600
Letters to the Editor
[7] Llinas R, Henderson GV. Images in clinical medicine. Tremor as a cause of pseudo-ventricular tachycardia. N Engl J Med 1999;341:1275. [8] Bhatia L, Turner DR. Parkinson's tremor mimicking ventricular tachycardia. Age Ageing 2005;34:410–1.
[9] Srikureja W, Darbar D, Reeder GS. Tremor-induced ECG artifact mimicking ventricular tachycardia. Circulation 2000;102:1337–8. [10] Chase C, Brady WJ. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 2000;18:312–6.
http://dx.doi.org/10.1016/j.ijcard.2014.03.090 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The link between sleep duration and inflammation: Effects on cardiovascular disease Alberto Dominguez-Rodriguez a,b,⁎, Pedro Abreu-Gonzalez b,c a b c
Hospital Universitario de Canarias, Servicio de Cardiología, Tenerife, Spain Instituto Universitario de Tecnologías Biomédicas, Tenerife, Spain Universidad de La Laguna, Departamento de Fisiología, Tenerife, Spain
a r t i c l e
i n f o
Article history: Received 27 January 2014 Accepted 14 March 2014 Available online 19 March 2014 Keywords: Sleep duration Inflammation Cardiovascular disease
To the Editor: We read with great interest the article of Cheng et al., about whether long working hours and short sleep duration, are associated with an increased risk of acute myocardial infarction or severe coronary heart diseases, independent of established psychosocial work-related factors [1]. They must be congratulated by your article. However, in the discussion the authors do not discuss the relationship that exists between the inflammation, sleep duration and cardiovascular disease. Inflammation is well established as a key mechanism in the development of cardiovascular disease [2–4]. Libby describes how the inflammatory process contributes to all stages of cardiovascular disease, from the development of atherosclerotic plaques in the vascular wall to end stage thrombotic complications [5]. Inflammation is a plausible mechanism linking sleep duration and cardiovascular disease. There is evidence that sleep loss is associated with inflammation [6–8] and negative cardiovascular outcomes [6–9]. Recently, observational and experimental sleep deprivation studies have shown an association between sleep loss and proinflammatory processes that promote the development of atherosclerotic plaques [6]. A study by van Leeuwen et al. assessed 13 healthy young men who were restricted to 4 h in bed for five nights, followed by two nights of recovery sleep. This study assessed Creactive protein at baseline, after sleep restriction, and after recovery. Following sleep restriction, C-reactive protein was increased when compared to baseline, and continued to increase during recovery. These studies suggest that shortened sleep produces an acute increase in C-reactive protein that is not immediately ameliorated by recovery [10]. Moreover, sex differences were reported for sleep duration and C-reactive protein among 4600
⁎ Corresponding author at: Hospital Universitario de Canarias, Department of Cardiology, Ofra s/n La Cuesta E-38320, Tenerife, Spain. Tel.: +34 922679040; fax: +34 922 678460. E-mail address: [email protected] (A. Dominguez-Rodriguez).
adults in the Whitehall II Study [11]. The authors reported a null association between short and long sleep duration and C-reactive protein among men in that cohort after adjusting for covariates. Among women, however, long sleep (≥ 9 h) was associated with a 35% increase in C-reactive protein levels after adjusting for covariates. A recent study utilizing the 2007–2008 National Health and Nutrition Examination Survey cohort had its goal to discern relationships between sleep duration and C-reactive protein in the American population (N = 5587). In a nationally representative sample of U.S. adults, a J-shaped relationship between C-reactive protein and sleep duration was demonstrated, such that those with very short or very long sleep duration were more likely to show elevated C-reactive protein. In addition, this pattern was only partially explained by sleep disorders and other medical comorbidities. Thus, the role of sleep duration in proinflammatory processes, as marked by C-reactive protein levels, is complex, but the current data suggest that extremes of sleep duration increase proinflammatory risk [12]. In summary, important bi-directional effects between inflammation and sleep exist and short and long term sleep deprivation may have different effects on markers of inflammation and cardiovascular outcomes. Therefore, in the article of Cheng et al. [1], the omission of this aspect important in the discussion would deprive at the medical community of potentially useful information. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Cheng Y, Du CL, Hwang JJ, Chen IS, Chen MF, Su TC. Working hours, sleep duration and the risk of acute coronary heart disease: a case–control study of middle-aged men in Taiwan. Int J Cardiol 2014;171:419–22. [2] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Inflammatory systemic biomarkers in setting acute coronary syndromes—effects of the diurnal variation. Curr Drug Targets 2009;10:1001–8. [3] Battistoni A, Rubattu S, Volpe M. Circulating biomarkers with preventive, diagnostic and prognostic implications in cardiovascular diseases. Int J Cardiol 2012;157:160–8. [4] Aldous SJ. Cardiac biomarkers in acute myocardial infarction. Int J Cardiol 2013;164:282–94. [5] Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83:456S–60S. [6] Grandner MA, Sands-Lincoln MR, Pak VM, Garland SN. Sleep duration, cardiovascular disease, and proinflammatory biomarkers. Nat Sci Sleep 2013;5:93–107. [7] Matthews KA, Zheng H, Kravitz HM, et al. Are inflammatory and coagulation biomarkers related to sleep characteristics in mid-life women?: study of women's health across the nation sleep study. Sleep 2010;33:1649–55. [8] Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis 2009;51:294–302.
Letters to the Editor [9] Miller MA. Association of inflammatory markers with cardiovascular risk and sleepiness. J Clin Sleep Med 2011;7(5 Suppl):S31–3. [10] van Leeuwen WM, Lehto M, Karisola P, et al. Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP. PLoS One 2009;4:e4589.
601
[11] Miller MA, Kandala NB, Kivimaki M, et al. Gender differences in the crosssectional relationships between sleep duration and markers of inflammation: Whitehall II study. Sleep 2009;32:857–64. [12] Grandner MA, Buxton OM, Jackson N, Sands-Lincoln M, Pandey A, Jean-Louis G. Extreme sleep durations and increased C-reactive protein: effects of sex and ethnoracial group. Sleep 2013;36:769–79.
http://dx.doi.org/10.1016/j.ijcard.2014.03.089 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Differential association of chronic obstructive pulmonary disease with myocardial infarction and ischemic stroke in a nation-wide cohort☆,☆☆ Li Yin a, Catarina Lensmar b,c, Erik Ingelsson a,d, Magnus Bäck b,c,⁎ a b c d
Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden Department of Medicine, Karolinska Institutet, Stockholm, Sweden Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden
a r t i c l e
i n f o
Article history: Received 5 February 2014 Accepted 15 March 2014 Available online 21 March 2014 Keywords: Atherosclerosis Cardiovascular risk Epidemiology Inflammation
Chronic obstructive pulmonary disease (COPD) has been associated with an increased risk of cardiovascular disease, which has been suggested to relate to both similar risk factors and to similar pathophysiological mechanisms [1–4]. The latter notion has also received support from pharmacoepidemiological studies, suggesting reduced cardiovascular risk by respiratory medications [5,6]. However, the full impact of COPD on myocardial infarction (MI) and stroke in a population-based cohort remains to be fully investigated. The aim of the present study was to outline the association of COPD with MI and stroke. To this end, we analyzed the prevalence and the association of COPD with incidence and recurrence of these outcomes in a nationwide population-based cohort of approximately 7 million Swedish residents integrating data from the Prescribed Drug-, Patient-, Cause of Death-, Income-, Educational- and Emigration Registers. The associations between COPD and outcome were examined by Cox proportional hazard models estimating the hazard ratio (HR) of COPD, after either partial adjustment for age, gender and socioeconomic factors (education level and income) or fully adjusted for all factors listed under the respective outcomes in Table 1. The average follow-up time was 3.5 years for incident events, and 2.9 and 2.7 years for recurrent MI and stroke, respectively. Events and event rates are shown in Supplementary Table 1. The cohort and statistical methods have been described in detail in
☆ All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation. ☆☆ Sources of funding: This work was supported by the Swedish Heart and Lung Foundation (20120474, 20120827, and 20100401), the Swedish Research Council (20112988 and 2009-2298) and the Swedish Foundation for Strategic Research (ICA080047). ⁎ Corresponding author at: Karolinska University Hospital, CMM L8:03, 171 76 Stockholm, Sweden. Tel.: + 46 8 51770000; fax: +46 8 313147. E-mail address: [email protected] (M. Bäck).
our previous studies [6–8], and an expanded methods section is provided as supplementary material. The prevalence of COPD was 4.18 (4.08–4.28)% in individuals with a prior MI, compared with 3.27 (3.17–3.36)% in those with a prior ischemic stroke, which was higher compared with the general population; 0.76 (0.75–0.76)%. Individuals with a COPD diagnosis exhibited a 4.7-fold higher prevalence of MI (4.71 [4.53–4.90]%), and a 3.8-fold higher prevalence of stroke (2.20 [2.07–2.32]) %, compared with prevalences previously reported in the general population of these cohorts [7]. COPD diagnosis was associated with an increased risk of incident MI, in both the partially and fully adjusted analyses (Fig. 1), which corroborates another nationwide cohort study, in which everdiagnosed COPD was associated with life-time risk increases of one quarter for MI [17]. In addition, we extend these findings by showing that COPD was also significantly associated with recurrent MI (Fig. 1). Similar higher rates of adverse outcomes previously reported in smaller cohorts were related to lower prescription rates of guideline-recommended medications for secondary prevention [9]. In the present study, we also establish that subjects with COPD and MI to a significantly lesser extent received secondary prevention in terms of acetylsalicylic acid, β-blockers and lipidlowering drugs (P b 0.001; Table 1). Nevertheless, the higher recurrence of MI in COPD subjects remained significant also in the fully adjusted analysis taking into account these differences in drug treatments, suggesting COPD as an independent risk factor in this aspect. Previous studies of COPD as a risk factor for stroke have generated contradictory results [10–13]. The present report is the first nationwide cohort study showing that COPD was associated with a significantly increased risk of both incident and recurrent stroke in the fully adjusted analyses (Fig. 1), albeit with a lower HR compared with that for MI (Fig. 1). Analyzing the differences in HRs as competing outcomes revealed that the COPD-associated HR for incident MI was statistically significant compared with that for incident stroke (P b 0.001). In addition, COPD was associated with a significantly higher HR for myocardial infarction compared with stroke in the cohorts of patients with either a previous stroke or a previous myocardial infarction (P = 0.0 4 a nd P b 0.0 01, respectively). The differential associations of COPD for MI and ischemic stroke are intriguing, since both outcomes reflect atherosclerotic vessel disease. Since ischemic stroke may in addition encompass cardiac emboli, which is commonly related to atrial fibrillation, the present
Letters to the Editor
[7] Llinas R, Henderson GV. Images in clinical medicine. Tremor as a cause of pseudo-ventricular tachycardia. N Engl J Med 1999;341:1275. [8] Bhatia L, Turner DR. Parkinson's tremor mimicking ventricular tachycardia. Age Ageing 2005;34:410–1.
[9] Srikureja W, Darbar D, Reeder GS. Tremor-induced ECG artifact mimicking ventricular tachycardia. Circulation 2000;102:1337–8. [10] Chase C, Brady WJ. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 2000;18:312–6.
http://dx.doi.org/10.1016/j.ijcard.2014.03.090 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The link between sleep duration and inflammation: Effects on cardiovascular disease Alberto Dominguez-Rodriguez a,b,⁎, Pedro Abreu-Gonzalez b,c a b c
Hospital Universitario de Canarias, Servicio de Cardiología, Tenerife, Spain Instituto Universitario de Tecnologías Biomédicas, Tenerife, Spain Universidad de La Laguna, Departamento de Fisiología, Tenerife, Spain
a r t i c l e
i n f o
Article history: Received 27 January 2014 Accepted 14 March 2014 Available online 19 March 2014 Keywords: Sleep duration Inflammation Cardiovascular disease
To the Editor: We read with great interest the article of Cheng et al., about whether long working hours and short sleep duration, are associated with an increased risk of acute myocardial infarction or severe coronary heart diseases, independent of established psychosocial work-related factors [1]. They must be congratulated by your article. However, in the discussion the authors do not discuss the relationship that exists between the inflammation, sleep duration and cardiovascular disease. Inflammation is well established as a key mechanism in the development of cardiovascular disease [2–4]. Libby describes how the inflammatory process contributes to all stages of cardiovascular disease, from the development of atherosclerotic plaques in the vascular wall to end stage thrombotic complications [5]. Inflammation is a plausible mechanism linking sleep duration and cardiovascular disease. There is evidence that sleep loss is associated with inflammation [6–8] and negative cardiovascular outcomes [6–9]. Recently, observational and experimental sleep deprivation studies have shown an association between sleep loss and proinflammatory processes that promote the development of atherosclerotic plaques [6]. A study by van Leeuwen et al. assessed 13 healthy young men who were restricted to 4 h in bed for five nights, followed by two nights of recovery sleep. This study assessed Creactive protein at baseline, after sleep restriction, and after recovery. Following sleep restriction, C-reactive protein was increased when compared to baseline, and continued to increase during recovery. These studies suggest that shortened sleep produces an acute increase in C-reactive protein that is not immediately ameliorated by recovery [10]. Moreover, sex differences were reported for sleep duration and C-reactive protein among 4600
⁎ Corresponding author at: Hospital Universitario de Canarias, Department of Cardiology, Ofra s/n La Cuesta E-38320, Tenerife, Spain. Tel.: +34 922679040; fax: +34 922 678460. E-mail address: [email protected] (A. Dominguez-Rodriguez).
adults in the Whitehall II Study [11]. The authors reported a null association between short and long sleep duration and C-reactive protein among men in that cohort after adjusting for covariates. Among women, however, long sleep (≥ 9 h) was associated with a 35% increase in C-reactive protein levels after adjusting for covariates. A recent study utilizing the 2007–2008 National Health and Nutrition Examination Survey cohort had its goal to discern relationships between sleep duration and C-reactive protein in the American population (N = 5587). In a nationally representative sample of U.S. adults, a J-shaped relationship between C-reactive protein and sleep duration was demonstrated, such that those with very short or very long sleep duration were more likely to show elevated C-reactive protein. In addition, this pattern was only partially explained by sleep disorders and other medical comorbidities. Thus, the role of sleep duration in proinflammatory processes, as marked by C-reactive protein levels, is complex, but the current data suggest that extremes of sleep duration increase proinflammatory risk [12]. In summary, important bi-directional effects between inflammation and sleep exist and short and long term sleep deprivation may have different effects on markers of inflammation and cardiovascular outcomes. Therefore, in the article of Cheng et al. [1], the omission of this aspect important in the discussion would deprive at the medical community of potentially useful information. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Cheng Y, Du CL, Hwang JJ, Chen IS, Chen MF, Su TC. Working hours, sleep duration and the risk of acute coronary heart disease: a case–control study of middle-aged men in Taiwan. Int J Cardiol 2014;171:419–22. [2] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Inflammatory systemic biomarkers in setting acute coronary syndromes—effects of the diurnal variation. Curr Drug Targets 2009;10:1001–8. [3] Battistoni A, Rubattu S, Volpe M. Circulating biomarkers with preventive, diagnostic and prognostic implications in cardiovascular diseases. Int J Cardiol 2012;157:160–8. [4] Aldous SJ. Cardiac biomarkers in acute myocardial infarction. Int J Cardiol 2013;164:282–94. [5] Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83:456S–60S. [6] Grandner MA, Sands-Lincoln MR, Pak VM, Garland SN. Sleep duration, cardiovascular disease, and proinflammatory biomarkers. Nat Sci Sleep 2013;5:93–107. [7] Matthews KA, Zheng H, Kravitz HM, et al. Are inflammatory and coagulation biomarkers related to sleep characteristics in mid-life women?: study of women's health across the nation sleep study. Sleep 2010;33:1649–55. [8] Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis 2009;51:294–302.
Letters to the Editor [9] Miller MA. Association of inflammatory markers with cardiovascular risk and sleepiness. J Clin Sleep Med 2011;7(5 Suppl):S31–3. [10] van Leeuwen WM, Lehto M, Karisola P, et al. Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP. PLoS One 2009;4:e4589.
601
[11] Miller MA, Kandala NB, Kivimaki M, et al. Gender differences in the crosssectional relationships between sleep duration and markers of inflammation: Whitehall II study. Sleep 2009;32:857–64. [12] Grandner MA, Buxton OM, Jackson N, Sands-Lincoln M, Pandey A, Jean-Louis G. Extreme sleep durations and increased C-reactive protein: effects of sex and ethnoracial group. Sleep 2013;36:769–79.
http://dx.doi.org/10.1016/j.ijcard.2014.03.089 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Differential association of chronic obstructive pulmonary disease with myocardial infarction and ischemic stroke in a nation-wide cohort☆,☆☆ Li Yin a, Catarina Lensmar b,c, Erik Ingelsson a,d, Magnus Bäck b,c,⁎ a b c d
Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden Department of Medicine, Karolinska Institutet, Stockholm, Sweden Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden
a r t i c l e
i n f o
Article history: Received 5 February 2014 Accepted 15 March 2014 Available online 21 March 2014 Keywords: Atherosclerosis Cardiovascular risk Epidemiology Inflammation
Chronic obstructive pulmonary disease (COPD) has been associated with an increased risk of cardiovascular disease, which has been suggested to relate to both similar risk factors and to similar pathophysiological mechanisms [1–4]. The latter notion has also received support from pharmacoepidemiological studies, suggesting reduced cardiovascular risk by respiratory medications [5,6]. However, the full impact of COPD on myocardial infarction (MI) and stroke in a population-based cohort remains to be fully investigated. The aim of the present study was to outline the association of COPD with MI and stroke. To this end, we analyzed the prevalence and the association of COPD with incidence and recurrence of these outcomes in a nationwide population-based cohort of approximately 7 million Swedish residents integrating data from the Prescribed Drug-, Patient-, Cause of Death-, Income-, Educational- and Emigration Registers. The associations between COPD and outcome were examined by Cox proportional hazard models estimating the hazard ratio (HR) of COPD, after either partial adjustment for age, gender and socioeconomic factors (education level and income) or fully adjusted for all factors listed under the respective outcomes in Table 1. The average follow-up time was 3.5 years for incident events, and 2.9 and 2.7 years for recurrent MI and stroke, respectively. Events and event rates are shown in Supplementary Table 1. The cohort and statistical methods have been described in detail in
☆ All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation. ☆☆ Sources of funding: This work was supported by the Swedish Heart and Lung Foundation (20120474, 20120827, and 20100401), the Swedish Research Council (20112988 and 2009-2298) and the Swedish Foundation for Strategic Research (ICA080047). ⁎ Corresponding author at: Karolinska University Hospital, CMM L8:03, 171 76 Stockholm, Sweden. Tel.: + 46 8 51770000; fax: +46 8 313147. E-mail address: [email protected] (M. Bäck).
our previous studies [6–8], and an expanded methods section is provided as supplementary material. The prevalence of COPD was 4.18 (4.08–4.28)% in individuals with a prior MI, compared with 3.27 (3.17–3.36)% in those with a prior ischemic stroke, which was higher compared with the general population; 0.76 (0.75–0.76)%. Individuals with a COPD diagnosis exhibited a 4.7-fold higher prevalence of MI (4.71 [4.53–4.90]%), and a 3.8-fold higher prevalence of stroke (2.20 [2.07–2.32]) %, compared with prevalences previously reported in the general population of these cohorts [7]. COPD diagnosis was associated with an increased risk of incident MI, in both the partially and fully adjusted analyses (Fig. 1), which corroborates another nationwide cohort study, in which everdiagnosed COPD was associated with life-time risk increases of one quarter for MI [17]. In addition, we extend these findings by showing that COPD was also significantly associated with recurrent MI (Fig. 1). Similar higher rates of adverse outcomes previously reported in smaller cohorts were related to lower prescription rates of guideline-recommended medications for secondary prevention [9]. In the present study, we also establish that subjects with COPD and MI to a significantly lesser extent received secondary prevention in terms of acetylsalicylic acid, β-blockers and lipidlowering drugs (P b 0.001; Table 1). Nevertheless, the higher recurrence of MI in COPD subjects remained significant also in the fully adjusted analysis taking into account these differences in drug treatments, suggesting COPD as an independent risk factor in this aspect. Previous studies of COPD as a risk factor for stroke have generated contradictory results [10–13]. The present report is the first nationwide cohort study showing that COPD was associated with a significantly increased risk of both incident and recurrent stroke in the fully adjusted analyses (Fig. 1), albeit with a lower HR compared with that for MI (Fig. 1). Analyzing the differences in HRs as competing outcomes revealed that the COPD-associated HR for incident MI was statistically significant compared with that for incident stroke (P b 0.001). In addition, COPD was associated with a significantly higher HR for myocardial infarction compared with stroke in the cohorts of patients with either a previous stroke or a previous myocardial infarction (P = 0.0 4 a nd P b 0.0 01, respectively). The differential associations of COPD for MI and ischemic stroke are intriguing, since both outcomes reflect atherosclerotic vessel disease. Since ischemic stroke may in addition encompass cardiac emboli, which is commonly related to atrial fibrillation, the present
