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where the symptom pattern and/or angiographic features raise suspicion about their clinical significance. 1 H. Kitazume, J. R. Kramer, D. Krauthamer, S. El Tobgi, W. L. Proudfit, and F. M. Sones, “Myocardial bridges in obstructive hypertrophic cardiomyopathy.,” American heart journal, vol. 106, no. 1 Pt 1, pp. 131–5, Jul. 1983. 2 F. Navarro-Lopez, J. Soler, J. Magriña, E. Esplugues, J. C. Pare, G. Sanz, and A. Betriu, “Systolic compression of coronary artery in hypertrophic cardiomyopathy.,” International journal of cardiology, vol. 12, no. 3, pp. 309–20, Sep. 1986. 3 C. Basso, G. Thiene, S. Mackey-Bojack, A. C. Frigo, D. Corrado, and B. J. Maron, “Myocardial bridging, a frequent component of the hypertrophic cardiomyopathy phenotype, lacks systematic association with sudden cardiac death.,” European heart journal, vol. 30, no. 13, pp. 1627–34, Jul. 2009. 4 S. A. Mohiddin, D. Begley, J. Shih, and L. Fananapazir, “Myocardial bridging does not predict sudden death in children with hypertrophic cardiomyopathy but is associated with more severe cardiac disease.,” Journal of the American College of Cardiology, vol. 36, no. 7, pp. 2270–8, Dec. 2000. 5 I. Olivotto, F. Cecchi, and M. H. Yacoub, “Myocardial bridging and sudden death in hypertrophic cardiomyopathy: Salome drops another veil.,” European heart journal, vol. 30, no. 13, pp. 1549–50, Jul. 2009. 6 J. Downar, W. G. Williams, C. McDonald, E. D. Wigle, and B. W. McCrindle, “Outcomes after ‘unroofing’ of a myocardial bridge of the left anterior descending coronary artery in children with hypertrophic cardiomyopathy.,” Pediatric cardiology, vol. 25, no. 4, pp. 390–3. 7 I. Olivotto, F. Cecchi, R. Bini, S. Favilli, B. Murzi, I. El-Hamamsy, and M. H. Yacoub, “Tunneled left anterior descending artery in a child with hypertrophic cardiomyopathy.,” Nature Clinical Practice Cardiovascular Medicine, vol. 6, no. 2. pp. 134–139, 2009. 8 A. T. Yetman, B. W. McCrindle, C. MacDonald, R. M. Freedom, and R. Gow, “Myocardial bridging in children with hypertrophic cardiomyopathy--a risk factor for sudden death.,” The New England journal of medicine, vol. 339, no. 17, pp. 1201–9, Oct. 1998. 9 F. Gori, C. Basso, and G. Thiene, “Myocardial infarction in a patient with hypertrophic cardiomyopathy.,” The New England journal of medicine, vol. 342, no. 8, pp. 593–4, Feb. 2000. 10 P. Sorajja, S. R. Ommen, R. a Nishimura, B. J. Gersh, A. J. Tajik, and D. R. Holmes, “Myocardial bridging in adult patients with hypertrophic cardiomyopathy,” Journal of the American College of Cardiology, vol. 42, no. 5, pp. 889–894, Sep. 2003. 11 J. Ge, a Jeremias, a Rupp, M. Abels, D. Baumgart, F. Liu, M. Haude, G. Görge, C. von Birgelen, S. Sack, and R. Erbel, “New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler.,” European heart journal, vol. 20, no. 23, pp. 1707–16, Dec. 1999. 12 M. S. Maron, I. Olivotto, B. J. Maron, S. K. Prasad, F. Cecchi, J. E. Udelson, and P. G. Camici, “The case for myocardial ischemia in hypertrophic cardiomyopathy.,” Journal of the American College of Cardiology, vol. 54, no. 9, pp. 866–75, Aug. 2009. 13 P. Knaapen, T. Germans, P. G. Camici, O. E. Rimoldi, P. A. Dijkmans, W. G. Van Dockum, J. W. R. Twisk, A. C. Van Rossum, A. A. Lammertsma, F. C. Visser, N. Heart, H. Campus, T. Erasmus, and P. Knaapen, “Determinants of Coronary Microvascu a myocardial bridge and regional ischemia might prove to be a difficult task in this setting however. Angiographic features of myocardial bridges including length of the tunneled segment, degree of systolic compression, and depth within the myocardium are not reliable predictors of their potential to cause ischemia 10. In addition, conventional angiography frequently fails to identify persistence of epicardial compression into variable periods of diastole (and hence more likelihood of causing ischemia) compared to other modalities such as intravascular ultrasound and intracoronary Doppler flow velocity measurements 11. It is therefore not advisable to rely on coronary angiography only to determine the physiological significance of myocardial bridges except in cases with very mild compression that is unequivocally limited to systole 7. Results of myocardial perfusion imaging on the other hand may be confounded by a number of factors in this subset of patients, including the presence of diffuse subendocardial ischemia, extensive microvascular disease, severe compression of septal perforators as well as patchy fibrosis, and should therefore be interpreted with caution 12–14. FFR has recently emerged as a simple, accurate, highly-reproducible and lesion-specific index of the physiological significance of fixed epicardial coronary stenosis, with strong evidence supporting its correlation with clinical outcomes 15–21. Its value in patients with “dynamic” epicardial coronary disease such as myocardial bridging is much less studied and remains limited to a few small series and case reports 22, 23. Furthermore, conventional FFR measurement – defined as the ratio of mean pressure distal to a lesion to mean proximal/aortic pressure – in the setting of coronary bridges is prone to fallacies related to cyclical changes in coronary flow and distal pressure. The “squeezing” of the blood column distal to bridged segment against a highly resistive microcirculation (during systole) causes overshooting of the distal coronary pressure compared to the proximal/ aortic pressure resulting in a negative pressure gradient across the myocardial bridge during systole. This surge in distal intracoronary systolic pressure increases the mean distal coronary pressure and consequently (falsely) increases the FFR values. In some instances, non-physiological values of >1 are obtained due to this phenomenon. This has been frequently referred to as “the FFR paradox”. To overcome this limitation, the ratio between diastolic pressures – rather than mean – has been proposed to evaluate the physiological significance of epicardial stenosis. This is demonstrated in the present report where “conventional” FFR was 0.91 while diastolic FFR was 0.76. This approach offers the added theoretical advantage of limiting evaluation of the effect of myocardial bridges to diastole, the period where coronary blood flow predominantly occurs. The additional use of incremental doses of i.v. dobutamine to increase contractility and heart rate can further enhance the diagnostic yield of this technique by simulating the effects of exercise on the myocardium and consequently augment the “squeezing” of the bridged segment prior to pressure measurements 22. The use of dobutamine was not deemed necessary in this patient given the low “non-augmented” diastolic FFR value. Successful surgical relief of the tunneled LAD segment led to normalization of diastolic FFR with restoration of concordance with “conventional” FFR measurements, which further supports the theory of the “FFR paradox”. Conclusion Myocardial bridges are frequently encountered in patients with HCM and are inconsequential in the majority of cases. However, it is crucial to accurately identify the small subset of patients where the presence of such bridges is associated with regional myocardial ischemia. Diastolic FFR measurement is a simple and highly reproducible tool that can reliably quantify the functional significance of such lesions in patients Cardiology Charity 54  AXIOM Innovations | December 2013 | www.siemens.com/angiography


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