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  • Title: [Increase in troponin levels after coronary angioplasty (PTCA) in stable angina pectoris].
    Author: Varvarovský I, Brtko M, Branny M.
    Journal: Vnitr Lek; 2004 Mar; 50(3):203-7. PubMed ID: 15125370.
    Abstract:
    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, lesions 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 antiaggregation treatment with acetyl salicylic acid (ASA) and ticlopidine did not lead to a lower incidence of cTnI elevation compared to treatment only with ASA. Heaviness in chest after PTCA has low positive and high negative predictive value for cTnI elevation.
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