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To the Editor:
We thank Doctors Thombs and Ziegestein for their commentary on our article.1 We trust that the following responses will answer their questions. But the short answer to their rhetorical query "Shouldn't we just ask?" is the following: only if you are untroubled by large proportions of your patients continuing to go unrecognized, untreated, and therefore, suffering emotionally, experiencing more symptoms,2,3 utilizing more resources,4-6 failing to comply to lifestyle changes,7-10 and, very likely, dying at higher rates.11,12 Because inquiry regarding stress/psychosocial issues is viewed (correctly) as a "time suck" for medical practitioners, and patients deny/minimize symptoms of depression/distress,13-18 the use of objective frequency-rating screening instruments by nonpsychiatric personnel is unavoidable. Regarding the other questions raised:
1. "Age at Initial Diagnosis is not the best criterion by which to select a screening instrument." Agreed. As noted in our Discussion section, the optimal criterion would be prospective prediction of hard outcomes. Until such a study comparing the candidate instruments in a single-sample, head-to-head fashion is published, we continue to believe that age at initial diagnosis is the optimal criterion for the reasons discussed. We need not wait until such a study is completed to begin the task. If such a study yielded different results, practice can change. The good is not the enemy of the perfect.
2. "The modest Sensitivity and Specificity observed do not justify screening." Thombs and Ziegelstein assume that the use of the Patient's Health Questionnaire-9 (PHQ9) is the end of the screening process proposed. As is the standard of care nationally, it is assumed that the positive patient would then be referred to someone to conduct a diagnostic psychosocial history and mental status exam, presumably a clinical health psychologist or consultation/liaison psychiatrist. This second step then determines if (and which) treatment recommendations are appropriate. (The cost of this second step is less than that of a standard treadmill test.)
3. "Patients benefit from screening only if appropriate and effective treatment is available." Surely, Thombs and Ziegelstein are not seriously arguing that effective treatment of depression/distress does not exist. If so, I suggest they acquaint themselves with the literature on treating depression19-22 and the best available evidence for treatment in cardiac populations, which we have recently summarized23 and have been buttressed by several recent studies.24,25 We doubt very much that any cardiologist practices in a community without mental health providers. It must become the goal of cardiac centers to cultivate referral/consultation relationships with one or more such providers to optimally serve their population.
4. "Age at death is not an outcome of interest." To whom? I assure Thombs and Ziegelstein that it is an outcome of interest to the patient! As a public health matter, age at death is universally accepted as reflective of the quality of care provided by national healthcare systems.26
5. "There is no evidence that age of CAD diagnosis can be successfully used as a sensitive and specific measure of mortality risk among cardiology patients regardless of the cutoff level used." Early-onset coronary heart disease (CHD) is known to be associated with a family history of early CHD/death27,28 and is assumed to reflect only partially understood genetic predispositions29 and high-risk lifestyles.
6. "A PHQ9 cutoff of 10 is poorly predictive of Major Depressive Disorder." As we (and others) have proven elsewhere,30 major depressive disorder is far too stringent a cutoff for predicting adverse cardiac outcomes in cardiac populations. Furthermore, because of the confounding of depression with anxiety/anger,31,32 many screening positive patients who do not have a primary depressive disorder will have other forms of emotional distress with adverse effects on CHD.12,23
7. "The authors did not provide any evidence that the PHQ9 cutoff they report is useful to detect cases of high psychosocial distress." As noted in the article, the PHQ9 is a verbatim copy of the criteria used in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, for diagnosing depression. Thus, it is arguably the most validated measure of psychosocial distress available and the "gold standard" for assessing depression.
Thus, we argue that ample evidence exists to meet the criteria that Thombs and Ziegelstein cite.
1. Depression/distress is not detected without screening.33-35
2. Depression/distress is prevalent in the population.12,23
3. Effective treatments are available.19-22
4. Failure to treat has adverse consequences for the patient.24,25,36-41
5. We can find no published data indicating that false-positives (which, because of the confounding of anger/anxiety, may not be false-positives but detection of anxiety/anger disorders) will lead to invasive or expensive testing, inappropriate treatment, or negative sequelae for the patient.
Furthermore screening with the PHQ9 is virtually cost-free, noninvasive, and user friendly for cardiac personnel at the bedside or in clinic. We stand by our original position. Imperfect though it may be, screening for depression and (because of the confounding of anxiety and anger31,32) distress can and should be performed by cardiac personnel with the PHQ9 and a cutoff of 10. Such a protocol represents a quantum leap improvement over current practice. We welcome empirical studies testing this belief, other screening systems (including leaving it up to cardiac practitioners alone), and the effect of treatment on both psychosocial and cardiac outcomes.
Mark W. Ketterer, PhD, ABPP Senior Bioscientific Staff, Henry Ford Hospital, Clinical Professor of Psychiatry and an Adjunct Associate Professor of Psychology, Wayne State University, Detroit, Michigan.
Mark W. Ketterer, PhD, ABPP
Senior Bioscientific Staff, Henry Ford Hospital, Clinical Professor of Psychiatry and an Adjunct Associate Professor of Psychology, Wayne State University, Detroit, Michigan.
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2. Ketterer MW, Mahr G, Cao JJ, Hudson M, Smith S, Knysz W. What's "unstable" in unstable angina? Psychosomatics. 2004;45:1-12. [Context Link]
3. Ketterer MW, Knysz W, Keteyian SJ, et al. Cardiovascular symptoms in cad patients are strongly correlated with emotional distress. Psychosomatics. In press. [Context Link]
4. Allison TG, Williams DE, Miller TD, et al. Medical and economic costs of psychologic distress in patients with coronary artery disease. Mayo Clin Proc. 1995;70:734-742. [Context Link]
5. Frasure-Smith N, Lesperance F. Depression and anxiety increase physician costs during the first post-MI year. Psychosom Med. 1998;60:99. [Context Link]
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13. Ketterer MW, Kenyon L, Foley BA, et al. Denial of depression as an independent correlate of coronary artery disease. J Health Psychol. 1996;1:93-105. [Context Link]
14. Ketterer MW, Huffman J, Lumley MA, et al. Five year follow up for adverse outcomes in males with at least minimally positive angiograms: the importance of "denial" in assessing psychosocial risk factors. J Psychosom Res. 1998;44:241-250. [Context Link]
15. Ketterer MW, Denollet J, Chapp J, et al. Men deny and women cry, but who dies? Do the wages of "denial" include early ischemic heart disease? J Psychosom Res. 2004;56:119-123. [Context Link]
16. Siegman AW, Townsend ST, Blumenthal RS, Sorkin JD, Civelek AC. Dimensions of anger and CHD in men and women: self ratings versus spouse ratings. J Behav Med. 1998;21(4):315-336. [Context Link]
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18. Smith TW, Uchino BN, Berg CA, et al. Hostile personality traits and coronary artery calcification in middle-ages and older married couples: different effects for self-reports versus spouse ratings. Psychosom Med. 2007;69:441-448. [Context Link]
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21. Hersch EK, Lazar SG. Cost-effectiveness of psychotherapy for depression. In: Spiegel D, ed. Efficacy and Cost-effectiveness of Psychotherapy. Washington, DC: American Psychiatric Press; 1999:125-134. [Context Link]
22. Nemeroff CB, Schatazberg AF. Pharmacological treatment of unipolar depression. In: Nathan PE, Gorman JM, eds. A Guide to Treatments That Work. Oxford, United Kingdom: Oxford University Press; 1998:212-225. [Context Link]
23. Ketterer MW, Knysz W, Khanal S, Hudson M. Cardiovascular disease. In: Blumenfield M, Strain JJ, eds. Psychosomatic Medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:109-119. [Context Link]
24. Lesperance F, Frasure-Smith N, Koszycki D, et al. Effects of citalopram and interpersonal psychotherapy on depression in patients with coronary artery disease: the Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) Trial. JAMA. 2007;297:411-420. [Context Link]
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28. Ketterer MW, Denollet J, Chapp J, et al. Familial transmissibility of early age at initial diagnosis in coronary heart disease (CHD): males only, and mediated by psychosocial/emotional distress? J Behav Med. 2004;27(1):1-10. [Context Link]
29. Pyeritz RE. Genetics and cardiovascular disease. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, PA: WB Saunders Co; 1997:1650-1686. [Context Link]
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