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Periprocedural myocardial infarction (PMI) represents a frequent complication in patients undergoing percutaneous coronary revascularization. Despite great attention focused on pharmacological prevention of periprocedural damage, very little is known about using biomarkers to potentially predict the risk of PMI. Larger platelets have been associated with enhanced reactivity, increased cardiovascular risk, and higher rates of complications after coronary stenting. The platelet–larger cell ratio (P-LCR) identifies the largest-sized fraction of platelets, the proportion potentially more closely related to thrombotic events. The present study evaluated the relationship between P-LCR and PMI. We included 1,285 patients undergoing PCI. Myonecrosis biomarkers were dosed at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined as troponin I increase by three times the upper limit of normal (ULN) or by 50 % of an elevated baseline value, whereas PMI was defined as an increase in creatine kinase MB by 3 × ULN or 50 % of baseline. We grouped patients according to tertile values of P-LCR (

Our goal was to estimate the role of high-density lipoprotein cholesterol (HDL-C) in predicting the prevalence and extent of coronary artery disease (CAD) in 3280 patients undergoing coronary angiography. Predictors of lower HDL levels (

Periprocedural myocardial infarction (PMI) still occurs in a large amount of percutaneous coronary interventions (PCI), mainly due to increased platelet activation. Platelet size has been suggested as an indicator of enhanced reactivity and platelet distribution width (PDW) could reflect morphologic changes in platelets, therefore affecting their function and potentially increasing the risk of complications after coronary stenting. Aim of the present study was to evaluate the relationship between PDW and PMI. We included 1,300 consecutive patients undergoing PCI. Myonecrosis biomarkers were dosed at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined as troponin I increase by three times the ULN or by 50 % of an elevated baseline value, whereas PMI as CKMB increase by three times the ULN or 50 % of baseline. We grouped patients according to tertiles values of PDW (

Item does not contain fulltext BACKGROUND: Periprocedural myocardial infarction (PMI) represents a relatively common complication of percutaneous coronary intervention (PCI). Mean platelet volume (MPV) has been proposed as a marker for platelet activation, as larger sized platelets have been associated with higher pro-thrombotic risk. Therefore, aim of the current study was to evaluate whether MPV is associated with increased risk of PMI after PCI. METHODS: We included 1056 consecutive patients undergoing PCI. We measured myonecrosis biomarkers at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined for troponin I increase by 3 times the ULN or by 50% if elevated at the time of the procedure. PMI was defined as CK-MB increase by 3 times the ULN or 50% if elevated at the time of the procedure. RESULTS: We grouped patients according to tertiles values of MPV (11.4 fl). High MPV was associated with diabetes (p = 0.025) and higher prevalence of cerebrovascular events (p = 0.005). MPV significantly related with haemoglobin levels (p < 0.001), but inversely to platelet count (p < 0.001) and higher presence of thrombus (p = 0.03). Larger sized platelets did not increase risk of periprocedural myonecrosis (p = 0.91; OR[95% CI] = 1.04[0.90-1.2], p = 0.64) or PMI (p = 0.09; OR[95%IC] = 1.13[0.93-1.37]; p = 0.20). Subgroup analysis confirmed no impact of MPV on periprocedural MI also in high-risk subsets of patients, such as those with ACS at presentation (OR[95%CI] = 1.09 [0.87-1.38]; p = 0.44), diabetes (OR[95% CI] = 1.02[0.71-1.47], p = 0.91), female gender (OR [95% CI] = 1.15 [0.78-1.71], p = 0.48), elderly patients (age >/= 75 years) (OR[95%CI] = 1.21[0.87-1.69], p = 0.25) or with renal failure (OR[95%CI] = 1.55[0.91-2.61], p = 0.1). CONCLUSIONS: This study demonstrates that MPV does not predict the risk of PMI in patients undergoing PCI.

Mean platelet volume (MPV) has been correlated with platelet reactivity, thus its changes might be used to monitor the effects of antiplatelet therapy. However, no data have been reported on platelet remodelling after antiplatelet therapy. The aim of the current study was to investigate the short-term effects of oral antiplatelet therapy on MPV. Our population is represented by 62 consecutive patients with acute coronary syndrome (ACS), who did not receive GpIIb-IIIa inhibitors. We measured MPV before starting dual antiplatelet therapy, at day 1, day 2, and day 3-5 from starting adjunctive antiplatelet therapy. We additionally analyzed the relationship between platelet aggregation and MPV at admission by Multiplate in patients who were on chronic aspirin therapy. We observed a significant paradoxical increase in MPV, with a reduction in platelet count. We observed at all time intervals a significant inverse relationship between MPV and platelet count (T0: r = -0.44, P < 0.0001; T1: r = -0.36, P = 0.006; T2: r = -0.3, P = 0.026; T3-5: r = -0.29, P = 0.046). No relationship was observed between MPV and the extent of platelet aggregation inhibition by aspirin. This study showed a paradoxical increase in MPV after starting antiplatelet therapy. In addition, we did not observe any relationship between baseline MPV and the extent of platelet aggregation inhibition by aspirin. Thus, larger MPV does not imply higher platelet reactivity and may not be considered to monitor platelet reactivity and the efficacy of antiplatelet therapies.

Transradial approach has significantly decreased the rate of access site bleeding in patients undergoing percutaneous coronary interventions (PCI), therefore potentially mitigating the benefits offered by bivalirudin in lowering major bleeding complications as compared to heparin. However, nonaccess site bleeding, that represent the majority of hemorrhagic complications, still carry negative prognostic consequences for these patients and no study has so far defined the exact impact of bivalirudin on nonaccess site bleeding, that was therefore the aim of present meta-analysis.Literature archives (Pubmed, EMBASE, Cochrane) and main scientific sessions were scanned comparing bivalirudin vs. heparin in patients undergoing PCI. Primary endpoint was the occurrence of nonaccess site bleeding within 30 days. Secondary endpoints were 30 days mortality and the occurrence of access-site bleeding.A total of nine randomized clinical trials were finally included, involving 32,587 patients, 55.8% randomized to bivalirudin. Bivalirudin significantly reduced the rate of nonaccess site bleeding (2.6 vs. 3.8%, OR [95% CI] = 0.68 [0.60-0.77], P 0.00001, PThe present meta-analysis shows that bivalirudin can provide a significant reduction of both access and nonaccess site bleeding in patients undergoing PCI. However, these hemorrhagic benefits did not impact on survival, and moreover, were significantly conditioned by the association of heparin with potent antithrombotic strategies, such as glycoprotein IIbIIIa inhibitors, rather than by heparin or bivalirudin alone. Therefore, we could not provide any clinical evidence for the routine use of bivalirudin as preferred anticoagulation strategy for PCI. © 2017 Wiley Periodicals, Inc.

Despite new-generations of drug-eluting stents (DESs), the optimal duration of dual antiplatelet therapy (DAPT) remains controversial. We performed a meta-analysis of randomized trials (RTs) evaluating the effectiveness and safety of shorter versus longer DAPT duration strategies in patients undergoing percutaneous coronary interventions with DES. Literature and main scientific session abstracts were searched. The primary end point was mortality. Secondary end points were (1) cardiovascular mortality, (2) nonfatal myocardial infarction, (3) definite/probable stent thrombosis (ST), and (4) major bleedings. We included 11 RTs (n = 32 372 patients). Shorter DAPT duration reduced mortality (odds ratio, OR [95% confidence interval, CI] = 0.85 [0.71-1], P = .05; p heterogeneity = 0.91). Similar results were observed when comparing 3 to 6 versus 12 months DAPT, while a significant increase in recurrent ischemic events was found for 6 to 12 months DAPT versus extended treatment (myocardial infarction: OR [95%CI] = 1.66 [1.37-2], P < .00001; phet = 0.13 and ST: OR [95%CI] = 2.47 [1.72-3.45], P < .00001; phet = 0.12), however, counterbalanced by a significant reduction in major bleeding (OR [95%CI] = 0.60 [0.47-0.76], P < .0001; phet = 0.38) and a trend in lower mortality. Thus, among selected patients undergoing DES implantation, a shorter DAPT strategy is associated with reduction in mortality and major bleeding but a higher risk of myocardial infarction and ST. A short duration (3-6 months) of DAPT appears as the safest strategy, while a prolonged duration (24-36 months) reduces thrombotic complications but with an excess in major bleeding complications.

Contains fulltext : 172736.pdf (Publisher’s version ) (Closed access) Residual high-on treatment platelet reactivity (HRPR) has been associated with a 2-9 fold increased risk of acute ischemic events in patients with acute coronary syndromes or coronary stenting. However, the mechanism of suboptimal platelet inhibition are still poorly understood. Aim of present study was to evaluate the role of the percentage of reticulated platelets on HRPR with ticagrelor. In patients treated with ASA (100-160 mg) and ticagrelor (90 mg twice a day) platelet reactivity and the reticulated platelets fraction (immature platelets fraction, IPF) were assessed at 30-90 days after acute coronary syndrome. Aggregation was assessed by multiple-electrode aggregometry. HRPR was defined as ADP test >417 AU*min. Our population is represented by 190 patients, divided according to tertiles values of IPF (/=4 %). Higher IPF was associated to a larger platelet volume and lower platelets count (p < 0.001), and inversely related with a history of previous coronary revascularization (p = 0.03). Twenty-one out of 190 (11.0 %) patients displayed HRPR. No difference in the levels of circulating IPF was found in patients with or without HRPR (p = 0.25), with no correlation between the rate of reticulated platelets and platelet reactivity at ADP test (r = -0.084, p = 0.26). In fact no association was observed between high levels of IPF and the occurrence of HRPR (adjusted OR[95 % CI] = 0.69[0.34-1,37], p = 0.28), even after correction for baseline differences. In patients treated with ticagrelor, the levels of circulating reticulated platelets assessed at 30-90 days post-ACS are not associated with platelet reactivity or the occurrence of HRPR.

Background/Aims: Coronary artery disease (CAD) is a major cause of mortality worldwide. Hyperhomocysteinemia has been identified as a risk factor for CAD due to increased thrombogenicity, oxidative stress status and endothelial dysfunction. Few data have been provided on the impact of diabetes on homocysteine and its relationship with the prevalence and extent of CAD in this high-risk subset of patients and therefore, this is the aim of this study. Methods: Our population is represented by a consecutive cohort of patients undergoing coronary angiography at Azienda Ospedaliera-Universitaria, ‘Maggiore della Carità', Novara, Italy from March 2007 to October 2012. Results: Diabetes was observed in a total of 1,125 out of 3,534 patients. Diabetes was associated with more advanced age, hypercholesterolemia, arterial hypertension, renal failure, previous myocardial infarction, coronary revascularization (p < 0.001, respectively) and smoking (p = 0.001). Patients with diabetes were more frequently on angiotensin-converting-enzyme inhibitors, angiotensin receptor blockers, beta-blockers, calcium-antagonists, diuretics, statins (p < 0.001, respectively), and acetylsalicylic acid (p = 0.004). Patients with diabetes displayed higher creatinine and triglycerides (p < 0.001), but lower total and high-density lipoprotein-cholesterol (p < 0.001) and haemoglobin (p < 0.001). Diabetes was associated with a significantly higher prevalence and extent of CAD and more complex lesions at angiography, including calcified lesion, total occlusions, in-stent restenosis. No significant difference was found in total homocysteine (tHcy) levels between diabetic and non-diabetic patients (p = 0.2). No difference in the percentage of patients with tHcy above the third tertile (≥18.2 nmol/ml) was observed between patients with or without diabetes (32.8 vs. 35%, p = 0.18; adjusted OR 0.88, 95% CI 0.73-1.05, p = 0.14). Among patients with diabetes, no significant association was found between tHcy, CAD (82.4 vs. 83.6 vs. 78.6%, p = 0.19) or severe CAD (33.2 vs. 33.1 vs. 36.9%, p = 0.18). Same results were observed after correction for baseline differences (adjusted OR 0.78, 95% CI 0.61-1.02, p = 0.11) for CAD and severe CAD (adjusted OR 0.92, 95% CI 0.76-1.13, p = 0.46). Conclusions: In our study, diabetes was not associated with higher tHcy levels. Furthermore, elevated tHcy is not a risk factor for CAD among patients with diabetes.

Contains fulltext : 172755.pdf (Publisher’s version ) (Closed access) Contrasting data have been reported so far on the role of reticulated platelets in suboptimal response to antiplatelet therapies. In particular, still unexplored is whether they may contribute to explain the higher risk of thrombotic complications observed in diabetic patients. Aim of the present study was to evaluate the impact of diabetes on the levels of reticulated platelets and its relationship with high residual on-treatment platelet reactivity (HRPR) in patients receiving dual antiplatelet therapy. In patients treated with ASA (100-160 mg) and clopidogrel (75 mg daily) or ticagrelor (90 mg twice a day) platelet reactivity and the reticulated platelets fraction (immature platelets fraction, IPF) were assessed at 30-90 days post-discharge for an acute coronary syndrome or elective PCI. Aggregation was assessed by multiple-electrode aggregometry. We included 386 patients, 158 (40.9 %) diabetics. The percentage of IPF was similar in diabetic and non diabetic patients, both at baseline (3.5 +/- 2.5 vs 3.6 +/- 2.7 %, p = 0.91) and at 30-90 days re-assessment (3.3 +/- 2.1 vs 3.5 +/- 2.5 %, p = 0.30), with diabetes not emerging as an independent predictor of IPF above III tertile (adjusted OR [95 %CI] = 0.58 [0.30-1.09], p = 0.10). Diabetic patients displayed an enhanced platelet reactivity and a higher rate of HRPR with ADP antagonists (32.8 vs 22.5 %, p = 0.009). However, no association was found between the percentage of IPF and platelet function (r = -0.004; p = 0.95 for ASPI test, r = -0.04; p = 0.59 for ADP-mediated aggregation), or the rate of HRPR for ADP antagonsist across IPF tertiles. Results were similar for diabetics both receiving clopidogrel and ticagrelor. Diabetic patients display a higher platelet reactivity and suboptimal response to ADP-antagonists. However, the rate of reticulated platelets is neither influenced by diabetic status nor associated with an increased platelet reactivity among diabetic patients receiving dual antiplatelet therapy for a recent acute coronary syndrome or PCI.

Background The optimal duration of dual antiplatelet therapy (DAPT) in acute coronary syndrome (ACS) patients treated with drug eluting stents (DES) is still under debate. Recent meta-analyses on ≤6months versus 12months DAPT suggest that bleeding rates can be reduced, without a higher rate of thrombotic complications. In particular, the COMBO dual therapy stent, being associated with early re-endothelialization, may allow for a reduction of the duration of DAPT without increasing the thrombotic risk, while reducing the risk of bleeding complications. Aim The aim of the REDUCE trial is to demonstrate the non-inferiority of a combined efficacy and safety endpoint of a short-term 3months DAPT strategy as compared to standard 12-month DAPT strategy in ACS patients treated with the COMBO stent. Design A prospective, multicenter, randomized study designed to enroll 1500 patients with ACS treated with the COMBO stent. Patients will be randomized before discharge in a 1:1 fashion to either 3 or 12months of DAPT. A clinical follow-up is scheduled at 3, 6, 12, and 24months. The primary endpoint is the time to event as defined by the occurrence of one of the following: all cause mortality, myocardial infarction, stent thrombosis, stroke, target vessel revascularization or bleeding (Bleeding Academic Research Council type II, III and V) within 12months. The study has recruited patients since July 2014, and the results are expected in 2017. Summary A reduction of the DAPT duration in ACS patients after PCI without affecting the thrombotic risk is an attractive option with regard to the associated bleeding risk. The REDUCE trial will be the first to investigate the efficacy and safety of a 3-month DAPT strategy compared to a 12-month DAPT strategy in an ACS only population treated with the COMBO stent.

Distal embolization is a relatively common complication in primary angioplasty and is associated with poor perfusion and higher mortality. The aim of this article is to critically review literature on thrombectomy devices to prevent distal embolization in patients undergoing primary angioplasty. Several manual and mechanical devices have been proposed. Although negative data have been observed with mechanical devices, significant impact on mortality has been observed with routine use of manual thrombectomy devices, due to an improvement in myocardial perfusion and reduction in distal embolization. Therefore, routine adjunctive manual thrombectomy devices should be recommended in the setting of ST-segment elevation myocardial infarction, whereas the use of larger manual thrombectomy devices (7F) or mechanical devices may be considered in patients with large thrombotic burden to provide more guarantees for complete thrombus removal.

SummaryIt has been shown that bleeding complications are associated with higher mortality rates among patients undergoing coronary angioplasty. Due to its properties, bivalirudin may provide benefits in terms of bleeding and thrombotic complications as compared to unfractionated heparin (UFH).The aim of the current study was to perform a meta-analysis of randomised trials to evaluate whether bivalirudin might offer benefits in terms of mortality as compared to UFH.We obtained results from all randomised trials evaluating the benefits of adjunctive bivalirudin as compared to UFH with or without Gp IIb-IIIa inhibitors among patients undergoing coronary angioplasty. The literature was scanned by formal searches of electronic databases (MEDLINE and CENTRAL) from January 1990 to October 2008.The following keywords were used: randomised trial, coronary angioplasty, stent, reperfusion, primary angioplasty, bivalirudin, direct thrombin inhibitors, hirulog. Primary endpoint was mortality. Secondary endpoint was infarction. Safety endpoint was the risk of major bleeding complications. No language restriction was applied.A total of nine randomised trials were included in the metaanalysis, with 15655 patients randomised to bivalirudin and 13104 patients randomised to UFH. We did not observe any difference in mortality between bivalirudin and UFH (1.73% vs 1.67%, p = 0.15) without any relationship between the baseline risk of mortality (r = 0.17, p = 0.71) or the reduction in major bleeding complications (r = –0.29, p = 0.53) and the benefits in mortality with bivalirudin. A trend in higher risk of myocardial infarction was observed with bivalirudin (6.9% vs 5.9%, p = 0.07, p het = 0.65). Bivalirudin was associated with a significant reduction in major bleeding complications (1.7% vs 3.4%, p < 0.0001), as compared to UFH.This meta-analysis shows that among patients undergoing coronary angioplasty, bivalirudin is associated with significant reduction in major bleeding complications. However, these benefits did not translate into benefits in mortality, with even a trend in higher risk of myocardial infarction.

Growing attention has been addressed to the cardiovascular effects of vitamin D, in order to prevent the vascular wall degeneration and the progression of atherosclerosis. Diabetes mellitus is an established risk factor for coronary artery disease, where the enhanced pro-inflammatory and pro-thrombotic status could render even more important the athero-protective effects of vitamin D. Therefore, we aimed to evaluate the impact of diabetes on vitamin D levels and its relationship with the extent of CAD.Consecutive patients undergoing non urgent coronary angiography were included. Admission samples were collected for vitamin D levels assessment. Significant coronary artery disease was defined as at least 1 vessel stenosis50%, severe coronary artery disease as left main and/or trivessel disease, as evaluated by quantitative coronary angiography.Patients included were 1859, among them 641 were diabetics (34.5%). Diabetic patients displayed older age, higher rate of renal failure, previous cardiovascular events, hypercholesterolemia, hypertension, glycaemia, HbA1c, creatinine, uric acid (p 0.001, respectively). Lower levels of haemoglobin, total cholesterol, high and low density lipoprotein cholesterol (p 0.001) were found in diabetics. Diabetic patients displayed significantly lower levels of vitamin D (p = 0.003), however diabetes did not emerge as an independent predictor of hypovitaminosis-D (adjusted OR [95% CI] = 0.95[0.72, 1.26], p = 0.72). In diabetics, lower vitamin D levels were associated to female gender (p = 0.003), glucose control and lower haemoglobin levels (p 0.001). Lower levels of vitamin D were related with the prevalence (adjusted OR [95% CI] = 1.54[1.12-2.12], p = 0.008) and severity (adjusted OR [95% CI] = 1.28[1.014-1.621], p = 0.038) of coronary artery disease.The present study shows that diabetes mellitus is not an independent predictor of hypovitaminosis-D. However, diabetic patients showed lower vitamin D levels that were independently associated with an increased prevalence and severity of coronary artery disease.

Mean platelet volume (MPV) has been proposed as a marker of platelet reactivity and cardiovascular disease. Chronic kidney disease (CKD) significantly favors the occurrence of cardiovascular events, by increasing the circulating levels of a wide spectrum of pro-oxidant and pro-thrombotic mediators. However, opposite alterations of platelet function, both enhanced aggregability and increased bleeding diathesis have been reported in these patients, with contrasting results on the effects of renal function on MPV and coronary artery disease, that were assessed in present study.In patients undergoing coronary angiography, MPV and renal function (serum creatinine and estimated Glomerular Filtration Rate, eGFR, by MDRD formula) were assessed at admission. Coronary artery disease (CAD) was defined as a stenosis50% in at least 1 coronary vessel, while severe CAD as left main or trivessel disease.Among 3712 patients, 1044 (28.1%) had chronic kidney disease. CKD was related with age, female gender, diabetes and glycemic control, history of myocardial infarction, cerebrovascular accidents, coronary artery bypass grafting and left ventricular dysfunction or arrhythmias as indication to angiography, therapy with angiotensin-receptor blockers, nitrates, diuretics and calcium-antagonists, but lower rate of smoking, lower fibrinogen levels, haemoglobin, total and HDL cholesterol (p0.001, respectively). CKD patients displayed increased severity and complexity of CAD (p0.001) and significantly larger platelet volume (p0.001), with CKD resulting as independent predictor of MPV above the median (≥10.85fl; Adjusted OR[95%CI]=1.56[1.23,1.99], p=0.002). Moreover, in the 1044 patients with renal failure, higher platelet volume (above the median value; ≥10.85fl) was associated with age (p=0.05), haemoglobin levels and platelet count (p0.001), but not to a higher prevalence or extent of coronary artery disease (CAD: adjusted OR[95%CI]=0.80[0.58-1.09], p=0.16; severe CAD, adjusted OR[95%CI]=1.07[0.81-1.41], p=0.65).Higher values of MPV are observed among patients with chronic kidney disease, inversely relating to eGFR. However, larger platelet size does not contribute to explain the increased severity of coronary artery disease observed among these patients.

Suboptimal platelet inhibition still represents an important challenge, especially for patients undergoing percutaneous coronary interventions (PCI). Chronic kidney disease (CKD) is a common comorbidity of patients with coronary artery disease, and may potentially influence platelet reactivity. So

Patients with coronary artery disease who undergo stent implantation and have concomitant indication for long term oral anticoagulation represent a considerable percentage of the overall population. To date there is still no consensus about the optimal antithrombotic strategy to choose in this kind

Background Acetylsalicylic acid (ASA) represents the basis of pharmacological therapy for cardiovascular prevention. However, several patients are excluded from the benefits of ASA for hypersensitivity problems, and controversies still exist on their management. The aim of present study was to evaluate the safety and efficacy of ASA desensitization protocols in patients requiring dual antiplatelet therapy for coronary artery disease. Methods Literature archives and main scientific sessions' abstracts were scanned for studies describing desensitization protocols for patients with ASA hypersensitivity. Primary endpoint was the tolerance of ASA maintenance therapy (protocol success). Secondary endpoints were: 1) the occurrence of hypersensitivity symptoms during the protocol, 2) the rate of ASA discontinuation at follow-up; 3) recurrent cardiovascular ischemic events. Results We finally selected 14 studies out of 335 initially screened citation, reporting complete data on protocol desensitization strategies, with a total of 256 patients. Among them 213 (83.2%) underwent an oral desensitization protocol, while 43 received endovenous ASA. The protocol was successfully completed in 238 out of 256 patients (92.9%), who were subsequently kept on chronic daily therapy with ASA. The weighted success proportion was wP [95%CI] = 93[89.8–96.1]%. Hypersensivity symptoms occurred during the desensitization protocol in 29 patients, with a pooled events rate of 11.3[7.5–15.2]%. All adverse reactions were safely faced with pharmacological interventions. In 11 of these patients, slowing the protocol or restarting another ASA challenge could successfully achieve the tolerance. The rate of ASA discontinuation and major cardiovascular events was extremely low (6.1 and 2.3% respectively). Conclusions Aspirin desensitization protocols represent a safe and effective option for the management of patients with a cardiovascular indication to ASA and history of allergy to ASA. Future randomized trials are certainly needed to confirm present findings and provide indications for the optimization of these protocols.

Item does not contain fulltext OBJECTIVE: High on-treatment platelet reactivity (HRPR) is associated with a two- to ninefold increased risk of recurrent ischemic events among patients receiving dual antiplatelet therapy (DAPT) for coronary artery disease. However, its determinants are still poorly understood. The aim of the present study was to assess the impact of mean platelet volume (MPV) on platelet reactivity in patients receiving DAPT after an acute coronary syndrome or PCI. METHODS: Patients treated with DAPT (acetylsalicylic acid [ASA] and clopidogrel or ticagrelor) were scheduled for platelet function assessment at 30 - 90 days post-discharge. By whole blood impedance aggregometry, HRPR was considered for ASPI test > 862 aggregation units (AU)*min (for ASA) and ADP test values >/= 417 AU*min (for ADP-antagonists). RESULTS: Our population is represented by a total of 487 patients on DAPT, divided according to MPV tertiles (< 10.4 fl; 10.4 - 11.29 fl; >/= 11.3 fl). Larger-sized platelets were associated with use of statins (p < 0.001) and beta-blockers (p = 0.03), higher hemoglobin levels (p = 0.002) and lower platelets count (p < 0.001). Higher platelet reactivity was observed at ASPI test in patients with higher MPV (r = 0.12, p = 0.008), but not for ADP-mediated aggregation (r = -0.007, p = 0.88). However, a low prevalence of HRPR was observed with ASA, with no impact of MPV tertiles (1.2 vs 1.1 vs 1.6%, p = 0.70, adjusted OR [95% CI] = 1.05 [0.51 - 1.77], p = 0.87). MPV did not influence the prevalence of HRPR for ADP-antagonists (25.9 vs 1 vs 26.5%, p = 0.89; adjusted OR [95% CI] = 1.1 [0.84 - 1.45], p = 0.50) with similar results among the 259 patients receiving clopidogrel (adjusted OR [95% CI] = 1.15 [0.82 - 1.62], p = 0.43) and the 228 patients on ticagrelor (adjusted OR [95% CI] = 1.46 [0.84 - 2.55], p = 0.18). CONCLUSION: In patients receiving DAPT, MPV does not affect the response to major antiplatelet therapies. In fact, MPV elevation does not influence the risk of HRPR with clopidogrel, ticagrelor or ASA.

Despite the demonstrated benefits of Prasugrel, a new generation thienopyridine, in the prevention of thrombotic complications after percutaneous coronary interventions (PCI) for Acute Coronary Syndromes (ACS), its use is still precluded to those many patients arriving to the cath lab pre-treated with Clopidogrel. Conclusive data on the strategy of switching from Clopidogrel to Prasugrel are still missing, therefore we aimed to perform a meta-analysis of current studies evaluating the safety and efficacy of switching from Clopidogrel to Prasugrel (PS) as compared to a standard thienopyridine therapy with Clopidogrel or Prasugrel in patients undergoing PCI. Literature archives and main scientific sessions' abstracts were scanned for studies comparing a switching strategy from Clopidogrel to Prasugrel vs. Prasugrel or Clopidogrel. Primary efficacy endpoint was overall mortality. Secondary endpoints were: non-fatal myocardial infarction and definite/probable stent thrombosis. Safety endpoint was the rate of major bleedings according to a per-protocol definition. A total of 12 studies, involving 3956 patients, were included. Among them, 1396 patients (35.3%), received Prasugrel after a Clopidogrel treatment (PS), while 2560 (64.7%) received either Prasugrel or Clopidogrel. The switch from Clopidogrel to Prasugrel was in the majority of the studies periprocedural. The mortality was numerically lower, but not statistically significant, in the PS group as compared with patients who did not switch (1.7% vs. 3.8%, OR [95% CI] = 0.68 [0.40,1.15], p = 0.15, phet = 0.61), without any relationship with patients' risk profile (r = -0.68 [-2.09, 0.73], p = 0.35). Similar results were obtained for secondary efficacy endpoints and at sensitivity analysis in the majority of subgroups evaluated. Moreover, the PS strategy did not increase major bleedings as compared with standard therapy (1.4% vs. 2.5%, OR [95% CI = 0.70 [0.39, 1.25], p = 0.23, phet = 0.6). The present meta-analysis confirms that, among patients undergoing PCI, switching from Clopidogrel to Prasugrel may be safely performed and therefore should be encouraged among patients eligible to Prasugrel.

The neutrophil to lymphocyte ratio (NLR), an inflammatory biomarker, may be of predictive and prognostic value for cardiovascular (CV) events. We evaluated the relationship of NLR with the prevalence and extent of coronary artery disease (CAD) in consecutive patients undergoing elective or urgent coronary angiography. Our population (n = 3738 patients) was divided into NLR quartiles. Higher NLR was associated with aging and established CV risk factors, previous percutaneous coronary revascularization, acute presentation, and more complex pharmacological therapy. The NLR was related to platelet count, white blood cell count, creatinine, glycemia, uric acid, and C-reactive protein (all P = .001) levels but inversely related to hemoglobin ( P < .001), total cholesterol ( P = .005), and triglycerides ( P < .001) levels. The NLR was associated with multivessel disease ( P < .001), anterior descending, right coronary arteries ( P < .001) or circumflex branch lesions ( P = .01), percentage of stenosis ( P < .001), coronary calcification ( P < .001), and intracoronary thrombus ( P < .001) but inversely with in-stent restenosis ( P < .001) and thrombolysis in myocardial infarction flow ( P = .04). The NLR was directly related to the prevalence of CAD ( P = .001) and severe CAD ( P < .001). In patients undergoing coronary angiography, the NLR is independently associated with the prevalence and severity of CAD.

Coronary perforation is a severe complication of percutaneous coronary intervention (PCI) with high mortality and morbidity. The incidence of coronary perforation in patients undergoing PCI ranges from 0.1% to 0.5%. The use of long balloon inflation and reversal anticoagulation is associated with high mortality, periprocedural myocardial infarction and emergency coronary bypass surgery. We present a case of severe coronary perforation treated with the dual catheter technique through the radial and femoral approach. The dual catheter technique enabled rapid delivery of a covered stent without losing control of the perforation site. Our patient did not show pericardial effusion, hemodynamic instability or need for emergency bypass surgery. About 1h after PCI, he developed acute stent thrombosis treated with thromboaspiration and biolimus-eluting stent implantation. At 2 years of follow-up, he was asymptomatic without evidence of exercise-induced ischemia. We conclude that the dual catheter technique is a safe and effective approach to treat PCI-induced severe coronary perforation, and may significantly improve patient outcome compared to historical series.

We have hypothesized that high red blood cells (RBC) count can potentially play an atheroprotective role in patients with coronary atherosclerosis. We, therefore, have investigated the relationship between high density lipoproteins cholesterol (HDL-C) and RBC levels in patients undergoing coronary angiography. Coronary artery disease (CAD) is a major cause of mortality. Impaired lipid profile represents a major risk factor for atherosclerosis. High density lipoprotein (HDL) is a key factor in atherosclerosis disease development. RBC can mimic HDL's reverse cholesterol transportation with a potential atheroprotective role. Coronary angiography has been evaluated in 3,534 patients. Fasting samples were collected for haematology and lipids levels assessment. Coronary disease was defined for at least 1 vessel stenosis50 %. Patients were divided according to HDL-C and RBC tertiles. Lower HDL-C was significantly associated to the prevalence of CAD (84.8 vs 78.5 vs 67.3 %, p ≤ 0.001; adjusted OR [95 % CI] = 1.55 [1.3-1.8], p0.001) and severe CAD (30 % vs 30 % vs 24.4 %, p = 0.002; adjusted OR [95 % CI] = 1.08 [1.01-1.16], p = 0.02), this relationship was maintained even dividing our population according to RBC tertiles (p0.001).In conclusion, HDL-C levels are directly related to RBC count and inversely to the prevalence and extent of coronary disease. Higher RBC levels can reduce the risk of CAD in patients with lower HDL-C levels, suggesting an important atheroprotective role.

Item does not contain fulltext Contrast-induced nephropathy (CIN) is a common complication in patients with impaired kidney function undergoing coronary angiography/angioplasty. We evaluated whether elevated homocysteine (known to be associated with free radical generation and oxidative stress) increases the risk of CIN. Patients (n = 876) with creatinine clearance /=0.5 mg/dL or >/=25% creatinine increase 24 to 48 hours post-PCI. A significant relationship was observed between homocysteine levels and the risk of CIN (P = .033), confirmed after correction for baseline confounding factors, adjusted odds ratio, OR (95% confidence interval, [CI]) = 1.68 (1.09-2.59), P = .019. This association was also significant applying the new definition of contrast-induced acute kidney injury (11.9% in group 1, 10.4% in group 2, and 22.8% in group 3; P < .001), adjusted OR (95% CI) = 1.96 (1.3-2.95), P = .001. Future studies are needed to confirm our findings and to define the role of homocysteine in CIN.

Item does not contain fulltext BACKGROUND: Alterations of glucose homeostasis have been reported to occur even in non-diabetic patients, thus increasing the risk of cardiovascular events and worsening the outcome after an acute myocardial infarction (AMI). Still debated is the role of impaired glucose control in patients undergoing percutaneous coronary intervention (PCI), as hyperglycemia, represents an important pro-thrombotic stimulus, increasing platelet reactivity and potentially procedural complications. Therefore, the aim of our study was to assess the association between glycosylated hemoglobin and periprocedural myocardial infarction (PMI) in non-diabetic patients undergoing PCI. METHODS: We included patients without history of diabetes undergoing elective PCI. PMI was defined as creatine kinase-MB increase by 3 times the upper limit normal or by 50% of an elevated baseline value, whereas periprocedural myonecrosis as Troponin I increase by 3x ULN or 50% of baseline. RESULTS: Our population is represented by 1199 patients, who were divided according to tertile values of glycosylated hemoglobin (HbA1c). Higher HbA1c was associated with ageing (p

Item does not contain fulltext INTRODUCTION: Dual antiplatelet therapy (DAPT) is considered essential in clinical management of patients undergoing percutaneous coronary revascularization or acute coronary syndromes. However, the optimal platelet inhibition is not always obtained, with high residual platelet reactivity (HRPR) increasing stent thrombosis and recurrent ischemic events. Aim of this study was to investigate the impact of body mass index (BMI) on platelet reactivity in patients on DAPT. METHODS: We included patients treated with acetylsalycilic acid (ASA) (100-160 mg) and clopidogrel (75 mg) or ticagrelor (90 mg twice a day) for acute coronary syndromes or drug-eluting stent implantation. Platelet reactivity was assessed at 30-90 days postdischarge by multiple-electrode aggregometry. HRPR for adenosine diphosphate (ADP) antagonists was defined as ADP test results >417 AU*min. HRPR for ASA was considered for ASPI test >862 AU*min. RESULTS: Our population is represented by 498 patients, 308 (61.8%) were treated with clopidogrel and 190 (38.2%) with ticagrelor. Overall, higher BMI was related with younger age (P = 0.003), higher prevalence of diabetes mellitus (P < 0.001), hypercholesterolemia (P = 0.017), hypertension (P < 0.001), chronic therapy with angiotensin-receptor blockers (P = 0.019), calcium channel blockers (P = 0.003). Higher values of BMI directly related with hemoglobin (P = 0.02), triglycerides (P < 0.001), glycemia (P = 0.035), HbA1c (P < 0.001), and inversely related with high-density lipoprotein cholesterol (P = 0.01). BMI did not influence the effectiveness of ASA, whereas it was associated to a nonsignificant trend for higher platelet reactivity (r = 0.08, P = 0.08) for ADP antagonists. In fact, 111 patients (22.3%) displayed HRPR at ADP test (>417 AU*min) with no statistically significant difference according to BMI {20.3% vs. 27.1% vs. 25.7%, P = 0.28; adjusted odds ratio [OR] [95% confidence interval (CI)] = 1.19 [0.86-1.64], P = 0.30}. However, results were different when considering separately patients receiving clopidogrel or ticagrelor. In the clopidogrel-treated subgroup, significantly higher ADP-mediated aggregation values were found in patients with higher BMI (r = 0.14, P = 0.023) that emerged as an independent predictor of HRPR with clopidogrel [OR (95% CI), 1.45 (1.01-2.12), P = 0.049]. On the contrary, no impact of BMI was observed in the ticagrelor-treated subgroup for platelet reactivity (r = -0.036, P = 0.62) or the prevalence of HRPR [adjusted OR (95% CI), 0.73 (0.39-1.36), P = 0.32]. CONCLUSIONS: This study shows that among patients treated with DAPT for coronary artery disease, higher BMI is related to increased platelet reactivity and a higher prevalence of HRPR in clopidogrel-treated patients while not significantly influencing the effectiveness of ticagrelor or ASA.

Background: Uncertainty still exists on the correct management of antithrombotic therapies after Transcatheter Aortic Valve Replacement (TAVR). Dual antiplatelet therapy (DAPT) is currently recommended on empirical basis, although having been claimed to increase bleedings without offering enhanced

Great interest has been focused in the last year on genetic predictors of cardiovascular risk. Glycoprotein IIb/IIIa (GP IIb/IIIa), fibrinogen receptor, is the final common pathway for aggregation and a key point for atherothrombosis. A single nucleotide polymorphism of IIIa subunit (Leu33Pro-PlA(1)/PlA(2) allele) has been suggested to increase aggregation and adhesion, however, contrasting reports have been reported so far on its effects on coronary artery disease (CAD). Aim of the current study was to perform a large meta-analysis including cohorts of patients undergoing coronary angiography in order to evaluate whether this polymorphism is associated with coronary artery disease. Literature archives (Pubmed, EMBASE, Cochrane) and main scientific sessions abstracts were scanned for data of consecutive cohorts of patients undergoing coronary angiography, where PlA genotype was assessed. Primary endpoint was the prevalence of CAD. Secondary endpoint was severity of CAD defined as prevalence of multivessel disease (≥2 vessels). Data from seven studies were extracted, including a final number of 6700 patients. Among them 1893 (28.3%) carried the PlA(2) polymorphism, 163 of them in homozygosis. Angiographically defined CAD was present in 3573 (74.3%) PlA(1)/PlA(1) patients and in 1430 (75.5%) PlA(2) carriers. PlA(2) polymorphism was not associated with an increased prevalence of coronary artery disease, (OR [95% CI] = 1.07 [0.95-1.21], p = 0.28, pheterogeneity = 0.39). Similar results were obtained for multivessel disease (OR [95% CI] = 1.07[0.95-1.20], p = 0.27, pheterogeneity = 0.12). Meta-regression analysis demonstrated a significant inverse relationship between the risk of CAD among the PlA(2) carriers and ageing (r = -0.044, (-0.09, -0.0008), p = 0.046). Present meta-analysis demonstrates that 33Leu → Pro substitution of GPIIIa does not influence the prevalence and extent of angiographically defined coronary artery disease in general population, although apparently playing a role among younger patients.

Periprocedural myocardial infarction still occurs in patients undergoing percutaneous coronary intervention. However, very little is known about the role of biomarkers possibly predicting this complication. Serum uric acid has been associated with enhanced inflammatory status, higher thrombotic risk and poorer outcome after percutaneous coronary intervention. We therefore, evaluated the association between uric acid levels and periprocedural myocardial infarction in patients undergoing percutaneous coronary intervention.We evaluated 1272 consecutive patients undergoing percutaneous coronary intervention. We measured myonecrosis biomarkers at intervals from 8 to 48 h after percutaneous coronary intervention. Periprocedural myonecrosis was defined as a troponin I increase by 3 times the upper limit normal (ULN) or by 50% of an elevated baseline value and periprocedural myocardial infarction as creatine kinase-Myocardial Band increase by 3 times the ULN or 50% of baseline.Patients were divided according to tertile values of uric acid (5.40, ≥ 6.70 mg/dL). Serum uric acid was related to age, male gender, hypertension, smoking, renal failure (p0.001), previous coronary artery bypass grafts (p = 0.05), therapy with ACE inhibitors (p = 0.001) and diuretics (p0.001), glycaemia (p = 0.001), creatinine (p0.001), haemoglobin (p = 0.002) and white blood cells (p = 0.02). Serum uric acid was inversely related to type C lesions (p = 0.03) and coronary thrombus (p = 0.02). SUA did not affect the risk of periprocedural myocardial infarction (p = 0.29; adjusted odds ratio = 1.11[0.93-1.32], p = 0.26) or periprocedural myonecrosis (p = 0.97; adjusted odds ratio = 0.99[0.86-1.14], p = 0.89). Results were confirmed at subgroup analyses of higher-risk subsets of patients.This is the first large study showing that serum uric acid is not associated with an increase in the risk of periprocedural myocardial infarction in patients undergoing percutaneous coronary revascularization.

Contrast induced nephropathy (CIN) is a common complication of coronary angiography/angioplasty. Prevention is the key to reduce the incidence of CIN and it begins with appropriate pre-procedural management. Statins have been shown to possess pleiotropic effects (anti-oxidant, anti-inflammatory and anti-thrombotic properties) and their effects on CIN were assessed in several studies with conflicting results. Aim of this meta-analysis is to evaluate the efficacy of short-term statins for the prevention of CIN in patients undergoing coronary angiography/percutaneous interventions. We performed formal searches of PubMed, EMBASE, Cochrane central register of controlled trials and major international scientific session abstracts from January 1990 to January 2014 of trials which compares short-term statins versus Placebo for the prevention of CIN in patients undergoing coronary angiography/angioplasty. Data regarding study design, statin dose, inclusion/exclusion criteria, number of patients, and clinical outcome was extracted by 2 investigators. Eight trials were included, with a total of 4734 patients. CIN occurred in 79/2,358 patients (3.3%) treated with statins versus 153/2,376 patients (6.4%) of the placebo group [OR 95% CI 0.50 (0.38-0.66), p < 0.00001; p het = 0.39]. Benefits were both observed with high-dose short-term statins [OR 95% CI 0.44 (0.30-0.65), p < 0.0001; p het = 0.16] and low-dose statins, [OR 95% CI 0.58 (0.39-0.88), p = 0.010; p het = 0.90]. By meta-regression analysis, no significant relationship was observed between benefits from statin therapy and patient's risk profile (p = 0.26), LDL cholesterol (p = 0.4), contrast volume (p = 0.94) or diabetes rate (p = 0.38). This meta-analysis showed that among patients undergoing coronary angiography/percutaneous intervention the use of short-term statins reduces the incidence of CIN, and therefore is highly recommended even in patients with low LDL-cholesterol levels.

Item does not contain fulltext Prasugrel has been shown to be superior to clopidogrel in the setting of ACS patients undergoing coronary angioplasty. However, few data have been reported so far on those patients who switch from clopidogrel to prasugrel after coronary angioplasty. Aim of the current study was to evaluate the safety of prasugrel loading dose administration in ACS patients undergoing PCI and pretreated with high-dose clopidogrel. From May 2010 to December 2011 150 ACS patients undergoing coronary angioplasty and pretreated with high-dose clopidogrel, were switched to prasugrel loading dose soon after the procedure. They were matched (ratio 1:2) according to sex and age with a group of 300 ACS patients undergoing angioplasty and treated with high-dose clopidogrel only from May 2010 to December 2011. All demographic clinical and angiographic were collected. Primary endpoint was the rate of major bleeding complications (according to ACUITY trial definition) at 30-day follow-up. Secondary endpoints were: TIMI major and minor bleeding, definite stent thrombosis, major adverse cardiac events (MACE) and Net adverse cardiac events (NACE) at 30-day followup. The two groups of patients showed similar baseline demographic, and clinical characteristics. Most of the patients had unstable angina or non-ST segment elevation myocardial infarction. Almost (about 95 %) all patients underwent radial approach. No difference was observed in major bleeding complications according to both ACUITY (2.0 vs 2.0 %) and TIMI Major (0.7 vs 1.3 %) definition. No difference between the two groups was observed in terms of in-stent thrombosis, MACE and NACE at 30-day follow-up. Our observational study showed that switching to prasugrel with loading dose soon after angioplasty among ACS patients who were pretreated with clopidogrel seems to be well tolerated without overt evidence of heightened major bleeding. Future large randomized trials are certainly needed to confirm these findings.

Diabetic patients undergoing percutaneous coronary interventions are still regarded as a very high risk category because of an increased platelet reactivity and risk of complications, especially in patients with inadequate glycaemic control. However, although its prognostic effect on long-term outcome is well-defined, still unclear is the effect of diabetes on the risk of periprocedural myocardial infarction in patients undergoing percutaneous coronary interventions, which was therefore the aim of our study.Myonecrosis biomarkers were dosed at intervals from 6 to 48 h after nonemergent percutaneous coronary interventions. Periprocedural myocardial infarction was defined as creatine kinase-MB increase by three times the upper limit normal or by 50% of an elevated baseline value, whereas periprocedural myonecrosis as troponin I increase by three times the upper limit normal or 50% of baseline.Of 1311 patients, diabetes mellitus was found in 458 patients (34.9%) and associated with age (p = 0.03), hypertension (p 0.001), renal failure (p = 0.01), previous MI (p = 0.03), previous coronary revascularization (p 0.001), higher fasting glycaemia and lower haemoglobin (p 0.001), more severe coronary disease (p 0.001), multivessel percutaneous coronary interventions (p = 0.03), coronary calcification (p = 0.003) and in-stent restenosis (p 0.001) but lower presence of thrombus (p = 0.03). Diabetic patients were receiving significantly more frequent specific pharmacological treatment at admission. Diabetic status did not influence the risk of periprocedural myocardial infarction or periprocedural myonecrosis [adjusted OR(95%CI) = 0.90(0.64-1.27), p = 0.57 and adjusted OR(95%CI) = 0.92(0.70-1.21), p = 0.55]. Amongst diabetic patients, we did not observe any effect of chronic glycaemic control on periprocedural myocardial infarction.Diabetic status, independent of chronic glycaemic control, is not associated with increased risk of periprocedural myocardial infarction and myonecrosis in patients undergoing percutaneous coronary interventions.

Item does not contain fulltext Acute coronary syndromes (ACSs) represent a high-risk condition, as enhanced platelet reactivity importantly influences myocardial perfusion and procedural results after percutaneous coronary intervention (PCI). In fact, higher rate of periprocedural myocardial infarction (PMI) and reduced event-free survival have been reported in these patients. The single nucleotide polymorphism Leu33Pro of platelet glycoprotein IIIa has been related to an increased platelet reactivity, a lower response to antiplatelet agents and higher risk of stent restenosis. Therefore, our aim was to evaluate the impact of this polymorphism on PMI in patients undergoing PCI for non-ST-segment elevation MI (NSTEMI). Our population is represented by 478 consecutive patients undergoing coronary angioplasty for NSTEMI. Cardiac biomarkers were monitored at intervals from 8 to 48 h after the procedure. Genetic analysis was performed to assess the presence of Leu33Pro polymorphism. A total of 156 patients (32.6%) were polymorphic. Clinical features did not differ according to genetic status, neither pharmacological treatment pre and during angioplasty. PlA carriers had lower rate of calcifications (P = 0.01) and higher coronary tortuosity (P = 0.03) at angiography and underwent more frequently to thrombectomy (P = 0.05). PCI-related complications did not differ according to genotype. Leu33Pro polymorphism was not associated with increased risk of periprocedural myonecrosis and PMI even after correction for baseline differences, [odds ratio (OR) (95% confidence interval (CI) = 0.70 (0.44-1.13), P = 0.15 for PMI and OR (95% CI) = 0.77 (0.53-1.11), P = 0.17 for myonecrosis, respectively]. Results were confirmed in high-risk subgroups of patients. In conclusion, among patients undergoing PCI for ACS, the polymorphism Leu33Pro of platelet glycoprotein IIIa is not associated with increased risk of PMI.

Item does not contain fulltext BACKGROUND: Eosinophils have been involved in a wide spectrum of pro-inflammatory and pro-thrombotic conditions, with the development of cardiovascular complications in a significant proportion of hypereosinophilic patients. However, no study has so far evaluated the impact of eosinophils levels on periprocedural myocardial infarction (PMI) in patients undergoing non-urgent percutaneous coronary interventions (PCI), that was, then, aim of current study. METHODS: In a consecutive cohort of patients, myonecrosis biomarkers were dosed at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined as troponin I increase by 3 times the ULN or by 50% of an elevated baseline value, whereas PMI as CKMB increase by 3 times the ULN or 50% of baseline. RESULTS: Our population is represented by 1543 patients who were divided according to tertiles of absolute eosinophils count (AEC 0.2 x 10^3/ml). Higher AEC was related to male gender (p = 0.002), arterial hypertension (p = 0.02), diabetes (p = 0.001), previous coronary revascularization (p = 0.003 for PCI, p = 0.03 for CABG), treatment with ARBs, beta-blockers, diuretics and ASA (p < 0.001), statins (p = 0.02), calcium antagonists (p = 0.05), glycosylated hemoglobin (p < 0001), creatinine levels (p = 0.001) and platelet count (p = 0.01), while inversely with acute presentation (p < 0.001), glycemia (p = 0.03), HDL-cholesterol and C-reactive protein (p = 0.02). AEC related with multivessel coronary artery disease (p = 0.05), lesion length (p = 0.01), drug eluting stents implantation (p = 0.001) and use of kissing balloon technique (p = 0.05), while inversely to intracoronary thrombus (p < 0.001) and thrombectomy (p = 0.04). AEC did not influence the occurrence of PMI (p = 0.06, adjusted OR [95% CI] = 1.06 [0.86-1.31], p = 0.57) or myonecrosis (p = 0.15, adjusted OR [95% CI] = 1.06 [0.88-1.27], p = 0.53). Results were confirmed at subgroup analysis in higher-risk subsets of patients. CONCLUSION: In patients undergoing non-urgent PCI, eosinophils levels are not associated with the occurrence of periprocedural myocardial infarction or myonecrosis.

Background Vitamin D (25-OH D3) deficiency represents a rising social and economic problem in Western countries. Vitamin D has been recently reported to modulate inflammatory processes, endothelium and smooth muscle cell proliferation and even platelet function, thus potentially modulating atherothrombosis. Great interest has been addressed on its impact on cardiovascular outcome, with contrasting results. The aim of current study was to evaluate the relationship between 25-OH D3 and the extent of coronary artery disease (CAD) in a consecutive cohort of patients undergoing coronary angiography. Materials and methods Patients undergoing elective coronary angiography were included in a cross-sectional study. Fasting samples were collected for 25-OH D3 levels assessment. Significant CAD was defined as at least 1 vessel stenosis > 50%, while severe CAD as left main and/or trivessel disease, as evaluated by quantitative coronary angiography. Results Hypovitaminosis D was observed in 70·4% of 1484 patients. Patients were divided according to vitamin D tertiles (

Diabetes is a major determinant of cardiovascular risk, mainly due to higher prothrombotic status and enhanced platelet reactivity. Mean platelet volume (MPV) has been suggested as indicator of platelet reactivity and moreover, diabetics have been shown to have larger MPV. The aim of our study was to evaluate the impact of diabetes and glycemic control on MPV in a large cohort of patients.Our population is represented by 3414 patients undergoing coronary angiography at Azienda Ospedaliera-Universitaria, "Maggiore della Carità", Novara, Italy. We obtained a fasting blood sample for glycemic assessment and for MPV evaluation. History of diabetes and pharmacological treatment, together with main cardiovascular risk factors were recorded. New diagnosis of diabetes was defined as nonfasting glucose200mg/dL, fasting glucose ≥126mg/dL, or HbA1c48mmol/L.Diabetes was observed in 1272 patients (37.2%). Diabetes was related to older age, waist circumference, arterial hypertension, smoking, hypercholesterolemia, renal failure, previous MI and PCI, therapy with ACE-inhibitors, ARBs, beta-blockers, diuretics, statins (respectively p0.001) and ASA (p=0.004). Diabetics had lower haemoglobin (p0.001), higher fibrinogen (p=0.001) and worst lipid profile (p0.001). MPV was related with diabetes mellitus (p0.001) and glycemic control (p=0.05; at linear regression r=0.07; p0.001 for fasting glycaemia; r=0.09; p0.001 for HbA1c, respectively). However, this relationship was not confirmed at multivariate analysis (OR[95%CI]=1.2[0.97-1.5], p=0.09 for diabetes, OR[95%CI]=1.05[0.96-1.15], p=0.25 for HbA1c). Independent predictors of MPV above median value (10.8fL) resulted to be age (OR[95%CI]=1.02[1.01-1.03], p=0.002), treatment with ARBs (OR[95%CI]=1.4[1.1-1.8], p=0.007) and haemoglobin levels (OR[95%CI]=1.2[1.15-1.23], p0.001), while inverse relationship was found with total cholesterol (OR[95%CI]=0.99[0.99-1], p=0.002).Larger MPV is associated with ageing, treatment with ARBs, cholesterol and haemoglobin levels. Diabetes mellitus and glycemic control are not independently associated with larger platelet size.

Item does not contain fulltext BACKGROUND: Contrast induced nephropathy (CIN) is a complication of coronary angiography/percutaneous intervention (PCI). It is known that diabetes is an independent risk factor for CIN, but we have no data regarding the association between CIN and glycemic levels in patients without diabetes. Aim of our study was to evaluate whether high level of glycated-haemoglobin in patients without diabetes is associated with an increased risk of CIN. METHODS: A total of 1324 patients without diabetes, undergoing elective/urgent coronary angiography/angioplasty were divided according to quartiles of baseline glycated-haemoglobin. CIN was defined as an absolute >/=0.5mg/dL or a relative >/=25% increase in creatinine level at 24-48h after the procedure. RESULTS: Patients with elevated glycated-haemoglobin were older, with hypertension, metabolic syndromes, previous history of AMI, PCI and CABG. They had higher gycaemia, fasting-glycaemia and triglycerides but lower HDL-cholesterol. Patients with higher glycated-haemoglobin were more often on therapy with statins, diuretics and calcium-antagonist at admission, had higher basal, 24 and 48h creatinine, lower creatinine clearance and lower ejection fraction. They had the highest incidence of PCI and contrast volume-eGFR rate. CIN occurred in 10.6% of patients with a linear association with glycated-haemoglobin (p=0.001). No relationship was found between glycaemia/fasting glycaemia at admission and CIN. The multivariate analysis confirmed the association between elevated glycated haemoglobin (above the median value 5.7%) and the risk of CIN after adjustment for baseline confounding factors (Adjusted OR [95% CI]=1.69 [1.14-2.51], p=0.009). In fact, the results were consistent in major high-risk subgroups. CONCLUSION: This is the first study showing that among patients without diabetes undergoing coronary angiography/PCI elevated glycated-haemoglobin but not glucose levels is independently associated with the risk of CIN.

The aim of the current study was to investigate whether the combination between mean platelet volume (MPV) and platelet distribution width (PDW) may improve the prognostic information in the prediction of prevalence and extent of coronary artery disease (CAD). We measured MPV and PDW in 2330 consecutive patients undergoing coronary angiography. Significant CAD was defined as stenosis more than 50% in at least one coronary vessel. We additionally measured carotid intima-media thickness (IMT) in 359 patients. Patients were grouped according to the median value of MPV (10.8fl) and PDW (13fl): Group 1 (MPV and PDW < 50th percentile; n = 958); Group 2 (MPV or PDW ≥50th percentile; n = 288); Group 3 (MPW and PDW ≥ 50th percentile; n = 1055). Patients in Group 3 were older (P < 0.001) with larger prevalence of diabetes (P = 0.024). Combined MPV-PWD was significantly associated with baseline glycemia (P < 0.001) and red blood cell count (P < 0.0001), but inversely related to platelet count (P < 0.0001). Combined MPV-PDW was inversely associated with the presence of thrombus, but directly related to the prevalence of chronic occlusion and worse TIMI flow. However, combined MPV-MPV was not associated with the prevalence of CAD [odds ratio (OR) (95% confidence interval (CI) = 0.99 (0.90-1.09), P = 0.87; adjusted OR (95%CI) = 0.95 (0.85-1.05), P = 0.3], or severe CAD [OR (95%CI) = 1.05 (0.95-1.16), P = 0.3; adjusted OR (95% CI) = 0.97 (0.87-1.08), P = 0.63]. No relationship was observed between IMT and the combination of PDW and MPW. This study showed that the combined information on MPV and PDW is not related to the extent of CAD and carotid IMT. Thus, both MPV and PDW can not be considered as a risk factor for CAD.

Abnormal glucose metabolism is a major determinant of coronary artery disease (CAD) and mortality in developed countries. Glycosylated hemoglobin (HbA1c) is a more stable, accurate parameter of glucose homeostasis than fasting glycemia, thus providing prognostic information in diabetics. However, its role and relationship with CAD remains unclear in non-diabetics.To evaluate the relationship between HbA1c and CAD in a consecutive cohort of patients without diabetes mellitus.Non-diabetic patients undergoing coronary angiography between April 2007 and October 2012 were included. Additionally carotid intima-media thickness (C-IMT) was evaluated during hospitalization in a consecutive cohort of patients.1,703 consecutive patients were included and divided according to HbA1c tertiles (5.5%, 5.5%-5.79%, ≥5.8%). HbA1c was associated with aging (p0.001); hypercholesterolemia (p=0.01); renal failure (p=0.006); hypertension (p=0.002); previous myocardial infarction (p=0.004); previous percutaneous coronary intervention (p=0.01); indication to angiography (p=0.01); use of angiotensin receptor blockers (p=0.01); beta-blockers (p=0.03); nitrates (p=0.02); statins (p=0.008); calcium antagonists (p=0.01); diuretics (p0.001); acetylsalicylic acid (p0.001); baseline glycemia (p0.001); triglycerides (p=0.02); and uric acid (p=0.04). HbA1c, but not fasting glycemia, was significantly associated with the prevalence of CAD (adjusted OR=1.51, 95% CI=1.15, 1.97, p=0.002), with 5.8% identified by the receiver operating characteristic (ROC) curve as the best cut-off value for CAD prediction. HbA1c was significantly associated with C-IMT and carotid plaques prevalence.Among non-diabetic patients, higher HbA1c even within the normal range is significantly associated with the risk of CAD. Future large studies are needed to evaluate whether more aggressive cardiovascular prevention can reduce the risk of CAD among patients with HbA1c ≥ 5.8%.

Platelets play a central role in the pathogenesis of coronary artery disease (CAD). Mean platelet volume (MPV) is an indicator of platelet activation, and has been demonstrated to be correlated with platelet reactivity. Diabetic patients have been shown to have larger MPV, that may contribute to higher platelet reactivity and atherothrombotic complications observed in these patients. Therefore, the aim of the current study was to investigate whether MPV is associated with platelet reactivity and the extent of CAD among diabetic patients. We performed a cohort study including 1016 consecutive diabetic patients undergoing coronary angiography at the University Hospital 'Maggiore della Carita', Novara, Italy. CAD is defined as stenosis above 50% in at least one coronary vessel at coronary angiography. Platelet reactivity was evaluated in 50 diabetic patients without history of CAD and who were free (in the past month) from medications which may affect platelet aggregation. Platelet aggregation was evaluated by light transmission aggregometry after stimulation with 1 μg/ml collagen type I. We additionally evaluated platelet surface expression of P-selectin after stimulation with U46619 (a stable synthetic analogue of the prostaglandin PGH2) and plasma concentration of thromboxane B2 (TxB2). Patients were grouped according to tertile values of MPV (10.6 fl, group 1; 10.6-11.3 fl, group 2;11.4 fl, group 3). MPV was associated with age (P=0.011), baseline fasting glucose (P=0.044), glycosylated haemoglobin (P=0.005), creatinine (P=0.052) and haemoglobin (P=0.003), but inversely related to platelet count (P0.001) and triglycerides (P=0.031). Larger MPV was associated with therapy with statins (P=0.012) and diuretics (P=0.021). CAD was observed in 826 patients (81.3%). MPV was not associated with the prevalence of CAD [odds ratio (OR), 0.85 (0.7-1.03), P=0.11]. The results were confirmed in terms of severe CAD [OR, 1.03 (0.88-1.21), P=0.7]. The absence of any significant relationship between MPV and CAD was confirmed after correction for baseline confounding factors [OR, 0.9 (0.75-1.08), P=0.19]. Finally, MPV was not related to platelet reactivity. This is the first study showing that in diabetic patients MPV is not related to platelet reactivity and the prevalence and extent of CAD. Therefore, MPV may not be considered a risk factor for CAD among diabetic patients.

Previous reports have shown that female gender is associated with impaired outcomes among patients with ST-segment elevation myocardial infarction (STEMI) treated by thrombolysis, mainly owing to a worst risk profile (more diabetes, more advanced age, and higher Killip class at presentation) compared to men. Still contrasting are data on the effect of gender on the outcome in patients with STEMI undergoing primary angioplasty. In particular, it is still unclear whether a larger infarct size might contribute to the explanation of the worse outcome in women. Therefore, the aim of the present study was to investigate gender-related differences in infarct size as evaluated by myocardial scintigraphy in a large cohort of patients with STEMI undergoing primary percutaneous coronary intervention. We included 830 patients with STEMI undergoing primary percutaneous coronary intervention. The infarct size was evaluated at 30 days using technetium-99m-sestamibi. A logistic regression analysis was performed to determine the relation between gender and infarct size (as percentage of patients above the median) after correction for baseline confounding factors. We also evaluated the presence of a potential age-gender interaction. A total of 183 patients (20.8%) were women. Female gender was associated with more advanced age and a greater prevalence of hypertension; previous infarction and smoking were more frequently observed in men. Female gender was associated with a smaller infarct size (p0.001) that was confirmed after correction for baseline confounding factors (adjusted odds ratio 0.48, 95% confidence interval 0.33-0.7, p0.001). No age-gender interaction was observed (p = 0.13). In conclusion, the results of the present study have shown that despite the presence of high-risk features at presentation, female gender was associated with a smaller infarct size than that in men, without any interaction between age and gender.

High on treatment platelet reactivity still represents a challenging issue, potentially vanishing the benefits of dual antiplatelet treatment in patients with coronary artery disease. Recent interests have emerged on potential protrombotic effect of parathyroid hormone (PTH). Aim of the present

Acute coronary syndrome represents one of the most common causes of admittance to emergency rooms in Western countries. Despite being in the majority of cases the mirror of coronary atherosclerosis, more rare causes could be hidden beyond this presentation, whose identification is often crucial for patients' outcome. We hereby present the case of a 44-year-old woman, with a history of relapsing-remitting multiple sclerosis in treatment with natalizumab, who was admitted to our division for an acute coronary syndrome. At arrival, anaemia and severe thrombocytopenia were observed; thus, no antiplatelet agent was administered. Within a few hours, aphasia occurred. Clinical presentation and the identification of schistocytes at blood smear led to the suspicion of thrombotic thrombocytopenic purpura, which was then confirmed by laboratory analysis. Immediate high-dose steroids and plasma exchange allowed discharging of the patient within a few days without neurological or cardiac sequelae.

Cardiovascular risk is still underestimated in women, experiencing higher mortality and worse prognosis after acute cardiovascular events. Gender differences have been reported in thrombotic and hemorrhagic risk during dual antiplatelet therapy (DAPT), thus suggesting a potential variability in

Statins represent a pivotal treatment in coronary artery disease (CAD), offering “pleiotropic” benefits in cardiovascular risk far beyond the lipid-lowering action. Vitamin D has been suggested as a potential mediator of the anti-atherosclerotic and anti-thrombotic effects of statins. Aim of