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This document aims to be an integral part of the SICI-GISE position document on standards and guidelines for cardiovascular diagnostic intervention laboratories published in October 2015. It was created with the aim of defining quality and quantitative standards by providing practical support for the structuring of a training course to reach high levels of assistance for nursing and technical personnel working within the catheterization laboratories. The competences detected are the expression of a highly specialized organizational and operational reality that combines technicality with a well-defined clinical assistance need as an expression of a real patient care. The Nurses & Technicians Area of SICI-GISE aimed at issuing a flexible and dynamic document based on technical and operational progress which, in addition to defining qualitative and quantitative standards, describes the underlying knowledge of the professionals of the sector operating in our laboratories. This is the first experience that, through a survey carried out in 2015, has been able to decline qualitative and quantitative data so as to provide resources and skills for measuring and improving assistance outcomes.

Coronary artery disease and type 2 diabetes are chronic diseases of substantial and growing prevalence. Although diabetes is a strong independent risk factor for cardiovascular events, this risk is not confined to glucose levels above the diagnostic threshold for diabetes. Rather, there is now a growing consensus that nondiabetic hyperglycemia measured by fasting glucose, postload glucose or glycated hemoglobin is a progressive, continuous risk factor for cardiovascular outcomes. Whether dysglycemia is a marker for a more complex metabolic condition or may directly contribute to excess cardiovascular risk is still a matter of debate. While strategies designed to normalize glucose levels in people with type 2 diabetes remain inconclusive, diabetes prevention trials suggest that along with reduction of the rate of conversion toward diabetes, a significant improvement in cardiovascular risk factors occurs. Moreover, a number of ongoing studies may provide answers to this question. Recognition that nondiabetic hyperglycemia is associated with an increased cardiovascular risk may suggest new ways for preventing cardiovascular disease.

Background: The glycoprotein IIIa (beta3 integrin) is an integral part of two glicoprotein receptors of platelets and, respectively, endothelium and vascular smooth muscle cells. The gene encoding the GPIIIa, a receptor for fibrinogen, vWF and fibronectin, shows polymorphism (PlA1/PlA2); the PlA2 allele has been associated with myocardial infarction, stroke and cardiovascular disease., Methods: Seven hundred and thirty-two subjects with type 1 diabetes and 605 subjects with type 2 were recruited. The prevalence of complications in type 1 diabetes was: microalbuminuria (uA) 17%, overt nephropathy (MA) 10%; background retinopathy (bR) 27%, proliferative retinopathy (pR) 22%; hypertension (HYP) 13%; coronary heart disease (CHD) 9%. The respective figures for type 2 diabetes were: uA 34%, MA 21%; bR 38%, pR 18%; HYP 80%; CHD 26%. A 247 bp fragment (exon 2) was amplified by PCR. For the detection of the point mutation CDGE (Constant Denaturing Gel Electrophoresis) after optimum denaturing conditions setting by DGGE (Denaturing Gradient GE) and/or RFLP by NciI digestion were employed., Results: In type 1 diabetes, PlA1PlA1/PlA1PlA2 distribution was 77/23%. No differences were found among normoalbuminuric (nA: 76/24%), microalbuminuric (uA: 79/21%) and macroalbuminuric subjects (MA: 75/25%, p=0.79) as well as among subjects with no retinopathy (Ret-) (74/26%), bR (76/24%) and pR (78/22%, p=0.81), and between HYP- (78/22%) and HYP+ (72/28%, p=0.27) as well as CHD- (76/24%) and CHD+ (75/25%, p=0.72). Systolic blood pressure, HbA1c and retinopathy were independent predictors of nephropathy. No contribution of diastolic BP, sex, BMI, duration of diabetes and PlA2 allele was found for the risk of nephropathy. In type 2 diabetes, PlA1PlA1/PlA1PlA2/PlA2PlA2 distribution was 74.4/23.3/2.3%, with no differences foud among nA (73/25/2%), uA (75/23/2%) and MA (81/17/2%, p=0.66). No significant difference was detected among subjects with Ret- (74/22/4%), bR (77/22/1%) and pR (77/22/1%, p=0.62). Also, no differences were found between HYP- (81/17/2%) and HYP+ (74/24/2%, p=0.28) as well CHD- (76/22/2%) and CHD+ (74/24/2%, p=0.93). Systolic BP, HbA1c, presence of retinopathy, gender and BMI were independent predictors of nephropathy. Diastolic BP, duration of diabetes and PlA2 allele did not contribute to the risk of nephropathy., Conclusions: The PlA1/PlA2 polymorphism of the GPIIIa gene does not contribute to the development of nephropathy or retinopathy in type 1 and type 2 diabetes. Furthermore, no association was found between the PlA1/PlA2 polymorphism, hypertension, and coronary heart disease.

The combination of high serum triglyceride levels and small low density lipoprotein particles, with a reduction in high density lipoprotein cholesterol levels has been named atherogenic lipoprotein phenotype or, simply, lipid triad. These lipid factors are commonly associated with peripheral resistance to the action of insulin, hyperinsulinism, central and visceral obesity, hypertension, hyperuricemia, hypercoagulability. The clustering of these nonlipid factors along with the lipid factors has been called metabolic syndrome. Insulin resistance plays a central role in the development of the lipid triad increasing the production of triglyceride-rich lipoproteins and decreasing their catabolism. There is currently great interest about the origins of the metabolic syndrome. One question under considerable research is whether genetic or acquired factors predominate in causing this syndrome. There seems to be little doubt that the metabolic syndrome taken as a whole constitutes a major risk factor for coronary heart disease. What is less certain is that each component of the syndrome is an independent risk factor. People with lipid triad are at very high risk of developing coronary heart disease, and careful management is warranted. Nonetheless, appropriate therapeutic strategies that will modify the metabolic syndrome as a whole are needed. More investigations about key metabolic steps that simultaneously affect multiple pathways will be required to yield a satisfactory therapy for high risk patients exhibiting the metabolic syndrome.

The effects on carbohydrate metabolism by four low-dose oral contraceptives were evaluated in four low-dose oral contraceptives were evaluated-66 young women randomly divided in four groups. In the various preparations there were a different dosage of estrogen (ethinylestradiol) together different doses and types of progestogen (desogestrel, gestodene, cyproterone acetate). After six months of treatment, in all groups a slight increase of glycemic and insulinemic responses during OGTT was observed; the significance was achieved with the preparation containing cyproterone acetate alone. Glycated hemoglobin did not change. Our results suggest that these new low-dose oral contraceptives induced negligible metabolic side effects.