Early signs of airflow restriction and cardiovascular damage in conditionally healthy smokers

Tobacco smoking is one of the most widespread and at the same time difficult to control risk factors for chronic noncommunicable diseases, which make the most significant contribution to the mortality. Smoking intensity, development of airflow restrictions, and damage to vascular endothelium are connected to the accelerated development of atherosclerosis. At the same time, there is no evidence of a possible relationship between the development of myocardial dysfunction and exposure to tobacco combustion products. It is of interest to study the incidence of airflow restrictions, arterial hypertension, and markers of early damage to target organs - the brachiocephalic arteries (BCA) and myocardium, in so-called relatively healthy smoking individuals. The aim of the study was to describe the incidence of airflow restrictions, hypertension, the state of the brachiocephalic arteries, and indicators of global and regional longitudinal strain of the left ventricle (GLSLV and RLSLV) in actively smoking conditionally healthy individuals. Methods. 100 active smokers were examined (smoking person index or ICH > 10 (17 ± 2 packs/year)) at the mean age of 48,80± 0,68years. 55% of the patients were male. The diagnosis of COPD was made based on spirometry values before and after the test with bronchodilators (400 mcg of salbutamol) (FEV1/FVC < 70% and FEV1 increase <12% of the initial values). Blood pressure measurement, duplex scanning of brachiocephalic arteries, transthoracic echocardiography with GLSLV and RLSLV with 17-segment division by Strain method were performed in all patients. Results. COPD was diagnosed in 35% of the patients, hypertension - in 45%. Evaluation of BCA showed increased thickness of intimamedia complex in the patients with hypertension (р= 0.002) and a significantly higher degree of stenosis and number of plaques in patients with concomitant COPD and hypertension. Type 1 diastolic dysfunction of LV was detected both in patients with hypertension and in the patients with COPD, but it was most common in the patients with concomitant COPD and hypertension. The GLSLV values did not change in all patients, but the RLSLV values depended on the segment (basal, medial, apical) and were significantly lower in the patients with concomitant COPD and hypertension. Conclusion. Tobacco combustion products not only are risk factors of airflow restriction and systemic vascular dysfunction, but also cause preclinical myocardial damage, a marker of which is a violation of the longitudinal strain of the left ventricle.

1. Christiani D.C. Vaping-Induced Lung Injury. N. Engl. J. Med. 2020; 382: 960-962. DOI: 10.1056/NEJMe1912032.

2. Bogdanov D.Ju., Kondrashova E.A., Kulakova N.V. et al. [Risk factors' characteristics of cardiovascular diseases in the population of Primorsk Region residents depending on the status of smoking and age (according to the data of the epidemiological study of ESSE-RF)]. Tihookeanskiy medicinskiy zhurnal. 2017; (4): 45-50 (in Russian).

3. Seimetz M., Parajuli N., Pichl A. et al. Inducible NOS inhibition reverses tobacco-smoke-induced emphysema and pulmonary hypertension in mice. Cell. 2011; 147 (2): 293-305. DOI: 10.1016/j.cell.2011.08.035.

4. Peinado V.I., Pizarro S., Barbera J.A. Pulmonary vascular involvement in COPD. Chest. 2008; 134 (4): 808-814. DOI: 10.1378/chest.08-0820.

5. Barberà J.A., Riverola A., Roca J. et al. Pulmonary vascular abnormalities and ventilation-perfusion relationships in mild chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 1994; 149 (2, Pt 1): 423-429. DOI: 10.1164/ajrccm.149.2.8306040.

6. Nevzorova V.A., Zaharchuk N.V., Brodskaya T.A. et al. [Evaluation of cardiovascular risk in chronic obstructive pulmonary disease using spirometry indices]. Sibirskoe meditsinskoe obozrenie. 2018; (2): 18-24 (in Russian).

7. Chuchalin A.G., Khaltaev N., Antonov N.S. et al. Chronic respiratory diseases and risk factors in 12 regions of the Russian Federation. Int. J. Chron Obstruct Pulmon Dis. 2014; 9 (1): 963-974. DOI: 10.2147/COPD.S67283.

8. Chevplyanskaya O.N., Dudarev M.V., Mel'nikov A.V. [Strain rate and the coronary blood flow in patients with high normal blood pressure]. Arterial'naya gipertenziya. 2016; 22 (3): 282-290. DOI: 10.18705/1607-419X-2016-22-3-282-290 (in Russian).

9. Li V.V., Timofeeva N.Yu., Zadionchenko V.S. et al. [Recent aspects of cardiac remodeling in patients with chronic obstructive pulmonary disease]. Ratsional'naya farmakoterapiya v kardiologii. 2018; 14 (3): 379-386. DOI: 10.20996/1819-6446-2018-14-3-379-386 (in Russian).

10. Collier P., Phelan D., Klein A. A test in context: Myocardial strain measured by speckle-tracking echocardiography. J.Am. Coll. Cardiol. 2017; 69 (8): 1043-1056. DOI: 10.1016/j.jacc.2016.12.012.

11. Nesukay E.G., Danilenko A.A. [Role of speckle tracking echocardiography in the diagnosis and treatment of cardiovascular diseases]. Arterial'naya gipertenziya. 2018; (2): 3343. DOI: 10.22141/2224-1485.2.58.2018.131064 (in Russian).

12. Edvardsen T., Haugaa K.H. Strain echocardiography: from variability to predictability. JACC Cardiovasc Imaging. 2017; 11 (1): 35-37. DOI: 10.1016/j.jcmg.2017.03.012.

13. Phelan D., Collier P., Thavendiranathan P. et al. Relative apical sparing of longitudinal strain using two-dimensional speckle-tracking echocardiography is both sensitive and specific for the diagnosis of cardiac amyloidosis. Heart. 2012; 98 (19): 1442-1448. DOI: 10.1136/heartjnl-2012-302353.

14. Senapati A., Sperry B.W., Grodin J.L. et al. Prognostic implication of relative regional strain ratio in cardiac amyloidosis. Heart. 2016; 102 (10): 748-754. DOI: 10.1136/heartjnl-2015-308657.

15. Mayanskaya S.D., Grebenkina I.A., Oshchepkova O.B., Mikhoparova O.Yu. [Intima-media thickness of common carotid artery as an early predictor of arterial hypertension in patients with hereditary load]. Vestnik sovremennoy klinicheskoy meditsiny. 2016; 9 (6): 67-72 (in Russian).

16. Agusti A. Thomas A. Neff lecture. Chronic obstructive pulmonary disease: a systemic disease. Proc. Am. Thorac. Soc. 2006; 3 (6): 478-481. DOI: 10.1513/pats.200603-058MS.

17. Agustl A.G.N., Noguera A., Sauleda J. et al. Systemic effects of chronic obstructive pulmonary disease. Eur. Respir. J. 2003; 21 (2): 347-360. DOI: 10.1183/09031936.03.00405703.

18. Brodskaya T.A., Gel'tser B.I., Nevzorova V.A., Motkina E.V. [Arterial and myocardial rigidity in patients with chronic obstructive pulmonary disease]. Kazanskiy meditsinskiy zhurnal. 2008; 89 (5): 642-647 (in Russian).

19. Arciniegas E., Frid M.G., Douglas I.S., Stenmark K.R. Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension. Am. J. Physiol. Lung Cell Mol. Physiol. 2007; 293 (1): L1-8. DOI: 10.1152/ajplung.00378.2006.

20. Voelkel N.F., Mizuno S., Bogaard H.J. The role of hypoxia in pulmonary vascular diseases: a perspective. Am. J. Physiol. Lung Cell Mol. Physiol. 2013; 304 (7): L457-465. DOI: 10.1152/ajplung.00335.2012.

21. Nevzorova V.A., Vakhrusheva S.E., Tilik T.V., Isaeva M.P. [Polymorphism of GSTP1 and EPHX1 genes in smokers and patients with chronic obstructive pulmonary disease stages I and II]. Pul'monologiya. 2013; (1): 32-37. DOI: 10.18093/0869-0189-2013-0-1-32-37 (in Russian).

22. Tilik T.V., Nevzorova V.A., Vakhrusheva S.E. et al. [Polymorphism of glutathione transferase genes in case of chronic obstructive lung disease associated with ischemic heart disease]. Tikhookeanskiy meditsinskiy zhurnal. 2010; (1): 13-15 (in Russian).

23. Llinàs L., Peinado V.I., Ramon Goni J. et al. Similar gene expression profiles in smokers and patients with moderate COPD. Pulm. Pharmacol. Ther. 2011; 24 (1): 32-41. DOI: 10.1016/j.pupt.2010.10.010.