Search

BACKGROUND: Optimal strategy for patients who need coronary revascularization before undeferrable non-cardiac surgery is still unknown. We performed a pilot study of dual antiplatelet therapy discontinuation followed by major non-cardiac surgery and endovascular aortic repair early after successful endothelial-progenitor cell-capture coronary stent deployment. METHODS AND RESULTS: Thirty consecutive patients underwent coronary angioplasty plus stenting, before upcoming endovascular or surgical procedures requiring early interruption of antiplatelet therapy. An optimal acute procedural result was observed in all patients. Antiplatelet therapy was stopped before surgery in all patients, achieving an average antiplatelet therapy time of 12.2 ± 3.9 days. Surgery was performed after antiplatelet therapy interruption at an average time interval from revascularization of 17.2 ± 3.9 days. No patient suffered cardiac events during the perioperative period. At thirty day follow-up after surgery there were no cardiac events in all patients. CONCLUSIONS: Our preliminary data might suggest a role for EPC-capture stent in patients requiring surgical procedures early after coronary stent placement. Further studies on larger population are needed to confirm the clinical impact of our findings.

Adaptive immune responses are involved in all stages of atherosclerotic plaque development, including plaque complication (i.e., rupture, ulceration, etc), which may lead to the clinical occurrence of Acute Coronary Syndromes (ACS) [1]. Unstable coronary plaques, in addition to macrophages, contain a 10-fold increase in T-lymphocytes, as compared to stable plaques [2]. T-cells produce and release cytokines, and, in turn, regulate macrophage activity [3]; thus, T-cell activation, through cytokine production, might play a pivotal role in the pathophysiology of plaque complication [4]. Several studies have focused on cytokine plasma levels in patients with ACS, demonstrating that many of these substances are elevated in the systemic blood of patients with ACS (for a review, see Ref. [5]), some of which may even correlate with an adverse prognosis [6]. However, most of these studies have measured cytokine levels in the peripheral blood, raising the issue that the local cytokine milieu is still largely unexplored. This is not a trivial issue, since the assessment of the local inflammatory milieu could contribute to a better understanding of different inflammatory and immune-mediated pathways determining different outcomes in patients affected by ACS [7]. Twenty-eight patients with a clinical diagnosis of ACS and 16 patients with Stable Angina (SA) undergoing coronary angiography were studied. After coronary angiography, a 6 F multipurpose catheter was positioned into the Coronary Sinus (CS); thereafter, blood samples (4.5 mL) were simultaneously obtained from the CS and the ascending aorta (Ao) and placed in pre-chilled Vacutainer tubes containing sodium citrate. Transcoronary cytokine levels (expressed as a Δ% of CS–Ao levels) were measured by LuminexTM technology [8]. We found that transcoronary serum levels of IL-1β, IL-2, IL-6, IL12p40/70, IL-15, and IFN-γ – all of which can be ascribed to a Th1related response – were all significantly increased with the exception of IL-2. (Fig. 1, panel A). On the contrary, transcoronary serum levels of IL-4, IL-5, IL-10, IL-13, (Th2-related response) did not change significantly in patients with ACS as compared to SA patients, with the exception of IL-10 transcoronary levels, which were significantly lower in the ACS group (Fig. 1, panel B). Finally, we have found a significant increase in the transcoronary blood levels of EGF, eotaxin, MCP-1, IP-10, RANTES, and TNF-α in the ACS patients, as compared to their SA counterparts (Fig. 2). Systemic inflammation has been associatedwith an altered pattern of cytokine profile in patients with ACS [5]. However, many large studies attempting to link specific cytokine/chemokine levels to ACS have been inconclusive [9], probably because the inflammatory responses accounting for the outcome of the lesion occur predominantly at the level of the complicated plaque, which may not be paralleled by similar changes in the peripheral blood. Therefore, consistent with this hypothesis, we have focused our attention on the local, i.e., intracoronary cytokine production profile in patients with ACS and compared it to patients with SA. In particular, we have observed that local cytokine release was characterized by an increase in the transcardiac levels of those substances which characterize a Th1-like type of immune response. In contrast, the local production of those cytokines which represent the “fingerprint” of the Th2-like response, did not change significantlywhen compared to that found in patients with SA. Interestingly, the transcoronary levels of IL-10, a cytokine able to down-regulate the inflammatory responses via multiple mechanisms, were even lower in ACS patients, as compared to those obtained in patients with SA. The observed increase in IP-10 and MCP-1 transcoronary blood levels also suggests that the recruitment of inflammatory cells is taking place locally, i.e., at the International Journal of Cardiology 176 (2014) 227–299

Primary percutaneous coronary intervention (PCI) is the standard of care in patients with acute ST-segment elevation myocardial infarction (STEMI), since it is associated with a mortality reduction as compared with thrombolytic therapy alone. At this regard, we have previously demonstrated that drug-eluting stents are more effective than bare-metal stents in reducing the need for repeat revascularization of target vessel, without safety concerns [1] and [2]. However, it is unclear whether there are differences in clinical outcomes between sirolimus- (SES) and paclitaxel-eluting stent (PES). Herein, we report a meta-analysis of randomized studies comparing SES versus PES in patients undergoing primary PCI.