Letters to the Editor
Multiple analysis revealed a significant interaction of physical activity with heart failure or myocardial ischemia (OR = 0.054, 95% CI: 0.003–0.95), indicating that subjects having moderate or vigorous physical activity and heart failure or myocardial ischemia had lower odds for having insomnia compared to individuals with heart problems and low physical activity levels. No significant interaction of physical activity status with mental health was found. Sleep disorders are quite frequent in cardiac patients that may result in both physical and psychological complications, consequently deteriorating even further their quality of life and health [4]. Our results suggest that cardiac patients suffering from insomnia might benefit from physical exercise. This conclusion must be tempered by the relatively small number of subjects with heart failure or myocardial ischemia in our study, which is reflected in a wide confidence interval; nevertheless, this is supportive evidence of the protective role of physical activity against insomnia in cardiac patients. Further research is necessary to explore the effects of physical activity on sleep disorders in this particularly vulnerable population.
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The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [8]. References [1] Driver HS, Taylor SR. Exercise and sleep. Sleep Med Rev 2000;4:387–402. [2] Lamberg L. Sleep disorders, often unrecognized, complicate many physical illnesses. JAMA 2000;284:2173–5. [3] Ohayon MM. Epidemiology of insomnia: what we know and what we still need to learn. Sleep Med Rev 2002;6:97–111. [4] Chen HM, Clark AP. Sleep disturbances in people living with heart failure. J Cardiovasc Nurs 2007;22:177–85. [5] Ware Jr JE, Sherbourne CD. The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30:473–83. [6] Soldatos CR, Dikeos DG, Paparrigopoulos TJ. The diagnostic validity of the Athens Insomnia Scale. J Psychosom Res 2003;55:263–7. [7] Craig CL, Marshall AL, Sjöström M, Bauman AE, Booth ML, Ainsworth BE, Pratt M, Ekelund U, Yngve A, Sallis JF, Oja P. International physical activity questionnaire: 12-country reliability and validity. Med Sci Sports Exerc 2003;35:1381–95. [8] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.
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Impedance cardiography versus invasive measurements of stroke volume index in patients with chronic heart failure Arne G. Kieback a,⁎, Adrian C. Borges b , Tania Schink c , Gert Baumann b , Michael Laule b a
Universitätsklinikum Greifswald, Klinik für Innere Medizin B, Friedrich-Loeffler-Street 23 a D-17475, Greifswald, Germany b Charité-Medizinische Klinik und Poliklinik Kardiologie und Angiologie, Berlin, Germany c Charité-Institut für Biometrie und Klinische Epidemiologie, Berlin, Germany Received 15 July 2008; accepted 30 November 2008 Available online 13 January 2009
Keywords: Impedance cardiography; Hemodynamics; Thermodilution; Right heart catheterization
Drug therapy of patients suffering from severe chronic heart failure (NYHA III–IV) can be optimized with invasive hemodynamic monitoring. In two studies examining vasodilator therapy in patients with acute congestive heart failure, invasive hemodynamic parameters were significantly improved while clinical changes were not yet significant [1,2]. But in the SUPPORT study [3], the risks associated with the use of Swan Ganz catheters seemed to outweigh the benefits. Binancy et al. examined ⁎ Corresponding author. E-mail address:
[email protected] (A.G. Kieback).
the effects of pulmonary artery catheterization-guided treatment in 433 patients with decompensated heart failure [4]. Mortality after 6 months did not differ between patient groups. A meta-analysis of 13 randomized controlled trials examining the benefits and harms of pulmonary artery catheters demonstrated neutrality for clinical outcomes [5]. A noninvasive alternative for hemodynamic monitoring is bioimpedance measurement. Moshkovitz et al. describe the development of newer algorithms for bioimpedance measurement in a review [6], which demonstrates lack of larger studies performed in patients with severe heart failure.
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Letters to the Editor
In 39 patients with pulmonary arterial hypertension, impedance cardiography correlated quite well with thermodilution and direct Fick method [7]. In a retrospective study of 64 patients with chronic heart failure, impedance cardiography parameters correlated well with changes in New York Heart Association class and 6-minute walk distance [8]. In 59 patients with stable chronic heart failure, impedance cardiography and invasive measurements were moderately correlated (r = 0.64) [9]. Albert et al. found a good correlation between bioimpedance and thermodilution measurements of cardiac output and cardiac index in 29 patients with advanced, decompensated chronic heart failure [10]. There are important limitations to impedance cardiography: Measurements were inaccurate under conditions of tachycardia, low cardiac output, and arrhythmias [11]. In a meta-analysis of 75 studies, correlation of the impedance method with other reference methods for cardiac output determination was insufficient in critically ill patients [12]. We assessed the hypothesis that non-invasive measurement of stroke volume index can replace invasive measurements in patients with chronic heart failure. After ethical approval, non-invasive impedance cardiography (ICG) measurements (using a BioZ.com® machine) together with invasive hemodynamic thermodilution (TD) measurements were performed in 13 patients. Inclusion criteria were admission to the cardiac intensive care unit due to severe chronic heart failure (NYHA III–IV). Noninvasive measurements were performed with the BioZ.com® machine. Invasive hemodynamic measurements were performed with the thermodilution method. The agreement between the ICG and TD values for the stroke volume index was defined as primary endpoint. Pearson's correlation coefficients were calculated to examine the correlation between ICG and TD measurements. Agreement was evaluated by plotting the differences between ICG and TD values for the stroke volume against the mean values of both measurements and by calculating the limits of agreement according to the Bland–Altman-method. Patient characteristics are shown in Table 1. A total of 42 paired measurements were obtained of the 13 patients. ICG curves were considered to be of good quality in 23 measurements (55%), insufficient in 10 measurements (24%) and indefinite in 9 measurements (21%). Table 1 Patient characteristics. Age–years Male sex–no. (%) Ischemic etiology of heart failure–no. (%) Mean NYHA class Left ventricular ejection fraction (%) Stroke volume index (TD)–ml/m2 ≤Second degree mitral valve insufficiency–no (%) ≤Second degree tricuspid valve insufficiency–no (%)
53.8 ± 12.2 12 (92) 8 (62) 3.2 ± 0.4 22.5 ± 8.0 26.6 ± 11.7 9 (69) 11 (85)
Fig. 1. Differences between thermodilution- and ICG-measurements plotted against mean values of both measurements.
Results of the evaluation of agreement of stroke volume index are displayed in Fig. 1 where differences between the ICG and TD values for the stroke volume are plotted against the mean values of both measurements and the limits of agreement are depicted. The mean difference (bias) between TD and ICG measurements is − 4.6 with a standard error of 11.2. The resulting limits of agreement are −27.0 and 17.7. Subgroup analyses considering only patients without or with only mild tricuspid regurgitation or good impedance curves yielded similar results. Correlation between non-invasive and invasive hemodynamic measurements was low (r = 0.29). The lack of agreement between both ways of hemodynamic measurement may be due to limitations of ICG in patients with very low cardiac index. Most studies in the available literature have shown a good correlation between ICG and invasive hemodynamic measurements, but few were dealing with patients who had very low stroke volume index. Negative results may not have been published. Studies including a greater number of patients with very low cardiac index are needed to find out if this technique works well in those patients. Packer et al. [13] followed 212 stable patients with heart failure over a period of 26 weeks. They retrospectively identified the ICG parameters velocity index, thoracic fluid content index and left ventricular ejection time as being predictive for short-term decompensation. The prospective validation of these parameters is currently been evaluated in a large-scale trial. We performed an open study in a small number of patients. For the calculation of the limits of agreement, we didn't take into account that the 42 measurements are clustered within patients. However, the point estimate of the mean difference is unbiased and the limits of agreement would be even wider when taking the clustering into account [14]. In conclusion, non-invasive measurements of stroke volume index using impedance cardiography did not result
Letters to the Editor
in sufficient agreement with invasive thermodilution measurements in this study with patients suffering from severe chronic heart failure. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [15]. References [1] Torre-Amione G, Young JB, Colucci W, et al. Hemodynamic and clinical effects of tezosentan, an intravenous dual endothelin receptor antagonist, in patients hospitalized because of acute decompensated heart failure. J Am Coll Cardiol 2003;42:140–7. [2] VMAC investigators. Intravenous nesiritide versus nitroglycerin for treatment of decompensated congestive heart failure: a randomized contolled trial. JAMA 2002;287:1531–40. [3] Connors Jr AF, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. JAMA 1996;276:889–97. [4] Binancy C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA 2005;294:1625–33. [5] Shah MR, Hasselblad V, Stevenson L, et al. Impact of the pulmonary artery catheter in critically ill patients. JAMA 2005;294:1664–70. [6] Moshkovitz Y, Kaluski E, Milo O, et al. Recent developments in cardiac output determination by bioimpedance: comparison with invasive cardiac output and potential cardiovascular applications. Curr Opin Cardiol 2004;19:229–37.
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[7] Yung GL, Fedullo PF, Kinninger K, Johnson W, Channick RN. Comparison of impedance cardiography to direct Fick and thermodilution cardiac output determination in pulmonary arterial hypertension. CHF 2004;10(2 suppl 2):7–10. [8] Vijayaraghavan K, Crum S, Cherukuri S, Barnett-Avery L. Association of impedance cardiography parameters with changes in functional and quality-of-life measures in patients with chronic heart failure. CHF 2004;10(2 suppl 2):22–7. [9] Drazner MH, Thompson B, Rosenberg PB, et al. Comparison of impedance cardiography with invasive hemodynamic measurements in patients with heart failure secondary to ischemic or nonischemic cardiomyopathy. Am J Cardiol 2002;89:993–5. [10] Albert NM, Hail MD, Li J, Young JB. Equivalence of the bioimpedance and thermodilution methods in measuring cardiac output in hospitalized patients with advanced, decompensated chronic heart failure. Am J Crit Care 2004;13(6):469–79. [11] Spinale FG, Reines HD, Crawford Jr FA. Comparison of bioimpedance and themodilution methods for determining cardiac output: experimental and clinical studies. Ann Thorac Surg 1988;45:421–5. [12] Fuller HD. The validity of cardiac output measurements by thoracic impedance: a meta-analysis. Clin Invest Med 1992;15:103–12. [13] Packer M, Abraham WT, Mehra MR, et al. Utility of impedance cardiography for the identification of short-term risk of clinical decompensation in stable patients with chronic heart failure. J Am Coll Cardiol 2006;47:2245–52. [14] Bland JM, Altman DG. Agreement between methods of measurement with multiple observations per individual. J Biopharm Stat 2007;17(4): 571–82. [15] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.
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Effect of L-arginine on circulating endothelial progenitor cells in hypercholesterolemic rabbits Shaghayegh Haghjooy Javanmard a,⁎, Yousof Gheisari a , Masoud Soleimani b , Mehdi Nematbakhsh a , Alireza Monajemi a a
Applied Physiology Research Center, Isfahan University of Medical Sciences, Hezar jerib Avenue, Isfahan, Iran b Hematology Department, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran Received 10 July 2008; accepted 30 November 2008 Available online 24 January 2009
Keywords: Atherosclerosis; Endothelial progenitor cells; L-arginine; Nitric Oxide
Atherosclerosis risk factors cause injury to endothelial cells as well as apoptosis and lead to a progressive loss of endothelial integrity [1]. In endothelial injury, adjacent
⁎ Corresponding author. Tel.: +98 311 7922295; fax: +98 311 6682006. E-mail address:
[email protected] (S.H. Javanmard).
endothelial cells proliferate, and re-endothelialize the denuded luminal surface[1]. Additionally, adult peripheral blood contains Endothelial Progenitors Cells (EPCs) which have a prominent role in the re-endothelization phenomena at sites of endothelial injury[2] and [3]. They can also affect surrounding cells through the secretion of angiogenic growth factors [4].