The aim of this study was to assess the effect of periprocedural antibiotic treatment with roxithromycin on circulating cell adhesion molecules and restenosis after coronary stent implantation.
Case-control study enrolling 25 consecutive patients submitted to coronary stenting for stable, single-vessel coronary artery disease, treated with 300 mg roxithromycin once daily for 5 days, starting 2 days before the procedure (group R). Twenty-five patients, matched for lesion site, length and diameter, as control group (group C). The serological status for Chlamydia pneumoniae (CP) infection (IgG, ELISA) was assessed in all patients. The plasma concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), E-selectin and C-reactive protein at 1 month after coronary stenting were compared with baseline values. Binary restenosis (> or = 50%) was also evaluated at 6 months.
sICAM-1 significantly decreased at 1 month in group R vs group C (371 +/- 181 vs 573 +/- 273 ng/ml, p = 0.005). This decrease was more evident in patients with a positive serology for CP (CP+) (group R 373 +/- 131 vs group C 597 +/- 255 ng/ml, p = 0.014). Antibiotic treatment had no effects on circulating E-selectin levels at 1 month (56.7 +/- 97 vs 49.8 +/- 62 ng/ml, p = 0.54). The restenosis rate (9/50, 18%) was similar in the two groups (group R 5/25 [20%], group C 4/25 [16%]). The restenosis rate was similar in the CP+ vs CP- group (6/35 [17%] vs 3/15 [20%]).
A short course of treatment with roxithromycin at the time of coronary stenting induces a significant reduction in the sICAM-1 levels at 1 month but apparently does not influence the restenosis rate.
Italian heart journal: official journal of the Italian Federation of Cardiology 09/2004; 5(9):667-72.
Inflammation plays an important role in the pathogenesis of acute coronary syndromes. The purpose of our study was to evaluate the time course and the clinical relevance of inflammatory markers in patients with unstable angina undergoing successful coronary stent implantation.
Fifty-six patients (33 with unstable and 23 with stable angina) scheduled for single vessel coronary angioplasty followed by successful stent implantation were studied. Blood samples for measurements of interleukin-6 (IL-6) and von Willebrand factor antigen (vWf) were taken immediately before coronary angioplasty and 24 hours and 1 month after the procedure. Patients were clinically examined 1 month after the procedure.
The mean levels of IL-6 before stenting were significaNtly higher in unstable than in stable angina patients (p = 0.002), whereas baseline values of vWf showed no difference between the two groups. In unstable angina, serum levels of IL-6 and of vWf did not change 24 hours after stent implantation, but significantly decreased 1 month after the procedure (p = 0.005 and p = 0.0015 respectively). In stable patients, serum levels of IL-6, but not of vWf, increased 24 hours after the procedure and returned to baseline levels 1 month after stent implantation (p = 0.046).
In unstable angina, successful treatment of the culprit lesion by coronary stenting results in a significant decrease in the serum levels of IL-6 and of vWf 1 month after the procedure, suggesting that, in this clinical condition, elevated levels of these parameters correlate with the instability of the atheromatous plaque and that their decrease after successful stent implantation is the result of plaque stabilization.
Italian heart journal: official journal of the Italian Federation of Cardiology 11/2002; 3(10):593-7.
Recent data show that markers of inflammation, endothelial perturbation as well as activation of the coagulation and fibrinolytic systems are altered in unstable angina. The purpose of this study was to compare the 30-day prognostic value of the indexes of inflammation [interleukin-6 (IL-6)], endothelial activation [von Willebrand factor antigen (vWf)], fibrinolysis [plasminogen activator inhibitor-1 (PAI-1)] and coagulation (F1 + 2), in a consecutive series of patients with non-ST elevation acute coronary syndromes.
Eighty-eight patients consecutively admitted to the coronary care unit because of chest pain occurring within the previous 24 hours were included in the study. Blood was drawn on admission to the coronary care unit and 72 hours thereafter for the assessment of plasma levels of IL-6, vWf, F1 + 2 and PAI-1. Troponin I serum levels were measured 6 to 12 hours after admission. All patients underwent coronary arteriography.
Patients were divided into two groups according to their 30-day outcome: 57 patients (group 1) had an uneventful outcome, whereas 31 patients had an adverse clinical event (4 died, 1 had a Q wave myocardial infarction and 26 had refractory angina). The baseline biochemical variables were similar between group 1 and group 2 patients. Seventy-two hours following admission, an increase in the serum levels of IL-6 was observed in 71% of group 2 patients and in 28% of group 1 patients (p = 0.0001). The other measured variables showed significant changes at 72 hours versus entry only in group 1 patients, and no significant difference between the two groups. The areas under the ROC curves were higher for IL-6 (0.72) than for the other variables (0.58 for F1 + 2, 0.52 for vWf and 0.54 for PAI-1). In a multivariate model, including clinical, angiographic, and biochemical variables, only the change in IL-6 over 72 hours was significantly associated with a worse 30-day outcome (odds ratio 8.472, 95% confidence interval 1.030-69.671).
This study shows that a mounting inflammatory process, as indicated by increasing levels of IL-6 over the first 72 hours after admission, is the most powerful predictor of the 30-day prognosis in patients with non-ST elevation acute coronary syndromes.
Italian heart journal: official journal of the Italian Federation of Cardiology 02/2002; 3(1):28-33.