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Background Patients with diabetes mellitus (DM) are at higher risk of restenosis and stent thrombosis after percutaneous coronary intervention and drug eluting stent (DES) positioning. Limited although interesting data are available on prognosis after revascularization with drug–coated balloon (DCB) in this group of patients. The aim of this study is to evaluate the prognostic impact of DCB use in patients affected by DM. Methods Patients with DM enrolled in a retrospective multicenter registry were identified and matched to a control population of diabetic patients treated with DES enrolled in another retrospective registry, according to a propensity score calculated on the independent predictors of main adverse cardiac events (MACE). The primary study endpoint was the occurrence of MACE, a composite of death, myocardial infarction, and target vessel revascularization. Secondary endpoints were the independent components of the primary endpoint, or target lesion failure (TLF). Results 150 patients were identified in the DCB group and matched with 150 DES–treated patients. However, patients treated with DCB displayed more often a previous cardiovascular history and received a more complete pharmacological therapy. Target vessel diameter and the percentage of stenosis were lower in DCB patients, whereas binary in–stent restenosis was more common. At a median follow–up of 545.5 days, MACE occurred in 54 (19.4%) of the patients, with no difference according to the PCI strategy. Although a trend toward higher TLF was found (p=0.06), overall death was significantly reduced in diabetic patients (3.6% vs 10.9%; adjusted HR[95%CI]= 0.27[0.08–0.91], p=0.03). Conclusion Although limited by some differences among the groups, the present propensity–matched study shows that, among patients with DM undergoing PCI for in–stent restenosis or de novo lesions, the use of DCB is associated to a similar rate of MACE and a possible increase in TLF, but a significantly improved survival as compared to use of DES.

Background The Academic Research Consortium for High Bleeding Risk (ARC–HBR) has recently proposed, by consensus, twenty clinical criteria for the assessment of the bleeding risk after percutaneous coronary intervention (PCI). A major criterion was defined as any individual clinical condition conferring in isolation a risk for major bleeding ≥4% up to 1 year after PCI; instead, a minor criterion was considered to confer a bleeding risk of Methods MEDLINE, COCHRANE, Web of Sciences, and SCOPUS were searched for studies aimed at validating the ARC–HBR criteria in patients treated with PCI. The primary outcome measure of this meta–analysis was major bleeding. Results The analysis included 10 studies encompassing 67,862 patients undergoing PCI; the HBR definition was fulfilled in 44.7% of the cases. The risk of major bleeding was significantly higher in HBR vs. Non–HBR group (RR, 2.56, 95% CI 2.28–2.89). The average C–statistic was 0.64 (95% CI 0.60–0.68), indicating modest discrimination. The risk of intracranial hemorrhage, gastrointestinal bleeding, fatal bleeding, ischaemic stroke, cardiac death and all–cause death was higher in HBR vs. Non–HBR group. Despite a higher incidence of myocardial infarction and stent thrombosis in patients deemed at HBR, the rate of target lesion revascularization was comparable between groups (RR, 1.01, 95% CI 0.88–1.16). When assessed in isolation, the mean cumulative incidence of major bleeding at 1 year exceeded the cut–off value of 4% for all the major criteria and for two out of six minor criteria, including age ≥75 years and moderate chronic kidney disease (CKD) (Figure). Conclusion The ARC–HBR definition identifies patients at higher risk of major bleeding and other adverse cardiovascular events after PCI. Almost all major criteria, but also two of the minor criteria, were individually associated with rates of major bleeding above 4% thus fulfilling the definition of major HBR criteria. These findings corroborate the ability of ARC–HBR major criteria in identifying PCI patients who are more likely to develop adverse events, but also suggest caution in the decision making of patients with isolated minor criteria, including age≥75 years and moderate CKD.

Introduction Drug coated balloons (DCB) have emerged for percutaneous coronary interventions (PCI) and mainly for in–stent restenosis or particular anatomies. However, the indications and the predictors of long–term failure of DCB have been poorly evaluated besides small–sized randomized clinical trials. Therefore, the aim of the present study was to provide a real–world analysis of the prognostic determinants and long–term outcomes among patients treated with DCB for any type of lesion and included in a comprehensive multicenter registry. Methods We included patients undergoing coronary angiography and PCI with DCB for in–stent restenosis or de novo lesions in 3 centers. Quantitative parameters for coronary lesions were calculated by an automatic edge–detection system. The primary study endpoint was the occurrence of major cardiovascular events (a composite of death, MI and target vessel revascularization) at the longest available follow–up. Secondary endpoints were the individual components of the primary endpoint, target lesion failure (TLF) or any acute coronary syndrome. Results Out of 281 patients treated with DCB, the 267 displaying a follow–up > 12 months were included, of whom 196 treated for in–stent restenosis and 71 with de novo lesions. At a median follow–up of 616 [368–1025] days, MACE occurred in 70 (26.2%) of the patients. No difference in clinical, demographic of angiographic features was observed between patients with or without an event, with the exception of a higher rate of in–stent restenosis (p = 0.04), longer and more type C lesions (p = 0.05 and p = 0.04) related with MACE. At multivariate Cox–regression, type C lesions emerged as the only independent predictor of MACE (adjusted OR[95%CI]= 1.83[1.13–2.97], p = 0.014), mainly driven by target vessel revascularization (adjusted OR[95%CI]= 1.78[1.05–2.95], p = 0.03) although not conditioning survival. However, in–stent restenosis emerged as a major determinant of TLF (adjusted OR[95%CI]= 2.59[1.17–5.75], p = 0.02). Conclusion The present registry shows that drug–coated balloons represent a potential treatment strategy even for de–novo lesions, especially in less complex cases. In fact, we observed an increased risk of MACE and target lesion failure in case of type C and restenotic lesions.

Background Vitamin D displays a broad spectrum of cardioprotective effects, preventing oxidative stress, inflammation and thrombosis and improving endothelial function. Previous studies have associated vitamin D deficiency with more extended and severe coronary artery disease (CAD) and worse outcome, and especially among patients with ST-segment elevation myocardial infarction (STEMI). Few data have been reported on the association of vitamin D levels with the features of infarct-related lesions and PCI outcomes. Aim We aimed at assessing the relationship between vitamin D and angiographic findings and the procedural results of primary percutaneous coronary intervention (pPCI) in STEMI. Methods A consecutive cohort of patients admitted for STEMI treated with pPCI were included. The levels of 25(OH)D were assessed at admission by chemiluminescence immunoassay kit LIAISON® Vitamin D assay. Hypovitaminosis D was defined for 25(OH)D Results We included in our study 450 patients, divided according to tertiles values of 25(OH)D. Lower vitamin D was associated to higher use of diuretics (p=0.02), higher levels of white blood cells and glycemia (p Conclusion The present study shows that among patients with STEMI undergoing pPCI, lower levels of vitamin D indepently predict the occurrence of slowflow/no-reflow phenomenon. Future dedicated studies will shed light on the prognostic implications of hypovitaminosis D in these patients and the potential therapeutic perspectives. Funding Acknowledgement Type of funding sources: None.

Item does not contain fulltext BACKGROUND: Gender differences in the thrombotic and bleeding risk have been suggested to condition the benefits of antithrombotic therapies in Acute Coronary Syndrome (ACS) patients, and mainly among those undergoing percutaneous coronary interventions with drug eluting stents (DES). The impact of gender on the optimal duration of dual antiplatelet therapy (DAPT) in ACS patients is still unexplored and was, therefore, the aim of the present sub-study. METHODS: REDUCE was a prospective, multicenter, randomized investigator-initiated study designed to enroll 1500 ACS patients after treatment with the COMBO Dual Stent Therapy, based on a noninferiority design. Patients were randomized in a 1:1 fashion to either 3 or 12 months of DAPT. Primary study endpoint was a composite of all-cause mortality, myocardial infarction, definite/probable stent thrombosis (ST), stroke, target-vessel revascularization (TVR) and bleedings (BARC II, III, V) at 12 months. Secondary endpoints were cardiovascular mortality and the individual components of the primary endpoint within 24 months. RESULTS: From June 2014 to May 2016 300 women and 1196 men were included in the study. Among them, 43.7% of females and 51.9% of males were assigned to the 3 months DAPT treatment. Baseline characteristics were well matched between the two arms, with the exception of a lower rate of TIMI flow

The immature platelet count (IPC) is a potential marker of platelet reactivity. We assessed the relationship between IPC during chronic dual antiplatelet therapy (DAPT) and the response to antiplatelet drugs (acetylsalycilic acid + clopidogrel/ticagrelor). We included 286 patients: 167 (58.4%) patients received ticagrelor and 119 (41.6%) received clopidogrel. At a median follow-up of 46.5 days, the variation in IPC displayed an absolute median (interquartile range [IQR]) of −11.9 × 103/µL (−182.7 to 160.8), corresponding to a median percentage change in IPC ([%ΔIPC] IQR) of −0.3% (−21.9% to 35.5%), with an increase in IPC levels in those on ticagrelor and a decrease in IPC levels in those on clopidogrel. We observed an inverse association of lower platelet reactivity at different tests and a higher increase in IPC ( r = −0.14, P = .04 for arachidonic acid test; r = −0.12, P = .05 for collagen test; and r = −0.13, P = .02 for adenosine diphosphate test [ADP]). The rate of poor effectiveness of ADP antagonists was the only independent predictor of a ΔIPC above the third tertile (odds ratio [95% confidence interval] = 0.55 [0.32-0.99]; P = .048). We showed that in patients treated with chronic DAPT, an increase in IPC is significantly related to lower levels of platelet reactivity.

Background Gender differences in the thrombotic and bleeding risk have been suggested to condition the benefits of antithrombotic therapies in Acute Coronary Syndrome (ACS) patients, and mainly among those undergoing percutaneous coronary interventions with drug eluting stents (DES). Therefore, the impact of gender on the optimal duration of dual antiplatelet therapy (DAPT) treated is still unclear and was therefore the aim of the present sub-study. Methods REDUCE is a prospective, multicenter, randomized, investigator-initiated study, designed to enroll 1500 ACS patients after treatment with the COMBO Dual Stent Therapy, based on a non-inferiority design. Patients were randomized in a 1:1 fashion to either 3 or 12 months of DAPT. Primary study endpoint was a composite of all-cause mortality, myocardial infarction, definite/probable stent thrombosis (ST), stroke, target-vessel revascularization (TVR) and bleeding (BARC II, III, V) at 12 months. Secondary endpoints were cardiovascular mortality and the individual components of the primary endpoint. Results From June 2014 to May 2016 300 women and 1196 men were randomized in the trial. Among them 43.7% of females and 51.9% of males were assigned to the 3 months DAPT treatment. Baseline characteristics were well matched between the two arms, but of a lower rate of TIMI flow Conclusions The present study shows that among ACS patients randomized in the REDUCE trial, a 3 months DAPT strategy offers comparable results as compared to a standard 12 months DAPT at 1-year follow-up in both male and female gender. Acknowledgement/Funding None

Item does not contain fulltext BACKGROUND AND AIM: High residual platelet reactivity (HRPR) is still an important challenge, despite the advent of new potent ADP-antagonists. Therefore it is of extreme importance to identify factors that can influence platelet activation. Serum uric acid (SUA) has been largely addressed in the past as a possible risk factor for coronary artery disease, with a possible association with platelets hyperreactivity. So far no studies have assessed the role of serum uric acid on the response to dual antiplatelet therapy. Therefore, the aim of our study was to evaluate the impact of uric acid levels on platelet function in patients treated with dual antiplatelet therapy (DAPT) with clopidogrel or ticagrelor. METHODS AND RESULTS: We scheduled for platelet function assessment at 30-90 days post-discharge patients treated with DAPT (ASA + clopidogrel or ticagrelor) for an ACS or elective percutaneous coronary intervention (PCI). Platelet function was assessed by whole blood impedance aggregometry (Multiplate((R))-Roche Diagnostics AG), HRPR was considered for ASPI test >862 AU( *)min (for ASA) and ADP test values >/=417 AU( *)min (for ADP-antagonists). RESULTS: We included a total of 493 patients (262 were on ASA and clopidogrel and 231 on ASA and ticagrelor). Patients were divided according to quartiles of serum uric acid levels measured at the time of platelet aggregation assessment (Group 1 6.9, n = 122). Patients with higher uric acid levels were older, more often smokers, with history of hypertension and previous coronary artery bypass surgery and renal failure and were more often on therapy with diuretics at admission. Patients with higher SUA had higher triglycerides and fibrinogen. Uric acid levels did not influence ASPI, COL, TRAP and ADP tests. High residual platelet reactivity (HRPR) was observed in 1.5% of patients treated with ASA, with no difference according to SUA quartiles (p = 0.60), confirmed at multivariate analysis after correction for baseline confounders (adjusted OR[95%CI] = 1.05 [0.44-2.52], p = 0.90). HRPR for ADP-antagonists was observed in 23.6% of patients, with no difference according to SUA quartiles (p = 0.47); this result was confirmed also after correction for baseline confounders (adjusted OR[95%CI] = 1.04 [0.84-1.28], p = 0.73). Moreover, no association was found between HRPR and uric acid levels both among patients treated with clopidogrel (p = 0.35) or ticagrelor (p = 0.74), that was confirmed after correction for baseline confounding factors (adjusted OR[95%CI] = 1.18 [0.90-1.55], p = 0.23) and (adjusted OR[95%CI] = 0.96 [0.63-1.47], p = 0.85). The absence of association between SUA and platelet reactivity was confirmed at linear regression analysis both with clopidogrel (r = 0.03, p = 0.55) or ticagrelor (r = -0.01, p = 0.85). CONCLUSION: This is the first large study showing that in patients receiving DAPT, uric acid levels do not influence response to ticagrelor and clopidogrel or the effectiveness of ASA.

Item does not contain fulltext BACKGROUND AND AIM: High density lipoproteins (HDL) have been addressed as a potential strategy for cardiovascular prevention, with great controversies on pharmacological approaches for HDL-elevation. Our aim was to compare HDL-rising treatment with niacin or CETP-inhibitors with optimal medical therapy in cardiovascular outcome. METHODS AND RESULTS: Randomized trials were searched. Primary endpoint was cardiovascular death, secondary were: non fatal myocardial infarction; coronary revascularization; cerebrovascular accidents and safety endpoints. As many as 18 randomized trials, for a total of 69,515 patients, were included. HDL-modifiers did not reduce cardiovascular mortality (2.3%vs3.4%; OR [95%CI] = 0.96 [0.87-1.05], p = 0.37, phet = 0.58), with no benefit from niacin/CETP inhibitors according to patients' risk profile (beta [95%CI] = -0.14 [-0.29 to 0.02], p = 0.09) or the amount of HDL increase (beta [95%CI] = 0.014 [-0.008 to 0.04], p = 0.21). Niacin but not CETP-I reduced myocardial infarction and coronary revascularization, but higher rate of SAE occurred with HDL-modifiers (OR [95%CI] = 1.24 [1.18-1.31], p < 0.00001, phet = 0.02), in particular new onset of diabetes with niacin and worsening of hypertension with CETP-inhibitors. CONCLUSIONS: Niacin and CETP inhibitors do not influence cardiovascular mortality. Significant benefits in MI and coronary revascularization were observed with niacin, despite the higher occurrence of diabetes.

Item does not contain fulltext BACKGROUND: Suboptimal platelet inhibition with antiplatelet treatments is associated with a severe prognosis in patients with coronary artery disease (CAD), and the identification of its determinants is still challenging. Homocysteine elevation has emerged as a prothrombotic factor, influencing coagulative status and endothelial function and potentially modulating platelet aggregation. We therefore aimed to evaluate the effects of homocysteine (Hcy) levels on platelet reactivity in patients receiving acetylsalicylic acid (ASA) with or without ADP antagonists. METHODS: Patients undergoing coronary angiography and receiving ASA (100-160 mg daily) for >7 days, with or without ADP antagonists, were included. Aggregation tests were performed by multiple electrode aggregometry. Suboptimal platelet inhibition was defined as on-treatment aggregation above the lower limit of normality. RESULTS: Our population is represented by 508 ASA-treated patients, 406 (80.1%) of whom on dual antiplatelet therapy (ASA and ADP antagonists). Hcy levels above the median (15.1 nmol/mL) were associated with male gender (P = 0.04), hypertension (P = 0.004), hypercholesterolemia (P = 0.03), aging, renal failure (P < 0.001, respectively), previous coronary bypass grafting (P = 0.04), therapy with calcium antagonists (P = 0.04) and diuretics (P = 0.001), and multivessel CAD (P = 0.03). Higher Hcy is directly related with serum creatinine and uric acid (P < 0.001). Suboptimal platelet inhibition was found in 16 patients (3.2%) for ASA and for ADP antagonists in 80 patients (19.7%). Hcy levels significantly affected suboptimal response to ASA, but not to ADP-mediated aggregation. In fact, a linear relationship was found between homocysteine and platelet reactivity after stimulation with arachidonic acid (r = 0.14, P = 0.004) and collagen (r = 0.12, P = 0.02), but not with ADP (r = 0.02, P = 0.77). Moreover, after correction for baseline differences, Hcy above the median was confirmed as an independent predictor of impaired ASA response [adjusted odds ratio (95% confidence interval) = 3.7 (1.08-12.4), P = 0.04]. CONCLUSIONS: Among patients with CAD, elevated homocysteine is an independent predictor of suboptimal response to ASA, but not to ADP antagonists.

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.

Item does not contain fulltext Contrast-induced nephropathy (CIN) is a common complication of coronary angiography/percutaneous coronary intervention (PCI). Identification of high-risk patients and optimal periprocedural management are key points to reduce the incidence of this iatrogenic complication. We evaluated the impact of gender on CIN after coronary angiography/PCI. We enrolled 2851 consecutive patients (730 females and 1851 males) undergoing coronary angiography/PCI. Baseline clinical and procedural characteristics were collected according to gender. CIN was defined as an absolute >/=0.5mg/dL or a relative >/=25% increase in creatinine level 24 to 48 hours after the procedure. The incidence of CIN was 12.6% and was significantly higher among females (15.6% vs 11.4%, odds ratio (OR) [95% confidence interval (CI)] = 1.42 [1.11-1.82]; P = .004), but this result was not confirmed at multivariate analysis after correction for all baseline confounders (adjusted OR [95% CI] = 1.14 [0.81-1.60]; P = 0.45). In conclusion, we showed that female gender is associated with an increased risk of CIN after coronary angiography/PCI. However, this finding was not confirmed after correction for baseline confounders. Therefore, the higher risk profile rather than female gender itself may contribute to the higher occurrence of CIN among women.

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.

Item does not contain fulltext BACKGROUND AND AIMS: New antithrombotic therapies have significantly improved the outcomes of patients with acute coronary syndrome (ACS), where the introduction of ticagrelor has provided the greatest mortality benefits. However, ticagrelor treatment has been associated with a potential increase in the serum uric acid (SUA) levels, which may influence endothelial dysfunction and prothrombotic status, thereby affecting the risk of acute cardiovascular events in patients requiring dual antiplatelet therapy (DAPT). The present study aimed to compare the impact of antiplatelet agents such as ticagrelor or clopidogrel on SUA levels and their effect on platelet reactivity. METHODS AND RESULTS: We included patients admitted for ACS or elective percutaneous coronary intervention (PCI) and discharged with ASA (acetylsalicylic acid; 100-160 mg) and clopidogrel (75 mg) or ticagrelor (90 mg twice a day). Chemistry was assessed at admission (baseline) and after a 30-90-day period of DAPT (together with platelet reactivity). The absolute and percentage variations of SUA after DAPT introduction were considered. Multiple-electrode aggregometry was used to assess platelet function. A total of 378 patients were enrolled, with 145 treated with aspirin and clopidogrel (AC) and 233 with aspirin and ticagrelor (AT). The AC patients were older (p = 0.003) and more often showed elective PCI as an indication to DAPT (

Item does not contain fulltext BACKGROUND AND AIM: There has been a surge of interest in the cardiovascular effects of vitamin D (25(OH)D), preventing the processes leading to vascular wall degeneration and coronary artery disease (CAD). Gender differences have been suggested for vitamin D status, with a higher rate of deficiency occurring especially in post-menopausal women, increasing the risk of bone fractures and osteoporosis. However, to date, few studies have evaluated the differences in 25(OH)D levels according to gender and their impact on the extent of CAD, which was therefore the aim of the present study. METHODS AND RESULTS: In patients undergoing coronary angiography, fasting samples were collected for the assessment of 25(OH)D levels. Significant CAD was defined as at least one vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. Of the 1811 patients included, 530 (29.3%) were females, who displayed older age (p < 0.001), higher rate of renal failure (p < 0.001), hypertension (p = 0.05), treatment with angiotensin-receptor blockers (p = 0.03) and diuretics (p < 0.001), acute presentation (p < 0.001), higher platelet count (p < 0.001), glycosylated haemoglobin (p = 0.02) and cholesterol (p = 0.001), but an inverse relationship with smoking (p < 0.001), previous cardiovascular events (p < 0.001), treatment with statins and acetylsalicylic acid (ASA) (p < 0.001), body mass index (p = 0.002), haemoglobin (p < 0.001), leucocytes (p = 0.03) and triglycerides (p < 0.001). Female gender was associated with lower vitamin D levels (14.5 +/- 10.9 vs. 15.9 +/- 9.5, p = 0.007) and independently associated with severe vitamin D deficiency (41.9% vs. 30.4%, p < 0.001; adjusted odds ratio (OR) (95% confidence interval (CI)) = 1.42 (1.08-1.87), p = 0.01). Lower tertiles of vitamin D were associated with an increased prevalence and severity of CAD in females (adjusted OR (95% CI = 1.26 (1.10-1.44), p = 0.001 for CAD; adjusted OR (95% CI) = 1.6 (1.39-1.87), p < 0.001 for severe CAD). In males, vitamin D status was independently related to the prevalence (adjusted OR (95% CI) = 1.28 (1.02-1.61), p = 0.03) of CAD, but not the extent of CAD (adjusted OR (95% CI) = 1.02 (0.86-1.2), p = 0.84). CONCLUSION: Gender significantly affects vitamin D status. The lower 25(OH)D levels observed in females, as compared to males, play a more relevant role in conditioning the severity of CAD.

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

Item does not contain fulltext BACKGROUND AND AIM: Clinical trials have reported lower mortality and repeated revascularization rate in diabetic patients treated with coronary artery bypass grafting (CABG) as compared to percutaneous revascularization. However, these studies were conducted in the era of bare-metal stents. Therefore, we performed a meta-analysis to compare CABG to PCI with drug-eluting stents (DES) in diabetic patients with multivessel and/or left main disease. METHODS AND RESULTS: The literature was scanned by formal search of electronic databases (Medline, EMBASE, and Cochrane databases), and major international scientific session abstracts from 2000 to 2013. Primary endpoint was mortality. A total of 14 (4 randomized and 10 non-randomized) trials were finally included, with a total of 7072 patients. Up to 5 years follow-up, CABG was associated with a reduction in mortality (7.3% vs 10.4%, OR[95%CI] = 0.65[0.55-0.77], p < 0.0001; phet = 0.00001), with similar results in both RCTs (OR[95%CI] = 0.64[0.50-0.82], p = 0.0005) and NRCTs (OR[95%CI] = 0.75[0.6-0.94)], p = 0.01) (p int = 0.93). A significant relationship was observed between risk profile and benefits in mortality with CABG (p < 0.001). CABG reduced target vessel revascularization (TVR; 5.2% vs 15.7%, OR[95%CI] = 0.30[0.25-0.36], p < 0.00001, p het = 0.02), with a relationship between risk profile and the benefits from CABG as compared to DES (p < 0.0001). CABG was associated with a lower rate of MACCE (14.9% vs 22.9%, OR[95%CI] = 0.59[0.51-0.67], p < 0.00001, p het

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.

Coronary artery disease (CAD) is the leading cause of mortality in developed countries. Abnormal glucose metabolism is a major determinant of CAD. Glycosilated haemoglobin might offer more advantages in terms of prognostic information being a more stable and accurate parameter to evaluate glucose homeostasis as compared to fasting glycaemia. The association of glycosilated haemoglobin with CAD is less clear, with few data reported in non diabetic patients. Therefore, the aim of the current study was to evaluate among a consecutive cohort of patients without diabetes mellitus the relationship between glycosilated haemoglobin and CAD. Methods: Our population is represented by a total of 1703 consecutive patients undergoing coronary angiography between April 2007 and October 2012, who did not meet the diagnostic criteria for diabetes mellitus, defined as previous diagnosis, specific treatment administration (oral or insulin), fasting glycemia > 126 mg/dL or HbA1c > 6.5%. We additionally evaluated IMT during hospitalization in 237 non diabetic patients. Results: Patients were divided according to tertiles of Glycosilated Haemoglobin ( 5.8%). Glycosilated haemoglobin was associated with ageing (p < 0.001), hypercholesterolemia (p = 0.01), renal failure (p = 0.006), hypertension (p = 0.002), previous MI (p = 0.004), previous PCI (p = 0.01), indication to angiography (p = 0.01), use of ARB (p = 0.01), beta-blockers (p = 0.03), nitrates (p = 0.02), statins (p = 0.008), calcium antagonist (0.01), diuretics (p < 0.001), ASA (p < 0.001), baseline glycaemia (p < 0.001), tryglicerides (p = 0.02) and uric acid (p = 0.04). Glycosilated Haemoglobin, but not resting glycaemia, was significantly associated with the prevalence of coronary artery disease (adjusted OR [95% CI] = 1.51[1.15-1.97], p= 0.002), with 5.8% identified by ROC curve as the best cut-off value in the prediction of CAD. IMT was measured in a consecutive cohort of 237 patients within hospitalization. Glycosilated haemoglobin was significantly associated with CIMT and prevalence of carotid plaques. Conclusions: This is one of the major study showing that among non-diabetic patients, high HbA1C, but not glycaemia, even within normal range, is significantly associated with the risk of proven CAD. Future large studies are certainly needed to further confirm our findings and to evaluate whether a more aggressive cardiovascular prevention can reduce the risk of CAD among patients with HbA1C > 5.8%.

Background Pro-thrombotic conditions importantly influence myocardial perfusion and procedural results after percutaneous coronary intervention (PCI). The neutrophil-to-lymphocyte ratio (NLR) has emerged as a predictor of cardiovascular events and of long-term prognosis, especially in ST-elevation myocardial infarction patients undergoing primary PCI. The aim of our study was to evaluate the role of NLR on periprocedural myocardial infarction (MI) in patients undergoing non-urgent PCI. Methods In a consecutive cohort of 1542 patients undergoing PCI, myonecrosis biomarkers were determined at 6, 12, 24 and 48 hours post-procedure. Patients were divided into quintiles according to NLR values. Periprocedural myonecrosis was defined as a troponin I increase of 3 times the upper limit of normal or as 50 % of an elevated baseline value, whereas periprocedural MI was defined as a CK-MB increase of 3 times the upper limit of normal or 50 % of baseline. Results Higher NLR was related to age, established risk factors and cardiovascular history. NLR was associated with severe coronary artery disease (p = 0.009), tighter stenosis (p