Association Between Prostatic Volume, Metabolic Syndrome and Left Ventricular Mass: A Cross Sectional Study
Clinical Medicine Research
Volume 6, Issue 4, July 2017, Pages: 121-126
Received: Apr. 11, 2017;
Accepted: Apr. 20, 2017;
Published: Jun. 1, 2017
Views 1902 Downloads 73
Ebenezer Adekunle Ajayi, Department of Medicine, Ekiti State University, Ado Ekiti, Nigeria
Patrick Temi Adegun, Department of Surgery, Ekiti State University, Ado Ekiti, Nigeria
Ganiyu Olusola Akanbi, Department of Radiology, Ekiti State University, Ado Ekiti, Nigeria
Akande Oladimeji Ajayi, Department of Medicine, Ekiti State University, Ado Ekiti, Nigeria
Peter Olufemi Areo, Department of Surgery, Ekiti State University, Ado Ekiti, Nigeria
Felix Olukayode Aina, Department of Family Medicine, Ekiti State University Teaching Hospital, Ado Ekiti, Nigeria
Samuel Ayokunle Dada, Department of Medicine, Ekiti State University, Ado Ekiti, Nigeria
Follow on us
Ageing in men is associated with increased prevalence of cardiovascular risk factors and benign prostatic hyperplasia (BPH) with both entities possibly representing downstream manifestations of a common pathogenesis. There is paucity of data on the association of BPH and left ventricular hypertrophy (LVH). This study evaluated relationship between prostate volume, common cardiovascular risk factors and LVH. It was a cross sectional, prospective, hospital-based study. Thirty patients with benign prostatic enlargement (BPE) and 30 age- matched male controls without BPE were studied. All the subjects had clinical, biochemical, prostate ultrasound and echocardiographic evaluation done. SPSS IBM 20 was used to analyze data. Mean age was 65.60 ± 8.11 years (range: 54-82years). Subjects with BPE compared to those without did not significantly differ in age (66.50± 7.75 vs. 64.70±8.49; p=0.39). Significantly higher percentage of subjects with BPE had abnormally low HDL-cholesterol and high blood pressure compared with subjects without BPE. Eight (26.7%) of subjects with BPE in contrast to none of the subjects without BPE had metabolic syndrome (Chi2 = 9.231; p=0.002). Left ventricular mass index were significantly higher in subjects with BPE than in those without. None of the subjects without BPE as compared with 7 (23.3%) of subjects with BPE had echocardiographic determined LVH. Echocardiographic indices that significantly correlated with prostatic volume were: LVPWd (r=0.326, p= 0.011), IVSTd (r= 0.267, p=0.039), LVMI(r=0.308, p= 0.017), LAD (r= 0.494, p <0.0001) and AOD (r= 0.352, p= 0.006). The conclusion was that BPE is associated with increased left ventricular mass index and metabolic syndrome, mostly driven by elevated blood pressure and low serum HDL-cholesterol.
Benign Prostatic Hypertrophy, Prostatic Volume, Left Ventricular Hypertrophy, Metabolic Syndrome, Left Ventricular Mass Index
To cite this article
Ebenezer Adekunle Ajayi,
Patrick Temi Adegun,
Ganiyu Olusola Akanbi,
Akande Oladimeji Ajayi,
Peter Olufemi Areo,
Felix Olukayode Aina,
Samuel Ayokunle Dada,
Association Between Prostatic Volume, Metabolic Syndrome and Left Ventricular Mass: A Cross Sectional Study, Clinical Medicine Research.
Vol. 6, No. 4,
2017, pp. 121-126.
Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/
) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Hammarsten J, Hogstedt B. Clinical, anthropometric, metabolic and insulin profile of men with fast annual growth rates of benign prostatic hyperplasia. Blood Press1999; 8:29–36.
Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. J Urol 1984; 132:474–9.
Holtgrewe HL. Economic issues and the management of benign prostatic hyperplasia. Urology 1995; 46:23–5.
Madersbacher S, Alivizatos G, Nordling J, Sanz CR, Emberton M, de la Rosette JJ. EAU 2004 guidelines on assessment, therapy and follow-up of men with lower urinary tract symptoms suggestive of benign prostatic obstruction (BPH guidelines). EurUrol 2004; 46:547–54.
Lee C, Kozlowski JM, Grayhack JT. Etiology of benign prostatic hyperplasia. UrolClin North Am 1995; 22:237–46.
Dahle SE, Chokkalingam AP, Gao YT, Deng J, Stanczyk FZ, Hsing AW. Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia. J Urol 2002; 168:599–604.
Hammarsten J, Hogstedt B. Hyperinsulinaemia as a risk factor for developing benign prostatic hyperplasia. EurUrol 2001; 39:151–8.
Ziada A, Rosenblum M, Crawford ED. Benign prostatic hyperplasia: an overview. Urology 1999; 53:1–6.
Parsons JK. Modifiable risk factors for benign prostatic hyperplasia andlower urinary tract symptoms: new approaches to old problems. J Urol2007; 178: 395–401.
Meigs JB, Mohr B, Barry MJ, Collins MM, McKinlay JB. Riskfactors for clinical benign prostatic hyperplasia in acommunity-based population of healthy aging men. J ClinEpidemiol 2001; 54:935–44.
Weisman KM, Larijani GE, Goldstein MR, Goldberg ME. Relationship between benign prostatic hyperplasia andhistory of coronary artery disease in elderly men. Pharmacotherapy 2000; 20:383–6.
McVary KT, Razzaq A, Lee C, Venegas MF, Rademaker A, McKenna KE. Growth of the rat prostate gland is facilitated by the autonomic nervous system. BiolReprod 1994; 51:99–107.
Frustaci A, Kajstura J, Chimenti C et al. Myocardial cell deathin human diabetes. Circ Res 2000; 87: 1123–1132.
Eaton CL. Aetiology and pathogenesis of benign prostatic hyperplasia. Curr Opin Urol 2003; 13:7–10.
Walz J, Graefen M, Chun FK, et al., High incidence of prostate cancer detected by saturation biopsy after previous negative biopsy series, Eur Urol. 2006, 498-505.
Troy BL, Pombo J, Rackley CE: Measurement of left ventricular wall thickness and mass by echocardiography. Circulation 1972; 45:602-611.
Sahn DJ, DeMaria A, Kisslo J, Weyman A: Recommendations regarding Quantitation in M-mode Echocardiography. Results of a survey of Echocardiographic measurements. Circulation 1978; 56:1072-1083.
Devereux RB: Detection of left ventricular hypertrophy by M-mode echocardiography. Anatomic validation, standardization, and comparison to other methods. Hypertension 1987; 9:1119-1126.
Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Chamber Quantification Writing Group; American Society of Echocardiography’s Guidelines and Standards Committee; European Association of Echocardiography. Recommendations for chamber quantification: A report from the American Society of Echocardiography’s Guidelines and Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am SocEchocardiogr. 2005; 18:1440-1463.
Alberti KG, Zimmet P, Shaw J. Metabolic syndrome-a new world-wide definition. A Consensus Statement from theInternational Diabetes Federation. DiabetMed 2006 May; 23(5):469-80.
Gacci M, Corona G, Vignozzi L, Salvi M, Serni S, De Nunzio C, et al. Metabolic syndrome and benign prostatic enlargement: a systematic review and meta-analysis. BJU Int 2015; 115: 24–3.
Vignozzi L, Gacci M, Cellai I et al. Fat boosts, while androgen receptor activation counteracts, BPH-associated prostate inflammation. Prostate 2013; 73: 789–800.
Vignozzi L, Rastrelli G, Corona G, Gacci M, Forti G, Maggi M. Benign prostatic hyperplasia: a new metabolic disease? J Endocrinol Invest. 2014; 37:313–22.