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A non-invasive left ventricular pressure-strain loop study on myocardial work in primary aldosteronism

Hypertension Research volume 44, pages 1462–1470 (2021)Cite this article

Abstract

We investigated the myocardial work derived from left ventricular pressure-strain loop in patients with primary aldosteronism or primary hypertension. We enrolled 50 patients with primary aldosteronism, 50 age- and sex-matched patients with primary hypertension, and 25 normotensive control subjects. We performed transthoracic echocardiography and speckle-tracking echocardiography-based left ventricular pressure-strain loop analysis to evaluate cardiac structure and function. Patients with primary aldosteronism and those with primary hypertension had similar clinic and ambulatory blood pressures, except that the former had a significantly (P = 0.03) higher nighttime systolic blood pressure. All subjects had normal left ventricular ejection fraction (66.4 ± 4.7%). Patients with primary aldosteronism had a greater left ventricular mass index than those with primary hypertension and the normal controls (111.0 ± 21.6 g/m2 versus 95.7 ± 17.7 and 77.9 ± 13.5 g/m2, respectively, P < 0.001). The global myocardial work index (GWI, 2336 ± 333, 2366 ± 288, and 2292 ± 249 mmHg%, respectively), and global constructive work (GCW, 2494 ± 325, 2524 ± 301, and 2391 ± 193 mmHg%, respectively), were comparable in the three groups (P ≥ 0.18). However, the global work efficiency (GWE) differed significantly (P < 0.001), being lowest in primary aldosteronism (91.1 ± 2.7%), intermediate in primary hypertension (93.5 ± 2.5%) and highest in controls (95.3 ± 1.5%). The opposite was true for the global wasted work (GWW) (205.6 ± 74.6, 142.0 ± 56.4 and 99.4 ± 33.7 mmHg%, respectively, P < 0.001). GWE was significantly correlated with the logarithmically transformed plasma concentration and the urinary excretion of aldosterone in patients with primary aldosteronism or primary hypertension (r = −0.43 for both, P < 0.001). The associations remained statistically significant (P ≤ 0.04) after further adjustment for several factors, including left ventricular mass index and clinic or nighttime blood pressure. In conclusion, GWE decreased and GWW increased in primary hypertension and further in primary aldosteronism, probably because of the adrenal aldosterone hypersecretion and the left ventricular mass index increase, while GWI and GCW were similar, indicating that similar and normalized total myocardial work might be a compensation in hypertension at the expense of work efficiency.

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References

  1. Käyser SC, Dekkers T, Groenewoud HJ, van der Wilt GJ, Carel Bakx J, van der Wel MC, et al. Study heterogeneity and estimation of prevalence of primary aldosteronism: a systematic review and meta-regression analysis. J Clin Endocrinol Metab. 2016;101:2826–35.

    Article  Google Scholar 

  2. Monticone S, Burrello J, Tizzani D, Bertello C, Viola A, Buffolo F, et al. Prevalence and clinical manifestations of primary aldosteronism encountered in primary care practice. J Am Coll Cardiol. 2017;69:1811–20.

    Article  Google Scholar 

  3. Chou CH, Hung CS, Liao CW, Wei LH, Chen CW, Shun CT, et al. IL-6 trans-signalling contributes to aldosterone-induced cardiac fibrosis. Cardiovasc Res. 2018;114:690–702.

    Article  CAS  Google Scholar 

  4. Reil JC, Tauchnitz M, Tian Q, Hohl M, Linz D, Oberhofer M, et al. Hyperaldosteronism induces left atrial systolic and diastolic dysfunction. Am J Physiol Heart Circ Physiol. 2016;311:H1014–23.

    Article  Google Scholar 

  5. Freel EM, Mark PB, Weir RA, McQuarrie EP, Allan K, Dargie HJ, et al. Demonstration of blood pressure-independent noninfarct myocardial fibrosis in primary aldosteronism: a cardiac magnetic resonance imaging study. Circ Cardiovasc Imaging. 2012;5:740–7.

    Article  Google Scholar 

  6. Yang Y, Zhu L, Xu J, Tang X, Gao P. Comparison of left ventricular structure and function in primary aldosteronism and essential hypertension by echocardiography. Hypertens Res. 2017;40:243–50.

    Article  Google Scholar 

  7. Shigematsu Y, Hamada M, Okayama H, Hara Y, Hayashi Y, Kodama K, et al. Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism. Hypertension. 1997;29:723–7.

    Article  CAS  Google Scholar 

  8. Redheuil A, Blanchard A, Pereira H, Raissouni Z, Lorthioir A, Soulat G, et al. Aldosterone-related myocardial extracellular matrix expansion in hypertension in humans: a proof-of-concept study by cardiac magnetic resonance. JACC Cardiovasc Imaging. 2020;13:2149–59.

    Article  Google Scholar 

  9. Cesari M, Letizia C, Angeli P, Sciomer S, Rosi S, Rossi GP. Cardiac remodeling in patients with primary and secondary aldosteronism: a tissue doppler study. Circ Cardiovasc Imaging. 2016;9:e004815.

    Article  Google Scholar 

  10. Brown NJ. Contribution of aldosterone to cardiovascular and renal inflammation and fibrosis. Nat Rev Nephrol. 2013;9:459–69.

    Article  CAS  Google Scholar 

  11. Chen YL, Xu TY, Xu JZ, Zhu LM, Li Y, Wang JG. A speckle tracking echocardiographic study on right ventricular function in primary aldosteronism. J Hypertens. 2020;38:2261–9.

    Article  CAS  Google Scholar 

  12. Wang D, Xu JZ, Chen X, Chen Y, Shao S, Zhang W, et al. Speckle-tracking echocardiographic layer-specific strain analysis on subclinical left ventricular dysfunction in patients with primary aldosteronism. Am J Hypertens. 2019;32:155–62.

    Article  CAS  Google Scholar 

  13. Russell K, Eriksen M, Aaberge L, Wilhelmsen N, Skulstad H, Remme EW, et al. A novel clinical method for quantification of regional left ventricular pressure-strain loop area: a non-invasive index of myocardial work. Eur Heart J. 2012;33:724–33.

    Article  Google Scholar 

  14. Russell K, Eriksen M, Aaberge L, Wilhelmsen N, Skulstad H, Gjesdal O, et al. Assessment of wasted myocardial work: a novel method to quantify energy loss due to uncoordinated left ventricular contractions. Am J Physiol Heart Circ Physiol. 2013;305:H996–1003.

    Article  CAS  Google Scholar 

  15. Funder JW, Carey RM, Mantero F, Murad MH, Reincke M, Shibata H, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101:1889–916.

    Article  CAS  Google Scholar 

  16. Chen SX, Du YL, Zhang J, Gong YC, Hu YR, Chu SL, et al. Aldosterone-to-renin ratio threshold for screening primary aldosteronism in Chinese hypertensive patients. ZhongHua Xin Xue Guan Bing Za Zhi. 2006;34:868–72.

    CAS  PubMed  Google Scholar 

  17. Morera J, Reznik Y. Management of endocrine disease: the role of confirmatory tests in the diagnosis of primary aldosteronism. Eur J Endocrinol. 2019;180:R45–58.

    Article  CAS  Google Scholar 

  18. Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L. et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28:1–39.

    Article  Google Scholar 

  19. Manganaro R, Marchetta S, Dulgheru R, Ilardi F, Sugimoto T, Robinet S, et al. Echocardiographic reference ranges for normal non-invasive myocardial work indices: results from the EACVI NORRE study. Eur Heart J Cardiovasc Imaging. 2019;20:582–90.

    Article  Google Scholar 

  20. Galli E, Leclercq C, Fournet M, Hubert A, Bernard A, Smiseth OA, et al. Value of myocardial work estimation in the prediction of response to cardiac resynchronization therapy. J Am Soc Echocardiogr. 2018;31:220–30.

    Article  Google Scholar 

  21. Cauwenberghs N, Tabassian M, Thijs L, Yang WY, Wei FF, Claus P, et al. Area of the pressure-strain loop during ejection as non-invasive index of left ventricular performance: a population study. Cardiovasc Ultrasound. 2019;17:15.

    Article  Google Scholar 

  22. Laine H, Katoh C, Luotolahti M, Yki-Järvinen H, Kantola I, Jula A, et al. Myocardial oxygen consumption is unchanged but efficiency is reduced in patients with essential hypertension and left ventricular hypertrophy. Circulation. 1999;100:2425–30.

    Article  CAS  Google Scholar 

  23. Chan J, Edwards NFA, Khandheria BK, Shiino K, Sabapathy S, Anderson B, et al. A new approach to assess myocardial work by non-invasive left ventricular pressure-strain relations in hypertension and dilated cardiomyopathy. Eur Heart J Cardiovasc Imaging. 2019;20:31–9.

    Article  Google Scholar 

  24. Brilla CG, Weber KT. Reactive and reparative myocardial fibrosis in arterial hypertension in the rat. Cardiovasc Res. 1992;26:671–7.

    Article  CAS  Google Scholar 

  25. Santos AB, Kraigher-Krainer E, Bello N, Claggett B, Zile MR, Pieske B, et al. Left ventricular dyssynchrony in patients with heart failure and preserved ejection fraction. Eur Heart J. 2014;35:42–7.

    Article  CAS  Google Scholar 

  26. Rao AD, Shah RV, Garg R, Abbasi SA, Neilan TG, Perlstein TS, et al. Aldosterone and myocardial extracellular matrix expansion in type 2 diabetes mellitus. Am J Cardiol. 2013;112:73–8.

    Article  CAS  Google Scholar 

  27. Frustaci A, Letizia C, Verardo R, Grande C, Francone M, Sansone L, et al. Primary aldosteronism-associated cardiomyopathy: clinical-pathologic impact of aldosterone normalization. Int J Cardiol. 2019;292:141–7.

    Article  Google Scholar 

  28. Drazner MH. The progression of hypertensive heart disease. Circulation. 2011;123:327–34.

    Article  Google Scholar 

  29. Nakamura M, Sadoshima J. Mechanisms of physiological and pathological cardiac hypertrophy. Nat Rev Cardiol. 2018;15:387–407.

    Article  CAS  Google Scholar 

  30. Kouzu H, Yuda S, Muranaka A, Doi T, Yamamoto H, Shimoshige S, et al. Left ventricular hypertrophy causes different changes in longitudinal, radial, and circumferential mechanics in patients with hypertension: a two-dimensional speckle tracking study. J Am Soc Echocardiogr. 2011;24:192–9.

    Article  Google Scholar 

  31. Fortuni F, Butcher SC, van der Kley F, Lustosa RP, Karalis I, de Weger A, et al. Left ventricular myocardial work in patients with severe aortic stenosis. J Am Soc Echocardiogr. 2021;34:257–66.

    Article  Google Scholar 

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Acknowledgements

The authors gratefully acknowledge the voluntary participation of all subjects.

Funding

The present study was financially supported by the Shanghai Municipal Commission of Health (grant 201840064). Drs. Yan Li and Ji-Guang Wang were also financially supported by grants from the National Natural Science Foundation of China (grants 91639203, 81770455, 82070432 and 82070435), the Ministry of Science and Technology (grants 2015AA020105-06 and 2018YFC1704902) and the Ministry of Health (grant 2016YFC0900902), Beijing, China, and from the Shanghai Commissions of Science and Technology (grant 19DZ2340200), Education (Gaofeng Clinical Medicine Grant Support 20152503) and Health (grant 2017BR025 and a special grant for “leading academics”).

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  1. Department of Cardiovascular Medicine, National Research Center for Translational Medicine, Centre for Cardiovascular Evaluations, Shanghai Key Laboratory of Hypertension, The Shanghai Institute of Hypertension, Department of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China

    Yi-Lin Chen, Ting-Yan Xu, Jian-Zhong Xu, Li-Min Zhu, Yan Li & Ji-Guang Wang

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  1. Yi-Lin Chen
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Contributions

Formal analysis: Y-LC, T-YX. Clinical data collection: L-MZ, J-ZX. Project administration: YL. Supervision: J-GW. Writing-original draft: Y-LC. Writing-review and editing: T-YX, J-GW.

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Correspondence to Ting-Yan Xu.

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Chen, YL., Xu, TY., Xu, JZ. et al. A non-invasive left ventricular pressure-strain loop study on myocardial work in primary aldosteronism. Hypertens Res 44, 1462–1470 (2021). https://doi.org/10.1038/s41440-021-00725-y

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