AUTHOR=Spicher Barbara , Fischer Kady , Zimmerli Zoe A. , Yamaji Kyohei , Ueki Yasushi , Bertschinger Carina N. , Jung Bernd , Otsuka Tatsuhiko , Bigler Marius R. , Gräni Christoph , von Tengg-Kobligk Hendrik , Räber Lorenz , Eberle Balthasar , Guensch Dominik P. 

TITLE=Combined Analysis of Myocardial Deformation and Oxygenation Detects Inducible Ischemia Unmasked by Breathing Maneuvers in Chronic Coronary Syndrome

JOURNAL=Frontiers in Cardiovascular Medicine

VOLUME=9

YEAR=2022

URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2022.800720

DOI=10.3389/fcvm.2022.800720

ISSN=2297-055X

ABSTRACT=<sec><title>Introduction</title><p>In patients with chronic coronary syndromes, hyperventilation followed by apnea has been shown to unmask myocardium susceptible to inducible deoxygenation. The aim of this study was to assess whether such a provoked response is co-localized with myocardial dysfunction.</p></sec><sec><title>Methods</title><p>A group of twenty-six CAD patients with a defined stenosis (quantitative coronary angiography &gt; 50%) underwent a cardiovascular magnetic resonance (CMR) exam prior to revascularization. Healthy volunteers older than 50 years served as controls (<italic>n</italic> = 12). Participants hyperventilated for 60s followed by brief apnea. Oxygenation-sensitive images were analyzed for changes in myocardial oxygenation and strain.</p></sec><sec><title>Results</title><p>In healthy subjects, hyperventilation resulted in global myocardial deoxygenation (-10.2 ± 8.2%, <italic>p</italic> &lt; 0.001) and augmented peak circumferential systolic strain (-3.3 ± 1.6%, <italic>p</italic> &lt; 0.001). At the end of apnea, myocardial signal intensity had increased (+9.1 ± 5.3%, <italic>p</italic> &lt; 0.001) and strain had normalized to baseline. CAD patients had a similar global oxygenation response to hyperventilation (−5.8 ± 9.6%, <italic>p</italic> = 0.085) but showed no change in peak strain from their resting state (-1.3 ± 1.6%), which was significantly attenuated in comparison the strain response observed in controls (<italic>p</italic> = 0.008). With apnea, the CAD patients showed an attenuated global oxygenation response to apnea compared to controls (+2.7 ± 6.2%, <italic>p</italic> &lt; 0.001). This was accompanied by a significant depression of peak strain (3.0 ± 1.7%, <italic>p</italic> &lt; 0.001), which also differed from the control response (<italic>p</italic> = 0.025). Regional analysis demonstrated that post-stenotic myocardium was most susceptible to de-oxygenation and systolic strain abnormalities during respiratory maneuvers. CMR measures at rest were unable to discriminate post-stenotic territory (<italic>p</italic> &gt;  0.05), yet this was significant for both myocardial oxygenation [area under the curve (AUC): 0.88, <italic>p</italic> &gt;  0.001] and peak strain (AUC: 0.73, <italic>p</italic> = 0.023) measured with apnea. A combined analysis of myocardial oxygenation and peak strain resulted in an incrementally higher AUC of 0.91, <italic>p</italic> &lt; 0.001 than strain alone.</p></sec><sec><title>Conclusion</title><p>In myocardium of patients with chronic coronary syndromes and primarily intermediate coronary stenoses, cine oxygenation-sensitive CMR can identify an impaired vascular and functional response to a vasoactive breathing maneuver stimulus indicative of inducible ischemia.</p></sec>