LETTER TO THE EDITOR
What is the mechanism of abnormal blood pressure response on exercise in hypertrophic cardiomyopathy?
Ross Campbell, BSc
Wales Heart Research Institute, Division of Cardiology, UWCM, Heath Park, Cardiff, Glamorgan CF 14 4XN, United Kingdom
Dante E. Manyari, MD,
William J. McKenna, MD and
Michael Frenneaux, MD
CampbellRI{at}cf.ac.uk
Ciampi et al. (1) recently reported a study on the mechanism of abnormal blood pressure response (ABPR) on exercise in hypertrophic cardiomyopathy (HCM). Their study suggests that ABPR is due to a profound impairment of cardiac output augmentation on exercise. Cardiac output was measured using a portable nuclear detector (nuclear VEST). Their results are in marked contrast to two previous published studies carried out by us.
In the first study Frenneaux et al. (2) evaluated cardiac output changes invasively and showed that ABPR was due to an exaggerated fall in systemic vascular resistance rather than a failure of cardiac output to increase appropriately. In the second study we showed that in patients with ABPR there was vasodilation in nonexercising vascular beds instead of the "normal" vasoconstrictor response (3). In the study by Ciampi et al. (1) we note that in all three groups of subjects (healthy controls, HCM, and ABPR HCM) cardiac output responses to exercise are markedly lower than would be expected from the published data. Furthermore, the HCM patients with ABPR have only marginally lower exercise duration than do subjects with a normal blood pressure response. Yet, in contrast, these patients demonstrate a dramatically lower cardiac output response.
The group with ABPR performed 8 min of exercise on a Bruce protocol. This should equate to a VO2 peak of approximately 20 to 25 ml/kg/min, which is similar to the measurement we have observed in an analogous group of patients with ABPR. In contrast, the observed increase in cardiac output of only 50% would be anticipated to lead to a VO2 peak of only 9 to 10 ml/kg/min. We should comment that we have tested the nuclear VEST technique for measuring cardiac output changes during exercise. The values we obtained were implausibly low, and we therefore abandoned the technique.
To the best of our knowledge, cardiac output measurements during exercise using the cardiac VEST technique have not been validated against established invasive measurements. Moreover, to ensure that the VEST was correctly positioned over the left ventricle (LV), the VEST detector was placed under gamma camera control with a 30-s static imaging obtained at the end of exercise (1). These control measures, however, were made in the supine position. Because exercise was performed in the upright posture, it is quite likely that some degree of displacement of the VEST relative to the LV took place. Although we greatly respect the work of this group, we suggest that the nuclear VEST cardiac data are incompatible with the observed exercise duration of these patients and that this must be due to an inherent inaccuracy of the technique during exercise, as used by both Ciampi et al. (1) and ourselves. Furthermore, given the very similar treadmill exercise duration of the HCM patients with and without ABPR, the hugely different cardiac output responses are unlikely to be valid. These observations suggest that the technique cannot even be used for the assessment of qualitative rather than quantitative differences.
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References
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1. Ciampi Q, Betocchi A, Lombardi R, et al. Hemodynamic determinants of exercise-induced abnormal blood pressure response in hypertrophic cardiomyopathy. J Am Coll Cardiol. 2002;40:278–284[Abstract/Free Full Text]
2. Frenneaux MP, Counihan PJ, Caforio ALP, Chikamori T, McKenna WJ. Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy. Circulation. 1990;82:1995–2002[Abstract/Free Full Text]
3. Counihan PJ, Frenneaux MP, Webb DJ, McKenna WJ. Abnormal vascular responses to supine exercise in hypertrophic cardiomyopathy. Circulation. 1991;84:686–696[Abstract/Free Full Text]
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