COPD and preclinical cardiovascular disease
https://doi.org/10.21886/2712-8156-2021-2-2-70-79
Abstract
Objective: to assess cerebral blood flow and reveal early myocardial remodeling in COPD patients with varying degrees of airflow restriction.
Materials and methods: the research included 105 patients with COPD from 1 to 4 degrees of severity, depending on the degree of restriction of FEV1 without CVD, diabetes mellitus, chronic kidney disease, obesity, other systemic and oncological diseases. Average age was 57.12 ± 0.68 years, men 45%. 5 groups were identified: mild severity of COPD (GOLD1, = 24), moderate (COLD2, n = 39), severe (GOLD3, n = 30), very severe (GOLD4, n = 12). Control group (n = 37) was tobacco free and CVD. Blood pressure and ultrasound tracranial dopplerography were performed in all groups. Transtoral echocardiography with assessment of global and local LV longitudinal deformation by the strain method and determination of left ventricular diastolic dysfunction (DDLV) was performed in GOLD1 and GOLD2 groups. Parameters of average values of deformation in basal, medial and apical segments are evaluated. Results were processed with Microsoft Excel 2016 and STATISTICA 10 (StatSoft, Inc., USA).
Results: arterial hypertension (AH) was detected in 56.4% of patients in the COLD2 group; 56.7% of patients in the GOLD3 group and 100% of patients in the GOLD4. Сhanges in cerebral blood flow were not found in the GOLD1-3 groups. Significant increase of linear blood flow rate of middle cerebral arteries and index of peripheral vascular resistance were detected in group GOLD4 relative to control and GOLD1-3 groups (p < 0.05). DDLV of 1 type was revealed in 27.7% of patients of COPD and was higher at patients with COPD and AH - 62.5% (χ²=11.5, р =0.009). Pathological patterns were identified at the level of the basal and medial parts of the left ventricle in patients with COPD.
Conclusion: preclinical signs of target organ involvement identified in COPD patients without cardiovascular disease. Changes in cerebral blood flow in the form of an increase in linear blood flow rate and peripheral vascular resistance index were detected in the GOLD4 group. DDLV of 1 type was detected in the GOLD1-2 groups and was found more frequently in the combination of COPD with AH. Pathological patterns were identified at the basal and medial left ventricular levels in a combination of COPD and AH. Changes in target organs indicate the need for an in-depth search to reclassify cardiovascular risk and identify an individual prevention plan.
About the Authors
V. A. NevzorovaRussian Federation
Vera A. Nevzorova, Dr. Sci. (Med.), Professor, Head of Institute Therapy and Instrumental Diagnostic
Vladivostok
N. V. Zakharchuk
Russian Federation
Natalya V. Zakharchuk, Dr. Sci. (Med.), associate professor of Institute Therapy and Instrumental Diagnostic
Vladivostok
E. U. Shapkina
Russian Federation
Elena U. Shapkina, Cand. Sci. (Med.), associate professor school of medicine
Vladivostok
E. A. Kondrashova
Russian Federation
Elena A Kondrashova, assistant of Institute Therapy and Instrumental Diagnostic
Vladivostok
D. V. Kondrashov
Russian Federation
Dmitry V. Kondrashov, student of the 6th year of the Faculty of Medicine
Vladivostok
References
1. Hawkins NM, Virani S, Ceconi C. Heart failure and chronic obstructive pulmonary disease: the challenges facing physicians and health services. Eur Heart J. 2013;34(36):2795-803. DOI: 10.1093/eurheartj/eht192
2. Agusti A, Calverley PM, Celli B, Coxson HO, Edwards LD, Lomas DA, et al. Characterisation of COPD heterogeneity in the ECLIPSE cohort. Respir Res. 2010;11(1):122. DOI: 10.1186/1465-9921-11-122
3. Berger JS, Sanborn TA, Sherman W, Brown DL. Effect of chronic obstructive pulmonary disease on survival of patients with coronary heart disease having percutaneous coronary intervention. Am J Cardiol. 2004;94(5):649-51. DOI: 10.1016/j.amjcard.2004.05.034
4. Anthonisen NR, Connett JE, Enright PL, Manfreda J; Lung Health Study Research Group. Hospitalizations and mortality in the Lung Health Study. Am J Respir Crit Care Med. 2002;166(3):333-9. DOI: 10.1164/rccm.2110093
5. Portegies ML, Lahousse L, Joos GF, Hofman A, Koudstaal PJ, Stricker BH, et al. Chronic Obstructive Pulmonary Disease and the Risk of Stroke. The Rotterdam Study. Am J Respir Crit Care Med. 2016;193(3):251-8. DOI: 10.1164/rccm.201505-0962OC
6. Truelsen T, Prescott E, Lange P, Schnohr P, Boysen G. Lung function and risk of fatal and non-fatal stroke. The Copenhagen City Heart Study. Int J Epidemiol. 2001;30(1):145-51. DOI: 10.1093/ije/30.1.145
7. Schroeder EB, Welch VL, Evans GW, Heiss G. Impaired lung function and subclinical atherosclerosis. The ARIC Study. Atherosclerosis. 2005;180(2):367-73. DOI: 10.1016/j.atherosclerosis.2004.12.012
8. Agarwal SK, Heiss G, Barr RG, Chang PP, Loehr LR, Chambless LE, et al. Airflow obstruction, lung function, and risk of incident heart failure: the Atherosclerosis Risk in Communities (ARIC) study. Eur J Heart Fail. 2012;14(4):414-22. DOI: 10.1093/eurjhf/hfs016
9. van Deursen VM, Urso R, Laroche C, Damman K, Dahlström U, Tavazzi L, et al. Co-morbidities in patients with heart failure: an analysis of the European Heart Failure Pilot Survey. Eur J Heart Fail. 2014;16(1):103-11. DOI: 10.1002/ejhf.30
10. Sitnikova MY, Lyasnikova EA, Yurchenko AV, Trukshina MA, Libis RA, Kondratenko VY, et al. [Results of Russian Hospital Chronic Heart Failure Registry in Three Subjects of Russian Federation]. Kardiologiia. 2015;55(10):5-13. (In Russian). DOI: 10.18565/cardio.2015.10.5-13
11. Uijl A, Lund LH, Vaartjes I, Brugts JJ, Linssen GC, Asselbergs FW, et al. A registry-based algorithm to predict ejection fraction in patients with heart failure. ESC Heart Fail. 2020;7(5):2388-2397. DOI: 10.1002/ehf2.12779
12. Ли В.В., Тимофеева Н.Ю., Задионченко В.С., Адашева Т.В., Высоцкая Н.В. Современные аспекты ремоделирования сердца у больных хронической обструктивной болезнью легких. Рациональная Фармакотерапия в Кардиологии. 2018;14(3):379-386. DOI: 10.20996/1819-6446-2018-14-3-379-386
13. Phelan D, Collier P, Thavendiranathan P, Popović ZB, Hanna M, Plana JC, 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):1442-8. DOI: 10.1136/heartjnl2012-302353
14. Senapati A, Sperry BW, Grodin JL, Kusunose K, Thavendiranathan P, Jaber W, et al. Prognostic implication of relative regional strain ratio in cardiac amyloidosis. Heart. 2016;102(10):748-54. DOI: 10.1136/heartjnl-2015-308657
15. Верещагин Н.В., Моргунов В.А., Гулевская Т.С. Патология головного мозга при атеросклерозе и артериальной гипертонии. М.: Медицина, 1997.
16. Лелюк В.Г., Лелюк С.Э. Церебральное кровообращение и артериальное давление. М.: Реальное время, 2004.
17. Шулутко Б.И., Алмазов В.А. Артериальная гипертензия 2000. - Ренкор, 2001.
18. Чевплянская О.Н., Дударев М.В., Мельников А.В. Продольная деформация левого желудочка и состояние коронарного кровотока у пациентов с высоким нормальным артериальным давлением. Артериальная гипертензия. 2016;22(3):282-290. DOI: 10.18705/1607-419X-2016-22-3-282-290
19. Gorter TM, van Veldhuisen DJ, Bauersachs J, Borlaug BA, Celutkiene J, Coats AJS, et al. Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2018;20(1):16-37. DOI: 10.1002/ejhf.1029
20. Задионченко В.С., Адашева Т.В., Федорова И.В., Нестеренко О.И., Миронова М.А. Артериальная гипертония и хроническая обструктивная болезнь легких: клиникопатогенетические параллели и возможности терапии. Российский кардиологический журнал. 2009;(6):62-68. eLIBRARY ID: 13039047
21. Малахов В. А., Завгородняя А. Н., Лычко В. С. и др. Проблема оксида азота в неврологии. Сумы : СумДПУ им. А. С. Макаренка, 2009.
22. Joannides R, Haefeli WE, Linder L, Richard V, Bakkali EH, Thuillez C, et al. Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo. Circulation. 1995;91(5):1314-9. DOI: 10.1161/01.cir.91.5.1314
23. Somers MJ, Harrison DG. Reactive oxygen species and the control of vasomotor tone. Curr Hypertens Rep. 1999;1(1):102-8. DOI: 10.1007/s11906-999-0080-z
24. Baker AH, Edwards DR, Murphy G. Metalloproteinase inhibitors: biological actions and therapeutic opportunities. J Cell Sci. 2002;115(Pt 19):3719-27. DOI: 10.1242/jcs.00063
25. Candelario-Jalil E, Yang Y, Rosenberg GA. Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia. Neuroscience. 2009;158(3):983-94. DOI: 10.1016/j.neuroscience.2008.06.025
26. Johnson C, Galis ZS. Matrix metalloproteinase-2 and -9 differentially regulate smooth muscle cell migration and cellmediated collagen organization. Arterioscler Thromb Vasc Biol. 2004;24(1):54-60. DOI: 10.1161/01.ATV.0000100402.69997. C3
27. Пыцкий В.И. Ремоделирование органов – типовой патологический процесс. Астма. 2010;11(2):65-74. eLIBRARY ID: 15798303
28. Бродская Т.А., Гельцер Б.И., Невзорова В.А., Моткина Е.В. Артериальная и миокардиальная ригидность у больных хронической обструктивной болезнью легких. Казанский медицинский журнал. 2008;89(5):642-647. eLIBRARY ID: 11911659
Supplementary files
Review
For citations:
Nevzorova V.A., Zakharchuk N.V., Shapkina E.U., Kondrashova E.A., Kondrashov D.V. COPD and preclinical cardiovascular disease. South Russian Journal of Therapeutic Practice. 2021;2(2):70-79. (In Russ.) https://doi.org/10.21886/2712-8156-2021-2-2-70-79