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Myocardial damage, coagulation activity and the response to thrombin inhibition in unstable coronary artery disease.

Oldgren, Jonas (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper,Kardiologi
Siegbahn, Agneta (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper
Grip, Lars, 1952 (författare)
Gothenburg University,Göteborgs universitet,Hjärt-kärlinstitutionen,Cardiovascular Institute
visa fler...
Linder, Rikard (författare)
Karolinska Institutet
Thygesen, Kristian (författare)
Wallentin, Lars (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper
visa färre...
 (creator_code:org_t)
2004
2004
Engelska.
Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 91:2, s. 381-7
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Unstable coronary artery disease is in most cases associated with plaque rupture, activation of the coagulation system and subsequent intracoronary thrombus formation which may cause myocardial cell damage. The aim of the present analysis was to assess the relation between troponin T, markers of coagulation activity, i.e. prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin and D-dimer, and ischemic events, i.e. death, myocardial (re-)infarction or refractory angina. 320 patients with unstable coronary artery disease were randomized to 72 hours infusion with inogatran, a low molecular weight direct thrombin inhibitor, or unfractionated heparin. Patients with elevated troponin levels had higher levels of prothrombin fragment 1+2, soluble fibrin and D-dimer before, during, and at 24 hours after cessation of anticoagulant treatment. These troponin-positive patients tended to have worse short-term clinical outcome, without relation to markers of coagulation activity. Troponin-negative patients with unchanged or early increased thrombin generation during treatment had a cluster of ischemic events within 24 hours after cessation of the study drug. The 30-day ischemic event rate was 19 % in troponin-negative patients with unchanged or early increased prothrombin fragment 1+2, and 5.7 % in patients with decreased prothrombin fragment 1+2, p=0.006, and similarly 15 % in troponin-negative patients with unchanged or early increased thrombin-antithrombin complex and 4.5 % in patients with decreased thrombin-antithrombin complex, p=0.02. In conclusion, in unstable coronary artery disease a troponin elevation indicates higher risk and higher coagulation activity. However, among the troponin negative patients, with a lower risk and lower coagulation activity, a part of the patients seem to be non-responders to treatment with a thrombin inhibitor expressed as unchanged or raised coagulation activity and a raised risk of ischemic events early after cessation of treatment.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kardiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)

Nyckelord

Adult
Aged
Biological Markers
blood
Blood Coagulation
drug effects
Coronary Arteriosclerosis
drug therapy
pathology
physiopathology
Glycine
administration & dosage
analogs & derivatives
pharmacology
Heparin
administration & dosage
Humans
Middle Aged
Myocardial Ischemia
blood
prevention & control
Piperidines
administration & dosage
pharmacology
Predictive Value of Tests
Risk Factors
Thrombin
antagonists & inhibitors
biosynthesis
Thrombophilia
blood
Treatment Failure
Treatment Outcome
Troponin T
blood
Adult

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