.

ACTS of Coronary Angioplasty 7

transluminal coronary angioplasty. Cathet Cardiovasc Diagn 34:

8. Anderson EF: Heparin resistance prior to cardiopulmonary by- pass. Anesthesiology 64:504-507, 1986.

9. Hillegass WB, Narins CR, Brott BC, Haura EB, Phillips HR, Stack RS, Califf RM: Activated clotting time predicts bleeding complications from angioplasty. J Am Coll Cardiol 23: 184A, February 1994.

10. Popma JJ, Satler LF, Pichard AD, Kent KM, Campbell A, Chuang YC, Clark C, Merritt AJ, Bucher TA, Leon MB: Vas- cular complications after balloon and new device angioplasty . Circulation 88: 1569-1578, 1993.

11. Reiner JS, Coyne KS, Lundergan CF, Ross AM: Bedside moni- toring of heparin therapy: comparison of activated clotting time to activated partial thromboplastin time. Cathet Cardiovasc Diagn

12. Blumenthal RS, Carter AJ, Resar JR, Coombs VJ, (310th ST, Dalal JA, Brinker JB: A comparison of bedside and hospital lab- oratory coagulation studies during and after coronary interven- tion. Cathet Cardiovasc Diagn (in press).

13. Becker RC, Cyr J, Corrao JM, Ball SP: Bedside coagulation monitoring in heparin-treated patients with active thromboembo- lic disease: A coronary care unit experience. Am Heart J 128: 719-723, 1994.

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REFERENCES

1. Ogilby JD, Kopelman HA, Klein LW, Agarwal JB: Adequate heparinization during PTCA: Assessment using activated clotting times. Cathet Cardiovasc Diagn 18:206-209, 1989.

2. Bull BS, Korpman RA, Huse WM, Briggs BD: Heparin therapy during extracorporeal circulation. I . Problems inherent in existing protocols. J Thorac Cardiovasc Surg 69:674-684, 1975.

3. Avendano A, Ferguson JJ: Comparison of hemochron and hemo- tec activated coagulation time target values during percutaneous transluminal coronary angioplasty . J Am Coll Cardiol 23:907- 910, 1994.

4. Ferguson JJ, Dougherty KG, Gaos CM, Bush HS, Marsh KC, Leachman DR: Relation between procedural activated coagula- tion time and outcome after percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 23:1061-1065, 1994.

5 . Narins CR, Hillegass WB, Nelson CL, Hanington RA, Phillips HR, Stack RS, Califf RM: Activated clotting time predicts abrupt closure risk during angioplasty. J Am Coll Cardiol 23:470A, 1994.

6 . Blumenthal RS, Wolff MR, Resar JR, Coombs VJ, Brinker JA: Preprocedural anticoagulation does not reduce angioplasty hepa- rin requirements. Am Heart J 125:1221-1225, 1993.

7. Wilson JM, Dougherty KG, Ellis KO, Ferguson JJ: Activated clotting times in acute coronary syndromes and percutaneous