open access

Vol 78, No 4 (2019)
Original article
Submitted: 2019-01-26
Accepted: 2019-02-06
Published online: 2019-03-01
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Influence of hereditary haemochromatosis on left ventricular wall thickness: does iron overload exacerbate cardiac hypertrophy?

K. Rozwadowska1, G. Raczak2, K. Sikorska3, M. Fijałkowski4, D. Kozłowski2, L. Daniłowicz-Szymanowicz2
·
Pubmed: 30835340
·
Folia Morphol 2019;78(4):746-753.
Affiliations
  1. Clinical Centre of Cardiology, University Clinical Centre, Gdańsk, Poland
  2. 2nd Department of Cardiology, Medical University of Gdańsk, Poland
  3. Department of Tropical Medicine and Epidemiology, Medical University of Gdańsk, Gdańsk, Poland
  4. 1st Department of Cardiology, Medical University of Gdańsk, Poland

open access

Vol 78, No 4 (2019)
ORIGINAL ARTICLES
Submitted: 2019-01-26
Accepted: 2019-02-06
Published online: 2019-03-01

Abstract

Background: The left ventricular (LV) hypertrophy increases the risk of heart failure. Hypertension and infiltrative cardiomyopathies are the well-known reasons of LV hypertrophy. The growing interest of scientists in this issue affects hereditary haemochromatosis (HH), which is characterised by the excess deposition of iron mostly due to HFE gene mutation. The aim of our study was to investigate the possible influence of HH on LV parameters in patients with early-diagnosed (early HH) and long-lasting and long-treated (old HH) disease. Materials and methods: Thirty nine early HH and 19 old HH patients were prospectively enrolled in the study; age- and sex-matched healthy volunteers constituted the appropriate control groups. All participants had echocardiography performed (including three-dimension volume and mass analysis); the iron turnover parameters were measured at the time of enrolment in every HH patients. Results: Echocardiographic parameters regarding to left atrium (LA), LV thickness, mass and long axis length were significantly higher, whereas LV ejection fraction was lower in early HH in comparison to healthy persons. In old HH patients the differences were similar to those mentioned before, except LV ejection fraction. The presence of hypertension in both HH groups did not influence echo parameters, as well as diabetes in old HH. The strongest correlation in all HH group was found between the time from HH diagnosis and LA, LV thickness and volumes parameters, but the correlations between iron turnover and echo parameters were non-existent. Conclusions: Hereditary haemochromatosis, not only long-lasting, but also early-diagnosed, could lead to exacerbation of LV wall thickness and cardiac hypertrophy. This effect is not simply connected with hypertension and diabetes that are frequent additional diseases in these patients, but with the time from HH diagnosis.

Abstract

Background: The left ventricular (LV) hypertrophy increases the risk of heart failure. Hypertension and infiltrative cardiomyopathies are the well-known reasons of LV hypertrophy. The growing interest of scientists in this issue affects hereditary haemochromatosis (HH), which is characterised by the excess deposition of iron mostly due to HFE gene mutation. The aim of our study was to investigate the possible influence of HH on LV parameters in patients with early-diagnosed (early HH) and long-lasting and long-treated (old HH) disease. Materials and methods: Thirty nine early HH and 19 old HH patients were prospectively enrolled in the study; age- and sex-matched healthy volunteers constituted the appropriate control groups. All participants had echocardiography performed (including three-dimension volume and mass analysis); the iron turnover parameters were measured at the time of enrolment in every HH patients. Results: Echocardiographic parameters regarding to left atrium (LA), LV thickness, mass and long axis length were significantly higher, whereas LV ejection fraction was lower in early HH in comparison to healthy persons. In old HH patients the differences were similar to those mentioned before, except LV ejection fraction. The presence of hypertension in both HH groups did not influence echo parameters, as well as diabetes in old HH. The strongest correlation in all HH group was found between the time from HH diagnosis and LA, LV thickness and volumes parameters, but the correlations between iron turnover and echo parameters were non-existent. Conclusions: Hereditary haemochromatosis, not only long-lasting, but also early-diagnosed, could lead to exacerbation of LV wall thickness and cardiac hypertrophy. This effect is not simply connected with hypertension and diabetes that are frequent additional diseases in these patients, but with the time from HH diagnosis.

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Keywords

hereditary haemochromatosis, echocardiography, left ventricular hypertrophy, heart siderosis, heart morphology, diabetes mellitus, arterial hypertension

About this article
Title

Influence of hereditary haemochromatosis on left ventricular wall thickness: does iron overload exacerbate cardiac hypertrophy?

Journal

Folia Morphologica

Issue

Vol 78, No 4 (2019)

Article type

Original article

Pages

746-753

Published online

2019-03-01

Page views

1887

Article views/downloads

1010

DOI

10.5603/FM.a2019.0025

Pubmed

30835340

Bibliographic record

Folia Morphol 2019;78(4):746-753.

Keywords

hereditary haemochromatosis
echocardiography
left ventricular hypertrophy
heart siderosis
heart morphology
diabetes mellitus
arterial hypertension

Authors

K. Rozwadowska
G. Raczak
K. Sikorska
M. Fijałkowski
D. Kozłowski
L. Daniłowicz-Szymanowicz

References (20)
  1. Andrews NC. Disorders of iron metabolism. N Engl J Med. 1999; 341(26): 1986–1995.
  2. Bellenger NG, Burgess MI, Ray SG, et al. Comparison of left ventricular ejection fraction and volumes in heart failure by echocardiography, radionuclide ventriculography and cardiovascular magnetic resonance; are they interchangeable? Eur Heart J. 2000; 21(16): 1387–1396.
  3. Borghetti G, von Lewinski D, Eaton DM, et al. Diabetic cardiomyopathy: current and future therapies. Beyond glycemic control. Front Physiol. 2018; 9: 1514.
  4. European Association For The Study Of The Liver. EASL clinical practice guidelines for HFE hemochromatosis. J Hepatol. 2010; 53(1): 3–22.
  5. Gradman AH, Alfayoumi F. From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease. Prog Cardiovasc Dis. 2006; 48(5): 326–341.
  6. Gulati V, Harikrishnan P, Palaniswamy C, et al. Cardiac involvement in hemochromatosis. Cardiol Rev. 2014; 22(2): 56–68.
  7. Hoffmann R, von Bardeleben S, ten Cate F, et al. Assessment of systolic left ventricular function: a multi-centre comparison of cineventriculography, cardiac magnetic resonance imaging, unenhanced and contrast-enhanced echocardiography. Eur Heart J. 2005; 26(6): 607–616.
  8. Lloyd-Jones DM, Larson MG, Leip EP, et al. Framingham Heart Study. Lifetime risk for developing congestive heart failure: the Framingham Heart Study. Circulation. 2002; 106(24): 3068–3072.
  9. Mitchell C, Rahko PS, Blauwet LA, et al. Guidelines for Performing a Comprehensive Transthoracic Echocardiographic Examination in Adults: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2019; 32(1): 1–64.
  10. Nadruz W. Myocardial remodeling in hypertension. J Hum Hypertens. 2015; 29(1): 1–6.
  11. Niederau C, Fischer R, Sonnenberg A, et al. Survival and causes of death in cirrhotic and in noncirrhotic patients with primary hemochromatosis. N Engl J Med. 1985; 313(20): 1256–1262.
  12. Olsson KS, Norrby A. Comment to: Hepcidin: from discovery to differential diagnosis. Haematologica 2008; 93:90-7. Haematologica. 2008; 93(6): e51; discussion e52.
  13. Quinlan GJ, Evans TW, Gutteridge JMC. Iron and the redox status of the lungs. Free Radic Biol Med. 2002; 33(10): 1306–1313.
  14. Rozwadowska K, Daniłowicz-Szymanowicz L, Fijałkowski M, et al. Can two-dimensional speckle tracking echocardiography be useful for left ventricular assessment in the early stages of hereditary haemochromatosis? Echocardiography. 2018; 35(11): 1772–1781.
  15. Stickel F, Osterreicher CH, Datz C, et al. Prediction of progression to cirrhosis by a glutathione S-transferase P1 polymorphism in subjects with hereditary hemochromatosis. Arch Intern Med. 2005; 165(16): 1835–1840.
  16. Strohmeyer G, Niederau C, Stremmel W. Survival and causes of death in hemochromatosis. Observations in 163 patients. Ann N Y Acad Sci. 1988; 526: 245–257.
  17. Tsushima RG, Wickenden AD, Bouchard RA, et al. Modulation of iron uptake in heart by L-type Ca2+ channel modifiers: possible implications in iron overload. Circ Res. 1999; 84(11): 1302–1309.
  18. Vasan R. The role of hypertension in the pathogenesis of heart failure. Arch Intern Med. 1996; 156(16): 1789.
  19. Weber T, Protogerou A. Left ventricular hypertrophy, arterial stiffness and blood pressure: exploring the Bermuda Triangle. J Hypertens. 2019; 37(2): 280–281.
  20. Williams B, Mancia G, Spiering W, et al. ESC Scientific Document Group . 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018; 39(33): 3021–3104.

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