Letters

the values of patients and families?” This points clinicians away from the role of an epidemiologist identifying barriers to remove or a marketer offering options to choose from and toward the role of a teacher who knows that a child would rather play ball than learn how to multiply yet can draw on skill and commitment to engage and equip that child for the next steps in life. Like a skilled teacher, a skilled clinician can make it possible for a patient and family to rise to the challenge of goalsof-care conversations and, therefore, make a huge difference for everyone in the family. Anthony L. Back, MD

tion and decision making at this challenging and important time in the lives of our patients.2 John J. You, MD, MSc Daren K. Heyland, MD Author Affiliations: Department of Medicine, McMaster University, Hamilton, Ontario, Canada (You); Department of Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, Ontario, Canada (You); Kingston General Hospital, Clinical Evaluation Research Unit, Kingston, Ontario, Canada (Heyland). Corresponding Author: John J. You, MD, MSc, Department of Medicine, McMaster University, 1280 Main St West, HSC-2C8, Hamilton, ON L8S 4K1, Canada ([email protected]). Conflict of Interest Disclosures: None reported.

Author Affiliation: Department of Medicine, University of Washington, Seattle Cancer Care Alliance, Seattle. Corresponding Author: Anthony L. Back, MD, Department of Medicine, Seattle Cancer Care Alliance, University of Washington, 825 Eastlake Ave E, Seattle, WA 98108 ([email protected]). Conflict of Interest Disclosures: None reported. Additional Information: The ideas in this letter reflect contributions by Kathryn Pollak, PhD, James Tulsky, MD, and Robert Arnold, MD. 1. You JJ, Downar J, Fowler RA, et al; Canadian Researchers at the End of Life Network. Barriers to goals of care discussions with seriously ill hospitalized patients and their families: a multicenter survey of clinicians. JAMA Intern Med. 2015;175(4):549-556.

In Reply We thank Back for his thoughtful letter. We agree that our findings are a reflection of clinicians’ perceptions about barriers to goals of care discussions. While clinicians’ beliefs may not always reflect patient realities, we believe that insight into the “headspace” of clinicians provides powerful knowledge to drive future change. The survey findings reported in our article were from a larger mixed methods study. We have recently completed a qualitative analysis of interviews with hospital-based clinicians that will provide further insights into clinicians’ perspectives about goals-of-care discussions. We agree with Back that the common perception among clinicians that patient factors are barriers to goals-of-care discussions likely reflects that these conversations are, indeed, quite difficult for patients and clinicians alike. We would like to clarify that we are not saying that patients are the barrier and need to be removed. Rather, as we discussed in our article, we fully agree that “our findings underscore and support recent calls for more and better training for all clinicians in having end-of-life discussions.”1 We need to equip clinicians with self-awareness of their own discomfort and with communication skills that enable them to guide patients and families through medical decision making during what is an understandably difficult and stressful time. Having said this, we believe that our results also reflect that patients and families are often underprepared to engage in goals-of-care discussions. Because of this, a further implication of our findings is that multifaceted approaches using decision-support tools to better prepare patients and families to engage in goals-of-care discussions, in combination with more communication skills training for clinicians, will maximize our ability to improve the quality of communica1578

Additional Information: We would like to acknowledge contributions of our colleagues, James Downar, MD, Jessica Simon, MD, Patricia Strachan, PhD, and Jennifer Kryworuchko, PhD, in drafting this letter. 1. You JJ, Downar J, Fowler RA, et al; Canadian Researchers at the End of Life Network. Barriers to goals of care discussions with seriously ill hospitalized patients and their families: a multicenter survey of clinicians. JAMA Intern Med. 2015;175(4):549-556. 2. You J, Heyland D; Canadian Researchers at the End of Life Network (CARENET). Improving decision-making about goals of care for hospitalized, elderly patients: a “multi-incubator” study (the IDECIDE study). http: //thecarenet.ca/our-projects/acute-care/160-improving-decision-makingabout-goals-of-care-for-hospitalized-elderly-patients-a-multi-incubator-unitstudy-the-idecide-study. Accessed May 13, 2015.

Dietary Sodium Intake and Risk of Cardiovascular Disease To the Editor In their article on the Health, Aging, and Body Composition (Health ABC) study, Kalogeropoulos and colleagues1 report that no association between salt intake and mortality or risk for cardiovascular disease (CVD) and heart failure (HF) in older adults was found based on self-reported estimated sodium intake with a food frequency questionnaire (FFQ). This result is not surprising since, compared with other ways of sodium intake assessment (ie, 24-hour urinary sodium excretion), it is known that FFQs are suboptimal tools to assess dietary sodium intake. Although we understand it is difficult to apply other ways of sodium intake assessment in this study, Kalogeropoulos and colleagues should be careful to draw conclusions purely based on the results of FFQs. Recently, from rigorous controlled trials, it has been reported that subjects on high-salt diets displayed a significantly higher number of monocytes compared with the same subjects on a lower-salt diet, indicating an association between dietary salt intake and monocytes.2,3 Interestingly, a few recent reports from CVD research indicate that monocytes and/or macrophages are actively involved in the progression of a variety of CVDs, such as coronary atherothrombosis and HF.4,5 These findings suggest there is an intrinsic link between salt intake, CVD, and HF. Based on these results, it can be predicted that salt intake, at least to a certain extent, may affect risk of CVD and HF. Buqing Yi, PhD Jens Titze, MD Alexander Choukèr, MD

JAMA Internal Medicine September 2015 Volume 175, Number 9 (Reprinted)

Copyright 2015 American Medical Association. All rights reserved.

Downloaded From: http://archinte.jamanetwork.com/ by a GAZI UNIVERSITESI User on 03/02/2016

jamainternalmedicine.com

Letters

Author Affiliations: Department of Anaesthesiology, Hospital of the University of Munich, Munich, Germany (Yi, Choukèr); Department of Nephrology and Hypertension, Friedrich-Alexander-University, Erlangen, Germany (Titze). Corresponding Author: Buqing Yi, PhD, Department of Anaesthesiology, Hospital of the University of Munich, Marchioninistrasse15, Munich, Munich D-81377, Germany ([email protected]). Conflict of Interest Disclosures: None reported. 1. Kalogeropoulos AP, Georgiopoulou VV, Murphy RA, et al. Dietary sodium content, mortality, and risk for cardiovascular events in older adults: the Health, Aging, and Body Composition (Health ABC) Study. JAMA Intern Med. 2015;175 (3):410-419. 2. Yi B, Titze J, Rykova M, et al. Effects of dietary salt levels on monocytic cells and immune responses in healthy human subjects: a longitudinal study. Transl Res. 2015;166(1):103-110. 3. Zhou X, Zhang L, Ji WJ, et al. Variation in dietary salt intake induces coordinated dynamics of monocyte subsets and monocyte-platelet aggregates in humans: implications in end organ inflammation. PLoS One. 2013;8(4):e60332. doi:10.1371/journal.pone.0060332. 4. Wyss CA, Neidhart M, Altwegg L, et al. Cellular actors, Toll-like receptors, and local cytokine profile in acute coronary syndromes. Eur Heart J. 2010;31(12): 1457-1469. 5. Ismahil MA, Hamid T, Bansal SS, Patel B, Kingery JR, Prabhu SD. Remodeling of the mononuclear phagocyte network underlies chronic inflammation and disease progression in heart failure: critical importance of the cardiosplenic axis. Circ Res. 2014;114(2):266-282.

To the Editor We read with interest the recent article titled “Dietary Sodium Content, Mortality, and Risk for Cardiovascular Events in Older Adults: The Health, Aging, and Body Composition (Health ABC) Study” by Kalogeropoulos et al1 published in your journal. Based on a 10-year prospective cohort study consisting of 2642 older adults aged 71 to 80 years, the authors found that higher dietary sodium (>2300 mg/d) was not statistically associated with 10-year mortality, incident cardiovascular disease (CVD), or incident heart failure (HF), compared with normal sodium intake (1500-2300 mg/d). However, the conclusions by Kalogeropoulos et al should be interpreted with caution because of several limitations of the study. First, as stated by the authors, the food frequency questionnaires used in this study are less accurate than the 24hour urinary excretion method for estimating sodium intake, with the correlation coefficient being less than 0.2.2 Thus, it is likely the authors underestimated the true sodium intake of participants. The Health ABC Study did not assess participants’ potassium intake. Potassium intake affects the association between sodium intake and risk of CVD and mortality.3-5 In the Japan Collaborative Cohort Study for Evaluation of Cancer Risks study, Umesawa et al3 reported that compared with the low sodium and high potassium intake groups, the hazard ratio (HR) (95% CI) of CVD risk for subjects who consumed both high sodium and high potassium was 1.19 (1.03-1.39); whereas for subjects who consumed high sodium but low potassium, the HR was 1.28 (1.08-1.53). We do not fully agree with the category of higher sodium intake. In Table 3, the higher sodium intake group was defined as sodium intake greater than 2300 mg/d,1 but we would like to see the dose-response association further categorized into subgroups such as 2300 to 3099 mg/d, 3100 to 3900 mg/d, and at least 3900 mg/d. Even the reference groups in Table 41 jamainternalmedicine.com

(ie, >3000 mg/d vs ≤3000 mg/d and >4000 mg/d vs ≤4000 mg/d) might be inappropriate. The authors only examined the association between health outcomes and sodium intake at baseline, but over the course of 10 years, study participants might have changed their sodium intake. If participants in the higher sodium intake group at baseline lowered their sodium intake during the follow-up period because of incidence of hypertension, those participants would be less likely to develop CVD or mortality. The strength of association between higher sodium intake at baseline and health outcomes was possibly attenuated by the study’s cohort. Finally, we also question the statistical power of the Health ABC Study. For the association between baseline dietary sodium intake and 10-year mortality, the authors showed that higher sodium intake was, in fact, marginally associated with risk of 10-year mortality (HR, 1.15 [0.99-1.35] in the covariate’s adjustment model). We believe that the HR will become statistically significant with the increase of statistical power. The power was even lower in the subgroup analyses by sex, race, and whether participants had hypertension. In addition, analysis of incident CVD was restricted to 1981 individuals without CVD at baseline. Zhihao Liu, MS Xiwen Zhang, MD Author Affiliations: Institute for Health Education, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, China (Liu); Department of Cardiology, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, China (Zhang). Corresponding Author: Xiwen Zhang, MD, Department of Cardiology, Huai’an First People’s Hospital, Nanjing Medical University, 6 W Beijing Rd, Huai’an, China ([email protected]). Conflict of Interest Disclosures: None reported. 1. Kalogeropoulos AP, Georgiopoulou VV, Murphy RA, et al. Dietary sodium content, mortality, and risk for cardiovascular events in older adults: the Health, Aging, and Body Composition (Health ABC) Study. JAMA Intern Med. 2015;175 (3):410-419. 2. McKeown NM, Day NE, Welch AA, et al. Use of biological markers to validate self-reported dietary intake in a random sample of the European Prospective Investigation into Cancer United Kingdom Norfolk cohort. Am J Clin Nutr. 2001; 74(2):188-196. 3. Umesawa M, Iso H, Date C, et al; JACC Study Group. Relations between dietary sodium and potassium intakes and mortality from cardiovascular disease: the Japan Collaborative Cohort Study for Evaluation of Cancer Risks. Am J Clin Nutr. 2008;88(1):195-202. 4. O’Donnell MJ, Yusuf S, Mente A, et al. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. 2011;306(20):2229-2238. 5. Yang Q, Liu T, Kuklina EV, et al. Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2011;171(13):1183-1191.

In Reply We thank Liu and Zhang as well as Yi and colleagues for their interest in our work. We agree that food frequency questionnaires (FFQ) underestimate sodium intake. However, if this underestimation is similar across the range of intake, then the overall dose-response association should be valid, albeit at higher actual levels of dietary sodium intake. The latter is supported by findings from recent large-scale studies that point to a higher J point than previously thought for (Reprinted) JAMA Internal Medicine September 2015 Volume 175, Number 9

Copyright 2015 American Medical Association. All rights reserved.

Downloaded From: http://archinte.jamanetwork.com/ by a GAZI UNIVERSITESI User on 03/02/2016

1579

Letters

the dose-response association between sodium intake and outcomes.1,2 On the other hand, limited precision does dilute regression estimates, and this might have weakened the association with the outcomes of interest in our study. We also agree that statistical power was limited in the high sodium intake group. We categorized sodium intake using cutoff points driven by the current US recommendations to facilitate clinical interpretation. We would have liked to analyze a very high sodium intake subgroup, but the number of participants was too small to provide stable estimates. The small numbers in the very high sodium subgroup are potentially related to underestimation of sodium intake with FFQ. On the other hand, the dose-response association across the range of reported intakes is evident in the spline graph (Figure 1) provided in the main article.3 The point about potassium is important and supported by the recently reported findings from O’Donnell and colleagues.2 To address this comment, we evaluated self-reported potassium intake in our cohort. The median daily intake was 2750 mg (2130-3500 mg/d), which is comparable to other cohorts.2,4 However, we did not observe any significant association (either crude or adjusted) between self-reported potassium intake and risk of mortality, cardiovascular disease, or heart failure in the Health ABC Study (unpublished data). This may have to do with the limitations of self-reporting as discussed above, or with the fact that our cohort consists of considerably older participants compared with the aforementioned cohorts.2,4 Of note, sodium and potassium intakes were estimated using an FFQ in the study by Umesawa and colleagues.4 We agree that changing dietary habits over time could have led to regression dilution in our cohort. Without multiple dietary assessments, we are not able to rule this out. However, after explicit testing, we did not observe any time-dependent effects of baseline dietary sodium intake on study outcomes. Finally, we agree that high sodium intake has important physiologic effects. However, the increase in monocytes observed by Yi and colleagues was evident only in the 12-g/d salt group,5 which corresponds to twice the amount of the currently recommended intake for the general population. Similarly, the high sodium intake group in the study by Zhou and colleagues6 was consuming 15 g/d of salt. These data actually are in concordance with the aforementioned large-scale studies that observed association with harm only at dietary sodium intake levels exceeding 4000 mg/d,1,2 highlighting the need for prospective clinical trials to establish optimal sodium intake levels. Andreas P. Kalogeropoulos, MD, MPH, PhD Vasiliki V. Georgiopoulou, MD, MPH Stephen B. Kritchevsky, PhD Author Affiliations: Emory Clinical Cardiovascular Research Institute, Emory University, Atlanta, Georgia (Kalogeropoulos, Georgiopoulou); Section on Gerontology and Geriatric Medicine, Wake Forest School of Medicine, WinstonSalem, North Carolina (Kritchevsky). Corresponding Author: Andreas P. Kalogeropoulos, MD, MPH, PhD, Emory Clinical Cardiovascular Research Institute, Emory University, 1462 Clifton Rd NE, Ste 535B, Atlanta, GA 30322 ([email protected]). Conflict of Interest Disclosures: None reported.

1580

1. O’Donnell MJ, Yusuf S, Mente A, et al. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. 2011;306(20):2229-2238. 2. O’Donnell M, Mente A, Rangarajan S, et al; PURE Investigators. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014;371(7):612-623. 3. Kalogeropoulos AP, Georgiopoulou VV, Murphy RA, et al. Dietary sodium content, mortality, and risk for cardiovascular events in older adults: the Health, Aging, and Body Composition (Health ABC) Study. JAMA Intern Med. 2015;175 (3):410-419. 4. Umesawa M, Iso H, Date C, et al; JACC Study Group. Relations between dietary sodium and potassium intakes and mortality from cardiovascular disease: the Japan Collaborative Cohort Study for Evaluation of Cancer Risks. Am J Clin Nutr. 2008;88(1):195-202. 5. Yi B, Titze J, Rykova M, et al. Effects of dietary salt levels on monocytic cells and immune responses in healthy human subjects: a longitudinal study. Transl Res. 2015;166(1):103-110. 6. Zhou X, Zhang L, Ji WJ, et al. Variation in dietary salt intake induces coordinated dynamics of monocyte subsets and monocyte-platelet aggregates in humans: implications in end organ inflammation. PLoS One. 2013;8(4):e60332. doi:10.1371/journal.pone.0060332.

Ongoing Attention to Injurious Inpatient Falls and Pressure Ulcers To the Editor The effectiveness of Centers for Medicare & Medicaid Services (CMS) performance-based payment strategies will shape efforts to improve the quality and value of care. Waters et al1 examined the effect of the Hospital-Acquired Conditions (HACs) Initiative, which denies incremental payment for 8 complications on 4 outcomes: central line–associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), hospital-acquired pressure ulcers (HAPUs), and injurious inpatient falls. They found an association with reductions in CLABSIs and CAUTIs but not injurious falls or stage III/IV HAPUs. Waters et al concluded that there is less evidence that changing hospital processes affects these other 2 outcomes, but we believe this conclusion may be missing key factors. Nursing leaders have advanced improvements in falls and HAPUs for nearly 2 decades. Central line-associated bloodstream infections and CAUTIs have more recently received attention and been added to National Healthcare Safety Network indicators. Waters et al1 report improvement in HAPU and fall rates prior to implementation of the HACs Initiative. This is consistent with prior reports using data from the Collaborative Alliance for Nursing Outcomes (CALNOC), the nation’s first registry of nursing-sensitive outcomes data. In 2010, CALNOC reported improvements in HAPU rates from 2001 to 2008,2 and in 2013, they reported continued improvements in HAPU rates from 2003 to 2010.3 Given that nursing leaders were steadily advancing improvements in these adverse outcomes, it is not surprising that the HACs Initiative had no additional effect. The authors did not examine the prevalence of stage II HAPUs, even though the National Quality Forum endorses measures for stage II HAPUs and higher.4 Stage III/IV HAPUs are rare in most hospitals, with Waters et al1 reporting a 2010 rate of about 0.4%, and CALNOC data reporting a similar rate that year, having dropped from 2.0% in 2003.3 The more common stage II HAPUs are clinically important, because appropriate interventions will prevent progression to stage III/IV. The

JAMA Internal Medicine September 2015 Volume 175, Number 9 (Reprinted)

Copyright 2015 American Medical Association. All rights reserved.

Downloaded From: http://archinte.jamanetwork.com/ by a GAZI UNIVERSITESI User on 03/02/2016

jamainternalmedicine.com

Dietary Sodium Intake and Risk of Cardiovascular Disease--Reply.

Dietary Sodium Intake and Risk of Cardiovascular Disease--Reply. - PDF Download Free
1KB Sizes 0 Downloads 11 Views