Elevation of Troponin Following Coronary Angioplasty
(PTCA) in Patients with Stable Angina Pectoris
Varvařovský I.1, Brtko M.2, Branny M.3
1Kardio-Troll, pracoviště invazivní kardiologie, Nemocnice Pardubice, přednosta prim. MUDr. Aleš Herman, Ph.D. 2Kardiochirurgická klinika Lékařské fakulty UK a FN, Hradec Králové, přednosta prof. MUDr. Jan Dominik, CSc. 3Kardiocentrum Nemocnice Podlesí, Třinec, přednosta prim. MUDr. Marian Branny |
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Summary:
Goal: To determine frequency of elevated troponin levels following PTCA in patients with stable
angina pectoris. To identify risk factors related to troponin elevation. Method: Multicentric prospective
study. Troponin I level (cTnI) was determined in a group of 261 patients treated for stable
angina pectoris with coronary angioplasty (PTCA) 12 hours after the intervention. A group of
patients with cTnI levels above the upper level of a normal range was compared to patients
without troponin elevation. Clinical, angiography, and peri-procedural indicators were assessed
and frequency of their incidence in both groups of patients was compared. Results: Elevation of
cTnI levels above the upper levels of the normal range was identified in 32 patients (12.3 %). There
were no differences in age, risk factors for ischemic heart disease (IHD), nor number of impaired
coronary arteries between this group of patients and the rest of them. Associated antithrombotic
treatment (acetylsalicylic acid + ticlopidine 87.5 % vs. 86.9 %, p = NS; low-molecular heparin for
PTCA 46.9 % vs. 57.2 %, p = NS) was comparable in both groups. On angiography, according to
ACC/AHA, lessions were worse in patients with elevated cTnI (2.73 vs. 2.33, p = 0.02). Troponin
elevation was significantly more often connected with calcification of coronary arteries (37.5 % vs.
17 %, p = 0.03), with intracoronary thrombus on angiography (15.6 % vs. 2.2 %, p = 0.05), and with
increased number of implanted stents (1.13 vs. 0.90, p = 0.03). Incidence of peri-procedural complications
(temporarily occluded artery, arterial dissection type C and worse, forced administration
of inhibitors GP IIb/IIIa) was comparable. Chest pain after PTCA was accompanied with
consecutive elevation of cTnI in 40 %, while in absence of chest pain cTnI was elevated only in
8 % of patients. Conclusion: Elevation of troponin after PTCA in stable angina pectoris is significantly
related to angiography findings in treated lesion. Elevation of cTnI is comparable both in
use of unfractionated heparin during PTCA and in use of low-molecular heparin during PTCA.
A combined antiaggreagation treatment with acetyl salicylic acid (ASA) and ticlopidine did not
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