- Email: [email protected]
Gender and COPD in Patients With Chronic Respiratory Insufficiency Requiring Domiciliary Oxygen Therapy
double blind, randomised, comparative trial. BMJ 2003; 327:891– 896 3 Ilowite J, Webb R, Friedman B, et al. Addition of montelukast or salmeterol to fluticasone for protection against asthma attacks: a randomized, double-blind, multicenter study. Ann Allergy Asthma Immunol 2004; 92:641– 648
differences were seen in comorbid conditions. However, women requiring LTOT were 10 years older compared to those with moderate COPD.1 Most importantly, our findings of lower FVC and total lung capacity in women at the time of LTOT initiation raise the possibility that gender differences might exist in the pathogenesis of COPD-related lung impairment. Further studies are needed to investigate this in more detail.
Gender and COPD in Patients With Chronic Respiratory Insufficiency Requiring Domiciliary Oxygen Therapy To the Editor: We read with interest the article in CHEST (October 2005)1 by de Torres et al in which the authors compared 53 FEV1-matched men and women, and found that women were younger, had better oxygenation, fewer comorbidities, poorer quality of life, and higher degree of dyspnea than men. However, since only 8% of patients had stage IV COPD,1 a question remains regarding gender differences in patients with the most severe disease. Therefore, readers may be interested in a similar analysis that we conducted among patients with very severe COPD. We studied 189 COPD patients (154 men and 35 women) with chronic respiratory insufficiency meeting the indication criteria for long-term oxygen therapy (LTOT). At the time of LTOT initiation, no age differences were seen between men and women (mean [⫾ SD] age, 67 ⫾ 8 vs 69 ⫾ 9 years, respectively). Whereas FEV1 did not differ between men and women, women had significantly lower FVC and TLC, and higher FEV1/FVC compared to men (Table 1). No gender differences were seen in arterial blood gases or nutritional status. The proportion of men and women with comorbid conditions was similar: arterial hypertension, 38% vs 50%, respectively; diabetes, 19% vs 13%, respectively; myocardial infarction, 18% vs 7%, respectively; and stroke, 6% vs 3%, respectively. Our results differ from those by de Torres et al1 in several aspects. First, unlike significant age differences in moderate COPD,1 men and women requiring LTOT were of similar age, implying that gender differences might exist in the rate of the annual decline in lung function. Indeed, a recent study2 points to such possibility. Second, women with moderate COPD had lower comorbidity scores than men,1 whereas at the time of LTOT initiation no gender
Table 1—Pulmonary Function Test Results in Men and Women at the Time of LTOT Initiation* Variables
Men (n ⫽ 154)
Women (n ⫽ 35)
p Value
FEV1, % predicted FVC, % predicted FEV1/FVC ratio, % RV, % predicted TLC, % predicted RV/TLC ratio, % Pao2, kPa Paco2, kPa BMI, kg/m2 Cholesterol, mmol/L
40 ⫾ 15 64 ⫾ 15 48 ⫾ 14 198 ⫾ 61 112 ⫾ 22 63 ⫾ 10 6.6 ⫾ 0.7 6.6 ⫾ 1.3 26 ⫾ 5 4.9 ⫾ 1.1
39 ⫾ 19 54 ⫾ 16 58 ⫾ 15 167 ⫾ 64 100 ⫾ 29 67 ⫾ 10 6.6 ⫾ 0.9 6.9 ⫾ 1.7 26 ⫾ 6 5.1 ⫾ 1.1
0.940 0.002 0.002 0.061 0.048 0.174 0.682 0.408 0.920 0.530
*Values are given as the mean ⫾ SD, unless otherwise indicated. RV ⫽ residual volume; TLC ⫽ total lung capacity; BMI ⫽ body mass index. www.chestjournal.org
Ruzena Tkacova, MD, PhD Stefan Toth, MD, PhD Pavol Joppa, MD P.J. Safarik University Kosice, Slovakia Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Ruzena, Tkacova, MD, PhD, L. Pasteur Teaching Hospital, Medical Faculty, P.J. Safarik University, Department of Respiratory Medicine, Rastislavova 43, Kosice 041 90, Slovakia; e-mail: [email protected]
References 1 de Torres JP, Casanova C, Herna´ndez C, et al. Gender and COPD in patients attending a pulmonary clinic. Chest 2005; 128:2012–2016 2 Watson L, Vonk JM, Lofdahl CG, et al. Predictors of lung function and its decline in mild to moderate COPD in association with gender: results from the Euroscop study. Respir Med 2006 (in press) To the Editor: We are pleased that Tkacova et al found our work (October 2005)1 interesting. As we pointed out, our findings are only applicable to the population included in our study sample (ie, women with mild-to-moderate COPD from the outpatient clinic at University Hospital clinic). The findings in a population of women and men requiring oxygen, as reported by Tkacova and coworkers, represent an even more selected group in whom the final expression of the disease may be due to many other phenotypic and mechanistic issues that cannot be extrapolated to patients without significant hypoxemia. Indeed, the data presented in that letter refer to a population of COPD patients with an uneven number of patients in both gender groups (154 men and 35 women) with similar degrees of airway obstruction (mean [⫾ SD] FEV1, 39 ⫾ 19% predicted) and, by definition, a similar degree of hypoxemia at the time of the initiation of long-term oxygen therapy (LTOT). By forcing both factors to be similar, it is not surprising that men and women had the same age, similar degrees of comorbidity, equal Pao2-Paco2 values, and the same body mass indexes. When we analyzed our database and evaluated only those patients in Global Initiative for Chronic Obstructive Lung Disease stages III and IV (28 men and 28 women) with exactly the same mean FEV1 (40 ⫾ 7% predicted), we still observed differences in the studied prognostic parameters (ie, men vs women), as follows: mean age, 64 ⫾ 7 vs 59 ⫾ 11 years (p ⬍ 0.05); mean modified Medical Research Council score of ⱖ 2, 11% vs 64%, respectively (p ⬍ 0.05); mean body mass index, 27 ⫾ 3 vs 23 ⫾ 3, respectively (p ⬍ 0.05); mean Pao2, 64 ⫾ 10 vs 72 ⫾ 11 mm Hg, respectively (p ⬍ 0.05); mean Paco2, 46 ⫾ 6 vs 40 ⫾ 5 mm Hg, respectively (p ⬍ 0.05); mean 6-min walk distance, 99 ⫾ 20 vs 84 ⫾ 21% predicted, respectively (p ⬍ 0.005); and mean Charlson scale, 4 (range, 3 to 8) vs 2 (range, 1 to 3) [p ⬍ 0.05]. We did not find differences in functional residual capacity percent predicted and all domains of the St. George Respiratory Questionnaire. The differences between our findings and those of Tkacova et al could be explained in part by the more natural heterogeneity of the CHEST / 129 / 3 / MARCH, 2006
827
disease in our patients compared to the more homogeneous population reported by those authors. We may speculate that when our women reach the need for LTOT they will be older and probably will have more comorbidities. This may explain partially the data indicating that women receiving LTOT live longer that their male counterparts.2 Actually, we believe the findings of Tkacova et al are complementary to ours. Taken together, both sets of data suggest that COPD runs for a longer symptomatic period in women since the women in our study expressed worse dyspnea, exercise capacity, and quality of life at earlier stages. However, as the disease progresses these gender differences could disappear, and, by the time some of the patients need oxygen, the gender differences may no longer exist. The most important issue is to begin to address the gender differences in the expression of the disease, since in the year 2000 for the first time more women than men died of COPD in the United States.3 We believe that data like these from Tkacova et al are desperately needed and welcomed so that we can increase our knowledge of this dreadful epidemic. Juan P. de Torres, MD Ciro Casanova, MD Hospital Universitario Nuestra Sen˜ora de Candelaria Santa Cruz, Tenerife, Spain Bartolome R. Celli, MD Caritas St. Elizabeth Health System Boston, MA
ventricular diastolic dysfunction are correlated with increasing body mass index or obesity.5–7 Indeed, those cardiac structural abnormalities, which are characterized by the presence of heart failure with preserved left ventricular systolic function, are also commonly observed in patients with diastolic heart failure.8 Preliminary work by Fukuta et al9 has shown that patients with diastolic heart failure might benefit from the use of statins, and the reported survival benefit might be explained by the effects of statins on cardiac hypertrophy,10 endothelial function and vascular tone,11 and systemic inflammation.12 Thus, it would be of interest to have the data on body mass index and body weight for patients with and without atrial fibrillation to further explain the results of the present study. Miguel A. Arias, MD, PhD Complejo Hospitalario de Jae´n Jae´n, Spain Joaquı´n Sa´nchez-Gila, MD Hospital Universitario Virgen de las Nieves Granada, Spain Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Miguel A. Arias, MD, PhD, Pza del Zodiaco No. 8, 5°B, 23009 Jae´n, Spain; e-mail: maapalomares@ secardiologia.es
References Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Juan P. de Torres, MD, Unidad de Investigacio´n Hospital Nuestra Sen˜ora de Candelaria, Carretera del Rosario s/n, Santa Cruz, Tenerife, Spain 38010; e-mail: [email protected]
References 1 de Torres JP, Casanova C, Hernandez C, et al. Gender and COPD in patients attending a pulmonary clinic. Chest 2005; 128:2012–2016 2 Miyamoto K, Aida A, Nishimura M, et al. Gender effects on prognosis of patients receiving long term home oxygen therapy. Am J Respir Crit Care Med 1995; 152:972–975 3 Mannino DM, Homa DM, Akinbami LJ, et al. Chronic pulmonary disease surveillance: United States, 1971–2000. MMWR Morb Mortal Wkly Rep 2002; 51:SS6
Obesity As a Risk Factor for Developing Postoperative Atrial Fibrillation To the Editor: We read with great interest the recent article by Amar et al (November 2005)1 on reduction in the incidence of postoperative atrial fibrillation with the preoperative use of statin independent of levels of early markers of inflammation. Obesity may influence the plasma levels of such markers, which are nowadays considered as an indicator of subclinical inflammation.2,3 Importantly, however, levels of the analyzed markers of inflammation are influenced by many variables, and they are not related to a single one. The risk of postoperative atrial fibrillation has been significantly associated with rising body mass index in a large cohort4 of postoperative patients without a history of atrial fibrillation, and that association was independent of a broad range of clinical, surgical, and demographic factors known to influence the risk of atrial fibrillation. Some factors that have been linked to an increasing incidence of atrial fibrillation such as left atrial enlargement, enhanced neurohormonal activation, and left 828
1 Amar D, Zhang H, Heerdt PM, et al. Statin use is associated with a reduction in atrial fibrillation after noncardiac thoracic surgery independent of C-reactive protein. Chest 2005; 128: 3421–3427 2 Das UN. Obesity, metabolic syndrome X, and inflammation. Nutrition 2002; 18:430 – 432 3 Visser M, Bouter LM, McQuillan GM, et al. Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999; 282:2131–2135 4 Zacharias A, Schwann TA, Riordan CJ, et al. Obesity and risk of new-onset atrial fibrillation after cardiac surgery. Circulation 2005; 112:3247–3255 5 Pritchett AM, Jacobsen SJ, Mahoney DW, et al. Left atrial volume as an index of left atrial size: a population-based study. J Am Coll Cardiol 2003; 41:1036 –1043 6 Engeli S, Sharma AM. The renin-angiotensin system and natriuretic peptides in obesity-associated hypertension. J Mol Med 2001; 79:21–29 7 Iacobellis G, Ribaudo MC, Leto G, et al. Influence of excess fat on cardiac morphology and function: study in uncomplicated obesity. Obes Res 2002; 10:767–773 8 Aurigemma GP, Gaasch WH. Clinical practice: diastolic heart failure. N Engl J Med 2004; 351:1097–1105 9 Fukuta H, Sane DC, Brucks S, et al. Statin therapy may be associated with lower mortality in patients with diastolic heart failure: a preliminary report. Circulation 2005; 112:357–363 10 Takemoto M, Node K, Nakagami H, et al. Statins as antioxidant therapy for preventing cardiac myocyte hypertrophy. J Clin Invest 2001; 108:1429 –1437 11 O’Driscoll G, Green D, Taylor RR. Simvastatin, an HMGcoenzyme A reductase inhibitor, improves endothelial function within 1 month. Circulation 1997; 95:1126 –1131 12 Plenge JK, Hernandez TL, Weil KM, et al. Simvastatin lowers C-reactive protein within 14 days: an effect independent of low-density lipoprotein cholesterol reduction. Circulation 2002; 106:1447–1452 To the Editor: The authors raise some important issues. Mean (⫾ SD) body mass index did not differ in our patients who either did or did not develop atrial fibrillation (AF) [28 ⫾ 5 vs 27 ⫾ 4, respectively; p ⫽ 0.3]. We have previously found1–3 no difference in weight Correspondence
differences were seen in comorbid conditions. However, women requiring LTOT were 10 years older compared to those with moderate COPD.1 Most importantly, our findings of lower FVC and total lung capacity in women at the time of LTOT initiation raise the possibility that gender differences might exist in the pathogenesis of COPD-related lung impairment. Further studies are needed to investigate this in more detail.
Gender and COPD in Patients With Chronic Respiratory Insufficiency Requiring Domiciliary Oxygen Therapy To the Editor: We read with interest the article in CHEST (October 2005)1 by de Torres et al in which the authors compared 53 FEV1-matched men and women, and found that women were younger, had better oxygenation, fewer comorbidities, poorer quality of life, and higher degree of dyspnea than men. However, since only 8% of patients had stage IV COPD,1 a question remains regarding gender differences in patients with the most severe disease. Therefore, readers may be interested in a similar analysis that we conducted among patients with very severe COPD. We studied 189 COPD patients (154 men and 35 women) with chronic respiratory insufficiency meeting the indication criteria for long-term oxygen therapy (LTOT). At the time of LTOT initiation, no age differences were seen between men and women (mean [⫾ SD] age, 67 ⫾ 8 vs 69 ⫾ 9 years, respectively). Whereas FEV1 did not differ between men and women, women had significantly lower FVC and TLC, and higher FEV1/FVC compared to men (Table 1). No gender differences were seen in arterial blood gases or nutritional status. The proportion of men and women with comorbid conditions was similar: arterial hypertension, 38% vs 50%, respectively; diabetes, 19% vs 13%, respectively; myocardial infarction, 18% vs 7%, respectively; and stroke, 6% vs 3%, respectively. Our results differ from those by de Torres et al1 in several aspects. First, unlike significant age differences in moderate COPD,1 men and women requiring LTOT were of similar age, implying that gender differences might exist in the rate of the annual decline in lung function. Indeed, a recent study2 points to such possibility. Second, women with moderate COPD had lower comorbidity scores than men,1 whereas at the time of LTOT initiation no gender
Table 1—Pulmonary Function Test Results in Men and Women at the Time of LTOT Initiation* Variables
Men (n ⫽ 154)
Women (n ⫽ 35)
p Value
FEV1, % predicted FVC, % predicted FEV1/FVC ratio, % RV, % predicted TLC, % predicted RV/TLC ratio, % Pao2, kPa Paco2, kPa BMI, kg/m2 Cholesterol, mmol/L
40 ⫾ 15 64 ⫾ 15 48 ⫾ 14 198 ⫾ 61 112 ⫾ 22 63 ⫾ 10 6.6 ⫾ 0.7 6.6 ⫾ 1.3 26 ⫾ 5 4.9 ⫾ 1.1
39 ⫾ 19 54 ⫾ 16 58 ⫾ 15 167 ⫾ 64 100 ⫾ 29 67 ⫾ 10 6.6 ⫾ 0.9 6.9 ⫾ 1.7 26 ⫾ 6 5.1 ⫾ 1.1
0.940 0.002 0.002 0.061 0.048 0.174 0.682 0.408 0.920 0.530
*Values are given as the mean ⫾ SD, unless otherwise indicated. RV ⫽ residual volume; TLC ⫽ total lung capacity; BMI ⫽ body mass index. www.chestjournal.org
Ruzena Tkacova, MD, PhD Stefan Toth, MD, PhD Pavol Joppa, MD P.J. Safarik University Kosice, Slovakia Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Ruzena, Tkacova, MD, PhD, L. Pasteur Teaching Hospital, Medical Faculty, P.J. Safarik University, Department of Respiratory Medicine, Rastislavova 43, Kosice 041 90, Slovakia; e-mail: [email protected]
References 1 de Torres JP, Casanova C, Herna´ndez C, et al. Gender and COPD in patients attending a pulmonary clinic. Chest 2005; 128:2012–2016 2 Watson L, Vonk JM, Lofdahl CG, et al. Predictors of lung function and its decline in mild to moderate COPD in association with gender: results from the Euroscop study. Respir Med 2006 (in press) To the Editor: We are pleased that Tkacova et al found our work (October 2005)1 interesting. As we pointed out, our findings are only applicable to the population included in our study sample (ie, women with mild-to-moderate COPD from the outpatient clinic at University Hospital clinic). The findings in a population of women and men requiring oxygen, as reported by Tkacova and coworkers, represent an even more selected group in whom the final expression of the disease may be due to many other phenotypic and mechanistic issues that cannot be extrapolated to patients without significant hypoxemia. Indeed, the data presented in that letter refer to a population of COPD patients with an uneven number of patients in both gender groups (154 men and 35 women) with similar degrees of airway obstruction (mean [⫾ SD] FEV1, 39 ⫾ 19% predicted) and, by definition, a similar degree of hypoxemia at the time of the initiation of long-term oxygen therapy (LTOT). By forcing both factors to be similar, it is not surprising that men and women had the same age, similar degrees of comorbidity, equal Pao2-Paco2 values, and the same body mass indexes. When we analyzed our database and evaluated only those patients in Global Initiative for Chronic Obstructive Lung Disease stages III and IV (28 men and 28 women) with exactly the same mean FEV1 (40 ⫾ 7% predicted), we still observed differences in the studied prognostic parameters (ie, men vs women), as follows: mean age, 64 ⫾ 7 vs 59 ⫾ 11 years (p ⬍ 0.05); mean modified Medical Research Council score of ⱖ 2, 11% vs 64%, respectively (p ⬍ 0.05); mean body mass index, 27 ⫾ 3 vs 23 ⫾ 3, respectively (p ⬍ 0.05); mean Pao2, 64 ⫾ 10 vs 72 ⫾ 11 mm Hg, respectively (p ⬍ 0.05); mean Paco2, 46 ⫾ 6 vs 40 ⫾ 5 mm Hg, respectively (p ⬍ 0.05); mean 6-min walk distance, 99 ⫾ 20 vs 84 ⫾ 21% predicted, respectively (p ⬍ 0.005); and mean Charlson scale, 4 (range, 3 to 8) vs 2 (range, 1 to 3) [p ⬍ 0.05]. We did not find differences in functional residual capacity percent predicted and all domains of the St. George Respiratory Questionnaire. The differences between our findings and those of Tkacova et al could be explained in part by the more natural heterogeneity of the CHEST / 129 / 3 / MARCH, 2006
827
disease in our patients compared to the more homogeneous population reported by those authors. We may speculate that when our women reach the need for LTOT they will be older and probably will have more comorbidities. This may explain partially the data indicating that women receiving LTOT live longer that their male counterparts.2 Actually, we believe the findings of Tkacova et al are complementary to ours. Taken together, both sets of data suggest that COPD runs for a longer symptomatic period in women since the women in our study expressed worse dyspnea, exercise capacity, and quality of life at earlier stages. However, as the disease progresses these gender differences could disappear, and, by the time some of the patients need oxygen, the gender differences may no longer exist. The most important issue is to begin to address the gender differences in the expression of the disease, since in the year 2000 for the first time more women than men died of COPD in the United States.3 We believe that data like these from Tkacova et al are desperately needed and welcomed so that we can increase our knowledge of this dreadful epidemic. Juan P. de Torres, MD Ciro Casanova, MD Hospital Universitario Nuestra Sen˜ora de Candelaria Santa Cruz, Tenerife, Spain Bartolome R. Celli, MD Caritas St. Elizabeth Health System Boston, MA
ventricular diastolic dysfunction are correlated with increasing body mass index or obesity.5–7 Indeed, those cardiac structural abnormalities, which are characterized by the presence of heart failure with preserved left ventricular systolic function, are also commonly observed in patients with diastolic heart failure.8 Preliminary work by Fukuta et al9 has shown that patients with diastolic heart failure might benefit from the use of statins, and the reported survival benefit might be explained by the effects of statins on cardiac hypertrophy,10 endothelial function and vascular tone,11 and systemic inflammation.12 Thus, it would be of interest to have the data on body mass index and body weight for patients with and without atrial fibrillation to further explain the results of the present study. Miguel A. Arias, MD, PhD Complejo Hospitalario de Jae´n Jae´n, Spain Joaquı´n Sa´nchez-Gila, MD Hospital Universitario Virgen de las Nieves Granada, Spain Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Miguel A. Arias, MD, PhD, Pza del Zodiaco No. 8, 5°B, 23009 Jae´n, Spain; e-mail: maapalomares@ secardiologia.es
References Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml). Correspondence to: Juan P. de Torres, MD, Unidad de Investigacio´n Hospital Nuestra Sen˜ora de Candelaria, Carretera del Rosario s/n, Santa Cruz, Tenerife, Spain 38010; e-mail: [email protected]
References 1 de Torres JP, Casanova C, Hernandez C, et al. Gender and COPD in patients attending a pulmonary clinic. Chest 2005; 128:2012–2016 2 Miyamoto K, Aida A, Nishimura M, et al. Gender effects on prognosis of patients receiving long term home oxygen therapy. Am J Respir Crit Care Med 1995; 152:972–975 3 Mannino DM, Homa DM, Akinbami LJ, et al. Chronic pulmonary disease surveillance: United States, 1971–2000. MMWR Morb Mortal Wkly Rep 2002; 51:SS6
Obesity As a Risk Factor for Developing Postoperative Atrial Fibrillation To the Editor: We read with great interest the recent article by Amar et al (November 2005)1 on reduction in the incidence of postoperative atrial fibrillation with the preoperative use of statin independent of levels of early markers of inflammation. Obesity may influence the plasma levels of such markers, which are nowadays considered as an indicator of subclinical inflammation.2,3 Importantly, however, levels of the analyzed markers of inflammation are influenced by many variables, and they are not related to a single one. The risk of postoperative atrial fibrillation has been significantly associated with rising body mass index in a large cohort4 of postoperative patients without a history of atrial fibrillation, and that association was independent of a broad range of clinical, surgical, and demographic factors known to influence the risk of atrial fibrillation. Some factors that have been linked to an increasing incidence of atrial fibrillation such as left atrial enlargement, enhanced neurohormonal activation, and left 828
1 Amar D, Zhang H, Heerdt PM, et al. Statin use is associated with a reduction in atrial fibrillation after noncardiac thoracic surgery independent of C-reactive protein. Chest 2005; 128: 3421–3427 2 Das UN. Obesity, metabolic syndrome X, and inflammation. Nutrition 2002; 18:430 – 432 3 Visser M, Bouter LM, McQuillan GM, et al. Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999; 282:2131–2135 4 Zacharias A, Schwann TA, Riordan CJ, et al. Obesity and risk of new-onset atrial fibrillation after cardiac surgery. Circulation 2005; 112:3247–3255 5 Pritchett AM, Jacobsen SJ, Mahoney DW, et al. Left atrial volume as an index of left atrial size: a population-based study. J Am Coll Cardiol 2003; 41:1036 –1043 6 Engeli S, Sharma AM. The renin-angiotensin system and natriuretic peptides in obesity-associated hypertension. J Mol Med 2001; 79:21–29 7 Iacobellis G, Ribaudo MC, Leto G, et al. Influence of excess fat on cardiac morphology and function: study in uncomplicated obesity. Obes Res 2002; 10:767–773 8 Aurigemma GP, Gaasch WH. Clinical practice: diastolic heart failure. N Engl J Med 2004; 351:1097–1105 9 Fukuta H, Sane DC, Brucks S, et al. Statin therapy may be associated with lower mortality in patients with diastolic heart failure: a preliminary report. Circulation 2005; 112:357–363 10 Takemoto M, Node K, Nakagami H, et al. Statins as antioxidant therapy for preventing cardiac myocyte hypertrophy. J Clin Invest 2001; 108:1429 –1437 11 O’Driscoll G, Green D, Taylor RR. Simvastatin, an HMGcoenzyme A reductase inhibitor, improves endothelial function within 1 month. Circulation 1997; 95:1126 –1131 12 Plenge JK, Hernandez TL, Weil KM, et al. Simvastatin lowers C-reactive protein within 14 days: an effect independent of low-density lipoprotein cholesterol reduction. Circulation 2002; 106:1447–1452 To the Editor: The authors raise some important issues. Mean (⫾ SD) body mass index did not differ in our patients who either did or did not develop atrial fibrillation (AF) [28 ⫾ 5 vs 27 ⫾ 4, respectively; p ⫽ 0.3]. We have previously found1–3 no difference in weight Correspondence