It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Cardiac magnetic resonance (CMR) is emerging as an important tool in the assessment of heart failure with preserved ejection fraction (HFpEF). This study sought to investigate the prognostic value of multiparametric CMR, including left and right heart volumetric assessment, native T1-mapping and LGE in HFpEF. In this retrospective study, we identified patients with HFpEF who have undergone CMR. CMR protocol included: cines, native T1-mapping and late gadolinium enhancement (LGE). The mean follow-up period was 3.2 ± 2.4 years. We identified 86 patients with HFpEF who had CMR. Of the 86 patients (85% hypertensive; 61% males; 14% cardiac amyloidosis), 27 (31%) patients died during the follow up period. From all the CMR metrics, LV mass (area under curve [AUC] 0.66, SE 0.07, 95% CI 0.54–0.76, p = 0.02), LGE fibrosis (AUC 0.59, SE 0.15, 95% CI 0.41–0.75, p = 0.03) and native T1-values (AUC 0.76, SE 0.09, 95% CI 0.58–0.88, p < 0.01) were the strongest predictors of all-cause mortality. The optimum thresholds for these were: LV mass > 133.24 g (hazard ratio [HR] 1.58, 95% CI 1.1–2.2, p < 0.01); LGE-fibrosis > 34.86% (HR 1.77, 95% CI 1.1–2.8, p = 0.01) and native T1 > 1056.42 ms (HR 2.36, 95% CI 0.9–6.4, p = 0.07). In multivariate cox regression, CMR score model comprising these three variables independently predicted mortality in HFpEF when compared to NTproBNP (HR 4 vs HR 1.65). In non-amyloid HFpEF cases, only native T1 > 1056.42 ms demonstrated higher mortality (AUC 0.833, p < 0.01). In patients with HFpEF, multiparametric CMR aids prognostication. Our results show that left ventricular fibrosis and hypertrophy quantified by CMR are associated with all-cause mortality in patients with HFpEF.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details


1 University of Sheffield, Department of Infection, Immunity and Cardiovascular Disease, Sheffield, UK (GRID:grid.11835.3e) (ISNI:0000 0004 1936 9262); Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, UK (GRID:grid.451052.7) (ISNI:0000 0004 0581 2008); University of East Anglia, Norwich Medical School, Norwich, UK (GRID:grid.8273.e) (ISNI:0000 0001 1092 7967)
2 University of Sheffield, Department of Infection, Immunity and Cardiovascular Disease, Sheffield, UK (GRID:grid.11835.3e) (ISNI:0000 0004 1936 9262)
3 Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, UK (GRID:grid.451052.7) (ISNI:0000 0004 0581 2008)
4 Leiden University Medical Centre, Leiden, The Netherlands (GRID:grid.10419.3d) (ISNI:0000000089452978)
5 University of Sheffield, Department of Infection, Immunity and Cardiovascular Disease, Sheffield, UK (GRID:grid.11835.3e) (ISNI:0000 0004 1936 9262); Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, UK (GRID:grid.451052.7) (ISNI:0000 0004 0581 2008)