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Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

We assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case's home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. We included 126 patients (median age: 67.0 years of age; IQR: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and C o levels were positively and significantly correlated with serum levels of C-reactive protein. We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory activation may explain these findings. [Display omitted] [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCA) represents a heterogeneous clinical conundrum accounting for about 6%-8% of all acute MI who are referred for coronary angiography. Current guidelines and consensus documents recommend that these patients are appropriately diagnosed, uncovering the causes of MINOCA, so that specific therapies can be prescribed. Indeed, there are a variety of causes that can result in this clinical condition, and for this reason diagnostic cardiac imaging has an emerging critical role in the assessment of patients with suspected or confirmed MINOCA. In last years, different cardiac imaging techniques have been evaluated in this context, and the comprehension of their strengths and limitations is of the utmost importance for their effective use in clinical practice. Moreover, recent evidence is clearly suggesting that a multimodality cardiac imaging approach, combining different techniques, seems to be crucial for a proper management of MINOCA. However, great variability still exists in clinical practice in the management of patients with suspected MINOCA, also depending on the availability of diagnostic tools and local expertise. Herein, we review the current knowledge supporting the use of different cardiac imaging techniques in patients with MINOCA, underscoring the importance of a comprehensive multimodality cardiac imaging approach and proposing a practical diagnostic algorithm to properly identify and treat the specific causes of MINOCA, in order to improve prognosis and the quality of life in these patients. [ABSTRACT FROM AUTHOR]

Angina pectoris may arise from obstructive coronary artery disease (CAD) or in the absence of significant CAD (ischemia with nonobstructed coronary arteries [INOCA]). Therapeutic strategies for patients with angina and obstructive CAD focus on reducing cardiovascular events and relieving symptoms, whereas in INOCA the focus shifts toward managing functional alterations of the coronary circulation. In obstructive CAD, coronary revascularization might improve angina status, although a significant percentage of patients present angina persistence or recurrence, suggesting the presence of functional mechanisms along with epicardial CAD. In patients with INOCA, performing a precise endotype diagnosis is crucial to allow a tailored therapy targeted toward the specific pathogenic mechanism. In this expert opinion paper, we review the evidence for the management of angina, highlighting the complementary role of coronary revascularization, optimal medical therapy, and lifestyle interventions and underscoring the importance of a personalized approach that targets the underlying pathobiology. • Angina pectoris may arise from obstructive CAD or in the absence of significant CAD. • Functional mechanisms may be involved in determining angina both in obstructive CAD and in ischemia with nonobstructed coronary arteries. • Revascularization and medical therapy play complementary roles in achieving optimal outcomes for patients with angina. • Management of angina is shifting toward a more personalized approach, moving away from the traditional one-size-fits-all strategy. [ABSTRACT FROM AUTHOR]

• Functional evaluation plays a key role to identify the mechanisms underlying myocardial ischemia also in patients with non-obstructive CAD. • Treatment of myocardial ischemia should be targeted to the underlying pathogenic mechanism, and for these reasons the use of an invasive functional approach may have important therapeutic implications. • Invasive functional assessment has important therapeutic and prognostic implications in patients with both acute and chronic coronary syndromes. [ABSTRACT FROM AUTHOR]

Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor highly expressed in coronary plaques, particularly in macrophages, and in activated platelets. Thus, a possible role in the pathogenesis of acute coronary syndrome (ACS) has been suggested. We evaluated systemic BDNF levels according to the different clinical presentations of ACS. Moreover, we assessed the relationship between BDNF levels and the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) and healed plaques along the culprit vessel. We enrolled consecutive patients presenting with ST-elevation myocardial infarction (STEMI) or non-ST-elevation (NSTE)-ACS. Serum BDNF levels were assessed by enzyme-linked immunosorbent assay. Plaque characteristics of the culprit vessel were assessed by OCT. Among 126 ACS patients (median age 68.00, interquartile range [IQR] 59.75-75.25 years, male 74.6%, 71 (56.3%) were NSTE-ACS and 55 (43.7%) were STEMI. BDNF levels were higher in STEMI patients compared to NSTE-ACS. OCT assessment was performed in 53 (42.1%) patients. Patients with MØI (n = 27) had higher BDNF levels compared to patients without MØI. Furthermore, patients with healed plaques (n = 13) had lower BDNF levels than patients without healed plaques. At multivariate regression analysis BDNF levels independently predicted the presence of MØI (odds ratio [OR] = 2.856; 95% confidence interval [CI] [1.151-7.090], P = 0.024) and the absence of healed plaques (OR = 0.438, 95% CI [0.185-0.992], P= 0.050). Among ACS patients, BDNF levels were higher in patients with STEMI. Moreover, BDNF levels were independently associated with MØI and with the absence of healed plaques along the culprit vessel, suggesting a possible role of BDNF in promoting plaque inflammation, destabilization and occlusive thrombosis. [ABSTRACT FROM AUTHOR]

Macrophages play a key role in coronary plaque destabilization. In-vitro human monocyte-derived macrophages (MDMs) are used to study macrophages infiltrating tissue. Optical coherence tomography (OCT) provides an in-vivo insight of the coronary arteries. We compared the MDMs morpho-phenotype and culprit plaque features at OCT in acute coronary syndrome (ACS) patients according to the underlying plaque pathobiology. Sixty-six patients undergoing coronary angiography and pre-angioplasty OCT of the culprit vessel were allocated to three groups according to mechanism of ACS at OCT and C-reactive protein levels (cut-off: 2 mg/Ll): 1) plaque rupture with systemic inflammation; 2) plaque rupture without systemic inflammation, 3) plaque with intact fibrous cap. A blood sample was collected to obtain MDMs, categorized as having "round" or "spindle" morphology. Thirty-two patients (48.5%) were assigned to Group 1, 10 (15.2%) to Group 2 and 24 (36.4%) to Group 3. The "round" MDMs were significantly more frequent in Group 1 (39.25 ± 4.98%) than in Group 2 (23.89 ± 3.10%) and Group 3 (23.02 ± 7.89%), p = 0.008. MDMs in Group 1 as compared to Groups 2 and 3 showed lower efferocytosis (8.74 ± 1.38 vs 9.74 ± 2.15 vs 11.41 ± 2.41; p = 0.012), higher tissue factor levels (369.84 ± 101.13 vs 301.89 ± 59.78 vs 231.74 ± 111.47; p = 0.001) and higher heme oxygenase-1 expression (678.78 ± 145.43 vs 419.12 ± 74.44 vs 409.78 ± 64.33; p = 0.008). MDMs of ACS patients show morpho-phenotypic heterogeneity with prevalence of pro-thrombotic and pro-oxidative properties in case of plaque rupture and systemic inflammation. Such MDMs subpopulation may take part to the cellular pathways leading to fibrous cap rupture with the subsequent thrombus formation. • Monocyte-derived macrophages to study macrophages infiltrating coronary plaques. • Optical Coherence Tomography to identify the mechanism of plaque destabilization. • Pro-thrombotic, oxidative macrophages are prevalent in ruptures with inflammation. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Over the last several decades, clinicians and clinical scientists have had growing interest in heart failure (HF) diagnosis and treatment. While HF with reduced ejection fraction (EF) is a well-known clinical entity with several therapeutic strategies proven to be successful, HF with preserved ejection fraction is a more heterogenous syndrome with a prevalence that has increased in the last two decades, without effective therapeutic strategies. Great strides have been made in the detection of predisposing risk factors and pathological mechanisms; however, pharmacological therapies have shown to be ineffective in reducing cardiovascular mortality in the HF with preserved EF (HFpEF) population, opening the way to the necessity of developing new precision medicine based approaches. On the other hand, novel therapies and device interventions still require refinements with the ultimate goal of offering new clinically treatments for the HFpEF population. The aim of the present review is to provide insights into the HFpEF pathophysiology, diagnostic pathways and the latest updates on treatment strategies and their potential future application in routine clinical practice. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction (EnD) is a hallmark feature of coronary artery disease (CAD), representing the key early step of atherosclerotic plaque development and progression. Percutaneous coronary intervention (PCI) is performed daily worldwide to treat symptomatic CAD, however a consistent proportion of patients remain symptomatic for angina despite otherwise successful revascularization. EnD plays a central role in the mechanisms of post-PCI angina, as it is strictly associated with both structural and functional abnormalities in the coronary arteries that may persist, or even accentuate, following PCI. The assessment of endothelial function in patients undergoing PCI might help to identify those patients at higher risk of future cardiovascular events and recurrent/persistent angina who might therefore benefit more from an intensive treatment. In this review, we address the role of EnD in determining angina after PCI, discussing its pathophysiological mechanisms, diagnostic approaches and therapeutic perspectives. [ABSTRACT FROM AUTHOR]

• Recurrent cerebral ischemia after PFO closure is not rare (0.92/100 patients/year). • Obesity, ROPE score < 7 and migraine were predictors of recurrent stroke/TIA. • Future studies are required to refine prevention of recurrent stroke after PFO closure. Transcatheter patent foramen ovale closure lowers recurrent stroke in patients with cryptogenic stroke or transient ischemic attack with an indication for closure. However, the incidence of recurrent stroke is not negligible and underlying pathophysiology remains largely unknown. We sought to evaluate the prevalence of recurrent ischemic neurological events and to assess its predictors after transcatheter patent foramen ovale closure. We enrolled consecutive patients who underwent patent foramen ovale closure for secondary prevention of neurological ischemic events at the University Hospital of Parma between 2006 and 2021. Clinical and procedure-related features were collected for each patient. The incidence of recurrent ischemic neurological events was assessed at follow-up. We enrolled a total of 169 patients with mean Risk of Paradoxical Embolism score at hospital admission of 6.4 ± 1.5. The primary indication was previous cryptogenic stroke (94 [55.6 %] subjects), followed by transient ischemic attack (75 [44.4 %]). Among patients with complete outcome data (n= 154), after a median follow-up of 112 months, recurrent cerebral ischemia occurred in 13 [8.4 %], with an annualized rate of 0.92/100 patients. The presence of obesity [OR 5.268, p = 0.018], Risk of Paradoxical Embolism score < 7 [OR 5.991, p = 0.035] and migraine [OR = 5.932 p = 0.012] were independent positive predictors of recurrent stroke/ transient ischemic attack after patent foramen ovale closure. The presence of obesity, Risk of Paradoxical Embolism score < 7 and migraine were independent positive predictors of recurrent ischemic neurological events after patent foramen ovale closure. [ABSTRACT FROM AUTHOR]

Patients with acute coronary syndrome (ACS) associated to high C-reactive protein (CRP) levels exhibit a higher risk of future acute ischemic events. Yet, the positive predictive value of CRP is too low to guide a specific treatment. Our study aims to identify a high-risk patient subset who might mostly benefit from anti-inflammatory treatment on the basis of the combination of optical coherence tomography (OCT) assessment of the culprit vessel and CRP serum levels. Patients admitted for ACS and undergoing pre-interventional OCT assessment of the culprit vessel were selected from "Agostino Gemelli" Hospital OCT Registry. The primary end-point was recurrent ACS (re-ACS). CRP levels ≥2 mg/L were considered abnormal. The overall study population consisted of 178 patients. Among these, 156 patients were included in the primary end-point analysis. The re-ACS rate was 23% at 3-year follow-up. High CRP (2.587, 95% CI:1.345–10.325, p = 0.031), plaque rupture (3.985, 95% CI:1.698–8.754, p = 0.009), macrophage infiltration (3.145, 95% CI:1.458–9.587, p = 0.012) and multifocal atherosclerosis (2.734, 95% CI:1.748–11.875, p = 0.042) were independent predictors of re-ACS. All patients (14/14) with high CRP and with all OCT high-risk features had re-ACS. At the other extreme, only 4 of the 82 patients with low CRP levels and lack of high-risk features at OCT examination exhibited re-ACS at follow-up. The combination of systemic evidence of inflammation and OCT findings in the culprit plaque identifies very high-risk ACS. Future studies are warranted to confirm these findings and to test an anti-inflammatory treatment in this patient subset. • High CRP and OCT features of the culprit vessel predict recurrent coronary events. • Patients with high-risk OCT features and high CRP experienced a recurrent ACS. • Our findings may contribute to individualize the secondary prevention of ACS. [ABSTRACT FROM AUTHOR]

Gender differences in the pathophysiology of atherosclerosis, cardiovascular risk factors, and diagnosis of coronary artery disease and valvular heart disease are well known. Such differences have also been outlined in the management and outcomes after acute coronary syndromes and valvular repair. Regarding the atherosclerotic process, pathological experimental studies suggest that plaque composition and burden may differ by gender. Female gender is associated with worse outcomes in the case of ischemic heart disease and, compared with men, women are less likely to undergo interventional cardiac procedures and sustain worse outcomes. In the setting of valvular heart disease (VHD), transcatheter aortic valve implantation (TAVI) and percutaneous edge-to-edge mitral valve repair are now well-established procedures with high success rates. In women with moderate to severe aortic stenosis, subgroup analyses in TAVI trials have demonstrated gender-related differences suggesting female gender as beneficial in terms of short-, mid-, and long-term outcomes. Similarly, several studies reported different procedural challenges and outcomes in males and females following surgical and percutaneous mitral valve repair. These diverse findings emphasize the necessity to provide gender-specific analyses of interventional methods. This review highlights gender differences in the epidemiology, pathophysiology, treatment options and clinical outcomes of the conditions mentioned above. • Gender differences in the pathophysiology and clinical presentation of coronary and valvular heart disease have been shown. • In the case of ischemic heart disease, females are less likely to receive timely and evidence-based treatment than males. • In female gender, percutaneous valvular interventions have shown similar (or even better) short- and long-term outcomes. • Further studies are necessary to investigate and solve open gender-related issues in contemporary interventional cardiology. [ABSTRACT FROM AUTHOR]

Abstract Background Over the last decade, the intra-coronary imaging (ICI) has emerged to guide percutaneous coronary intervention (PCI), thus overcoming the limitations of "luminology" offered by angiography. Methods In this review, we aim at purely focusing on the clinical implications of the employment of ICI in the routine practice, thus providing suggestions for future applications. In particular, we will describe the principal contributions and implications of ICI in the following different clinical settings: 1) assessment of clinical and imaging outcomes of PCI; 2) guiding PCI before and after stent implantation; 3) identification of mechanisms of stent failure. Results Several studies showed the capability of ICI in assessing the clinical and imaging outcomes of PCI. In particular, they have compared the ICI-guided PCI with the angiography-guided procedures, emphasizing the advantages of using imaging. Indeed, ICI can characterize the coronary plaque, provide a precise estimation of the coronary stenosis, select the appropriate method of intervention, and optimize stent deployment and lesion coverage. Finally, ICI has been shown to be useful to point out the mechanisms of stent failure. Conclusions. ICI can facilitate decision-making in patients with unclear angiographic findings, guide-selected interventions and optimize the final PCI results in complex lesions or. in high-risk patients. Finally, by the identification of specific mechanisms of stent failure, the ICI can allow to adopt a tailored therapy for the singles cases. Highlights • Intra-coronary imaging (ICI) allows to assess clinical and imaging outcomes; • ICI allows to characterize the coronary plaque; • ICI allows to optimize stent deployment; • ICI allows to identify the mechanisms of stent failure. [ABSTRACT FROM AUTHOR]

Recent randomized trials comparing coronary artery bypass graft (CABG) with percutaneous coronary intervention (PCI) utilizing drug-eluting stents in patients with left main disease (LMD) and/or multivessel disease (MVD), reported conflicting results. We performed a study level meta-analysis comparing the 2 interventions for the treatment of LMD or MVD. Using electronic databases, we retrieved 6 trials, between January, 2010 and December, 2022. Five-years Kaplan-Meier curves of endpoints where reconstructed. Comparisons were made by cox-linear regression frailty model and by landmark analysis. A random-effect method was applied. A total of 8269 patients were included and randomly assigned to CABG (n = 4135) or PCI (n = 4134). During 5-years follow-up, PCI showed a higher incidence of all-cause mortality (hazard ratio [HR] 1.28; 95% confidence interval [CI], 1.11-1.47; P < 0.0001]), myocardial infarction (HR 1.84; 95% CI, 1.54-2.19; P < 0.0001) and repeat coronary revascularization (HR 1.96; 95% CI, 1.72-2.24; P < 0.0001). There was no long-term difference between the 2 interventions for cardiovascular death (P = 0.14) and stroke (P = 0.20), although the incidence of stroke was higher with CABG within 30-days from intervention (P < 0.0001). PCI was associated with an increased risk for composite endpoints (P < 0.0001) and major cerebral and cardiovascular events. (P < 0.0001). In conclusion, at 5-year follow-up, in patients with LMD and/or MVD there was a significant higher incidence of all-cause mortality, myocardial infarction and repeat revascularization with PCI compared to CABG. The incidence of stroke was higher with CABG during the postprocedural period, but no difference was found during 5-years follow-up. Longer follow-up is mandatory to better define outcome difference between the 2 interventions. [ABSTRACT FROM AUTHOR]

Takotsubo syndrome (TTS) is an acute reversible form of myocardial dysfunction that is often associated with serious adverse in-hospital complications, including acute heart failure, cardiogenic shock and life-threatening arrythmias. In the absence of randomized clinical trials, its management in the acute phase is based on empirical supportive pharmacological and non-pharmacological measures.In this review article, we aimed at providing an overview of the acute clinical manifestations of patients presenting with TTS, highlighting the predictors of a worse short-term outcome, along with the challenges in therapeutic management of TTS-related complications in the acute care setting. [ABSTRACT FROM AUTHOR]

Background: Natriuretic peptides are diagnostic/prognostic biomarkers in major cardiovascular diseases. We aimed at assessing the predictive role of N-terminal pro-A-type (NT-proANP) and pro-B-type (NT-proBNP) natriuretic peptides levels toward cardiovascular outcome in both stable and unstable coronary artery disease (CAD) patients after percutaneous coronary intervention (PCI) in a non-primary PCI setting.Methods: A total of 395 patients undergoing PCI with stent implantation for either stable angina (SA) or non ST-elevation acute coronary syndrome (NSTE-ACS) were enrolled. Pre-procedural NT-proANP and NT-proBNP levels were measured. Occurrence of major adverse cardiac events (MACEs), composite of cardiac death, non-fatal myocardial infarction, and clinically driven target lesion revascularization (c-TLR), was the endpoint of the study. Follow up mean time was 48.53±14.69months.Results: MACEs occurred in forty-four patients (11%) during follow up. Both NT-proANP levels [3170 (2210-4630) vs 2283 (1314-3913) fmol/mL, p=0.004] and NT-proBNP levels [729 (356-1353) vs 511 (267-1006) fmol/mL, p=0.04] were significantly higher in patients with MACEs compared to patients without MACEs. Similar results were found when considering hard MACEs (myocardial infarction and cardiac death). NT-proANP levels were significantly higher in patients with c-TLR compared with patients without c-TLR [3705 (2766-5184) vs 2343 (1340-3960) fmol/mL, p=0.021]. At multivariate analysis, NT-proANP levels were a significant predictor of MACEs (HR 1.09, 95% CI 1.03-1.18, p=0.04). Kaplan-Meyer curves revealed that patients with elevated NT-proANP levels (>2.100fmol/mL) had a lower MACE free survival (p=0.003).Conclusions: Both NT-proANP and NT-proBNP levels were higher in CAD patients experiencing MACEs following PCI in a non-primary setting. Notably, only NT-proANP levels significantly affected prognosis after PCI. [ABSTRACT FROM AUTHOR]

Background Lipoprotein Lp(a) has been shown to be an independent risk factor for coronary artery disease (CAD). However, its association with CAD burden in patients with ACS is largely unknown, as well as the association of Lp(a) with lipid rich plaques prone to rupture. Aim We aim at assessing CAD burden by coronary angiography and plaque features including thin cap fibroatheroma (TCFA) by optical coherence tomography (OCT) in consecutive patients presenting with acute coronary syndrome (ACS) and obstructive CAD along with serum Lp(a) levels. Methods This study comprises an angiographic and an OCT cohort. A total of 500 ACS patients (370 men, average age 66 ± 11) were enrolled for the angiographic cohort and 51 ACS patients (29 males, average age 65 ± 11) were enrolled for the OCT cohort. Angiographic CAD severity was assessed by Sullivan score and by Bogaty score including stenosis score and extent index. OCT plaque features were evaluated at the site of the minimal lumen area and along the culprit segment. Results In the angiographic cohort, at multivariate analysis, Lp(a) was a weak independent predictor of Sullivan score (p < 0.0001), stenosis score (p < 0.0001) and extent index (p < 0.0001). In the OCT cohort, patients with higher Lp(a) levels (≥30 md/dl) compared to patients with lower Lp(a) levels (<30 md/dl) exhibited a higher prevalence of lipidic plaque at the site of the culprit stenosis (67% vs. 27%; P = 0.02), a wider lipid arc (135 ± 114 vs 59 ± 111; P = 0.03) and a higher prevalence of TCFA (38% vs. 10%; P = 0.04). Conclusions Among patients with ACS, raised Lp(a) levels are associated with an increased atherosclerotic burden and it identifies a subset of patients with features of high risk coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Aim : To assess eosinophil cationic protein (ECP) and C-reactive protein (CRP) serum levels at three time points according to different stent types. Methods : 54 patients (age 64 ± 10 years, male 78%), undergoing Bare Metal Stent (BMS) ( n = 11), mammalian Target Of Rapamycin (mTOR)-inhibitor DES ( n = 27) and mTOR-inhibitor bioabsorbable DES (BES) ( n = 16) implantation for stable angina (SA) or non-ST-elevation acute coronary syndromes (NSTE-ACS), were prospectively enrolled. ECP and CRP serum levels were assessed before revascularization, at 1-month and at 1-year after the procedure. Moreover, 21 patients found to have inducible ischemia or angina symptoms at 6 month-stress test underwent 1-year follow-up (FU) angiography. Results : Baseline and 1-month ECP levels were similar among the 3 groups, whilst 1-year ECP was significantly higher in m-TOR-DES [8.61 (6.55–19.77) μg/ml] compared with m-TOR-BES [2.03 (1.78–5.53) μg/ml] and BMS-treated patients [2.23 (1.45–8.95) μg/ml] ( p = 0.02), without significant difference between BES and BMS. CRP was similar among the 3 groups at all time points. 1-year ECP significantly correlated with late loss in patients undergoing FU angiography ( r = 0.64, p = 0.002), while CRP did not ( p = NS). Conclusions : Our finding suggests that mTOR-DES stent type is associated with an increase of ECP levels at 1-year, possibly reflecting a persistent eosinophil activation triggered by permanent polymer. [ABSTRACT FROM AUTHOR]