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J Am Coll Cardiol, 2003; 41:2102-2104, doi:10.1016/S0735-1097(03)00411-X © 2003 by the American College of Cardiology Foundation |
a Univ Federico II, Facolta di Medicina, Via Caravaggio, 73, I-80126 NaplesItaly
sandro.betocchi{at}unina.it
As for the statement, various studies have evaluated the accuracy and the reproducibility of measurements obtained by VEST (4–7). In our laboratory, Pace et al. (8) demonstrated that the VEST-derived values of ejection fraction and peak filling rate are accurate and repeatable (8). Imbriaco et al. (9) showed that VEST is accurate in measuring cardiac hemodynamic responses to different cardiac stimulations (handgrip, tilt test, and nitrate administration). The researchers measured changes from baseline to peak response in ejection fraction, stroke volume, and cardiac output, and they found that these changes are similar in two different studies (coefficient of repeatability: 7.0, 7.0, and 7.6, respectively). Dr. Campbell is correct in saying that a validation of VEST-measured cardiac output in comparison with invasive techniques has never been performed; this is not crucial, though. The VEST does not measure absolute cardiac output; rather, it measures changes relative to baseline, and these changes are reproducible (9). In addition, measurements are derived from counts and are geometry-independent; therefore, exercise-induced changes in left ventricular (LV) shape would not affect the accuracy of measurements.
Second, VEST monitoring has also been used by others to assess LV function changes during routine activities and could detect silent ischemic episodes (10–12). Follow-up demonstrated a highly significant relationship between the occurrence of silent LV dysfunction, assessed by VEST, and cardiac events (13,14). Kayden et al. (15) monitored LV systolic function by VEST during left anterior descending coronary angioplasty. The investigators showed a fall in ejection fraction during balloon inflation, with an increase in end-systolic volume. During VEST monitoring, Volpe et al. (16) showed that cardiac adaptations to acute volume loading are compromised in patients with dilated cardiomyopathy. A drop in ejection fraction occurred during exercise and mental stress test in hypertensive patients with LV hypertrophy, as compared to a nearly normal response in patients without hypertrophy (17,18). Two studies demonstrated that LV dysfunction during exercise or dobutamine infusion is a common phenomenon in patients with hypertrophic cardiomyopathy (HCM), and these studies postulated that it was due to myocardial ischemia (19,20). Finally, our group studied the hemodynamic adaptation by VEST during handgrip in patients with HCM with or without obstruction (21) and also during head-up tilt test in patients with and without history of syncope (22). To the best of our knowledge, no fewer than 64 studies have evaluated LV hemodynamics by using VEST monitoring in various cardiac diseases and settings. All these studies have shown that hemodynamic changes by VEST correlate well with an array of physiological and clinical findings.
Third, Dr. Campbell reports that investigators had "implausibly low" cardiac output changes during exercise with VEST and "abandoned the technique." It is suggested that in our study the "implausibly low" cardiac output changes are due to unnoticed displacement of the device relative to the left ventricle, as exercise was performed in the orthostatic position and positioning of the device in the supine position. We respectfully disagree: positioning of the device was performed in the orthostatic position. Although this was not clearly stated in our report (1), we referred to a previous study for technical details (4). Because VEST position was checked twice—before and at the end of the study—it is unlikely that it was correct at the beginning and at the end of the protocol, but not during it. Besides, as outlined in our report, a sudden shift >10% in the average counts was considered a sign of inadequate data acquisition (as it is associated with detector’s movement or malfunction [4,8]).
As for syllogism, in our study (1), maximum increase in cardiac output was not reported: data reflect changes in cardiac output at peak exercise. Because cardiac output rises to a given level of exercise, it then declines (slightly in controls and more in patients); thus, reported increase in cardiac output is less than the maximum. We do not consider the actual increase in cardiac output to be implausibly low in our sedentary controls: maximum cardiac output ranged from 162% to 377% of baseline, with a mean of 230 ± 67%. Even if there was a systematic underestimation of cardiac output changes during exercise, it would be impossible to explain solely on the basis of such hypothetical (and in our view unproved) underestimation why patients with HCM and abnormal blood pressure response (ABPR) to exercise would increase cardiac output less than would controls and patients with HCM and normal blood pressure response.
Second, Dr. Campbell performs an estimate of peak oxygen consumption based on the duration of exercise. It is not clear to us how that can be accomplished. In a series of 28 patients with HCM in whom expired gases were analyzed during exercise, we found no correlation between exercise duration in minutes and peak or % of predicted oxygen consumption (r = 0.31, p = 0.11; r = 0.22, p = 0.25, respectively). If exercise duration was an accurate estimate of peak oxygen consumption, we wonder why anyone would measure expired gases. Although we concur that peak oxygen consumption is related to cardiac output, we believe that exercise duration bears no correlation with cardiac output. In the above-mentioned series of 28 patients, only one patient had exercise-induced hypotension, and 9 patients had a flat blood pressure response to exercise. In these patients, peak oxygen consumption was significantly less than in patients with HCM and normal blood pressure response to exercise (% of predicted: 73 ± 14 vs. 93 ± 25%, p = 0.027). A paper from St. George’s Hospital Medical School dealt with oxygen consumption in HCM (23): interestingly, investigators found that patients with ABPR had lower peak oxygen consumption than did those with normal response. These data are in agreement with ours, and they are consistent with a blunted cardiac output increase in that subgroup of patients. Furthermore, a study appeared in JACC a few years ago outlining a mechanism for ABPR to exercise in HCM that is consistent with our data: Yoshida et al. (23) proved that those patients are the ones in whom a greater degree of exercise-induced subendocardial ischemia develops.
In conclusion, we believe that the discrepancy between our study (1) and the studies by Frenneaux et al. (2,3) exists, but it cannot be explained on the basis of an inadequacy of VEST in measuring cardiac hemodynamics, as we had outlined in the Discussion section of our original report (24).
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