Long-term serial changes in platelet activation indices following sirolimus elution and bare metal stent implantation in patients with stable coronary artery disease.

BACKGROUND: Platelet activation is crucial in the development of stent thrombosis following percutaneous coronary intervention (PCI). We carried out a long-term assessment of multiple factors implicated in the thrombotic process and monitored markers of platelet activation after the implantation of sirolimus-eluting stents (SES) in patients with stable coronary artery disease (CAD). Additionally, we compared these findings with those after bare-metal stent (BMS) implantation. METHODS: A cohort of 47 consecutive patients, aged <70 years, with severe stenosis (>70% narrowing of the lumen) of one major epicardial coronary artery and stable CAD underwent successful elective PCI. Patients were randomly allocated to SES (n = 25) or BMS (n = 22). Venous blood was obtained 24 hours before and 24 hours, 48 hours, 1 month, and 6 months after PCI for measurements of plasma levels of sP-selectin, von Willebrand Factor (vWF), fibrinogen, d-dimer, sCD40, factor VIII, b-thromboglobulin (b-TG) and platelet factor 4 (PF-4). RESULTS: There were no significant differences between the two groups in levels of fibrinogen or d-dimers in peripheral blood. However, we observed a significant kinetic effect (p<0.001) and stent-effect (p<0.015) on vWF levels and a significant kinetic effect (p = 0.012) on factor VIII, sP-selectin (p = 0.04), b-TG (p<0.001), and PF4 (p = 0.016). A trend towards a significant stent effect on sCD40 was also detected (p = 0.06). CONCLUSIONS: SES and BMS did not show significant differences in relationship to markers of platelet activation and coagulation in patients with stable CAD. Although some markers showed an increase after stent implantation, they returned to the initial levels 6 months later.

Hypertrophic and antihypertrophic microRNA levels in peripheral blood mononuclear cells and their relationship to left ventricular hypertrophy in patients with essential hypertension.

MicroRNAs regulate several aspects of physiological and pathologic cardiac hypertrophy, and they represent promising therapeutic targets in cardiovascular disease. We assessed the expression levels of the microRNAs miR-1, miR-133a, miR-26b, miR-208b, miR-499, and miR-21, in 102 patients with essential hypertension and 30 healthy individuals. All patients underwent two-dimensional echocardiography. MicroRNA expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. Hypertensive patients showed significantly lower miR-133a (5.06 ± 0.50 vs. 13.20 ± 2.15, P < .001) and miR-26b (6.76 ± 0.53 vs. 9.36 ± 1.40, P = .037) and higher miR-1 (25.99 ± 3.07 vs. 12.28 ± 2.06, P = .019), miR-208b (22.29 ± 2.96 vs. 8.73 ± 1.59, P = .016), miR-499 (10.06 ± 1.05 vs. 5.70 ± 0.91, P = .033), and miR-21 (2.75 ± 0.15 vs. 1.82 ± 0.20, P = .002) expression levels compared with healthy controls. In hypertensive patients, we observed significant negative correlations of miR-1 (r = -0.374, P < .001) and miR-133a (r = -0.431, P < .001) and significant positive correlations of miR-26b (r = 0.302, P = .002), miR-208b (r = 0.426, P < .001), miR-499 (r = 0.433, P < .001) and miR-21 (r = 0.498, P < .001) expression levels with left ventricular mass index. Our data reveal that miR-1, miR-133a, miR-26b, miR-208b, miR-499, and miR-21 show distinct expression profiles in hypertensive patients relative to healthy individuals and they are associated with clinical indices of left ventricular hypertrophy in hypertensive patients. Thus, they may be related to heart hypertrophy in hypertensive patients and are possibly candidate therapeutic targets in hypertensive heart disease.