, Volume 196, Issue 2, pp 195–200 | Cite as

Cardiovascular Studies in Patients with Chronic Obstructive Pulmonary Disease Due to Biomass Smoke or Tobacco

  • Rafael Golpe
  • Pilar Sanjuán-López
  • Irene Martín-Robles
  • Carlos González-Juanatey
  • Luis Pérez-de-Llano
  • José L. López-Campos


Background and Objective

The cardiovascular effects of biomass smoke exposure in patients with chronic obstructive pulmonary disease are not well characterized, and few studies have assessed the possible differences between patients with disease caused by biomass smoke and tobacco. The aim of this study was to search for differences in cardiovascular variables between both types of the disease.


Twenty subjects (15 men, 5 women) with chronic obstructive pulmonary disease caused by tobacco were matched one to one for sex, age, and forced expiratory volume in 1 s to 20 patients with biomass-related disease. Echocardiography and carotid ultrasound studies were performed. Flow-mediated endothelium-dependent vasodilatation and endothelium-independent vasodilatation were also measured.


There were no significant differences between groups in any of the echocardiographic variables, nor in the intima–media carotid thickness, the number of carotid plaques, or the percentage of endothelium-dependent or endothelium-independent vasodilation. A high percentage of patients in both groups showed an abnormal flow-mediated endothelium-dependent vasodilatation pattern.


The study does not support the hypothesis of a different cardiovascular effect of biomass or tobacco smoke exposure in patients with chronic obstructive pulmonary disease. Cardiovascular comorbidity should be assessed in patients with biomass-associated disease, similarly to subjects with tobacco-related disease.


COPD Biomass smoke Tobacco Cardiovascular diseases 



This research was supported by Fundación Ramón Domínguez [Grant Number: O-023].

Author Contributions

RG: conception and design, obtained funding, recruitment of patients, data analysis and interpretation, drafting the manuscript, had full access to all of the data in the study, and takes responsibility for the integrity of the data. PS-L: recruitment of patients, acquisition of data, and critical revision of the manuscript for important intellectual content. IM-R: recruitment of patients, acquisition of data, and critical revision of the manuscript for important intellectual content. CG-J: conception and design, acquisition of data, drafting the manuscript, and critical revision of the manuscript for important intellectual content. LP-d-L: conception and design, obtained funding, study supervision, and drafting the manuscript. JLL-C: provided material support and critical revision of the manuscript for important intellectual content.

Compliance with Ethical Standards

Conflict of interest

The authors report no conflict of interest in this work.

Ethical Approval

The study was performed in accordance with the 1964 Declaration of Helsinki and its later amendments and it was approved by our ethical committee (Comité Autonómico de Ética de la Investigación de Galicia, Registry Number: 2012/003).

Informed Consent

Informed written consent was obtained from all the subjects, prior to the inclusion in the study.


  1. 1.
    Salvi S, Barnes PJ (2010) Is exposure to biomass smoke the biggest risk factor for COPD globally? Chest 138:3–6CrossRefPubMedGoogle Scholar
  2. 2.
    Sin DD, Man SF (2003) Why are patients with chronic obstructive pulmonary disease at increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic obstructive pulmonary disease. Circulation 107:1514–1519CrossRefPubMedGoogle Scholar
  3. 3.
    Ruiz-Vera T, Pruneda-Álvarez LG, Ochoa-Martínez AC, Ramírez-GarcíaLuna JL, Pierdant-Pérez M, Gordillo-Moscoso AA et al (2015) Assessment of vascular function in Mexican women exposed to polycyclic aromatic hydrocarbons from wood smoke. Environ Toxicol Pharmacol 40:423–429CrossRefPubMedGoogle Scholar
  4. 4.
    Buturak A, GenÇ A, Ulus OS, Duygu E, Ökmen AS, Uyarel H (2011) Evaluation of the effects of chronic biomass fuel smoke exposure on peripheral endothelial functions: an observational study. Anadolu Kardiyol Derg 11:492–497PubMedGoogle Scholar
  5. 5.
    Caravedo MA, Herrera PM, Mongilardi N, de Ferrari A, Davila-Roman VG, Gilman RH et al (2016) Chronic exposure to biomass fuel smoke and markers of endothelial inflammation. Indoor Air 26:768–775CrossRefPubMedGoogle Scholar
  6. 6.
    Sertogullarindan B, Gumrukcuoglu HA, Sezgi C, Akil MA (2012) Frequency of pulmonary hypertension in patients with COPD due to biomass smoke and tobacco smoke. Int J Med Sci 9:406–412CrossRefPubMedPubMedCentralGoogle Scholar
  7. 7.
    Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017. Accessed 12 June 2017
  8. 8.
    Beevers G, Lip GYH, O’Brien E (2001) ABC of hypertension, 4th edn. BMJ Books, LondonGoogle Scholar
  9. 9.
    Berger M, Haimowitz A, Van Tosh A, Berdoff RL, Goldberg E (1985) Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 6:359–365CrossRefPubMedGoogle Scholar
  10. 10.
    Kircher BJ, Himelman RB, Schiller NB (1990) Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 66:493–496CrossRefPubMedGoogle Scholar
  11. 11.
    Gonzalez-Juanatey C, Llorca J, Vazquez-Rodriguez TR, Diaz-Varela N, Garcia-Quiroga H, Gonzalez-Gay MA (2008) Short-term improvement of endothelial function in rituximab-treated rheumatoid arthritis patients refractory to tumor necrosis factor α blocker therapy. Arthritis Care Res 59:1821–1824CrossRefGoogle Scholar
  12. 12.
    Esper RJ, Nordaby RA, Vilariño JO, Paragano A, Cacharrón JL, Machado RA (2006) Endothelial dysfunction: a comprehensive appraisal. Cardiovasc Diabetol 5:4CrossRefPubMedPubMedCentralGoogle Scholar
  13. 13.
    Touboul PJ, Hennerici MG, Meairs S, Adams H, Amarenco P, Bornstein N et al (2012) Mannheim carotid intima-media thickness and plaque consensus (2004-2006-2011). An update on behalf of the Advisory Board of the 3rd, 4th and 5th watching the risk symposia, at the 13th, 15th and 20th European stroke conferences, Mannheim, Germany, 2004, Brussels, Belgium, 2006 and Hamburg, Germany, 2011. Cerebrovasc Dis 34:290–296CrossRefPubMedPubMedCentralGoogle Scholar
  14. 14.
    Eickhoff P, Valipour A, Kiss D (2008) Determinants of systemic vascular function in patients with stable COPD. Am J Respir Crit Care Med 178:1211–1218CrossRefPubMedGoogle Scholar
  15. 15.
    Golpe R, Sanjuán-López P, Cano-Jiménez E, Castro-Añón O, Pérez de Llano LA (2014) Distribution of clinical phenotypes in patients with chronic obstructive pulmonary disease caused by biomass and tobacco smoke. Arch Bronconeumol 50:318–324CrossRefPubMedGoogle Scholar
  16. 16.
    Camp PG, Ramírez-Venegas A, Sansores RH, Alva LF, McDougall JE, Sin DD et al (2014) COPD phenotypes in biomass smoke- versus tobacco smoke-exposed Mexican women. Eur Respir J 43:725–734CrossRefPubMedGoogle Scholar
  17. 17.
    Golpe R, Mateos-Colino A, Testa-Fernández A, Pena-Seijo M, Rodríguez-Enríquez M, González-Juanatey C et al (2016) Blood pressure profile and hypertensive organ damage in COPD patients and matched controls. The RETAPOC study. PLoS ONE 11(6):e0157932CrossRefPubMedPubMedCentralGoogle Scholar
  18. 18.
    Solleiro-Villavicencio H, Quintana-Carrillo R, Falfán-Valencia R, Vargas-Rojas MI (2015) Chronic obstructive pulmonary disease induced by exposure to biomass smoke is associated with a Th2 cytokine production profile. Clin Immunol 161:150–155CrossRefPubMedGoogle Scholar
  19. 19.
    Golpe R, Martín-Robles I, Sanjuán-López P, Cano-Jiménez E, Castro-Añón O, Mengual-Macenlle N et al (2017) Prevalence of major comorbidities in chronic obstructive pulmonary disease caused by biomass smoke or tobacco. Respiration 94:38–44CrossRefPubMedGoogle Scholar
  20. 20.
    Sandoval J, Salas J, Martínez-Guerra ML, Gómez A, Martínez C, Portales A et al (1993) Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation. Chest 103:12–20CrossRefPubMedGoogle Scholar
  21. 21.
    Moran-Mendoza O, Pérez-Padilla JR, Salazar-Flores M, Vázquez-Alfaro F (2008) Wood smoke associated lung disease: a clinical, functional, radiological, and pathological description. Int J Tuberc Lung Dis 12:1092–1098PubMedGoogle Scholar
  22. 22.
    Rivera RM, Cosio MG, Ghezzo H, Salazar M, Pérez-Padilla R (2008) Comparison of lung morphology in COPD secondary to cigarette and biomass smoke. Int J Tuberc Lung Dis 12:972–977PubMedGoogle Scholar
  23. 23.
    Feary JR, Rodrigues LC, Smith CJ, Hubbard RB, Gibson JE (2010) Prevalence of major comorbidities in subjects with COPD and incidence of myocardial infarction and stroke: a comprehensive analysis using data from primary care. Thorax 65:956–962CrossRefPubMedGoogle Scholar

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© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Servicio de NeumologíaHospital Universitario Lucus AugustiLugoSpain
  2. 2.Servicio de CardiologíaHospital Universitario Lucus AugustiLugoSpain
  3. 3.Unidad Médico-Quirúrgica de Enfermedades RespiratoriasHospital Universitario Virgen del RocíoSevilleSpain
  4. 4.Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES)Instituto de Salud Carlos IIIMadridSpain

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