Advertisement

Click here for more guidelines.

 
 




CME Topic Collections Past Issues Search Current Issue Home
     

J Am Coll Cardiol, 2001; 38:921-922
© 2001 by the American College of Cardiology Foundation
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McCrindle, B. W.
Right arrow Articles by Yetman, A. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McCrindle, B. W.
Right arrow Articles by Yetman, A. T.

LETTER TO THE EDITOR

Myocardial bridging of the left anterior descending coronary artery in children with hypertrophic cardiomyopathy

Brian W. McCrindle, MD, MPH, FACCa and Anji T. Yetman, MDa

a The Hospital for Sick Children, 555 University Ave, Toronto, Ontario M5G 1X8, Canada

brian.mcctindle{at}sickkids.on.ca


We read with interest the study by Mohiddin et al. (1) in a recent issue of the Journal. The article appears to be a correction and expansion of data published previously in a letter to the editor of the New England Journal of Medicine (2), in response to our article on the same subject (3). Many of the criticisms we had in our response (4) regarding their published letter still hold concerning their follow-up article. Our article provided evidence that significant myocardial bridging of the left anterior descending coronary artery (LAD), characterized by greater than 90% systolic compression of the middle third of the LAD with ongoing compression during a mean of 50% of diastole, was associated with myocardial ischemia in children with hypertrophic cardiomyopathy. Such ischemia was manifested clinically as chest pain and as an increased risk of ventricular tachycardia and cardiac arrest. The presence of bridging as defined was not significantly associated with echocardiographic indices of severity of the hypertrophic cardiomyopathy. We reported anectodal evidence that surgical division of bridges reduced ischemia and its clinical consequences.

These findings are in contrast with those of Mohiddin et al. (1) for several reasons. The two studies would appear to be examining similar populations, although Mohiddin and colleagues did not examine for potential selection bias of catheterized patients. A major difference rests in the definition of bridging used by Mohiddin et al., in that they included all noted bridges of the coronary arteries, as well as systolic compression of septal branches of the LAD. The degree of systolic compression was significantly less than in our patients. The importance of systolic compression of septal branches is unknown, and it would be difficult to assess in the presence of important LAD bridging and underfilling of septal perforators. There would be expected to be important colinearity (correlation) between the presence of LAD bridging and septal perforator compression, which would complicate entry of both variables into multivariable models.

Likewise, significant colinearity would be expected between septal wall thickness and septal perforator compression. It would appear that LV outflow gradients were skewed in distribution and would require a normalizing data transformation before analysis. The analysis and conclusions are therefore flawed. It is suspected that further analysis restricted to their subgroup of patients with near complete systolic compression of the proximal to mid-LAD would show similar findings to our study.

Our greatest concern is that the investigators have not performed a comparable study and have not provided comparable evidence to refute our finding that significant bridging of the LAD is an important and treatable cause of myocardial ischemia and sudden death in selected children with hypertrophic cardiomyopathy. Uncritical acceptance of their findings may mislead clinicians and patients. We reassert that resolution of this controversy will require a well-designed prospective cohort study, followed by a clinical trial of surgical division of clinically significant myocardial bridges.


    References
 Top
 References
 
1. Mohiddin SA, Begley D, Shih J, Fananapazir L. Myocardial bridging does not predict sudden death in children with hypertrophic cardiomyopathy but is associated with more severe cardiac disease. J Am Coll Cardiol. 2000;36:2270–2278[Abstract/Free Full Text]

2. Mohiddin SA, Begley D, Fananapazir L. Myocardial bridging in children with hypertrophic cardiomyopathy. (letter)N Engl J Med. 1999;341:288–289[CrossRef][Medline]

3. Yetman AT, McCrindle BW, MacDonald C, Freedom RM, Gow R. Myocardial bridging in children with hypertrophic cardiomyopathy—a risk factor for sudden death. N Engl J Med. 1998;339:1201–1209[CrossRef][Medline]

4. Yetman AT, McCrindle BW, Gow RM. Myocardial bridging in children with hypertrophic cardiomyopathy. (letter response)N Engl J Med. 1999;341:289–290





This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McCrindle, B. W.
Right arrow Articles by Yetman, A. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McCrindle, B. W.
Right arrow Articles by Yetman, A. T.

 
  CME Topic Collections Past Issues Search Current Issue Home

Advertisement