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Background Analysis of left ventricular (LV) mechanical dyssynchrony may provide incremental prognostic information regarding cardiac resynchronization therapy (CRT) response in addition to QRS width alone. Our objective was to quantify LV dyssynchrony using feature tracking post processing of routine cardiovascular magnetic resonance (CMR) cine acquisitions (FT-CMR) in comparison to speckle tracking echocardiography. Methods We studied 72 consecutive patients who had both steady-state free precession CMR and echocardiography. Mid-LV short axis CMR cines were analyzed using FT-CMR software and compared with echocardiographic speckle tracking radial dyssynchrony (time difference between the anteroseptal and posterior wall peak strain). Results Radial dyssynchrony analysis was possible by FT-CMR in all patients, and in 67 (93%) by echocardiography. Dyssynchrony by FT-CMR and speckle tracking showed limits of agreement of strain delays of ±84 ms. These were large (up to 100% or more) relative to the small mean delays measured in more synchronous patients, but acceptable (mainly <25%) in those with mean delays of >200 ms. Radial dyssynchrony was significantly greater in wide QRS patients than narrow QRS patients by both FT-CMR (radial strain delay 230 ± 94 vs. 77 ± 92* ms) and speckle tracking (radial strain delay 242 ± 101 vs. 75 ± 88* ms, all *p < 0.001). Conclusions FT-CMR delivered measurements of radial dyssynchrony from CMR cine acquisitions which, at least for the patients with more marked dyssynchrony, showed reasonable agreement with those from speckle tracking echocardiography. The clinical usefulness of the method, for example in predicting prognosis in CRT patients, remains to be investigated. [ABSTRACT FROM AUTHOR]

An abstract on cardiac magnetic resonance (CMR) insights on the association of the right ventricular systolic dysfunction in patients with severe ischemic cardiomyopathy is presented.

An abstract regarding the prediction of diastolic dysfunction in advanced ischemic cardiomyopathy beyond ejection fraction cardiac magnetic resonance (CMR) assessment is presented.

Background: Heart failure (HF) most commonly occurs in patients who have had a myocardial infarction (MI), but factors other than MI size may be deterministic. Fibrosis of myocardium remote from the MI is associated with adverse remodeling. We aimed to 1) investigate the association between remote myocardial fibrosis, measured using cardiovascular magnetic resonance (CMR) extracellular volume fraction (ECV), and HF and death following MI, 2) identify predictors of remote myocardial fibrosis in patients with evidence of MI and determine the relationship with infarct size., Methods: Multicenter prospective cohort study of 1199 consecutive patients undergoing CMR with evidence of MI on late gadolinium enhancement. Median follow-up was 1133 (895-1442) days. Cox proportional hazards modeling was used to identify factors predictive of the primary outcome, a composite of first hospitalization for HF (HHF) or all-cause mortality, post-CMR. Linear regression modeling was used to identify determinants of remote ECV., Results: Remote myocardial fibrosis was a strong predictor of primary outcome (χ 2 : 15.6, hazard ratio [HR]: 1.07 per 1% increase in ECV, 95% confidence interval [CI]: 1.04-1.11, p < 0.001) and was separately predictive of both HHF and death. The strongest predictors of remote ECV were diabetes, sex, natriuretic peptides, and body mass index, but, despite extensive phenotyping, the adjusted model R 2 was only 0.283. The relationship between infarct size and remote fibrosis was very weak., Conclusion: Myocardial fibrosis, measured using CMR ECV, is a strong predictor of HHF and death in patients with evidence of MI. The mechanisms underlying remote myocardial fibrosis formation post-MI remain poorly understood, but factors other than infarct size appear to be important., Competing Interests: Declaration of competing interests The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Christopher Miller reports financial support was provided by National Institute for Health and Care Research. Christopher Miller reports financial support was provided by Guerbet. Christopher Miller reports equipment, drugs, or supplies were provided by Roche. Christopher Miller reports financial support was provided by British Heart Foundation. Christopher Miller reports a relationship with HAYA therapeutics that includes consulting or advisory, PureTech Health that includes consulting or advisory, Amicus Therapeutics Inc that includes funding grants, Roche that includes funding grants, Univar Solutions that includes funding grants, Novartis that includes consulting or advisory, Boehringer Ingelheim Ltd that includes consulting or advisory, Lilly Alliance that includes consulting or advisory, and AstraZeneca PLC that includes consulting or advisory. Erik Schelbert reports a relationship with HAYA therapeutics that includes consulting or advisory, PureTech Health that includes consulting or advisory, and Amicus Therapeutics Inc that includes funding grants and travel reimbursement. Joao L. Cavalcante reports a relationship with Abbott Vascular Inc that includes consulting or advisory and funding grants, Boston Scientific Corp that includes consulting or advisory and funding grants, Edwards Lifesciences Corporation that includes consulting or advisory and funding grants, Medtronic that includes consulting or advisory and funding grants, WL Gore and Associates that includes consulting or advisory and funding grants, Circle Cardiovascular Imaging Inc that includes funding grants, Siemens Healthineers that includes funding grants, 3Mension that includes funding grants, Medis that includes funding grants, and Ziosoft that includes funding grants. Theresa McDonagh reports a relationship with Novartis that includes speaking and lecture fees, AstraZeneca Pharmaceuticals LP that includes speaking and lecture fees, and Vifor Pharma Ltd that includes speaking and lecture fees. Fredrika Fröjdh and Martin Ugander were supported in part by grants from the Swedish Research Council, Swedish Heart and Lung Foundation, Stockholm County Council, and Karolinska Institutet. Martin Ugander is the principal investigator on a research and development agreement regarding cardiovascular magnetic resonance between Siemens and Karolinska University Hospital. Timothy C. Wong was supported by an American Heart Association Scientist Development grant and a Children’s Cardiomyopathy Foundation grant. Josephine Naish has a part-time appointment at Bioxydyn Ltd. The remaining authors have nothing to disclose. The other authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)