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European Heart Journal Advance Access originally published online on February 7, 2006
European Heart Journal 2006 27(6):757-758; doi:10.1093/eurheartj/ehi777
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

The heart, the brain, and the Kounis syndrome: reply

Roy C. Ziegelstein

Department of Medicine
B-1-North
Johns Hopkins University School of Medicine
Johns Hopkins Bayview Medical Center
4940 Eastern Avenue
Baltimore
MD 21224-2780
USA
E-mail address: rziegel{at}jhmi.edu

Brett D. Thombs

Department of Psychiatry and
Behavioral Sciences
Johns Hopkins University School of Medicine
Johns Hopkins Bayview Medical Center
Baltimore
MD
USA

Kounis et al.1 are correct that in our editorial,2 we noted with respect to the brain and the heart, ‘the twain have met,’ but we did not elaborate very much on the mechanisms connecting the two. This was deliberate. There are many more potential mechanisms that might connect the brain and the heart than could reasonably fit in an editorial. Kounis et al.1 describe some of these in their letter. While their discussion is superb, it is really only scratching the surface. For example, platelet activation is not mentioned at all, and the behavioural link between depression and cardiac disease (i.e. one mediated by an increased prevalence of cigarette smoking among depressed individuals or by the poor adherence to medications and risk-reducing behaviours, which is common in patients with depression3) is not even noted. It must also be pointed out that even after these are mentioned, we still have only focused on one side of the road connecting the brain and the heart, ignoring the possibility that poor cardiac function leads to depression rather than the other way round.

The study by van Melle et al.4 is very important because it shows that the severity of left ventricular dysfunction is significantly related to the severity of depressive symptoms in patients with myocardial infarction. This at least suggests the possibility that heart damage may be primary, and the mood disturbance follows. We agree with Kounis et al. that characterizing the mechanisms connecting the brain and the heart—as well as their direction—is critical, because the implication that left ventricular dysfunction might lead to depression is that if the former is treated appropriately, the latter may improve.

Acknowledgement

R.C.Z. is supported by the Miller Family Scholar Program.

References

  1. Kounis NG, Kounis GN, Kouni SN, Soufras GD. The heart, the brain and the Kounis syndrome. Eur Heart J 2006, doi:10.1093/eurheartj/ehi776.
  2. Ziegelstein RC, Thombs BD. The brain and the heart: the twain meet. Eur Heart J 2005;26:2607–2608.[Free Full Text]
  3. Ziegelstein RC, Fauerbach JA, Stevens SS, Romanelli J, Richter DP, Bush DE. Patients with depression are less likely to follow recommendations to reduce cardiac risk during recovery from a myocardial infarction. Arch Intern Med 2000;160:1818–1823.[Abstract/Free Full Text]
  4. van Melle JP, de Jonge P, Ormel J, Crijns HJGM, van Veldhuisen DJ, Honig A, Schene AH, van den Berg MP; for the MINT-IT investigators. Relationship between left ventricular dysfunction and depression following myocardial infarction. Eur Heart J 2005;26:2650–2656.[Abstract/Free Full Text]

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This Article
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