Rafal Wojnar

Trimetazidine Limits the Effects of Myocardial Ischaemia During Percutaneous Coronary Angioplasty

Summary 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 ± 26.2s with trimetazidine vs. 32 ± 15.0s, for control group (p = 0.03). The time to pain relief after deflation was 19.3 ± 11.4s with trimetazidine vs. 28.2 ± 16.8s (p = 0.001). Trimetazidine administered a few days before PTCA appears to be a cardioprotective agent for the prevention of myocardial ischaemia.

Outcomes of primary coronary angioplasty and angioplasty after initial thrombolysis in the treatment of 374 consecutive patients with acute myocardial infarction

BACKGROUND In patients with acute myocardial infarction (MI), the efficacy of thrombolysis is low. Angioplasty after failed thrombolysis (rescue percutaneous coronary angioplasty [PTCA]) has been associated with an increase in the incidence of inhospital complications. It has been proposed that these complications result from the procedure itself. Thus, the aim of this study was to compare the efficacy, inhospital complications, and mortality rate of patients with MI who are treated with primary PTCA and PTCA after initial thrombolysis (rescue or immediate rescue) in an experienced clinical center specializing in percutaneous coronary interventions. METHODS AND RESULTS The study group consisted of consecutive patients with MI treated with primary PTCA (n = 195) or PTCA after initial thrombolysis (n = 179). The study was performed in a referral center with a 24-hour catheter-laboratory service. The success rate of the procedure was 90.5% and 88.2% in the PTCA after initial thrombolysis group and primary PTCA group, respectively. The groups did not differ in the frequency of reocclusion, emergency surgical revascularization (coronary artery bypass grafting), or stroke. In patients without cardiogenic shock, the inhospital mortality rates were 3.2% and 0.6% in the rescue and immediate rescue group and primary PTCA group, respectively (not significant). In a subgroup of patients with cardiogenic shock, the mortality rate was 36.0% in the initial thrombolysis PTCA group and 30.8% in the primary PTCA group. However, after successful PTCA in this subgroup, the mortality rate dropped to 18% and 10%, respectively. CONCLUSIONS After initial thrombolysis, PTCA is safe, effective, and likely to restore grade 3 Thrombolysis In Myocardial Infarction flow in about 90% of patients. When available, immediate rescue PTCA should be performed in all patients, including patients with cardiogenic shock.

Plasma Pentraxin 3 May Be a More Sensitive Marker of Inflammatory Response Than High-Sensitivity C-Reactive Protein After Bare-Metal Stent Compared to Drug-Eluting Stent Implantation

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.

No predictive value of serum interleukin-6 and transforming growth factor-β1 in identifying patients with a first restenosis, recurrent restenosis or a history of restenosis

BACKGROUND The efficacy of percutaneous coronary intervention (PCI) is limited by the need for repeat revascularization resulting from restenosis. The restenosis rate after treatment for in-stent restenosis (recurrent restenosis) is high (> 30%). Numerous studies have suggested the predictive value of interleukin 6 (IL-6) and transforming growth factor beta1 (TGF-beta1). METHODS We sought to determine whether serum levels of IL-6 and TGF-beta1 could help identify individuals with recurrent restenosis. Thirty seven patients with a history of stent implantation were enrolled and divided into three groups: (1) patients with a current, first restenosis (n = 9); (2) patients with current restenosis and at least one prior restenosis (recurrent restenosis) (n = 11), and (3) patients with a history of restenosis, but without current restenosis (n = 17). RESULTS The baseline profile was similar in all three groups. The median (25th-75th percentile) concentrations of IL-6 were: group 1 - 2.8 (1.4-5.5); group 2 - 2.6 (0.6-8.6); group 3 - 2.4 (0.9-4.7) p = 0.69 and TGF-beta1: group 1 - 3.6 (0.2-14.4); group 2 - 4.2 (1.8-57.6); group 3 - 6.6 (2.8-30.0) p = 0.57. Moreover we found no correlation, either between diameter stenosis and IL-6 (R = 0.10; p = 0.38) or TGF-beta1 (R = 0.10; p = 0.57). Both IL-6 (AUC 0.59 p = 0.4 and AUC 0.51 p = 0.9) and TGF-beta1 (AUC 0.64 p = 0.2 and AUC 0.50 p = 0.9) failed to provide significant results in receiver-operating characteristic analysis. CONCLUSION We report that there is no association between the severity of diameter stenosis (restenosis) and IL-6 or TGF-beta1 concentrations. Our findings might suggest that levels of IL-6 and TGF-beta1 have no predictive value for identifying patients with recurrent restenosis.