rubrica

Cause ed epidemiologia analitica

  • Lorenzo Richiardi1

  1. Università di Torino

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Ricerca bibliografica periodo dal 1 febbraio 2014– 15 aprile 2014

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Stringa: ("italy"[MeSH Terms] OR "italy"[All Fields]) AND ("2014/02/01"[PDat] : "2014/04/15"[PDat]) AND (“Case-Control” [All fields] OR “Cohort”[all fileds] OR “Cross-sectional”[All fields]) AND ("risk"[All Fields] OR "association"[all fields] OR "epidemiologic factors"[MeSH Terms]) and (“odds ratios”[all fields] OR “odds ratio”[all fields] OR “ORs”[all fields] OR “rate ratio”[all fileds] OR “rate ratios”[all fileds] OR “RR”[all fileds] OR “RRs” [all fileds] OR “risk ratio”[all fields] OR “risk ratios”[all fields] OR “prevalence ratio*” [all fields] OR “prevalence ratios” [all fields] OR “hazard ratio” [all fields] OR “hazard ratios” [all fields] OR “HR”[all fields] OR “HRs”[all fields]) NOT "Clinical Trials as Topic"[Mesh] NOT "Sensitivity and Specificity"[Mesh] NOT "Comorbidity"[Mesh] NOT "Predictive Value of Tests"[Mesh] NOT "Prognosis"[Mesh] NOT "Review"[publication type] NOT "Population Surveillance"[Mesh]

FOCUS: pat. Cardiovascolari
AND ("cardiovascular diseases"[MeSH Terms] OR (cardiovascular*[title/abstract] AND diseas*[title/abstract]))

1. J Cardiovasc Med (Hagerstown). 2014 Apr 11. [Epub ahead of print] Lipoprotein-associated phospholipase A2 single-nucleotide polymorphisms and cardiovascular events in patients with coronary artery disease. Maiolino G(1), Lenzini L, Pedon L, Cesari M, Seccia TM, Frigo AC, Rossitto G, Caroccia B, Rossi GP.
Author information: (1)aDepartment of Medicine - DIMED - Internal Medicine 4 bDivisione di Cardiologia, Ospedale di Cittadella, Cittadella cDepartment of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.

Abstract AIMS: We tested the hypothesis that variations in the PLA2G7 gene encoding the lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzyme deemed to have proatherogenic activity, affect the Lp-PLA2 levels and predicts cardiovascular events. METHODS: Using a prospective cohort study design, we investigated incident cardiovascular events as a function of the PLA2G7 gene for rs1805017, rs1805018, and rs1051931 single-nucleotide polymorphisms (SNPs) in 643 randomly selected white patients from the GENICA Study, who at baseline underwent coronary angiography, measurement of Lp-PLA2 mass and activity. Cardiovascular event-free survival was compared across the genotypes by Cox regression, propensity score matching, and haplotype analysis. RESULTS: The rs1805018 SNP did not follow the Hardy-Weinberg equilibrium and was not further explored. The rs1805017 GG genotype had a lower Lp-PLA2 mass and a higher Lp-PLA2 activity, thus suggesting that this SNP is functional. Long-term follow-up (median 7.8 years) was obtained in 75% of the cohort and allowed recording of incident cardiovascular events in 25.8% of the patients. On Cox regression analysis, the common rs1805017 GG genotype predicted acute myocardial infarction (AMI) [hazard ratio 1.75, 95% confidence interval (CI) 1.03-2.99, P = 0.041]; this finding was confirmed on propensity score matching (82.6% AMI-free survival in GG vs. 94.4% in GA + AA, P = 0.003). The rs1805017 and rs1051931 G/G haplotype was also associated with AMI (52.7 vs. 42.2%, P = 0.026) and cardiovascular event incidence (49.5 vs. 41.7%, P = 0.025). CONCLUSION: In high-risk coronary artery disease patients of European ancestry, the PLA2G7 rs1805017 GG genotype is associated with increased Lp-PLA2 plasma activity and AMI.

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2. J Nutr Health Aging. 2014 Mar;18(3):314-21. doi: 10.1007/s12603-013-0392-1. Lifestyle habits and mortality from all and specific causes of death: 40-year follow-up in the Italian Rural Areas of the Seven Countries Study. Menotti A(1), Puddu PE, Lanti M, Maiani G, Catasta G, Fidanza AA.
Author information: (1)P.E. Puddu, MD, PhD, FESC, FACC, Laboratory of Biotechnologies Applied to Cardiovascular Medicine, Department of Cardiovascular, Respiratory, Nephrological, Anesthesiological and Geriatrical Sciences, Sapienza, University of Rome, Viale del Policlinico, 155, Roma 00161, Italy.Tel. +39.06.49972659; Fax. +39.06.4453891; e-mail: paoloemilio.puddu@uniroma1.it.

Abstract OBJECTIVES: Three lifestyle factors were investigated in a population study to explore their relationships with a long-term mortality. MATERIAL AND METHODS: In a cohort of 1564 men aged 45-64 and examined in 1965 within the Italian Rural Areas of the Seven Countries Study, smoking habits, physical activity at work and eating habits (as derived from factor analysis) were determined. During the follow-up 693 men died in 20 years and 1441 in 40 years. RESULTS: In Cox proportional hazards models men smoking cigarettes (versus never smokers), those having a sedentary activity (versus the very active) and those following the Diet Score 1, indexing an unhealthy Diet (versus men with a Diet close to the healthy Mediterranean style) had highly significant hazards ratios (HR) in relations with 20- and 40-year mortality from all causes, coronary heart disease (CHD), cardiovascular disease (CVD) and cancer. HR for all causes in 40 years were 1.44 (95% confidence intervals, CI, 1.27 and 1.64) for smokers, 1.43 (CI 1.23 and 1.67) for sedentary people, and 1.31 (CI 1.15 and 1.50) for men with unhealthy diet. Larger HR were found for CHD, CVD and cancers deaths. Combination of 3 unhealthy risk factors versus their absence was associated with 4.8-year life loss in the 20-year follow-up and 10.7-year in the 40-year follow-up. CONCLUSIONS: Lifestyle behavior linked to physical activity and smoking and eating habits is strongly associated with mortality and survival in middle aged men during long-term follow-up.

3. De Luca G(1), Secco GG, Cassetti E, Verdoia M, Bellomo G, Marino P; on behalf of the Novara Atherosclerosis Study Group (NAS). Haemoglobin levels do not correlate with the extent of coronary artery disease: results from a large cohort study. Coron Artery Dis. 2014 Mar 7. [Epub ahead of print]
Author information: (1)aDivision of Cardiology bClinical Chemistry, Azienda Ospedaliera-Universitaria 'Maggiore della Carità', Eastern Piedmont University, Novara, Italy.

Abstract 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<0.001), there was a predominance of women (P<0.0001), and patients had diabetes (P<0.0001), hypertension (P=0.024), renal failure (P<0.0001), previous coronary artery bypass graft (P<0.0001), previous cerebrovascular accident (P=0.039) and platelet count (P<0.0001). In terms of angiographic features, low Hb levels were associated with a larger prevalence of calcified lesions (P<0.001), but a lower prevalence of thrombus-containing lesions (P<0.001). Hb was not associated with the prevalence of CAD [odds ratio (OR) (95% confidence interval (CI))=0.96 (0.89-1.04), P=0.35], whereas an association was observed with the severity of CAD [OR (95% CI)=0.92 (0.85-0.99), P=0.032] that was not confirmed after correction for baseline confounding factors [OR (95% CI)=0.98 (0.89-1.09), P=0.76]. Similar findings were observed for mean corpuscular volume and red blood cell count. CONCLUSION: This study showed that Hb levels are not associated with the prevalence and extent of CAD.

4. Wang M(1), Beelen R(2), Stafoggia M(3), Raaschou-Nielsen O(4), Andersen ZJ(5), Hoffmann B(6), Fischer P(7), Houthuijs D(7), Nieuwenhuijsen M(8), Weinmayr G(9), Vineis P(10), Xun WW(11), Dimakopoulou K(12), Samoli E(12), Laatikainen T(13), Lanki T(14), Turunen AW(14), Oftedal B(15), Schwarze P(15), Aamodt G(15), Penell J(16), De Faire U(16), Korek M(16), Leander K(16), Pershagen G(16), Pedersen NL(17), Östenson CG(18), Fratiglioni L(19), Eriksen KT(4), Sørensen M(4), Tjønneland A(4), Bueno-de-Mesquita B(20), Eeftens M(21), Bots ML(22), Meliefste K(2), Krämer U(23), Heinrich J(24), Sugiri D(23), Key T(25), de Hoogh K(26), Wolf K(27), Peters A(27), Cyrys J(28), Jaensch A(29), Concin H(30), Nagel G(31), Tsai MY(32), Phuleria H(32), Ineichen A(32), Künzli N(32), Probst-Hensch N(32), Schaffner E(32), Vilier A(33), Clavel-Chapelon F(33), Declerq C(34), Ricceri F(35), Sacerdote C(36), Marcon A(37), Galassi C(36), Migliore E(36), Ranzi A(38), Cesaroni G(3), Badaloni C(3), Forastiere F(3), Katsoulis M(39), Trichopoulou A(39), Keuken M(40), Jedynska A(40), Kooter IM(40), Kukkonen J(41), Sokhi RS(42), Brunekreef B(43), Katsouyanni K(12), Hoek G(2). Long-term exposure to elemental constituents of particulate matter and cardiovascular mortality in 19 European cohorts: results from the ESCAPE and TRANSPHORM projects. Environ Int. 2014 May;66:97-106. doi: 10.1016/j.envint.2014.01.026. Epub 2014 Feb 18.
Author information: (1)Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. Electronic address: M.Wang@uu.nl. (2)Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. (3)Department of Epidemiology, Lazio Regional Health Service, Rome, Italy. (4)Danish Cancer Society Research Center, Copenhagen, Denmark. (5)Danish Cancer Society Research Center, Copenhagen, Denmark; Center for Epidemiology and Screening, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. (6)IUF, Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany; University of Düsseldorf, Düsseldorf, Germany. (7)National Institute of Public Health and the Environment, Bilthoven, The Netherlands. (8)Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Consortium for Biomedical Research in Epidemiology and Public Health (CIBER en Epidemiología y Salud Pública - CIBERESP), Madrid, Spain. (9)University of Düsseldorf, Düsseldorf, Germany; Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany. (10)MRC-HPA Centre for Environment and Health, Department of Epidemiology and Biostatistics, Imperial College London, London, United Kingdom. (11)MRC-HPA Centre for Environment and Health, Department of Epidemiology and Biostatistics, Imperial College London, London, United Kingdom; University College London, London, United Kingdom. (12)Department of Hygiene, Epidemiology and Medical Statistics, Medical School, University of Athens, Athens, Greece. (13)National Institute for Health and Welfare, Kuopio, Finland; Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. (14)National Institute for Health and Welfare, Kuopio, Finland. (15)Norwegian Institute of Public Health, Oslo, Norway. (16)Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. (17)Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. (18)Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. (19)Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden. (20)National Institute of Public Health and the Environment, Bilthoven, The Netherlands; School of Public Health, Imperial College London, London, United Kingdom. (21)Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands; Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. (22)Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. (23)IUF, Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany. (24)Institute of Epidemiology I, Helmholtz Zentrum München, German Research Center of Environmental Health, Neuherberg, Germany. (25)Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom. (26)MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, Imperial College London, London, United Kingdom. (27)Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. (28)Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; University of Augsburg, Environmental Science Center, Augsburg, Germany. (29)Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany. (30)Agency for Preventive and Social Medicine, Bregenz, Austria. (31)Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany; Agency for Preventive and Social Medicine, Bregenz, Austria. (32)Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland. (33)Inserm, Centre for Research in Epidemiology and Population Health (CESP), U1018, Nutrition, Hormones and Women's Health Team, Villejuif, France; University Paris Sud, UMRS 1018, Villejuif, France; IGR, Villejuif, France. (34)French Institute for Public Health Surveillance (InVS) 12, Saint-Maurice, France. (35)Human Genetics Foundation - HuGeF, Turin, Italy. (36)Unit of Cancer Epidemiology, AO Citta' della Salute e della Scienza, University of Turin and Center for Cancer Prevention, Turin, Italy. (37)Unit of Epidemiology & Medical Statistics, Department of Public Health and Community Medicine, University of Verona, Italy. (38)Environmental Health Reference Centre, Regional Agency for Environmental Prevention of Emilia-Romagna, Modena, Italy. (39)Hellenic Health Foundation, Athens, Greece. (40)TNO, Netherlands Organisation for Applied Scientific Research, Utrecht, The Netherlands. (41)Finnish Meteorological Institute, Helsinki, Finland. (42)University of Hertfordshire College Lane, Hatfield, United Kingdom. (43)Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands; Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands.

Abstract BACKGROUND: Associations between long-term exposure to ambient particulate matter (PM) and cardiovascular (CVD) mortality have been widely recognized. However, health effects of long-term exposure to constituents of PM on total CVD mortality have been explored in a single study only. AIMS: The aim of this study was to examine the association of PM composition with cardiovascular mortality. METHODS: We used data from 19 European ongoing cohorts within the framework of the ESCAPE (European Study of Cohorts for Air Pollution Effects) and TRANSPHORM (Transport related Air Pollution and Health impacts--Integrated Methodologies for Assessing Particulate Matter) projects. Residential annual average exposure to elemental constituents within particle matter smaller than 2.5 and 10 μm (PM2.5 and PM10) was estimated using Land Use Regression models. Eight elements representing major sources were selected a priori (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc). Cohort-specific analyses were conducted using Cox proportional hazards models with a standardized protocol. Random-effects meta-analysis was used to calculate combined effect estimates. RESULTS: The total population consisted of 322,291 participants, with 9545 CVD deaths. We found no statistically significant associations between any of the elemental constituents in PM2.5 or PM10 and CVD mortality in the pooled analysis. Most of the hazard ratios (HRs) were close to unity, e.g. for PM10 Fe the combined HR was 0.96 (0.84-1.09). Elevated combined HRs were found for PM2.5 Si (1.17, 95% CI: 0.93-1.47), and S in PM2.5 (1.08, 95% CI: 0.95-1.22) and PM10 (1.09, 95% CI: 0.90-1.32). CONCLUSION: In a joint analysis of 19 European cohorts, we found no statistically significant association between long-term exposure to 8 elemental constituents of particles and total cardiovascular mortality.

5. Garatachea N(1), Emanuele E(2), Calero M(3), Fuku N(4), Arai Y(5), Abe Y(5), Murakami H(6), Miyachi M(6), Yvert T(7), Verde Z(7), Zea MA(8), Venturini L(2), Santiago C(7), Santos-Lozano A(9), Rodríguez-Romo G(10), Ricevuti G(2), Hirose N(5), Rábano A(8), Lucia A(11). ApoE gene and exceptional longevity: Insights from three independent cohorts. Exp Gerontol. 2014 May;53:16-23. doi: 10.1016/j.exger.2014.02.004. Epub 2014 Feb 15.
Author information: (1)Faculty of Health and Sport Science, University of Zaragoza, Ronda Misericordia 5, 22001 Huesca, Spain; Hospital Universitario 12 de Octubre, Research Institute (i+12), Avda. de Córdoba s/n, 28041 Madrid, Spain. Electronic address: nuria.garatachea@unizar.es. (2)Department of Health Sciences, University of Pavia, Via Bassi, 21, I-27100 Pavia, Italy. (3)Fundación CIEN, Fundación Reina Sofía, Instituto de Salud Carlos III, Calle Valderrebollo 5, 28031 Madrid, Spain; UFIEC, Fundación CIEN-Fundación Reina Sofía, and CIBERNED - Instituto de Salud Carlos III, Madrid, Spain. (4)Department of Genomics for Longevity and Health, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo 173-0015, Japan. (5)Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. (6)Department of Health Promotion and Exercise, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, 162-8636 Tokyo, Japan. (7)European University of Madrid, Villaviciosa de Odón, 28670 Madrid, Spain. (8)Fundación CIEN, Fundación Reina Sofía, Instituto de Salud Carlos III, Calle Valderrebollo 5, 28031 Madrid, Spain. (9)Department of Biomedical Sciences, University of León, Campus de Vegazana s/n, 24071 León, Spain; Hospital Universitario 12 de Octubre, Research Institute (i+12), Avda. de Córdoba s/n, 28041 Madrid, Spain. (10)INEF, Universidad Politécnica, c/ Martín Fierro s/n, 28040 Madrid, Spain. (11)European University of Madrid, Villaviciosa de Odón, 28670 Madrid, Spain; Hospital Universitario 12 de Octubre, Research Institute (i+12), Avda. de Córdoba s/n, 28041 Madrid, Spain.

Abstract The ApoE gene is associated with the risk of Alzheimer or cardiovascular disease but its influence on exceptional longevity (EL) is uncertain. Our primary purpose was to determine, using a case-control design, if the ApoE gene is associated with EL. We compared ApoE allele/genotype frequencies among the following cohorts: cases (centenarians, most with 1+ major disease condition; n=163, 100-111years) and healthy controls (n=1039, 20-85years) from Spain; disease-free cases (centenarians; n=79, 100-104years) and healthy controls (n=597, age 27-81years) from Italy; and cases (centenarians and semi-supercentenarians, most with 1+ major disease condition; n=729, 100-116years) and healthy controls (n=498, 23-59years) from Japan. Our main findings were twofold. First, the ε4-allele was negatively associated with EL in the three cohorts, with the following odds ratio (OR) values (adjusted by sex) having been found: 0.55 (95% confidence interval (CI): 0.33, 0.94), P=0.030 (Spain); 0.41 (95%CI: 0.18, 0.99), P=0.05 (Italy); and 0.35 (95%CI: 0.26, 0.57), P<0.001 (Japan). Second, although no association was found in the Spanish cohort (OR=1.42 (95%CI: 0.89, 2.26), P=0.145), the ε2-allele was positively associated with EL in the Italian (OR=2.14 (95%CI: 1.18, 3.45), P=0.01) and Japanese subjects (OR=1.81 (95%CI: 1.25, 2.63), P=0.002). Notwithstanding the limitations of case-control designs, our data suggest that the ApoE might be a candidate to influence EL. The ε4-allele appears to decrease the likelihood of reaching EL among individuals of different ethnic/geographic origins. An additional, novel finding of our study was that the ε2-allele might favor EL, at least in the Italian and Japanese cohorts.

6. Yang J(1), Farioli A(2), Korre M(1), Kales SN(1). Modified mediterranean diet score and cardiovascular risk in a North American working population. PLoS One. 2014 Feb 4;9(2):e87539. doi: 10.1371/journal.pone.0087539. eCollection 2014.
Author information: (1)Department of Environmental Health, Environmental & Occupational Medicine & Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America ; The Cambridge Health Alliance, Harvard Medical School, Cambridge, Massachusetts, United States of America. (2)Department of Environmental Health, Environmental & Occupational Medicine & Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America ; Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.

Abstract INTRODUCTION: Greater adherence to a Mediterranean diet is linked to lower risk for cardiovascular morbidity/mortality in studies of Mediterranean cohorts, older subjects, and/or those with existing health conditions. No studies have examined the effects of this dietary pattern in younger working populations in the United States. We investigated the effects of Mediterranean diet adherence on cardiovascular disease (CVD) biomarkers, metabolic syndrome and body composition in an occupationally active, non-Mediterranean cohort. METHODS: A cross-sectional study in a cohort of 780 career male firefighters, ages 18 years or older, from the United States Midwest. No dietary intervention was performed. A modified Mediterranean diet score (mMDS) was developed for assessment of adherence to a Mediterranean dietary pattern from a previously administered life-style questionnaire that examined pre-existing dietary habits. Clinical data from fire department medical examinations were extracted and analyzed. RESULTS: Obese subjects had significantly lower mMDS, and they reported greater fast/take-out food consumption (p<0.001) and intake of sweetened drinks during meals (p = 0.002). After multivariate adjustment, higher mMDS was inversely related to risk of weight gain over the past 5 years (odds ratio [OR]: 0.57, 95% confidence interval [CI]: 0.39-0.84, p for trend across score quartiles: 0.01); as well as the presence of metabolic syndrome components (OR: 0.65, 95% CI: 0.44-0.94, p for trend across score quartiles: 0.04). Higher HDL-cholesterol (p = 0.008) and lower LDL-cholesterol (p = 0.04) were observed in those with higher mMDS in linear regression after multivariate adjustment for age, BMI and physical activity. CONCLUSIONS: In a cohort of young and active US adults, greater adherence to a Mediterranean-style dietary pattern had significant inverse associations with metabolic syndrome, LDL-cholesterol and reported weight gain, and was significantly and independently associated with higher HDL-cholesterol. Our results support the potential effectiveness of this diet in young, non-Mediterranean working cohorts, and justify future intervention studies.

7. Puddu PE(1), Bilancio G(2), Terradura Vagnarelli O(3), Lombardi C(4), Mancini M(5), Zanchetti A(6), Menotti A(7). Serum uric acid and eGFR_CKDEPI differently predict long-term cardiovascular events and all causes of deaths in a residential cohort. Int J Cardiol. 2014 Feb 15;171(3):361-7. doi: 10.1016/j.ijcard.2013.12.029. Epub 2013 Dec 22.
Author information: (1)Department of Cardiovascular, Respiratory, Nephrological, Anesthesiological and Geriatric Sciences, Sapienza University of Rome, Viale del Policlinico 155, I-00161 Rome, Italy. Electronic address: paoloemilio.puddu@uniroma1.it. (2)Department of Medicine and Surgery, University of Salerno, Via Salvador Allende 43, 84081 Baronissi (SA), Italy. Electronic address: giancarlo.bilancio@gmail.com. (3)Centre of Preventive Medicine, Gubbio, Italy. Electronic address: oscar.terradura@gmail.com. (4)Department of Medicine and Surgery, University of Salerno, Via Salvador Allende 43, 84081 Baronissi (SA), Italy. Electronic address: cinlomb@inwind.it. (5)Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy. Electronic address: mariomancini30@virgilio.it. (6)Istituto Auxologico Italiano, Milan, Italy; University of Milan, Milan, Italy. Electronic address: alberto.zanchetti@unimi.it. (7)Associazione per la Ricerca Cardiologica, Via Latina 49, 00179 Roma, Italy. Electronic address: menottia@tin.it.

Abstract OBJECTIVES: Serum uric acid (SUA) and estimated glomerular filtration rate (eGFR) were separately assessed as risk factors for incident coronary hard (CHDH), cardiovascular disease (CVDH) or all-cause (ALL) deaths but never concomitantly in a residential cohort. MATERIAL AND METHODS: Men and women aged 35-74years, totaling 2888 subjects were followed 13.5-19.5years for incident CVDH, CHDH and ALL deaths. Systematic comparisons among different end-points were based on: age, gender, systolic blood pressure (SBP), total and HDL cholesterol, cigarette consumption, body mass index, blood glucose, SUA, eGFR from the Chronic Kidney Disease Prognosis Consortium (eGFR_CKDEPI) and (eGFR_CKDEPI)(2). RESULTS: Significant (p<0.00001) differences in SUA quintiles were seen for SBP, total and HDL cholesterol, body mass index and eGFR_CKDEPI whereas cigarettes and blood glucose were not statistically different. There were increasingly larger proportions of all events in SUA quintiles (0.05>p<0.0001). Among 4 major continuous variables, SUA was largely accurate (ROC>0.610) to predict all end-points whereas eGFR_CKDEPI was the worse univariate predictor. Multivariately, age, gender, SBP and cigarettes were significant predictors for all end-points. Total cholesterol was a significant predictor only for CHDH events. Blood glucose and SUA were contributors for CVDH events (RR, for 1mg/dl of SUA, 1.09, 95%CI 1.01-1.17), CVD deaths (RR 1.11, 95%CI 1.03-1.20) and ALL deaths (RR 1.08, 95%CI 1.03-1.14) whereas (eGFR_CKDEPI)(2) was for ALL deaths only (RR 1.02, 95%CI 1.00-1.04). CONCLUSION: SUA is a predictor of long-term incidence of cardiovascular events and deaths and all-cause mortality and should be considered for risk predictive purposes and instruments whereas eGFR_CKDEPI only predicts all-cause mortality by a U-shaped relation.

8. Grosso G(1), Pajak A(2), Mistretta A(3), Marventano S(4), Raciti T(5), Buscemi S(6), Drago F(7), Scalfi L(8), Galvano F(7). Protective role of the Mediterranean diet on several cardiovascular risk factors: evidence from Sicily, southern Italy. Nutr Metab Cardiovasc Dis. 2014 Apr;24(4):370-7. doi: 10.1016/j.numecd.2013.09.020. Epub 2013 Nov 1.
Author information: (1)Department of G.F. Ingrassia, Section of Hygiene and Public Health, University of Catania, Catania, Italy; Department of Clinical and Molecular Biomedicine, Section of Pharmacology and Biochemistry, University of Catania, Catania, Italy. (2)Department of Epidemiology and Population Studies, Institute of Public Health, Faculty of Medical Care, Jagellonian University Medical College, Krakow, Poland. (3)Department of G.F. Ingrassia, Section of Hygiene and Public Health, University of Catania, Catania, Italy. Electronic address: anmist@unict.it. (4)Department of G.F. Ingrassia, Section of Hygiene and Public Health, University of Catania, Catania, Italy. (5)Provincial Health Authority of Catania, Catania, Italy. (6)Department of Internal Medicine, University of Palermo, Palermo, Italy. (7)Department of Clinical and Molecular Biomedicine, Section of Pharmacology and Biochemistry, University of Catania, Catania, Italy. (8)Department of Food Science, "Federico II" University Medical School, Naples, Italy.

Abstract BACKGROUND AND AIMS: Epidemiological studies conducted in European countries demonstrated that the adoption of a Mediterranean diet protect against clustered risk factors but those evaluating such benefits specifically in southern Italy are scarce. Thus, the aim of this study was to assess the association between the adherence to the Mediterranean diet and cardiovascular risk factors obesity, diabetes, and hypertension. METHODS AND RESULTS: A cross-sectional population-based survey including 3090 subjects was conducted in Sicily, southern Italy. Food intake was evaluated through a validated food frequency questionnaire and adherence to the dietary pattern was assessed using the MedDietScore. Linear and logistic regression models were performed to estimate odds ratios (ORs) and respective confidence intervals (CIs). After adjusting for confounding factors such as age and gender, participants in the highest tertile of the MedDietScore were less likely to be obese (OR 0.35, 95% CI: 0.24-0.51), hypertensive (OR 0.73, 95% CI: 0.55-0.97), and diabetic (OR 0.43, 95% CI: 0.24-0.77). Linear inverse relation between the MedDietScore and BMI (r(2) = 0.34, P < 0.001), waist circumference (r(2) = 0.17, P < 0.001), and waist-to-hip ratio (r(2) = 0.06, P < 0.001) was found. CONCLUSION: Despite the prevalence rates of nutrition-related diseases are high in Sicily, greater adherence to the Mediterranean dietary pattern is still associated with a better health status.

Breve commento a cura di L. Richiardi
L’effetto della dieta mediterranea su malattie cardiovscolari e tumori e’ stata oggetto di molti studi in diverse popolazioni, ma, come fanno notare gli autori di questo studio trasversale, sono stati condotti meno studi nel Sud Italia. Lo studio include circa tremila persone con almeno 18 anni reclutate a Catania e Lentini. Erano disponibili informazioni su stile di vita e caratetristiche demografiche, sulla dieta tramite FFQ, sulle caratteristiche antropomentriche, sulle malattie cardiovascolari e diabete e sulla pressione arteriosa. L’aderenza alla dieta mediterranea era inversamente associata all’indice di massa corporeo, alla circonferenza vita, all’obesita’ ed al diabete, mentre non c’era associazione con la pressione arteriosa. I risultati sono di interesse ed in linea con l’atteso in base alla letteratura, anche se non si puo’ escludere causalita’ inversa tra gli esiti misurati e la dieta.

9. Shah R(1), Gayat E(2), Januzzi JL Jr(3), Sato N(4), Cohen-Solal A(5), diSomma S(6), Fairman E(7), Harjola VP(8), Ishihara S(9), Lassus J(10), Maggioni A(11), Metra M(12), Mueller C(13), Mueller T(14), Parenica J(15), Pascual-Figal D(16), Peacock WF(17), Spinar J(15), van Kimmenade R(18), Mebazaa A(10); GREAT (Global Research on Acute Conditions Team) Network. Body mass index and mortality in acutely decompensated heart failure across the world: a global obesity paradox. J Am Coll Cardiol. 2014 Mar 4;63(8):778-85. doi: 10.1016/j.jacc.2013.09.072. Epub 2013 Dec 4.
Author information: (1)Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts. (2)Department of Anesthesiology and Intensive Care, Lariboisière University Hospital, Assistance Publique-Hôpitaux de Paris, Université Paris Diderot, Paris, France. (3)Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts. Electronic address: jjanuzzi@partners.org. (4)Internal Medicine, Cardiology, and Intensive Care Medicine, Nippon Medical School Musashi-Kosugi Hospital, Tokyo, Japan. (5)Biomarkers and Heart Diseases, UMR-942, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France. (6)Emergency Department, Sant'Andrea Hospital, University La Sapienza, Rome, Italy. (7)Sociedad Argentina de Cardiologia, Area de Investigacion SAC Azcuenaga, Buenos Aires, Argentina. (8)Division of Emergency Care, Helsinki University Central Hospital, Helsinki, Finland. (9)Department of Cardiology, Steel Memorial Yawata Hospital, Kitakyushu, Japan. (10)Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. (11)ANMCO Research Center, Firenze, Italy. (12)Cardiology, Department of Experimental and Applied Medicine, University of Brescia, Brescia, Italy. (13)Department of Internal Medicine, University Hospital, Basel, Switzerland. (14)Department of Laboratory Medicine, Konventhospital Barmherzige Brueder, Linz, Austria. (15)Department of Internal Medicine and Cardiology, University Hospital Brno, Faculty of Medicine, Masaryk University, Brno, Czech Republic. (16)Cardiology Service, Virgen de la Arrixaca Hospital, Department of Medicine, Faculty of Medicine, University Murcia, Murcia, Spain. (17)Baylor College of Medicine, Houston, Texas. (18)University Medical Center, Utrecht, Utrecht, the Netherlands. Comment in J Am Coll Cardiol. 2014 Mar 4;63(8):786-7.

Abstract OBJECTIVES: This study sought to define the relationship between body mass index (BMI) and mortality in heart failure (HF) across the world and to identify specific groups in whom BMI may differentially mediate risk. BACKGROUND: Obesity is associated with incident HF, but it is paradoxically associated with better prognosis during chronic HF. METHODS: We studied 6,142 patients with acute decompensated HF from 12 prospective observational cohorts followed-up across 4 continents. Primary outcome was all-cause mortality. Cox proportional hazards models and net reclassification index described associations of BMI with all-cause mortality. RESULTS: Normal-weight patients (BMI 18.5 to 25 kg/m(2)) were older with more advanced HF and lower cardiometabolic risk. Despite worldwide heterogeneity in clinical features across obesity categories, a higher BMI remained associated with decreased 30-day and 1-year mortality (11% decrease at 30 days; 9% decrease at 1 year per 5 kg/m(2); p < 0.05), after adjustment for clinical risk. The BMI obtained at index admission provided effective 1-year risk reclassification beyond current markers of clinical risk (net reclassification index 0.119, p < 0.001). Notably, the "protective" association of BMI with mortality was confined to persons with older age (>75 years; hazard ratio [HR]: 0.82; p = 0.006), decreased cardiac function (ejection fraction <50%; HR: 0.85; p < 0.001), no diabetes (HR: 0.86; p < 0.001), and de novo HF (HR: 0.89; p = 0.004). CONCLUSIONS: A lower BMI is associated with age, disease severity, and a higher risk of death in acute decompensated HF. The "obesity paradox" is confined to older persons, with decreased cardiac function, less cardiometabolic illness, and recent-onset HF, suggesting that aging, HF severity/chronicity, and metabolism may explain the obesity paradox.

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