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344 Letters to the Editorvasa vasorum of atherosclerotic plaque: angiographic results in a rabbit atheromaticmodel. Hellenic J Cardiol 2006;47:710.7 Stefanadis C, Toutouzas K, Stefanadi E, Tsiamis E, Vavuranakis M, Kipshidze N. Avastin-eluting stent: long-term angiographic and clinical follow up. Hellenic J Cardiol 2008;49:18890.8 Stefanadis C, Toutouzas K, Tsiamis E, Vavuranakis M, Stefanadi E, Kipshidze N. First-in-man study with bevacizumab-eluting stent: a new approach for the inhibition of atheromatic plaque neovascularisation. EuroIntervention 2008;3: 4604.0167-5273/$ see front matter 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.10.115Relationship of aortic stiffness, central systolic blood pressure and left atriumenlargement in general middle and aged populationSheng Kang a, Hui-min Fan a, Jue Li b, Lie-ying Fan c, Ming Chen a, Zhong-min Liu a,and Heart Failure Risk Factors Investigation Project collaborative group (HFRFIP collaborative group)a Center of Cardiology, Shanghai East Hospital, Chinab Department of Epidemiology, Tongji University Medical School, Chinac Department of Clinical Laboratory, Shanghai East Hospital, Chinaa r t i c l e i n f oArticle history:Received 23 October 2011Accepted 29 October 2011Available online 23 November 2011Keywords:Left atrial diameterCentral aortic systolic blood pressurePulse wave velocity Left atrial enlargement has been proposed as a predictor of atrialbrillation, stroke, congestive heart failure, and cardiovascular death1. Recently, it is reported that left atrial diameter (LAD) is increasedand independently associated with arterial stiffness in patients withobstructive sleep apnea 2. Central aortic systolic blood pressure (CSBP) is taken at the root ofthe aorta in the heart, the pulse wave represents a local blood pressurechange caused by the passage of blood from the left ventricle into theaorta, accompanied by the wave action through the artery. Severalprospective studies have conrmed that CSBP is concurrent closely related to heart, brain and kidney damage, and its ability to predict cardiovascular events may be superior to peripheral arterial pressure 3,4, besides, higher aortic stiffness assessed by pulse wave velocity (PWV) is associated with increased risk for a rst cardiovascular event in community 5. Thus, this study was aimed to investigate the performances ofaortic stiffness (PWV) and wave reection (CSBP) to detect left atrialenlargement. From July to end of August 2009,1929 subjects completed the cross-sectional investigation including questionary, systolic blood pressure(SBP), diastolic blood pressure (DBP), PWV, CSBP, brain natriuretic Corresponding author at: Center of Cardiology, Shanghai East Hospital, Jimo Rd 150,200120 Shanghai, China. Tel.: +86 21 38804518.peptide (BNP) and LAD measurements in Lujiazui community,Shanghai. 23 of the subjects were (aged 47 to 81 years; 10 males and 13females) randomly completed the re-survey during a week for qualitycontrol. Currently, Omron HEM-9000AI radial arterial pulse wavemonitor (OMRON Corp., Tokyo, Japan) is the rst automatedtonometer to provide an estimate of CSBP, thus we used it to detectCSBP and peripheral arterial pressure following the manipulationprocedure. The methods and quality controls of echocardiography, PWV and laboratory measurements including TC, HDL-C, LDL-C, BNP, FBS and HbA1C were reported in our previous study 6. According to American Society of Echocardiographys Guidelines 7, we set LAD enlargement standard as N38 mm for female and N40 mm for male. Statistical analysis was performed using a SPSS software package(SPSS 16.0, USA). Reproducibility of measurements were presentedusing BlandAltman plot, and made with MedCalc Software (Version11.2, Belgium). Clinical characteristics of population between LAD normal groupand LAD enlargement group were shown in Table 1. Coefcient of Repeatability (CR) for LAD was equal to 7.72 in Fig.1(A), another CR for PWV was calculated to 172.16 in Fig.1(B), and CR for CSBP was calculated to 29.49 in Fig. 1(C), we did not nd any systematic bias, and the two measurements indicated the good repeatability. PWV and CSBP were signicantly correlated with LAD respectively(Pearson correlation r=0.224, P=0.000) and (Pearson correlationr=0.273, P=0.000) in Fig. 2(A) and (B).Adjusted for those variables (P0.1) in Table 1 and the knownpredisposing factors of increased arterial stiffness and increased LAdimensions (myocardial infarction history) in multiple logistic-regression model, PWV and CSBP were independently correlated withLAD enlargement (Odd Ratio=1.001 1.000 to 1.001, P=0.044 andOdd Ratio=1.029 1.005 to 1.053, P = 0.019 respectively). This study was rst to suggest that increasing large artery stiffness(PWV) and aortic pressure wave reections (CSBP) are closelyindependently associated with LAD enlargement in general middleand aged population. The enlarged atria are more inclined to atrial brillation because a larger area allows for more re-entry circuits 8. The latest relevant guidelines reported that atrial brillation would be increased following LAD increased N40 mm 9,10. Therefore, our ndingsnot only suggest that increasing PWV and CSBP are closely associatedwith LAD enlargement, but also imply that increasing PWV and CSBPLetters to the Editor 345Table 1The clinical characteristics of subjects without LAD or with LAD enlargement.Characherisitc Overall subjects(n=1929)LAD normalgroup(n=1713)LADenlargementgroup(n=214)PvalueAge (years) 57.6 9.8 57.0 9.6 62.3 9.7 0.00Gender 32.2 31.5 37.4 0.08(male %) History (%) Diabetes 7.9 7.2 13.7 0.00 Hypertension 35.5 32.5 59.4 0.00 Dyslipidemia 21.9 20.8 30.7 0.00 Myocardial infarction 0.5 0.5 1.0 0.21 Valvular heart 3.4 3.3 4.2 0.03diseaseSmoking 0.44 Never smoking 79.1 79.4 76.9Ever smoking 5.3 5.1 7.1 Current smoking 15.6 15.5 16.0Drinking 0.24 Never drinking 86.6 87.1 82.5Ever drinking 2.4 2.2 3.3 Current drinking 11.1 10.8 14.2 Coronary artery 4.6 3.9 10.4 0.00disease PCI 0.4 0.3 1.4 0.01 CABG 0.2 0.2 0.5 0.37BMI (kg/m2) 24.1 3.3 23.8 3.1 26.6 3.6 0.00 SBP (mm Hg) 133.8 22.0 132.3 21.5 145.8 22.4 0.00 DBP (mm Hg) 75.7 11.7 75.2 11.4 79.3 13.2 0.00 CSBP (mm Hg) 138.9 22.0 137.3 21.2 151.6 24.7 0.00 PWV (cm/s) 1570.8 338.4 1549.9 328.0 1742.2 372.5 0.00 FBS (mmol/L) 5.4 1.3 5.3 1.2 5.8 1.9 0.00 TC (mmol/L) 5.2 1.0 5.2 1.0 5.3 1.0 0.23 HDL-C (mmol/L) 1.3 0.3 1.3 0.3 1.2 0.3 0.00 LDL-C (mmol/L) 3.1 1.1 3.1 1.1 3.2 0.9 0.24 BNP (pg/ml) 53.0 50.0 80.0 0.00 (31.0, 86.0) (30.0, 80.0) (39.0, 155.5)HbA1C (%) 6.0 1.9 5.9 2.0 6.3 1.3 0.03LAD (mm) 34.2 4.8 33.1 3.6 42.4 5.5 0.00PVWT (mm) 8.0 1.1 7.9 1.0 8.7 1.4 0.00IVST (mm) 8.5 1.4 8.4 1.3 9.1 1.6 0.00LVMI (g/m2) 86.584.8 98.8 0.00 (73.8, 100.5) (72.8, 98.5) (85.8, 116.2)LVEF (%) 65.0 3.3 65.2 3.2 63.2 3.6 0.00 Note: PCI, percutaneous coronary intervention; CABG, coronary artery bypass grafting; BMI, body mass index; FBS, fasting blood sugar; TC, total cholesterol; LDL, low-density lipoprotein cholesterol; HDL, high-density lipoprotein cholesterol; HbA1C, glycated hemoglobin; PVWT, posterior left ventricular wall thickness; IVST, interventricular septal thickness; LVMI, left ventricular mass index; LVEF, left ventricular ejection fraction. Continuous variables (mean SD) were made with 2- tailed unpaired t test, classied variables (proportion) were done with chi-squaretest, but skewed distributional BNP and LVMI (median and inter-quartile) wereperformed with MannWhitney U test.may predict for atrial brillation and other cardiovascular events in future. Noticeably, we found that PWV and CSBP were signicantly associated with LAD respectively in Fig. 2(A) and (B). Importantly, plasma BNP served as a biomarker for increasing left ventricular pressure and preclinical diastolic dysfunction in patients with normal systolic function 11, and we also found that BNP increased signicantly in LAD enlargement group compared with LAD normal group (Table 1), thereby suggesting that aortic stiffness and wavereections (PWV and CSBP) may initially induce abnormal left ventricular pressure, and further increase left atrial pressure and diameter. In conclusion, increased aortic stiffness and central systolic bloodpressure are independently associated with left atrial enlargement ingeneral middle and aged population. The noninvasive techniques used Fig. 1. The Bland and Altman plot displays a scatter diagram of the differences plotted against the averages of the two measurements. Horizontal lines are drawn at the mean difference, and at the limits of agreement, which are dened as the mean differenceplus and minus 1.96 times the standard deviation of the differences. (A). Repeatabilityof LAD measurements (LAD1 and LAD2); (B). Repeatability of PWV measurements(PWV1 and PWV2); (C). Repeatability of CSBP measurements (CSBP1 and CSBP2).in the present study are available to monitor arterial stiffness andwave reection changes in future clinical study. The study was funded by Heart Failure Risk Factors InvestigationProject (PKJ2010-Y05), and carried out by a collaborative group, wespecially appreciated staff to support our study. The authors of this346 Letters to the EditorFig. 2. (A). Correlation of PWV with LAD in 1929 subjects.(B). Correlation of CSBP with LAD in 1929 subjects.Letters to the Editor 347 manuscript have certied that they comply with the Principles of EthicalPublishing in the International Journal of Cardiology (Shewan and Coats2010; 144: 12).References1 Abhayaratna WP, Seward JB, Appleton CP, et al. Left atrial size: physiologic determinants and clinical applications. J Am Coll Cardiol 2006;47:235763. 2 Drager LF, Bortolotto LA, Pedrosa RP, Krieger EM, Lorenzi-Filho G. Left atrial diameter is independently associated with arterial stiffness in patients with obstructive sleep apnea: potential implications for atrial brillation. Int J Cardiol 2010;144:2579. 3 Mancia G, De Backer G, Dominiczak A, et al. The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007;25:110587.4 Williams B, Lacy PS, Thom SM, et al. Differential impact of blood pressure- lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation 2006;113:121325.5 Vlachopoulos C, Aznaouridis K, Stefanadis C. Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis. J Am Coll Cardiol 2010;55:131827.6 Kang S, Fan HM, Li J, et al. Relationship of arterial stiffness and early mild diastolic heart failure in general middle and aged population. Eur Heart J 2010;31:2799807.7 Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantication: a report from the American Society of Echocardiographys Guidelines and Standards Committee and the Chamber Quantication Writing Group, developed in conjunction with the European Association of Echocardio- graphy, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:144063.8 Allessie MA, Konings K, Kirchhof CJ, Wijffels M. Electrophysiologic mechanisms of perpetuation of atrial brillation. Am J Cardiol 1996;77:10A23A.9 Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J 2008;29:2388442.10 Fuster V, Rydn LE, Cannom DS, et al. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial brillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in partnership with the European Society of Cardiology and in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. J Am Coll Cardiol 2011;57:e10198.11 Ommen SR, Nishimura RA, Appleton CP, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular lling pressures: a comparative simultaneous Doppler- catheterization study. Circulation 2000;102:178894.0167-5273/$ see front matter 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.10.135No evidence for an association of AB0 blood group and manifestation ofthrombotic microangiopathiesChristoph Sucker a,c,1, Andreas Fusshoeller b,1, Firuseh Dierkes b, Bernd Grabensee b, Rdiger E. Scharf a, Rainer B. Zotz a, Jens Litmathe da Department of Hemostasis and Transfusion Medicine, Heinrich Heine University Medical Center, Duesseldorf, Germanyb Department of Nephrology, Heinrich Heine University Medical Center, Duesseldorf, Germanyc LaboMed Coagulation Centre, Berlin, Germanyd Dept. of Thoracic- and Cardiovascular Surgery, Heart and Vascular Center Oldenburg, Germanya r t i c l e i n f oArticle history:Received 7 September 2011Revised 24 October 2011Accepted 29 October 2011Available online 16 November 2011Keywords:ThrombosisMicroangiopathyABO blood groupDear Sirs, Since many years, AB0 blood group has been known to inuence on the manifestation of arterial and venous thrombotic disease 13. Inparticular, individuals carrying a Non-0-blood group (A, B, AB) appearedto have a higher risk for thrombotic events compared to those with A, B,or AB blood groups. This effect was attributed to higher factor VIII and Corresponding author at: LaboMed Coagulation Centre Berlin, Nurnberger Strasse 7b/c, 10789 Berlin, Germany.E-mail address: suckerlabomed.de (C. Sucker).1 Both authors equally contributed to this work. von Willebrand factor (vWF) plasma levels compared to individuals with the 0 blood group 4, 5. In a study enrolling 1117 healthy individuals, plasma vWF levels were lowest in group O (me