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Ann Thorac Surg 2003;75:1549
© 2003 The Society of Thoracic Surgeons

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Original article: cardiovascular

Invited commentary

^a Division of Cardiothoracic Surgery, The Children’s Hospital of Philadelphia, 34th Street and Civic Center Blvd, Philadelphia, PA 19104, USA

(Email: decampli{at}email.chop.edu).

Sheil and colleagues have described a method that purportedly detects coronary artery endothelial dysfunction during controlled cardiac ischemia. The technique, which involves imaging sonicated albumin microbubbles, has been previously used in adult cardiac surgery. Prior studies in the laboratory showed that these microbubbles attach to neutrophils. Their persistence in coronary arteries indicates adherence of neutrophils to the vascular endothelium, which implies endothelial injury. This paper’s contribution is to demonstrate the safety and efficacy of this technique in the clinical pediatric population.

While vascular endothelial dysfunction has been shown to be part of the spectrum of myocardial injury following ischemia, it is unlikely to account entirely for ischemic myocardial dysfunction, with direct myocyte injury being the other important consideration. How tightly does this qualitative measure of endothelial dysfunction correlate with subsequent clinical myocardial dysfunction following controlled ischemia or prolonged exposure to cardiopulmonary bypass? Even if this correlation is tight, the method’s clinical utility is unproven. What does one do with the result during an actual clinical case? The better home for the method may be in the laboratory, where it might serve as a real-time indicator of endothelial dysfunction in studies of strategies for protecting the myocardium from ischemic injury.

The next questions to answer are as follows: (1) What is the detailed mechanism underlying the phenomenon? (2) In controlled studies of myocardial ischemia, what is the relationship between microbubble transit time and post-ischemic ventricular function (as measured, eg, by load-independent indices of contractility)? (3) Do specific interventions (eg, cardioplegia administration) that improve ventricular function also shorten transit time? Depending upon these answers, the method may prove to be a simple, real-time way of evaluating myocardial protective strategies in the laboratory or in clinical studies.

This paper’s other impact is that it reopens the book on the problem of pediatric myocardial protection. While the literature is rife with contributions on the subject from the early 1990’s, the contributions recently have diminished. The clinical impact of decade-old strategies such as blood cardioplegia, leukocyte depletion, Na⁺–H⁺ exchange inhibition, K⁺–ATP channel activation, Ca⁺⁺ channel blockade, PAF antagonism, Mg⁺⁺ supplementation, nitric oxide, or amino acid enhancement in pediatric cardiac surgery remains unclear. While overall results of congenital cardiac surgery have improved dramatically in the past decade, a cadre of operations requiring longer ischemic times or involving the preoperatively impaired myocardium have been introduced. Clinically demonstrated advances in myocardial protection would enhance improvement in the outcome following these most difficult operations. The topic should be resurrected.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): William M. DeCampli Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by DeCampli, W. M. Search for Related Content PubMed Articles by DeCampli, W. M.