We thank Gibson et al.1 for their interest in our article. The authors have raised important issues. We agree that the uptake of myocardial contrast echocardiography (MCE) for stress echocardiography within the UK has been low.2 This may be surprising given the wealth of data that has accumulated over the past decade, demonstrating the clinical, prognostic, and practical value of performing MCE stress echocardiography using exercise, dobutamine, and dipyridamole techniques. There have been multiple large prospective and multicentre studies, which have demonstrated that MCE stress echocardiography is safe and comparable with single-photon emission computed tomography (SPECT) for the detection of coronary artery disease3,4 with consistent superior sensitivity in the intermediate high-risk population. Furthermore, assessment of myocardial perfusion with MCE stress echocardiography has advantages compared with analysis of wall motion alone. The addition of MCE perfusion imaging during stress echocardiography performed with either dobutamine or exercise or high-dose dipyridamole improved the sensitivity for the detection of coronary artery disease over wall motion analysis alone and provided incremental prognostic information.5,6,7 Indeed, a large randomized trial clearly established both diagnostic and prognostic advantages of myocardial perfusion with MCE over optimal wall motion assessment.8,9 Our survey preceded the publications of these large studies. Even then, 10% of the stress echocardiography labs were performing stress echocardiography (SE) with MCE.2 It is now recommended in the latest European Society of Cardiology guidelines for stable angina, as pointed out by the authors, that MCE should be used to enhance the performance of SE. In our institution, we routinely perform MCE in nearly all stress echocardiography studies for the assessment of myocardial ischaemia. We have several echocardiography fellows, already competent in stress echocardiography, who have been trained to perform myocardial perfusion assessment using MCE under supervision of an expert within 3–4 months of commencing training in our unit. Therefore, we believe the technique, with appropriate training, could be incorporated into the majority of echocardiography laboratories, where stress echocardiography is already being performed. Vasodilator MCE (low-dose dipyridamole, adenosine, and regadenoson), as Gibson et al. pointed out, may be used instead of inotropic stress as it is rapid (only 15 min) and thus can improve throughput of patients in a time-constrained environment. However, outcome data are sparse, and there is no study showing its equivalence to inotropic stress (where wall motion gives additional information to that obtained by vasodilator stress only). Notwithstanding, we do use it in our lab when dobutamine/exercise is not feasible. We hope to repeat our study in 5 years' time to assess temporal changes in stress echocardiography practice. With the evidence base that has accumulated, we expect that the use of MCE stress echocardiography will have substantially grown. However, it is important for the experts in the field and the responsible societies (national and international) in conjunction with the relevant industries to raise both the awareness of MCE and to provide support (teaching and training courses) to the echocardiography labs to perform quality work. Conflict of interest: None declared.
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Bhattacharyya et al. (2013) studied this question.
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