CLINICAL STUDIES
Changes of hemostasis, endogenous fibrinolysis, platelet activation and endothelins after percutaneous transluminal coronary angioplasty in patients with stable angina
Markus Borries, MDa,a,
Michael Heins, MD*,
Yuriko Fischer, MDa,
Hugo Stiegler, MDa,
Ansgar Peters, MDa,
Hans Reinauer, MD*,
Frank C. Schoebel, MD,
Bodo E. Strauer, MD, FACCa and
Matthias Leschke, MDa
a Klinik für Kardiologie, Pneumologie und AngiologieHeinrich-Heine-Universität, Düsseldorf, Germany
* Institut für Klinische Chemie und Laboratoriumsdiagnostik, Heinrich-Heine-Universität, Düsseldorf, Germany
Manuscript received September 14, 1998;
revised manuscript received March 15, 1999,
accepted April 22, 1999.
Reprint requests and correspondence: Dr. Markus Borries, Heinrich-Heine-Universität Düsseldorf, Klinik für Kardiologie, Pneumologie und Angiologie, Moorenstr. 5, 40225 Düsseldorf, Germany Markus.Borries{at}uni-duesseldorf.de
OBJECTIVES
This study investigated parameters of endogenous fibrinolysis, activation of coagulation and platelets, and endothelin levels before and after elective percutaneous transluminal coronary angioplasty (PTCA) in patients with stable coronary artery disease (CAD).
BACKGROUND
Abrupt vessel closure is a serious short-term complication after PTCA and is often unforeseeable. Detailed insight into the effect of PTCA on hemostasis, platelets and the release of vasoconstrictive substances, which are among the mainly discussed mechanisms of abrupt vessel closure, is needed to enhance the safety of coronary intervention.
METHODS
Plasma levels of markers of platelet activity, coagulation, endogenous fibrinolysis and endothelins were determined in 20 patients with stable CAD undergoing elective PTCA. The blood specimens were drawn before, immediately after, 1 h after intervention and on the next morning.
RESULTS
All patients showed an initially uncomplicated PTCA. Regarding the efficacy of anticoagulation after receiving 15.000 IU heparin during PTCA, two groups were compared. In eight patients with ineffective anticoagulation production of thrombin and platelet activation directly after and 1 h after PTCA was significantly higher compared with 12 patients with effective anticoagulation. Despite the strong activation of coagulation, only a low fibrinolytic response could be observed. Endothelins rose significantly after PTCA in both groups but stayed longer on higher levels in patients with distinct thrombin generation. Three of the eight patients without sufficient heparin treatment suffered abrupt vessel closure.
CONCLUSIONS
Initially uncomplicated dilation of coronary arteries leads to systemically measurable activation of coagulation and platelets in patients with ineffective doses of heparin and release of endothelins in all patients. Therefore, individual adjustment of anticoagulation and platelet inhibition in combination with effective antivasospastic substances are needed in every patient before, during and after initially uncomplicated PTCA to prevent this serious complication.
|
Abbreviations and Acronyms
| | APTT | = activated partial thromboplastin time | | AT | = antithrombin | | beta-TG | = beta-thromboglobulin | | CAD | = coronary artery disease | | F1+2 | = prothrombin fragment 1+2 | | PAI | = plasminogen activator inhibitor | | PAP | = plasmin- 2-antiplasmin complex | | PTCA | = percutaneous transluminal coronary angioplasty | | TAT | = thrombin-antithrombin complex | | t-PA | = tissue plasminogen activator |
|
|