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      Impact of caffeine on myocardial perfusion reserve assessed by semiquantitative adenosine stress perfusion cardiovascular magnetic resonance

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          Abstract

          Background

          Adenosine is used in stress perfusion cardiac imaging to reveal myocardial ischemia by its vasodilator effects. Caffeine is a competitive antagonist of adenosine. However, previous studies reported inconsistent results about the influence of caffeine on adenosine's vasodilator effect. This study assessed the impact of caffeine on the myocardial perfusion reserve index (MPRI) using adenosine stress cardiovascular magnetic resonance imaging (CMR). Moreover, we sought to evaluate if the splenic switch-off sign might be indicative of prior caffeine consumption.

          Methods

          Semiquantitative perfusion analysis was performed in 25 patients who underwent: 1) caffeine-naïve adenosine stress CMR demonstrating myocardial ischemia and, 2) repeat adenosine stress CMR after intake of caffeine. MPRI (global; remote and ischemic segments), and splenic perfusion ratio (SPR) were assessed and compared between both exams.

          Results

          Global MPRI after caffeine was lower vs. caffeine-naïve conditions (1.09 ± 0.19 vs. 1.24 ± 0.19; p <  0.01). MPRI in remote myocardium decreased by caffeine (1.24 ± 0.19 vs. 1.49 ± 0.19; p <  0.001) whereas MPRI in ischemic segments (0.89 ± 0.18 vs. 0.95 ± 0.23; p = 0.23) was similar, resulting in a lower MPRI ratio (=remote/ischemic segments) after caffeine consumption vs. caffeine-naïve conditions (1.41 ± 0.19 vs. 1.64 ± 0.35, p = 0.01). The SPR was unaffected by caffeine (SPR 0.38 ± 0.19 vs. 0.38 ± 0.18; p = 0.92).

          Conclusion

          Caffeine consumption prior to adenosine stress CMR results in a lower global MPRI, which is driven by the decreased MPRI in remote myocardium and underlines the need of abstinence from caffeine. The splenic switch-off sign is not affected by prior caffeine intake.

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          Most cited references 32

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          Magnetic resonance perfusion measurements for the noninvasive detection of coronary artery disease.

          With MRI, an index of myocardial perfusion reserve (MPRI) can be determined. We assessed the value of this technique for the noninvasive detection of coronary artery disease (CAD) in patients with suspected CAD. Eighty-four patients referred for a primary diagnostic coronary angiography were examined with a 1.5 T MRI tomograph (Philips-ACS). For each heartbeat, 5 slices were acquired during the first pass of 0.025 mmol gadolinium-diethylenetriamine pentaacetic acid/kg body weight before and during adenosine vasodilation by using a turbo-gradient echo/echo-planar imaging-hybrid sequence. MPRI was determined from the alteration of the upslope of the myocardial signal intensity curves for 6 equiangular segments per slice. Receiver operating characteristics were performed for different criteria to differentiate ischemic and nonischemic segments. Prevalence of CAD was 51%. Best results were achieved when only the 3 inner slices were assessed and a threshold value of 1.1 was used for the second smallest value as a marker for significant CAD. This approach yielded a sensitivity of 88%, specificity of 90%, and accuracy of 89%. The determination of MPRI with MRI yields a high diagnostic accuracy in patients with suspected CAD.
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            Improved detection of coronary artery disease by stress perfusion cardiovascular magnetic resonance with the use of delayed enhancement infarction imaging.

            We tested a pre-defined visual interpretation algorithm that combines cardiovascular magnetic resonance (CMR) data from perfusion and infarction imaging for the diagnosis of coronary artery disease (CAD). Cardiovascular magnetic resonance can assess both myocardial perfusion and infarction with independent techniques in a single session. We prospectively enrolled 100 consecutive patients with suspected CAD scheduled for X-ray coronary angiography. Patients had comprehensive clinical evaluation, including Rose angina questionnaire, 12-lead electrocardiography, C-reactive protein, and calculation of Framingham risk. Cardiovascular magnetic resonance included cine, adenosine-stress and rest perfusion-CMR, and delayed enhancement-CMR (DE-CMR) for infarction imaging. Matched stress-rest perfusion defects in the absence of infarction by DE-CMR were considered artifactual. All patients underwent X-ray angiography within 24 h of CMR. Ninety-two patients had complete CMR examinations. Significant CAD (> or =70% stenosis) was found in 37 patients (40%). The combination of perfusion and DE-CMR had a sensitivity, specificity, and accuracy of 89%, 87%, and 88%, respectively, for CAD diagnosis, compared with 84%, 58%, and 68%, respectively, for perfusion-CMR alone. The combination had higher specificity and accuracy (p < 0.0001), owing to incorporating the exceptionally high specificity (98%) of DE-CMR. Receiver operating characteristic curve analysis demonstrated the combination provided better performance than cine, perfusion, or DE-CMR alone. The accuracy was high in single-vessel and multivessel disease and independent of CAD location. Multivariable analysis including standard clinical parameters demonstrated the combination was the strongest independent CAD predictor. A combined perfusion and infarction CMR examination with a visual interpretation algorithm can accurately diagnose CAD in the clinical setting. The combination is superior to perfusion-CMR alone.
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              High-resolution magnetic resonance myocardial perfusion imaging at 3.0-Tesla to detect hemodynamically significant coronary stenoses as determined by fractional flow reserve.

              The objective of this study was to compare visual and quantitative analysis of high spatial resolution cardiac magnetic resonance (CMR) perfusion at 3.0-T against invasively determined fractional flow reserve (FFR). High spatial resolution CMR myocardial perfusion imaging for the detection of coronary artery disease (CAD) has recently been proposed but requires further clinical validation. Forty-two patients (33 men, age 57.4 ± 9.6 years) with known or suspected CAD underwent rest and adenosine-stress k-space and time sensitivity encoding accelerated perfusion CMR at 3.0-T achieving in-plane spatial resolution of 1.2 × 1.2 mm(2). The FFR was measured in all vessels with >50% severity stenosis. Fractional flow reserve <0.75 was considered hemodynamically significant. Two blinded observers visually interpreted the CMR data. Separately, myocardial perfusion reserve (MPR) was estimated using Fermi-constrained deconvolution. Of 126 coronary vessels, 52 underwent pressure wire assessment. Of these, 27 lesions had an FFR <0.75. Sensitivity and specificity of visual CMR analysis to detect stenoses at a threshold of FFR <0.75 were 0.82 and 0.94 (p < 0.0001), respectively, with an area under the receiver-operator characteristic curve of 0.92 (p < 0.0001). From quantitative analysis, the optimum MPR to detect such lesions was 1.58, with a sensitivity of 0.80, specificity of 0.89 (p < 0.0001), and area under the curve of 0.89 (p < 0.0001). High-resolution CMR MPR at 3.0-T can be used to detect flow-limiting CAD as defined by FFR, using both visual and quantitative analyses. Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Andreas.seitz@rbk.de
                Philipp.kaesemann@rbk.de
                Maria.chatzitofi@rbk.de
                Stephanie.loebig@rbk.de
                Gloria.tauscher@rbk.de
                Raffi.bekeredjian@rbk.de
                Udo.sechtem@rbk.de
                Heiko.mahrholdt@rbk.de
                Simon.greulich@med.uni-tuebingen.de
                Journal
                J Cardiovasc Magn Reson
                J Cardiovasc Magn Reson
                Journal of Cardiovascular Magnetic Resonance
                BioMed Central (London )
                1097-6647
                1532-429X
                24 June 2019
                24 June 2019
                2019
                : 21
                Affiliations
                [1 ]ISNI 0000 0004 0603 4965, GRID grid.416008.b, Department of Cardiology, Robert Bosch Medical Center, ; Auerbachstraße 110, 70376 Stuttgart, Germany
                [2 ]ISNI 0000 0001 0196 8249, GRID grid.411544.1, Department of Cardiology and Angiology, , University Hospital Tübingen, ; Tübingen, Germany
                Article
                542
                10.1186/s12968-019-0542-7
                6589875
                31230593
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001646, Robert Bosch Stiftung;
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

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