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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.
- American College of Cardiology
- Mohiddin S.A.,
- Begley D.,
- Shih J.,
- Fananapazir L.
- Yetman A.T.,
- McCrindle B.W.,
- Gow R.M.