Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41384329&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Diffusion Tensor CMR Assessment of the Microstructural Response to Dobutamine Stress in Health and Comparison With Patients With Recovered Dilated Cardiomyopathy #MMPMID41384329
Khalique Z; Scott AD; Ferreira PF; Molto M; Nielles-Vallespin S; Pennell DJ
Circ Cardiovasc Imaging 2025[Dec]; ? (?): e018226 PMID41384329show ga
BACKGROUND: Contractile reserve assessment assesses myocardial performance and prognosis. The microstructural mechanisms that facilitate increased cardiac function have not been described, but can be studied using diffusion tensor cardiovascular magnetic resonance. Resting microstructural contractile function is characterized by reorientation of aggregated cardiomyocytes (sheetlets) from wall-parallel in diastole to a more wall-perpendicular configuration in systole, with the diffusion tensor cardiovascular magnetic resonance parameter E2A defining their orientation, and sheetlet mobility defining the angle through which they rotate. We used diffusion tensor cardiovascular magnetic resonance to identify the microstructural response to dobutamine stress in healthy volunteers and then compared with patients with recovered dilated cardiomyopathy (rDCM). METHODS: In this first-of-its-kind prospective observational study, 20 healthy volunteers and 32 patients with rDCM underwent diffusion tensor cardiovascular magnetic resonance at rest, during dobutamine, and on recovery. RESULTS: In healthy volunteers, both diastolic and systolic E2A increased with dobutamine stress (13+/-3 degrees to 17+/-5 degrees ; P<0.001 and 59+/-11 degrees to 65+/-7 degrees ; P=0.002). Sheetlet mobility remained unchanged (45+/-11 degrees to 49+/-10 degrees ; P=0.19), but biphasic mean E2A increased (36+/-6 degrees to 41+/-4 degrees ; P<0.001). In rDCM, diastolic E2A at rest was higher than in healthy volunteers (20+/-8 degrees versus 13+/-3 degrees , P<0.001), and sheetlet mobility was reduced (34+/-12 degrees versus 45+/-11 degrees ; P<0.001). During dobutamine stress, rDCM diastolic and systolic E2A increased compared with rest (20+/-8 degrees to 24+/-10 degrees ; P=0.001 and 54+/-13 degrees to 63+/-11 degrees ; P=0.005). However, sheetlet mobility in patients with rDCM failed to increase with dobutamine to healthy levels (39+/-13 degrees versus 49+/-10 degrees ; P=0.005). CONCLUSIONS: This is the first report describing how the myocardial microstructure facilitates cardiac reserve. In health, sheetlet mobility moves further toward the wall-perpendicular plane to drive increased contractility, rather than increased magnitude of sheetlet mobility. Despite clinical recovery in patients with rDCM, microstructural function at rest and during dobutamine remains impaired. Further understanding of microstructural remodeling at rest and during stress may help refine risk stratification of patients with rDCM at risk of relapse.