Introduction 1 4 1 3 5 2 4 4 6 7 10 11 The addition of a perfusion sequence on peak-dose dobutamine may further enhance the interpretation of dobutamine stress CMR, by ruling out false positive findings, through the combined strength of both methods. The purpose of this study is to assess whether the addition of perfusion imaging to dobutamine stress CMR at peak-dose dobutamine reduces the number of false-positive dobutamine stress CMR examinations. Materials and methods Patient population Between September 2004 and April 2006, 124 consecutive patients were referred from the department of Cardiology for a dobutamine stress CMR. The study was approved by the local ethical committee. Informed consent was obtained prior to the study, after the nature of the procedure had been explained. All patients had chest pain and an inconclusive diagnosis of coronary artery disease by means of history, ECG recordings at rest and, if performed, during a bicycle exercise test. Patients with an acute coronary syndrome, atrial fibrillation, severe arterial hypertension (>220/120), CMR-incompatible metallic implants or known claustrophobia were not eligible. Protocol for dobutamine stress CMR with myocardial perfusion on peak-dose dobutamine 4 Termination criteria for dobutamine stress CMR were the development of new wall motion abnormalities (NWMA) or worsening WMA, a fall of systolic blood pressure of more than 40 mmHg, marked hypertension above 240/120 mmHg, severe chest pain, ventricular arrhythmias and intolerable side effects. NWMA are indicative of myocardial ischemia. ® During the examination a radiologist present in the MR suite to monitor the condition of the patient and to visually evaluate the images. When NWMA’s with a corresponding perfusion deficit were seen, a coronary angiography (CAG) was performed within 3 weeks. Patients with NWMA’s and a normal first pass perfusion on peak stress entered follow-up. Image analysis 4 Wall Motion Score Index (WMSI) was derived as the mean score of all segments of all short-axis images. WMSI data from the combined analysis of the cine and tagging images were determined from baseline and peak stress images. The first pass perfusion images on peak-dose dobutamine were visually analyzed by an experienced radiologist and cardiologist in a consensus reading after the wall motion analysis by the same physicians. A perfusion abnormality, corresponding to the coronary artery distribution areas, in at least two segments at consecutive short-axis slices or one segment of the most apical slice of the left ventricle was defined as myocardial ischemia. Follow-up Follow-up data were obtained in September 2006. The present status of the patient was determined by review of the hospital records or contacting the patient’s general physician. The date of the last review was used to calculate follow-up time. Evaluated end points were non-fatal myocardial infarction (angina of >30 min duration and either 2 mm ST segment elevation in two consecutive ECG leads or a rise in creatine kinase level and its myoglobine fraction two times the upper limit of normal), cardiac death (death in the presence of acute myocardial infarction, significant cardiac arrhythmias or refractory congestive heart failure) and coronary revascularization. Results Patient population From the 124 consecutively included patients, in nine patients the examination could not be completed due to: intolerable side effects (nausea, vomiting) in four patients, claustrophobia in three patients. Two patients were excluded due to insufficient image quality, one of whom had an irregular rhythm with triggering difficulties, and the other patient was unable to sustain breath holds. 1 Table 1 Demographic and hemodynamic data Variable Mean or % Age, years 61 ± 11 Female, % 29.6 Previous myocardial infarction, % 38.0 Revascularization, % 31.0 Rest wall motion abnormalities (RWMA), % 40.9 Body weight, kg 78 ± 12 Resting diastolic blood pressure, mmHg 87 ± 11 Peak diastolic blood pressure, mmHg 78 ± 12 Resting systolic blood pressure, mmHg 152 ± 26 Peak systolic blood pressure, mmHg 151 ± 31 Resting heart rate, bpm 79 ± 15 Peak heart rate, bpm 119 ± 21 a 12,030 ± 3,545 Rate-pressure product at peak stress 17,935 ± 4,807 Wall Motion Score Index (WMSI) at baseline 1.18 ± 0,32 Wall Motion Score Index (WMSI) at peak dose 1.21 ± 0.34 Values are expressed as mean ± SD or percentage a RWMA = Rest Wall Motion Abnormality; WMSI = Wall Motion Score Index Dobutamine stress CMR with myocardial perfusion on peak-dose dobutamine Eighteen of the 115 patients (16%) had NWMA of whom 14 (78%) showed perfusion deficits on peak-dose dobutamine in the corresponding segments. Four patients (22%) with NWMA did not have a perfusion deficit. In these four patients, NWMA were attributable to a LBBB as could be confirmed with an independent (stress) ECG. Two of these were inducible LBBB, not known prior to the examination. CAG was positive for the corresponding segments in the 14 patients (100%) with NWMA and a corresponding perfusion deficit. 1 2 Fig. 1 Flow chart illustrating course of the study and outcome NWMA = New Wall Motion Abnormality; LBBB = Left Bundle Branch Block; CAG = Coronary Angiogram  Fig. 2 A B C D  Follow-up results (median 13.5 months, range 6–20 months) were obtained from all patients with NWMA’s and a normal first-pass perfusion. None of these patients had cardiac events or revascularizations at follow-up. Discussion . 4 4 12 17 12 14 18 19 20 4 21 Absolute specificity values cannot be given with this study, because a CAG was not performed in case of a negative dobutamine stress examination. The outcome of the dobutamine stress CMR and myocardial perfusion on peak-dose dobutamine was used as a direct arbiter for subsequent clinical follow-up. In this respect follow-up was considered the reference standard. None of the patients with NWMA’s and a normal myocardial perfusion had an adverse outcome at follow-up. Therefore, it is reasonable to state that adding first pass myocardial perfusion imaging on peak-dose dobutamine increases the specificity of dobutamine stress CMR in this patient group. 12 12 22 23 Long term follow-up will provide information about the case in which a small perfusion abnormality was seen inferior without NWMA. Whether this abnormality is a “true” abnormality or an artefact is unclear. This patient did not have any adverse cardiac event at 14 months follow-up. 13 24 25 In a clinical post-infarct setting, delayed contrast enhancement imaging may provide valuable diagnostic information. To our opinion, this would in our study not have provided additional information regarding the fact whether a NWMA was caused by myocardial ischemia or a non-ischemic cause, and guide the necessity for an invasive coronary angiogram. Cine and grid tagging images were acquired at rest to look for rest wall motion abnormalities. New wall motion abnormalities in this setting would represent myocardial ischemia (whether or not in the presence of a previous myocardial infarction). Delayed contrast enhancement imaging was therefore not performed in this protocol. In this protocol we only acquired stress first-pass perfusion images. Perfusion imaging at rest may be very useful in stress-rest perfusion imaging studies, but the main focus in this protocol is on a normal perfusion in case of NWMA. A rest perfusion exam would in this context not provide additional information (the rest perfusion exam will also be normal). In this way the protocol is not unnecessarily prolonged and a second bolus injection of gadolinium-DTPA can be omitted. Conclusion Good agreement exists between the absence of NWMA and a normal myocardial perfusion. Furthermore, a perfusion sequence on peak-dose dobutamine can help decide whether a NWMA is caused by ischemia or is due to a LBBB. First pass myocardial perfusion during peak-dose dobutamine can be used as an additional tool to reduce the number of false-positive NWMA’s, to improve the detection of myocardial ischemia.