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J Am Coll Cardiol Intv, 2009; 2:368-369, doi:10.1016/j.jcin.2009.02.007
© 2009 by the American College of Cardiology Foundation
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Letter to the Editor

Reply

Ruchira Glaser, MD, MSCE*


I thank Dr. Dominguez-Rodriguez and colleagues for their interest in our paper (1) and appreciate the additional insight provided in their letter regarding the potential role of inflammation, and its diurnal patterns, in the differences in outcomes observed in patients undergoing primary percutaneous coronary intervention (PCI) during off hours versus routine hours. We agree that the role of inflammation and risk for plaque rupture and adverse short-term cardiovascular outcomes has become increasingly clear. In fact, in a prior report (2), we found that presentation with acute coronary syndrome as an indication for PCI was a potent independent risk factor for new lesion progression during the subsequent year; this finding further supports the role of inflammation, particularly in acute coronary syndrome patients.

In the present study (1), operators were more likely to state that a lesion did not respond appropriately during off hours when procedural success was not achieved. Although lesion characteristics by angiography were similar in both groups, flow characteristics were less favorable before PCI during off hours. Changes in inflammatory factors could certainly contribute to this finding, though phenomena such as platelet aggregation and activity changes with time have been previously described (3,4). In this regard, a study of blood markers of inflammation during off hours versus routine hours may prove valuable in establishing a link between inflammation and differential outcomes during off hours.

The possible role of inflammation highlights again our findings that multiple factors may be associated with poorer outcomes during off-hours PCI, including possible operator fatigue, a potentially modifiable risk factor. As health care policy is shaped, it is the understanding of other potential factors beyond door-to-balloon time, both institutional and biologic, that may ultimately improve outcomes in myocardial infarction.

* University of Pennsylvania School of Medicine, Medicine-Cardiology, 9 Founders Cardiology-HUP, 3400 Spruce Street, Philadelphia, Pennsylvania 19106 (Email: ruglaser{at}gmail.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. Glaser R, Selzer F, Faxon DP, et al. Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention Circulation 2005;111:143-149.[Abstract/Free Full Text]
  3. Tofler GH, Brezinski D, Schafer AI, et al. Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death N Engl J Med 1987;316:1514-1518.[Web of Science][Medline]
  4. Andreotti F, Davies GJ, Hackett DR, et al. Major circadian fluctuations in fibrinolytic factors and possible relevance to time of onset of myocardial infarction, sudden cardiac death and stroke Am J Cardiol 1988;62:635-637.[CrossRef][Web of Science][Medline]

Related Article

Cross-Talk Between Primary Percutaneous Coronary Intervention, Arterial Inflammation, and Light/Dark Patterns
Alberto Dominguez-Rodriguez, Francisco Bosa-Ojeda, and Pedro Abreu-Gonzalez
J. Am. Coll. Cardiol. Intv. 2009 2: 368. [Full Text] [PDF]




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