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J Am Coll Cardiol Intv, 2009; 2:368, doi:10.1016/j.jcin.2009.01.007
© 2009 by the American College of Cardiology Foundation
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Letter to the Editor

Cross-Talk Between Primary Percutaneous Coronary Intervention, Arterial Inflammation, and Light/Dark Patterns

Alberto Dominguez-Rodriguez, MD, PhD*, Francisco Bosa-Ojeda, MD, PhD, Pedro Abreu-Gonzalez, PhD


We read with great interest the recent article by Glaser et al. (1). The authors should be congratulated for this well-conducted study. However, we would like to point out an important aspect in the interpretation of these findings.

Recent research has shown that inflammation plays a key role in coronary artery disease and other manifestations of atherosclerosis. Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes (2). The implication or association of physiological rhythms with peak activity at a certain time of day or night may be suspected, given that the onset of cardiovascular accidents follows a circadian pattern (3). Likewise, we have previously reported that in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention, day/night rhythms of inflammatory markers may be abnormal (4–6). A reciprocal link exists between inflammation and thrombosis. A better understanding of arterial inflammation will enhance our ability to prognosticate risk and effectively design therapy. Therefore, the presence of variability during the 24 h of inflammatory and immunologic functions, would, hypothetically, have a profound effect on the practice of primary percutaneous coronary intervention.

* Coronary Care Unit, Department of Cardiology, University Hospital of Canarias, Ofra s/n La Cuesta E-38320, Tenerife, Spain (Email: adrvdg{at}hotmail.com).


    REFERENCES
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 REFERENCES
 

  1. Glaser R, Naidu SS, Selzer F, et al. Factors associated with poorer prognosis for patients undergoing primary percutaneous coronary intervention during off-hours: biology or systems failure? J Am Coll Cardiol Intv 2008;1:681-688.[Abstract/Free Full Text]
  2. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease N Engl J Med 2005;352:1685-1695.[CrossRef][Web of Science][Medline]
  3. Hernandes Fernandes E, Coelho D, Missel Correa JR, Kumpinski D. Circadian alterations of the cardiovascular system Rev Esp Cardiol 2000;53:117-122.[Web of Science][Medline]
  4. Dominguez-Rodriguez A, Abreu-Gonzalez P, Garcia-Gonzalez MJ, De la Rosa A, Vargas M, Marrero F. Light/dark pattern of the proinflammatory cytokines in acute myocardial infarction Rev Esp Cardiol 2003;56:555-560.[CrossRef][Web of Science][Medline]
  5. Dominguez-Rodriguez A, Garcia-Gonzalez M, Abreu-Gonzalez P, Ferrer J, Kaski JC. Relation of nocturnal melatonin levels to C-reactive protein concentration in patients with ST-segment elevation myocardial infarction Am J Cardiol 2006;97:10-12.[Web of Science][Medline]
  6. Dominguez-Rodriguez A, Abreu-Gonzalez P, Garcia-Gonzalez MJ, Samimi-Fard S, Kaski JC, Reiter RJ. Light/dark patterns of soluble vascular cell adhesion molecule-1 in relation to melatonin in patients with ST-segment elevation myocardial infarction J Pineal Res 2008;44:65-69.[Web of Science][Medline]

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Ruchira Glaser
J. Am. Coll. Cardiol. Intv. 2009 2: 368-369. [Full Text] [PDF]




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