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This open-label, randomised, controlled study is aimed at assessing the effect of pre-treatment with the metabolic agent trimetazidine on the degree of ischaemia during percutaneous transluminal coronary angioplasty (PTCA). Overall 44 patients with one-vessel coronary artery stenosis (> 70%) in the medial part of the left anterior descending artery were included. One group (n = 22) was pre-treated with oral trimetazidine. The other group (n = 22) was the control. All patients (n = 44) were administered aspirin and conventional treatment. All patients underwent PTCA; stents were implanted in 11 trimetazidine patients and in seven control patients. The mean ST-segment elevation during all balloon inflations was significantly lower in the trimetazidine group than in the control group (-1.66 +/- 1.50 mm vs. 3.29 +/- 1.59 mm, p = 0.001). Maximal ST-segment elevations and mean ST elevation values during sequential balloon inflations were also significantly lower with trimetazidine (p = 0.018). The mean amplitude of the T-wave alterations during all balloon inflations was significantly lower with trimetazidine (3.09 +/- 2.39 mm vs. 6.83 +/- 4.31 mm; p = 0.001). Similarly, the maximal amplitude of the T-wave alterations was 4.50 +/- 2.90 mm with trimetazidine vs. 9.25 +/- 4.97 mm in control patients (p = 0.0005). Angina and rhythm disturbances were more frequent in the control group. Time from balloon inflation to onset of angina was 50 +/- 26.2 s with trimetazidine vs. 32 +/- 15.0 s, for control group (p = 0.03). The time to pain relief after deflation was 19.3 +/- 11.4 s with trimetazidine vs. 28.2 +/- 16.8 s (p = 0.001). Trimetazidine administered a few days before PTCA appears to be a cardioprotective agent for the prevention of myocardial ischaemia.

Despite high efficacy of percutaneous coronary intervention (PCI), in-stent restenosis proves to be a significant problem of therapy. Restenosis concerns around 30% of patients. Studies have suggested that restenosis is initiated by cells which participate in intense inflammatory reaction caused by stent implantation. Atherosclerotic plaque rupture during stent implantation and PCI-associated injury of the vessel wall lead to hemorrhage and release of various cytokines. They are probably responsible for quick recurrence of vascular lumen stenosis (restenosis). Interleukin-6 (IL-6) is known as a main pro-inflammatory cytokine, whereas Transformig Growth Factor-β1 (TGF-β1) has anti-inflammatory properties. The study population comprised 36 patients with myocardial infarction treated with PCI with stent implantation. They underwent control coronary angiography after 12 months. At this time plasma concentration of IL-6 and TGF-β was measured in peripheral blood. Serum IL-6 concentration in the analyzed population correlates with lumen loss (p<0.01) and the severity of stenosis (p<0.001). No such correlation was found between serum TGF-β1 concentration and lumen loss (p=NS) or the severity of stenosis (p=NS). The IL-6 plasma concentration may be a marker of in-stent restenosis in patients after PTCA, while the concentration of TGF-β1 is not associated with the occurrence of restenosis at one year of follow-up.

C-reactive protein (CRP) and pentraxin 3 (PTX3) are members of a highly conserved pentraxin superfamily. CRP is synthesized in the liver and may represent a systemic response to local inflammation. PTX3 is synthesized locally at the inflammatory sites and may represent a marker for local inflammation at sites of vessel injury. We compared plasma high-sensitivity CRP (hsCRP) and PTX3 concentrations after bare-metal stent (BMS) and drug-eluting stent (DES) implantation. Fifty-three patients with stable coronary artery disease who underwent percutaneous coronary intervention were divided into 2 groups: 1-24 patients (BMS group) and 2-29 patients (DES group). Patients were scheduled for an elective, 6-month clinical follow-up. Major adverse cardiovascular events (MACEs) (death, myocardial infarction, target vessel revascularization) were assessed. Baseline clinical characteristics were similar in both groups. Patients after BMS implantation had a higher median PTX3 concentration 1.02 ng/mL compared to patients after DES implantation 0.80 ng/mL, P=0.045. Median hsCRP concentrations were similar in both groups: 0.9 mg/L versus 0.89 mg/L, respectively. Six-month follow-up was available in 33 patients. Four out of 33 patients had MACEs during follow-up. The cut-off value to predict MACEs for PTX3 was >1.16 ng/mL (P=0.004) and for hsCRP was >0.95 mg/L (P<0.001). Patients after DES implantation showed significantly lower plasma PTX3 levels compared with patients after BMS implantation. hsCRP showed no difference between the study groups. PTX3 may be a more sensitive marker of local inflammatory response due to vessel injury by BMS than hsCRP. DES implantation may attenuate the early inflammatory response. Lower PTX3 levels may reflect potent anti-inflammatory properties of DES.