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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

Item does not contain fulltext BACKGROUND AND AIM: Contrast Induced Nephropathy (CIN) is a common complication of procedures that require the use of contrast media, and seems to be mediated by oxidative stress and reactive oxygen species generation. Hyperuricemia is characterized by inhibited nitric oxide system and enhanced synthesis of reactive oxygen species. However, few studies have so far investigated the association between hyperuricemia and CIN that is therefore the aim of the current study among patients undergoing coronary angiography or percutaneous intervention. METHODS AND RESULTS: We analyzed a total of 1950 patients with Creatinine clearance /= 7.0 mg/dL, n = 643). CIN was defined as an absolute >/= 0.5 mg/dl or a relative >/= 25% increase in the serum creatinine level at 24 or 48 h after the procedure. Patients with higher uric acid levels were older, previous smokers, with higher prevalence of hypertension and diabetes, but with lower family history of CAD. They had more often history of a previous CABG and baseline renal dysfunction. Patients of the third Tertile had also higher levels of white blood cells, higher triglycerides and lower HDL-cholesterol and higher percentage of dilated cardiomyopathy/valvular disease as indication for angiography and consequently a lower prevalence of PCI. Patients with higher SUA were more often on therapy with ACE inhibitors and diuretics, but less often with statins, nitrate, ASA and Clopidogrel at admission. The occurrence of CIN was observed in 251 patients (12.9%), and was significantly associated with uric acid levels (12.3% in Group 1, 10.4% in Group 2 and 16.0% in Group 3; p = 0.04). Similar results were observed when the analysis was performed according to each tertiles values in both male and female gender. The association between elevated uric acid (>/= 7 mg/dl) and CIN was confirmed by multivariate analysis after correction for baseline confounding (Adjusted OR [95%CI] = 1.42 [1.04-1.93], p = 0.026). Similar results were observed across major subgroups of high-risk patients, such as patients with diabetes, female gender, renal failure, hypertension, and elderly. CONCLUSIONS: This is the first large study showing that among patients undergoing coronary angiography or percutaneous interventions elevated uric acid level is independently associated with an increased risk of CIN.

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.

Background and aim Pro-thrombotic status and platelet hyperreactivity still represent an important challenge for periprocedural myocardial infarction (PMI) after coronary stenting. Hyperhomocysteinemia has been suggested to increase the risk of cardiovascular events. The genetic variant of methylenetetrahydrofolate reductase (MTHFR) 677 C > T has been associated to reduced function of the enzyme, thus inducing hyperhomocysteinemia. In our study we investigated whether MTHFR 677 C > T polymorphism is associated with increased risk of periprocedural MI in patients undergoing coronary stenting. Methods and results We included 778 patients undergoing PCI. Homocysteinemia and genetic status were assessed at admission for all patients. Myonecrosis biomarkers were dosed at intervals from 6 to 48 h, PMI was defined as CKMB increase by 3 times the ULN or 50% of pre-PCI value, periprocedural myonecrosis for troponin I increase by 3 times the ULN or by 50% of the baseline. As many as 521 patients carried the MTHFR-T allele. No difference was found for main demographical and clinical features nor for biochemistry parameters, but for higher rate of statins treatment ( p = 0.03) in T-carriers. Polymorphic patients displayed significantly higher levels of homocysteine ( p = 0.005), with additive effect of the mutated T-alleles. Angiographic and procedural features were similar according to genetic status. MTHFR677T was not associated with periprocedural myocardial infarction (adjusted OR = 0.97[0.67–1.4], p = 0.87) or myonecrosis (adjusted OR = 1.03[0.83–1.36], p = 0.82). Same results were found at subgroup analysis in higher-risk subsets of patients. Conclusion Our study showed that among patients undergoing PCI, MTHFR 677 C > T polymorphism is associated to higher homocysteine levels, but does not influence the risk of periprocedural myocardial infarction.

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 (

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 (

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.

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.

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.

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.

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.

OBJECTIVES Even though anaemia has been shown to be a risk factor for adverse cardiovascular disease, there is scarce evidence of its relationship with angiographically proven coronary artery disease (CAD). The aim of this study was to evaluate the relationship between haemoglobin (Hb) levels and the extent of CAD. MATERIALS AND METHODS We measured Hb, mean corpuscular volume and red blood cell count in 2363 consecutive patients undergoing coronary angiography. Patients were divided into four groups according to quartile values of Hb (≤12.2 g/dl, group 1; 12.3-13.5 g/dl, group 2; 13.6-14.6 g/dl, group 3; >14.6 g/dl, group 4). RESULTS Patients with lower Hb were older (P

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.

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.

Few reports have so far investigated the relationship between fibrinogen levels and the extent of coronary artery disease (CAD) as evaluated by coronary angiography, that is therefore the aim of the current study. We measured fibrinogen in 2,121 consecutive patients undergoing coronary angiography. Patients were divided in 5 groups based on quintiles of fibrinogen levels. Significant CAD was defined as stenosis >50% in at least 1 coronary vessel. We additionally measured carotid intima-media thickness (CIMT) in a subgroup of 359 patients. Patients with elevated fibrinogen were older (P = 0.038), with larger prevalence of diabetes (P = 0.027), female gender (P < 0.0001), hypertension (P < 0.001), chronic renal failure (P < 0.0001), previous CVA (P = 0.036), less often with family history of CAD (P = 0.019) and previous PCI (P < 0.0001), more often presenting with ACS (P < 0.0001), more often on nitrates (P < 0.0001), clopidogrel (P = 0.009) and diuretics (P < 0.0001). Fibrinogen levels were linearly associated with baseline glycaemia (P < 0.017), WBC count (P < 0.0001), creatinine (P < 0.0001), and Platelet count (P < 0.0001) but inversely associated with RBC count (P < 0.0001). Fibrinogen levels were associated with CAD (P = 0.001), especially for extremely high levels (5th percentile, P < 0.0001). At multivariate analysis, after correction for baseline confounding factors, high fibrinogen level (5th percentile) was still associated with the prevalence of CAD (P = 0.034). Furthermore, fibrinogen levels were related with maximal CIMT (r = 0.12; P = 0.01), with larger prevalence of carotid plaques in patients with higher fibrinogen levels (5th quintile) as compared to remaining patients (P = 0.046). This study showed that high fibrinogen level is significantly associated with CAD and carotid atherosclerosis.

It has been postulated that large platelets may be an indicator of platelet activation, and thus be related to the extent of coronary artery disease (CAD). Platelet distribution width (PDW) directly measures the variability in platelet size. However, no data has been so far reported on this index and CAD. Thus, the aim of the current study was to investigate whether PDW is associated with the extent of CAD. We measured PDW in 1882 consecutive patients undergoing coronary angiography. Significant CAD was defined as stenosisgt;50% in at least one coronary vessel. We additionally measured Carotid Intima-Media Thickness (IMT) in 359 patients. Patients with higher PDW were older (p = 0.012), with higher weight (plt; 0.0001) and waist (plt; 0.0001), larger prevalence of diabetes (p = 0.014), dilated cardiomyopathy or valvular heart disease (plt; 0.0001) and less often family history of CAD (p = 0.021), more often on statins (p = 0.005), and diuretics (p = 0.016). PDW was significantly associated with baseline glycaemia (p = 0.002) and Red Blood Cell count (plt; 0.0001), but inversely related to platelet count (plt; 0.0001). PDW was not associated with the prevalence of coronary artery disease (OR [95% CI] = 0.91 [0.81#x2013;1.04], p = 0.16; adjusted OR [95% CI] = 0.96 [0.82#x2013;1.12], p = 0.56). No relationship was observed between IMT and PDW as tertiles or as continuous variable (Mean IMT: r = 0.04; p = 0.46; Maximal IMT: r = 0.036, p = 0.49). This study showed that PDW is not related to the extent of CAD and carotid IMT. Thus, PDW can not be considered as a risk factor for CAD.

Background Hyperuricemia may be involved in the atherosclerotic process due to endothelial dysfunction and facilitation of smooth muscle cell proliferation. However, debates still exist on the independent role of hyperuricemia, due to its association with several cardiovascular risk factors, such as hypertension, hyperlipidemia, obesity and insulin resistance. Thus, the aim of the current study was to investigate in a consecutive cohort of patients undergoing coronary angiography whether hyperuricemia is associated with the extent of coronary artery disease. Methods and Results Our population is represented by a total of 1901 consecutive patients undergoing coronary angiography between May 2007 and January 2010 at the Azienda Ospedaliera "Maggiore della Carita", Novara, Italy. We additionally evaluated platelet aggregation by PFA-100 (Collagen/Epinefrine) and Multiplate. Quantitative coronary angiography and analysis of IMT were performed by experienced cardiologists who had no knowledge of the patients' clinical information. Higher uric acid was associated with advanced age, larger prevalence of male gender, diabetes, renal insufficiency, hypertension, previous CABG and MI, but with a lower prevalence of family history of CAD. Patients with high uric acid were more often on calcium antagonists, ace-inhibitors, angiotensin receptor antagonists, and, as expected, on diuretics. A significant relationship was observed between uric acid and the prevalence (OR [95% CI] = 1.18 [1.04–1.32], p = 0.01) and severity of CAD (OR [95% CI] = 1.17 [1.03–1.33], p = 0.014). However, the relationship disappeared after correction for baseline confounding factors for both prevalence (OR [95% CI] = 1.06 [0.93–1.21], p = 0.35) and extent of CAD (OR [95% CI] = 1.0 [0.87–1.15], p = 0.96). No relationship was observed between acid uric and IMT ( p = 0.73) analyzed in 359 consecutive patients. Finally, there was no relationship between uric acid and platelet aggregation in patients with or without aspirin therapy, as measured by PFA-100 and Multiplate. Conclusions Our study showed that uric acid is not associated with platelet aggregation, the extent of coronary artery disease and IMT. Thus, waiting for the results of additional large studies, uric acid may not be considered as a risk factor for coronary artery disease, and its reduction by specific therapies may not be recommended to prevent coronary artery disease and atherosclerosis.