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High dose adenosine stress perfusion cardiovascular magnetic resonance (CMR) imaging for detection of coronary artery disease
© Weerackody et al; licensee BioMed Central Ltd. 2010
Published: 21 January 2010
CMR perfusion (CMRP) imaging using adenosine is increasingly used for the assessment of patients with known or suspected coronary artery disease. At a standard dose adenosine is well tolerated with a good safety profile but on occasion fails to produce a significant haemodynamic response. This may potentially lead to the misdiagnosis of significant ischaemia. We therefore examined whether using a higher dose in these patients to induce a haemodynamic response would lead to the identification of additional perfusion defects.
We prospectively recruited from 1230 consecutive patients undergoing CMRP. First pass CMRP was performed on a Philips Achieva CV 1.5 T MR scanner (Philips, The Netherlands), with standardised acquisition protocol with standard dose adenosine (SDA) at 140 µg/kg/min for 3 minutes. 3 short axis slices of 10 mm thickness were acquired per cardiac cycle using a single shot prospectively gated balanced TFE sequence (TR 2.5 ms, TE 1.3 ms, Flip angle 50° and voxel size 2.8 × 2.8 mm2) after the administration of a 0.1 mmol/Kg bolus of intravenous Gadolinium. Heart rate (HR) and blood pressure (BP) were recorded at baseline and during stress. Non responders were defined as those patients with a normal CMRP scan and blunted haemodynamic response (maximum HR increase <10 beats per minute and fall in systolic BP (SBP) <10 mmHg). CMRP in this group was then repeated with high dose adenosine (HDA) at 175 µg/kg/min for 3 minutes. CMRP images were interpreted by 2 independent experienced observers. Coronary angiographic data was analysed by an experienced interventionist who was blinded to the perfusion data. Results obtained at SDA and HDA (expressed as mean value value ± SD) were compared using the student t test.
Patient characteristics (n = 51)
62 ± 10.3
Known coronary artery disease
Haemodynamic response to adenosine stress (n = 51)
Systolic BP (mmHg)
136 ± 19
137 ± 23
133 ± 23
Heart rate (bpm)
68 ± 14
72 ± 16
82 ± 17 (P < 0.01)
Rate pressure product (bpm × mmHg/1000)
9.24 ± 2.4
9.89 ± 2.8
10.9 ± 2.5 (P < 0.01)
HDA achieved significant haemodynamic end-points with no significant clinical adverse events. Additional perfusion defects in the non responders at SDA were found using HDA. The perfusion defects correlated with significant coronary stenoses. The use of HDA may be important in certain patients where there is little or no haemodynamic response to SDA.
This article is published under license to BioMed Central Ltd.