The effect of spironolactone on left ventricular hypertrophy in patients with arterial hypertension and chronic obstructive pulmonary disease

Влияние спиронолактона на гипертрофию миокарда левого желудочка у больных артериальной гипертензией и хроническим обструктивным заболеванием легких
Pavel Kravchun 1, Valentina Delevskaya 1
More Detail
1 Kharkov National Medical University, Kharkov, Ukraine
J CLIN MED KAZ, Volume 3, Issue 37, pp. 43-46.
OPEN ACCESS 4084 Views 2864 Downloads
Download Full Text (PDF)

ABSTRACT

The Aim: To investigate the effect of spironolactone on echocardiograhic parameters of the heart in patients with arterial hypertension combined with chronic obstructive pulmonary disease.
Methods: A total of 80 patients, 41 patients, who received the basic therapy of arterial hypertension and chronic obstructive pulmonary disease (controls), and 39 patients, who additionally received spironolactone in a dose of 50 mg for 3 months, were included in the study. All the patients underwent spirometry and echocardiography before and after the treatment.
Results. The obtained results showed, that addition of spironolactone to the basic treatment of patients with arterial hypertension and chronic obstructive pulmonary disease led to the reduction of the left ventricular myocardial wall thickness, left ventricular myocardial mass and its dimensions (P < 0.05), the increase of its contractility along with decrease of pulmonary hypertension (P < 0.05).
Conclusion. Еру use of spironolactone in the basic treatment of patients with arterial hypertension and chronic obstructive pulmonary disease results in positive changes of structural and functional characteristics of the left ventricle of myocardium, prevents further adverse remodeling of the cardiovascular system and the progression of cardiac dysfunction.
Keywords: spironolactone, left ventricular dimensions of myocardium, chronic obstructive pulmonary disease, arterial hypertension

CITATION

Kravchun P, Delevskaya V. The effect of spironolactone on left ventricular hypertrophy in patients with arterial hypertension and chronic obstructive pulmonary disease. Journal of Clinical Medicine of Kazakhstan. 2015;3(37):43-6.

REFERENCES

  • Katholi R. E., Couri D. M. Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications, Int. J. Hypertens, 2011. – Article ID 495349, 10 p. http://dx.doi.org/10.4061/2011/495349.
  • Rutten F. H. Diagnosis and management of heart failure in COPD, Eur. Respir. Monogr, 2013, No. 59, pp. 50-63.
  • Rusinaru D., Saaidi I., Godard S. et al. Impact of chronic obstructive pulmonary disease on long-term outcome of patients hospitalized for heart failure, Am. J. Cardiol, 2008, No. 101, pp. 353-8.
  • Pitt В., Zannad F., Kemme W. J. The effect of spironolactone on morbidity and mortality in patients with severe heart failure, N. Engl. J., 1999, No. 341, pp. 709-717.
  • Kurrelmeyer K. M., Ashton Y., Xu J. et al. Effects of spironolactone treatment in elderly women with heart failure and preserved left ventricular ejection fraction, J. Card. Fail., 2014, No. 20, pp. 560-8.
  • Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2014, http://www.goldcopd.org.
  • Mancia G., Fagard R., Narkiewicz K., et al. Task Force Members. ESH/ESC Guidelines for the management of arterial hypertension: 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, 2013, No. 31, pp. 1281-357.
  • Devereux R. B., Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method, Circulation, 1977, No. 55, pp. 613.
  • Tsang T. S, Abhayaratna W. P., Barnes M. E., et al. Prediction of cardiovascular outcomes with left atrial size: is volume superior to area or diameter?, J. Am. Coll. Cardiol, 2006, No. 47, pp. 1018-23.
  • Mann D. L. Left ventricular size and shape: determinants of mechanical signal transduction pathways, Heart Fail Rev, 2005, No. 10, pp. 95-100.
  • Maron B. A., Zhang Y. Y., White K., et al. Aldosterone inactivates the endothelin-B receptor via a cysteinyl thiol redox switch to decrease pulmonary endothelial nitric oxide levels and modulate pulmonary arterialhypertension, Circulation, 2012, No. 126, pp. 963-74.