Fredrika Fröjdh1, Yaron Fridman2, Patrick Bering3, Aatif Sayeed3, Maren Maanja1, Louise Niklasson1, Eric Olausson1, Hongyang Pi3, Ali Azeem3, Timothy C Wong4, Peter Kellman5, Brian Feingold6, Adam Christopher7, Miho Fukui8, João L Cavalcante8, Christopher A Miller9, Javed Butler10, Martin Ugander11, Erik B Schelbert12. 1. Department of Clinical Physiology, Karolinska University Hospital, and Karolinska Institutet, Stockholm, Sweden. 2. Asheville Cardiology Associates, Mission Hospital, Asheville, North Carolina. 3. UPMC Cardiovascular Magnetic Resonance Center, UPMC, Pittsburgh, Pennsylvania. 4. UPMC Cardiovascular Magnetic Resonance Center, UPMC, Pittsburgh, Pennsylvania; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Heart and Vascular Institute, UPMC, Pittsburgh, Pennsylvania; Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, Pennsylvania. 5. National Heart Lung and Blood Institute, Bethesda, Maryland. 6. Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. 7. Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. 8. Minneapolis Heart Institute, Abbott Northwestern Hospital, Minneapolis, Minnesota. 9. Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom; Manchester University NHS Foundation Trust, Wythenshawe, Manchester, United Kingdom; Wellcome Centre for Cell-Matrix Research, Division of Cell-Matrix Biology & Regenerative Medicine, School of Biology, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom. 10. Department of Medicine, University of Mississippi, Jackson, Mississippi. 11. Department of Clinical Physiology, Karolinska University Hospital, and Karolinska Institutet, Stockholm, Sweden; Kolling Institute, Royal North Shore Hospital, and Sydney Medical School, Northern Clinical School, University of Sydney, Sydney, Australia. 12. UPMC Cardiovascular Magnetic Resonance Center, UPMC, Pittsburgh, Pennsylvania; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Heart and Vascular Institute, UPMC, Pittsburgh, Pennsylvania; Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, Pennsylvania. Electronic address: schelberteb@upmc.edu.
Abstract
OBJECTIVES: This study examined how extracellular volume (ECV) and global longitudinal strain (GLS) relate to each other and to outcomes. BACKGROUND: Among myriad changes occurring in diseased myocardium, left ventricular imaging metrics of either the interstitium (e.g., ECV) or contractile function (e.g., GLS) may consistently associate with adverse outcomes yet correlate minimally with each other. This scenario suggests that ECV and GLS potentially represent distinct domains of cardiac vulnerability. METHODS: The study included 1,578 patients referred for cardiovascular magnetic resonance (CMR) without amyloidosis, and it quantified how ECV associated with GLS in linear regression models. ECV and GLS were then compared in their associations with incident outcomes (death and hospitalization for heart failure). RESULTS: ECV and GLS correlated minimally (R2 = 0.04). Over a median follow-up of 5.6 years, 339 patients experienced adverse events (149 hospitalizations for heart failure, 253 deaths, and 63 with both). GLS (univariable hazard ratio: 2.07 per 5% increment; 95% CI: 1.86 to 2.29) and ECV (univariable hazard ratio: 1.66 per 4% increment; 95% CI: 1.51 to 1.82) were principal variables associating with outcomes in univariable and multivariable Cox regression models. Similar results were observed in several clinically important subgroups. In the whole cohort, ECV added prognostic value beyond GLS in univariable and multivariable Cox regression models. CONCLUSIONS: GLS and ECV may represent principal but distinct domains of cardiac vulnerability, perhaps reflecting their distinct cellular origins. Whether combining ECV and GLS may advance pathophysiological understanding for a given patient, optimize risk stratification, and foster personalized medicine by targeted therapeutics requires further investigation.
OBJECTIVES: This study examined how extracellular volume (ECV) and global longitudinal strain (GLS) relate to each other and to outcomes. BACKGROUND: Among myriad changes occurring in diseased myocardium, left ventricular imaging metrics of either the interstitium (e.g., ECV) or contractile function (e.g., GLS) may consistently associate with adverse outcomes yet correlate minimally with each other. This scenario suggests that ECV and GLS potentially represent distinct domains of cardiac vulnerability. METHODS: The study included 1,578 patients referred for cardiovascular magnetic resonance (CMR) without amyloidosis, and it quantified how ECV associated with GLS in linear regression models. ECV and GLS were then compared in their associations with incident outcomes (death and hospitalization for heart failure). RESULTS: ECV and GLS correlated minimally (R2 = 0.04). Over a median follow-up of 5.6 years, 339 patients experienced adverse events (149 hospitalizations for heart failure, 253 deaths, and 63 with both). GLS (univariable hazard ratio: 2.07 per 5% increment; 95% CI: 1.86 to 2.29) and ECV (univariable hazard ratio: 1.66 per 4% increment; 95% CI: 1.51 to 1.82) were principal variables associating with outcomes in univariable and multivariable Cox regression models. Similar results were observed in several clinically important subgroups. In the whole cohort, ECV added prognostic value beyond GLS in univariable and multivariable Cox regression models. CONCLUSIONS: GLS and ECV may represent principal but distinct domains of cardiac vulnerability, perhaps reflecting their distinct cellular origins. Whether combining ECV and GLS may advance pathophysiological understanding for a given patient, optimize risk stratification, and foster personalized medicine by targeted therapeutics requires further investigation.
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