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Patients with coronary artery disease who undergo stent implantation and have concomitant indication for long-term oral anticoagulation represent a considerable proportion of the overall population. To date there is still no consensus about the optimal antithrombotic strategy to choose in this kind of patients, due to the difficult balance between an increased risk of bleeding and thromboembolic complications. Therefore, the aim of this study was to perform a meta-analysis to evaluate the risk and benefits of triple antithrombotic therapy versus dual antithrombotic therapy in patients undergoing coronary stent implantation, requiring long-term oral anticoagulation. We performed formal searches of PubMed, EMBASE, Cochrane central register of controlled trials and major international scientific session abstracts from January 1990 to September 2015 regarding the use of triple antithrombotic therapy (TT) versus dual therapy (DT) in patients undergoing percutaneous coronary stent implantation that required chronic oral anticoagulation. Data regarding study design, inclusion/exclusion criteria, number of patients, and selected endpoints was extracted by 2 investigators. Disagreements were resolved by consensus. Sixteen trials with a total of 21716 patients undergoing coronary stent implantation with indication to long term oral anticoagulation, were finally included. A total of 6950 received TT, whereas 14766 received DT alone. The follow-up period ranged from 180 to 730 days. Data regarding mortality were available in 21658 patients (99.7 %). All cause mortality was observed in 10.4 % patients in TT versus 16.3 % in DT (OR [95 % CI] =0.73 [0.66–0.80], p

Intracoronary thrombus is a common finding in acute coronary syndromes and often correlates with adverse prognosis and complications during percutaneous coronary interventions (PCIs). Bivalirudin, a direct thrombin inhibitor, is one of the recommended antithrombotic treatments for PCI in ST-elevation myocardial infarction (STEMI). The intracoronary administration of a bivalirudin loading dose, even if off-label, offers theoretical advantages over the standard intravenous route, providing a very high drug concentration in the infarct-related artery without increasing the total dose of the drug administered. After the description in case reports of such an approach, a larger scale experience was recently reported in a large cohort of patients with STEMI treated during primary PCI with a bivalirudin intracoronary loading dose followed by the standard intravenous maintenance infusion. As a control group, a propensity score-matched cohort of patients undergoing primary PCI treated with intravenous bivalirudin in the same institution was selected. Compared with the intravenous bolus, the intracoronary administration of bivalirudin was associated with improved ST-segment resolution, lower post-procedural peak CK-MB levels, and better Thrombolysis in Myocardial Infarction (TIMI) frame count values, without difference in bleeding rates. Thus, this new promising antithrombotic strategy, based on the intracoronary administration of a bivalirudin loading dose during primary PCI, appeared safe, improved myocardial reperfusion, and mitigated enzymatic myocardial infarct size compared with the standard intravenous protocol. Randomized trials are warranted to confirm these results and evaluate the possible long-term clinical benefits.

Contrasting data have been reported on bivalirudin as an anticoagulation strategy during percutaneous coronary interventions, offering theoretical benefits on bleeding complications but raising concerns on a potential increase in the risk of stent thrombosis. We performed an updated meta-analysis to evaluate the efficacy and safety of bivalirudin compared with unfractionated heparin in patients undergoing percutaneous interventions for acute coronary syndromes.Literature archives and main scientific sessions were scanned. The primary efficacy endpoint was 30-day overall mortality. Secondary endpoints were stent thrombosis and major bleeding. A prespecified analysis was conducted according to clinical presentation.Twelve randomized trials were included, involving 32 746 patients (52.5% randomized to bivalirudin). Death occurred in 1.8% of the patients, with no differences between bivalirudin and heparin (odds ratio = 0.91; 95% confidence interval, 0.77-1.08; P = .28; P for heterogeneity = .41). Similar results were obtained for patients with non-ST-segment elevation and in ST-segment elevation myocardial infarction. A significantly higher rate of stent thrombosis was observed with bivalirudin (odds ratio = 1.42; 95% confidence interval, 1.09-1.83; P = .008; P for heterogeneity = .09). Bivalirudin was associated with a significant reduction in the rate of major bleeding (odds ratio = 0.60; 95% confidence interval, 0.54-0.75; P.00001; P for heterogeneity.0001), which, however, was related to the differential use of glycoprotein IIb/IIIa inhibitors (r = -0.02 [-0.033 to -0.0032]; P = .02) and did not translate into survival benefits.In patients undergoing percutaneous coronary interventions, bivalirudin is not associated with a reduction in mortality compared with heparin but does increase stent thrombosis. The reduction in bleeding complications observed with bivalirudin does not translate into survival benefits but is rather influenced by a differential use of glycoprotein IIb/IIIa inhibitors.

Suboptimal platelet inhibition still represents an important challenge, especially for patients undergoing percutaneous coronary interventions (PCIs). However, very few are known so far on the predictors of high-residual platelet reactivity (HRPR) despite antiplatelet strategies. Increasing attention has been paid in the last years to the role of vitamin D in atherothrombosis. Therefore, the aim of our study was to evaluate the impact of vitamin D levels on platelet function in patients treated with dual antiplatelet therapy (DAPT). Patients treated with DAPT (ASA and clopidogrel or ticagrelor) after a recent acute coronary syndrome (ACS) or elective PCI were scheduled for platelet function assessment at 30-90 days post-discharge. Platelet function was assessed by whole blood impedance aggregometry (Multiplate®-Roche Diagnostics AG), HRPR was considered for ASPI test values862 AU*min (for ASA) and adenosine diphosphate (ADP) test values ≥417 AU*min (for ADP-antagonists). Fasting samples were obtained for main chemistry parameters and vitamin D level assessment. Our population is represented by 503 patients, who were divided according to vitamin D quartiles (≤9.1; 9.2-14.4; 14.5-21.7;21.7 ng/ml). Lower vitamin D levels related with age (p = 0.04), diabetic status (p = 0.05), and previous coronary surgery (p = 0.007), therapy with beta-blockers and statins (p = 0.01 and p = 0.02). Vitamin D inversely related to the levels of total cholesterol (p = 0.01), triglycerides (p0.001), hemoglobin (p = 0.05), and HbA1c (p0.001). Significantly higher platelet reactivity was observed after platelet stimulation with ADP (p = 0.01), but not with other platelet activators. The prevalence of HRPR for ASA was low (1.2%) and not conditioned by Vitamin D levels (adjusted OR[95%CI] = 1.56[0.71-3.5], p = 0.27). HRPR with ADP-antagonists was observed in 26% of patients, and the rate increased with lower vitamin D quartiles (37.3% vs 22.2% vs 24.4% vs 20.2%, p = 0.005, adjusted OR[95%CI] = 1.23[1.02-1.49], p = 0.04). An absolute increase in HRPR with lower vitamin D levels was similarly observed among patients receiving ticagrelor (adjusted OR[95% CI] = 1.40[0.95-2.06], p = 0.08), and those on clopidogrel (adjusted OR[95%CI] = 1.31[0.99-1.75], p = 0.06). Thus, lower vitamin D levels are associated with higher platelet reactivity and impaired effectiveness of ADP-antagonists, while not influencing the effectiveness of ASA. Future studies will tell whether vitamin D supplementation can reduce platelet reactivity, overcoming the phenomenon of resistance to antiplatelet agents.

Item does not contain fulltext BACKGROUND: Low response to antiplatelet agents has been associated to an increased risk of thrombotic complications and recurrent ischemic events. Platelet size has been proposed as a potential marker of platelet reactivity. Therefore, the aim of the present study was to evaluate the impact of platelet Larger Cell Ratio (p-LCR) on platelet aggregation and the prevalence of residual high-on treatment platelet reactivity (HRPR) in patients receiving dual antiplatelet therapy (DAPT) after a recent acute coronary syndrome or coronary revascularization. METHODS: Patients treated with DAPT (ASA and clopidogrel or ticagrelor) were scheduled for platelet function assessment at 30-90 days post-discharge. HRPR was considered for ASPI test >862 AU*min (for ASA) or ADP test values >/=417 AU*min (for ADP-antagonists) using impedance aggregometry. RESULTS: Our population consisted of 530 patients receiving DAPT, who were divided in tertiles according to values of p-LCR (< 27.6; 27.6-34.7; >/=34.7 l). p-LCR was related with use of beta-blockers (p = 0.02) and statins (p = 0.002), and inversely with acute presentation (p = 0.05). Higher platelet count (p < 0.001) and haemoglobin levels (p = 0.001) were observed in higher p-LCR tertiles. The prevalence of HRPR for ASA was low and not significantly different across tertiles of p-LCR (1.1 vs 1.1 vs 1.7 %, p = 0.66; adjusted OR[95%CI] = 1.68[0.66-4.29], p = 0.27). Moreover, p-LCR did not influence the occurrence of HRPR for ADP-antagonists (24.4 % vs 20.9 % vs 25.6 %%, p = 0.80, adjusted OR[95%CI] = 0.88[0.67-1.17], p = 0.38) and similar results were obtained when considering separately patients receiving clopidogrel (adjusted OR[95%CI] = 1.21[0.86-1.69], p = 0.29) or ticagrelor (adjusted OR[95%CI] = 1.17[0.69-2], p = 0.56). CONCLUSION: In patients receiving DAPT for coronary artery disease, p-LCR does not impact platelet reactivity. Larger platelets did not influence the prevalence of high-on treatment platelet reactivity with the antiplatelet agents ASA, clopidogrel or ticagrelor.

Item does not contain fulltext Bivalirudin has gained ground against unfractionated heparin (UFH) in percutaneous coronary interventions (PCI), due to a reported better safety profile. However, whether bivalirudin may provide also advantages in clinical outcome beyond the known benefits in major bleedings, is still a debated matter and was, therefore, the aim of present meta-analysis of randomized trials, evaluating efficacy and safety of bivalirudin as compared with UFH in PCI. METHODS AND STUDY OUTCOMES: Literature archives (Pubmed, EMBASE, Cochrane) and main scientific sessions were scanned. Primary endpoint was overall mortality. Secondary endpoints were: 1) mortality within 30-days; 2) overall and within 30-days non fatal myocardial infarction; 3) overall and within 30-days stent thrombosis. Safety endpoints were major bleedings (per protocol definition or TIMI classification). A prespecified analysis was conducted according to clinical presentation (Elective, ACS, STEMI). RESULTS: A total of 22 randomized clinical were finally included, involving 40156 patients randomized to bivalirudin (52.9%) or to UFH (47.1%). Death occurred in 1100 (2.8%) of patients, with no difference between bivalirudin and UFH (2.7% vs 2.8% OR[95%C]=0.94[0.83,-.06], p=0.32, phet=0.48). The results did not change according to clinical presentation. By meta-regression analysis, the effects on mortality were not related to patients risk profile (r=-0.38(-0.89-0.14), p=0.15) or the reduction in bleeding complications (r=-0.008(-0.86-0.85), p=0.98). A significant increase in short-term stent thrombosis was observed with bivalirudin (OR[95%CI]=1.42 [1.10-1.83], p=0.006). However, Bivalirudin significantly reduced bleedings according to both study protocol definition (OR[95%CI]=0.62[0.56-0.69],p

BACKGROUND Despite improvements in pharmacological and mechanical devices, the risk of periprocedural myocardial infarction (PMI) is still high, particularly in prothrombotic conditions. Hyperhomocysteinemia has been associated with enhanced platelet function, impaired endothelial function and prothrombotic status, thus increasing the risk of cardiovascular events. No study has, so far, investigated the relationship between homocysteine levels and the risk of periprocedural MI in patients undergoing percutaneous coronary intervention (PCI), and this is therefore the aim of the current study. METHODS In 1150 patients undergoing PCI, homocysteinemia was assessed at admission. Cardiac biomarkers were measured at intervals from 8 to 48 h after PCI. Periprocedural myonecrosis was defined by a troponin I increase to three times the upper limit of normal (ULN) or by 50% if elevated at the time of the procedure. PMI was defined as a CK-MB increase to three times the ULN or of 50% if elevated at the time of the procedure. RESULTS We grouped patients according to tertile values of homocysteine. Higher homocysteine levels were associated with older age (P

Background Early escalation from clopidogrel to new generation P2Y12 inhibitors is common practice in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). Real-world data about this strategy, however, are limited. Methods From 2012 to 2015, 1,057 consecutive STEMI patients treated with pPCI in an Italian hub-and-spoke network were prospectively included in an observational registry (RENOVAMI, ClinicalTrials.gov Identifier: NCT01760382). We compared the prevalence, predictive factors and in-hospital outcomes of patients escalated to a new generation P2Y12 inhibitor within the first 24 hours from pPCI with those continuing on admission antiplatelet therapy. Results In the first 24 hours after pPCI, 165 patients (15.6%) were escalated from clopidogrel to a new generation P2Y12 inhibitor, while de-escalation to clopidogrel was occasional (19 patients, 1.8%) and switch between new generation P2Y12 inhibitors was rare (8 patients, 0.8%, all from ticagrelor to prasugrel). Drug eluting stent use (adjusted odds ratio [OR], 2.19, 95% confidence interval [CI], 1.55–3.08, p = 0.0002) and impaired renal function (adjusted OR, 0.19, 95% CI, 0.05–0.77, p = 0.02) were the only independent predictive factors for the decision to escalate. After adjustment for potential confounders, escalation did not predict in-hospital outcomes, whereas the overall use of new generation P2Y12 inhibitors was correlated with a better in-hospital survival (adjusted hazard ratio, 0.47, 95% CI, 0.25–0.91, p = 0.03). Moreover, escalation did not influence bleeding rates. Conclusions In this prospective registry of STEMI patients treated with pPCI and contemporary antiplatelet therapy, early escalation to a new generation P2Y12 inhibitor appeared safe and did not significantly affect in-hospital bleeding rates.

Background. Substantial improvements have been achieved with percutaneous coronary intervention (PCI) for the treatment of acute coronary syndromes (ACS). Nevertheless, bleeding still affects outcomes. The radial approach for PCI has shown important benefits on access site complications, but is still not achieving universal consensus as first choice in acute settings. Therefore, we performed a comprehensive meta-analysis of randomized trials comparing radial vs femoral approach in PCI for ACS. Methods. The literature and main scientific session abstracts were scanned for randomized studies comparing radial vs femoral approach for PCI in ACS. Primary endpoint was mortality within 30-days. Secondary endpoints were: 1) Major Adverse Cardiovascular Events (MACE), 2) major bleeding, and, 3) vascular complications. Results. We included 17 randomized trials, enrolling 19325 patients. A total of 9635 patients were randomized to the radial approach and 9690 to the femoral approach. The radial approach was associated with a significant reduction in mortality (1.8 vs 2.5%, odds ratio, OR [95% CI] = 0.72 [0.59,0.88], p = 0.001, pheterogeneity = 0.31) and in major bleeding complications compared with the femoral approach (1.5 vs 2.6%, OR [95% CI] = 0.57 [0.47, 0.71], p < 0.00001, pheterogeneity = 0.59), with similar advantages observed for both ST-elevation myocardial infarction and non-ST segment elevation ACS. MACE occurrence and vascular complications were also reduced with the radial approach (OR [95% CI] = 0.82 [0.74, 0.92], p = 0.0005, and OR [95% CI] = 0.52 [0.47, 0.58], p < 0.00001, respectively). Our results were not influenced by patient risk profile or the antithrombotic strategy applied. Conclusion. Our meta-analysis shows that among ACS patients undergoing PCI, the radial approach is associated with a significant reduction in mortality, major bleeding complications, MACE and vascular complication compared with the femoral approach.

Item does not contain fulltext BACKGROUND: Serum uric acid (SUA) elevation has been largely addressed in the past as a possible risk factor for cardiovascular disease. However, uric acid has not clearly emerged as independent risk factor for coronary artery disease. Several studies in literature have assessed sex-related differences in the association between elevated SUA levels and cardiovascular events with conflicting results. Therefore, aim of the current study was to evaluate the relationship between uric acid levels and the extent of coronary artery disease in male and female patients undergoing coronary angiography. METHODS: Our population is represented by 3520 consecutive patients undergoing coronary angiography from March 2007 to October 2012. Patients were divided according to Tertiles of SUA (Males, Group 1, /=6.8 mg/dL-0.40 mmol/mol, n = 851), (Females, Group 1, /= 6.3 mg/dL-0.37 mmol/mol, n = 370). Fasting samples were collected for uric acid levels assessment. Coronary disease was defined for at least 1 vessel stenosis >50% as evaluated by QCA. Severe coronary disease was defined as three-vessel disease and/or left main disease. RESULTS: Among 3520 patients, we identified 2442 men (69.4%) and 1078 women (30.6%). Males had higher levels of uric acid than women (6.33 +/- 1.7 vs 5.8 +/- 1.9 - p < 0.001). The association between elevated uric acid (>/=7 mg/dl or 0.42 mmol/l) and male gender was confirmed after correction for baseline confounding factors (Adjusted OR = 1.28 [1.01-1.62], p = 0.004). Males displayed a significantly higher prevalence and extent of CAD (p < 0.001) and more complex coronary lesions (p < 0.001). However, no significant relationship was observed between uric acid and CAD (Adjusted OR [95%CI] = 0.90 [0.76-1.06], p = 0.22) or severe CAD (Adjusted OR [95%CI] = 0.89 [0.79-1.01], p = 0.08). Among females, higher SUA levels were significantly associated with higher prevalence of severe CAD (p < 0.001) (Adjusted OR [95% CI] = 1.29 [1.03-1.62], p = 0.03). CONCLUSION: Our study showed that uric acid levels are significantly higher in men. However, high uric acid levels are associated with severe CAD only in women. Future large studies are certainly needed to confirm our findings and to evaluate the effects of SUA lowering therapies on cardiovascular prevention and outcome, especially in women.

Item does not contain fulltext Elderly patients represent a high risk category among subjects with atherosclerosis, due to the presence of comorbidities and suboptimal response to antiplatelet drugs. Mean platelet volume (MPV) has been indicated as a marker of platelet reactivity, with contrasting data on its role on coronary artery disease. Aim of the present study was to evaluate the impact of age on the MPV and its role on the extent of coronary artery disease (CAD). METHODS: Our population is represented by a cohort of 3750 patients undergoing coronary angiography. Elderly were defined according to age >/= 75 years. MPV was measured at admission. Significant coronary artery disease was defined as a stenosis >50% in at least 1 coronary vessel, while severe CAD was defined as left main and/or three-vessel disease. RESULTS: A total of 1170 out of 3750 (31.2%) patients were >/= 75 years old. Advanced age was associated with female gender (p/=10.85fl) at multivariate analysis (adjusted OR [95% CI]=1.18 [1.01-1.40], p=0.04). Among the elderly, MPV value above the median (>/=10.85fl) was not associated with a higher prevalence of coronary artery disease (77.3 vs. 79.4%, p=0.39, adjusted OR [95% CI]=0.94 [0.66-1.33], p=0.71), or higher prevalence of severe CAD (35.2 vs. 32.4%, p=0.28, adjusted OR [95% CI]=1.34 [0.99-1.82], p=0.06). CONCLUSION: Advanced age was directly associated with larger mean platelet volume that, however, did not contribute to explain the higher prevalence and extent of coronary artery disease observed in elderly patients.

Item does not contain fulltext BACKGROUND: Previous reports have suggested an association between elevated fibrinogen and CAD. Few studies have so far investigated the impact of diabetes on fibrinogen levels and its association with coronary artery disease (CAD) and platelet reactivity in diabetic patients that are therefore the aims of the current study. METHODS: We measured fibrinogen in 3280 consecutive patients undergoing coronary angiography. Samples were collected at admission for fibrinogen levels assessment. Coronary disease was defined for at least 1 vessel stenosis >50% as evaluated by QCA. RESULTS: Diabetes was observed in 1201 out of 3280 patients. Diabetic patients were older with more hypercholesterolemia, hypertension, higher BMI, more renal failure, previous MI or coronary revascularization (p

Contains fulltext : 153289.pdf (Publisher’s version ) (Closed access) Leukocytes have been involved in the pathogenesis of atherosclerosis, and recent attention has been raised on eosinophils, that have been claimed for a wide number of cardiovascular pathologies, affecting endocardium, myocardium and vascular walls. However, few data have been reported so far on the relationship between absolute eosinophils count (AEC) and the prevalence and extent of coronary artery disease (CAD), that was the aim of present study. Consecutive patients undergoing non-urgent coronary angiography were included. Haematological parameters were measured at admission. 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. Our population is represented by 3,742 patients, divided according to tertiles values of AEC (0.2 x 10(3)/microl). Higher eosinophils values were significantly associated to male gender, main established cardiovascular risk factors, previous percutaneous or surgical coronary revascularization, antihypertensive and antiplatelet therapy at admission but inversely with acute presentation. Higher AEC was directly related with platelets count (p < 0.001), haemoglobin levels (p = 0.02), white blood cells count (p = 0.02), higher serum creatinine (p < 0.001), triglycerides (p < 0.001) and glycosylated haemoglobin (p < 0.001), while inversely with HDL cholesterol (p < 0.001). AEC was associated with multivessel disease (p = 0.03), chronic occlusions (p = 0.01), in-stent restenosis (p = 0.002), while inversely with the presence of intracoronary thrombus (p < 0.001). A significant relationship was found between AEC and the prevalence of coronary artery disease (p = 0.049), but not for the extent of more severe LM/trivessel CAD (p = 0.31). At multivariate analysis no independent role of eosinophils was found for CAD (adjusted OR [95 % CI] = 1.02 [0.91-1.15], p = 0.70), or severe CAD (adjusted OR [95 % CI] = 0.99 [0.89-1.1], p = 0.9), even when considering separately acute and elective patients. In conclusion, among patients undergoing coronary angiography, higher eosinophils levels are not independently associated with the prevalence and extent of coronary artery disease, but appear confounded by their link with major cardiovascular risk factors.

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 (

Item does not contain fulltext INTRODUCTION: Primary angioplasty has improved survival as compared to thrormbolysis. However, bleeding complications still represent the Achille's heel, mainly related to access site. Although the radial approach is getting larger consensus for elective percutaneous procedures, its safety and advantages in the setting of ST-segment elevation (STEMI) is controversial. Therefore, the aim of the current study was to perform a comprehensive meta-analysis of randomized and non randomized trials comparing radial vs transfemoral approach in primary angioplasty for STEMI. METHODS: The literature was scanned by formal searches of electronic databases (MEDLINE, Pubmed) from January 1990 to October 2012. No language restrictions were enforced. RESULTS: A total of 27 trials were finally included, with 29,194 patients (4685 enrolled in 11 randomized trials and 24,509 in 15 non randomized trials). A total of 10,052 patients underwent radial approach and 19,142 patients underwent femoral approach. A total of 2499 patients (8.6%) had died at follow-up. Radial approach was associated with a significant reduction in short-term mortality (5.2% vs 10.3%, OR [95% CI]=0.55 [0.40, 0.76], p

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.

Item does not contain fulltext BACKGROUND: Statins represent a pivotal treatment in coronary artery disease, offering a reduction in cardiovascular risk even beyond their lipid-lowering action. However, the mechanism of these "pleiotropic" benefits of statins is poorly understood. Vitamin D has been suggested as a potential mediator of the anti-inflammatory, anti-thrombotic and vascular protecting effects of statins. Aim of present study was to assess the impact of a high-intensity statin therapy on vitamin D levels and platelet function in patients with coronary artery disease. METHODS: Patients discharged on dual antiplatelet therapy and high-intensity statins after an ACS or elective PCI were scheduled for main chemistry and vitamin D levels assessment at 30-90days post-discharge. Vitamin D (25-OHD) dosing was performed by chemiluminescence method through the LIAISON(R) Vitamin D assay (Diasorin Inc). Platelet function was assessed by Multiplate(R) (multiple platelet function analyser; Roche Diagnostics AG). RESULTS: Among 246 patients included, 142 were discharged on a new statin therapy or with an increase in previous dose (Inc-S), while 104 were already receiving a high-dose statin at admission, that remained unchanged (Eq-S). Median follow-up was 75.5days. Patients in the Inc-S group were younger (p=0.01), smokers (p

Background Pre-hospital ticagrelor, given less than 1 h before coronary intervention (PCI), failed to improve coronary reperfusion in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary PCI. It is unknown whether a longer interval from ticagrelor administration to primary PCI might reveal any improvement of coronary reperfusion. Methods We retrospectively compared 143 patients, pre-treated in spoke centers or ambulance with ticagrelor at least 1.5 h before PCI (Pre-treatment Group), with 143 propensity score-matched controls treated with ticagrelor in the hub before primary PCI (Control Group) extracted from RENOVAMI, a large observational Italian registry of more than 1400 STEMI patients enrolled from Jan. 2012 to Oct. 2015 ( ClinicalTrials.gov id: NCT01347580 ). The median time from ticagrelor administration and PCI was 2.08 h (95% CI 1.66–2.84) in the Pre-treatment Group and 0.56 h (95% CI 0.33–0.76) in the Control Group. TIMI flow grade before primary PCI in the infarct related artery was the primary endpoint. Results The primary endpoint, baseline TIMI flow grade, was significantly higher in Pre-treatment Group (0.88 ± 1.14 vs 0.53 ± 0.86, P = 0.02). However in-hospital mortality, in-hospital stent thrombosis, bleeding rates and other clinical and angiographic outcomes were similar in the two groups. Conclusions In a real world STEMI network, pre-treatment with ticagrelor in spoke hospitals or in ambulance loading at least 1.5 h before primary PCI is safe and might improve pre-PCI coronary reperfusion, in comparison with ticagrelor administration immediately before PCI.

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.

Even though platelet volume has been supposed to be indicator of platelet activation, contrasting results have been reported on its relationship with the extent of coronary artery disease (CAD). No data have been so far reported on Platelet-Large Cell Ratio (P-LCR). Thus, the aim of the current study was to investigate whether P-LCR is associated with CAD. We measured P-LCR in 1882 consecutive patients undergoing coronary angiography. Significant CAD was defined as stenosis >50% in at least 1 coronary vessel. We additionally measured Carotid Intima-Media Thickness (IMT) in 359 patients. The relationship between P-LCR and platelet aggregation was evaluated by PFA-100 and Multiplate. Patients with higher P-LCR were older (P = 0.038), with larger prevalence of diabetes (P < 0.0001), dilated cardiomyopathy or valvular heart disease (P = 0.004) and less often family history of CAD (P = 0.045), more often on statins (P = 0.002), and diuretics (P = 0.016). P-LCR was significantly associated with baseline glycaemia (P = 0.001) and RBC count (P < 0.001), but inversely related to platelet count (P < 0.0001). P-LCR was not associated with the prevalence of CAD (adjusted P = 0.3) or its severity. In addition, P-LCR was not related to Carotid IMT or platelet aggregation in patients with or without aspirin therapy. This study showed that P-LCR is not related to platelet aggregation, aspirin resistance, the extent of CAD and carotid IMT. Thus, P-LCR can not be considered as a marker of platelet reactivity or a risk factor for CAD.

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.

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.

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.

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.

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.