Abstract
Objectives
We aimed to determine the long-term prognostic significance of global longitudinal strain (GLS) assessed using cardiovascular magnetic resonance feature tracking (CMR-FT) in a large cohort of heart transplant recipients.
Background
In heart transplant recipients, GLS assessed using echocardiography has shown promise in the prediction of clinical outcomes. We hypothesized that CMR-FT GLS is independently associated with long-term outcomes in heart transplant recipients.
Methods
In a cohort of consecutive heart transplant recipients that underwent routine CMRs for clinical surveillance, CMR-FT GLS was calculated from three long-axis cine CMR images. We investigated associations between GLS and a composite endpoint of death or major adverse cardiac events (MACE): retransplantation, non-fatal myocardial infarction, coronary revascularization, and heart failure hospitalization.
Results
One hundred and fifty-two heart transplant recipients (age 54±15 years; 29% women; 5.0±5.4 years after heart transplantation) were included. The median GLS was −11.5% (IQR −13.6%, −9.2%). Over a median follow-up of 2.6 years, 59 recipients reached the composite endpoint. On Kaplan-Meier analyses, recipients with GLS worse than the median had a higher estimated cumulative incidence of the composite endpoint compared with recipients with GLS better than the median (log-rank p=0.004). On multivariable Cox proportional hazards regression, GLS was independently associated with the composite endpoint after adjustment for cardiac allograft vasculopathy, history of rejection, left ventricular ejection fraction (LVEF), right ventricular EF, and presence of myocardial fibrosis, with a hazard ratio of 1.15 for every 1% worsening in GLS (95% CI 1.06-1.24; p<0.001). Similar results were seen in subgroups of recipients with LVEF>50% and with no myocardial fibrosis. GLS provided incremental prognostic value over other variables in the multivariable model as determined by the log-likelihood chi-square test.
Conclusions
In a large cohort of heart transplant recipients, CMR-FT GLS was independently associated with the long-term risk of death or MACE.
Keywords: Heart transplantation, prognosis, strain, cardiac magnetic resonance imaging
INTRODUCTION
In appropriately selected patients, heart transplantation improves survival and provides a favorable quality of life (1). Heart transplantation outcomes have significantly improved because of advances in immunosuppressive therapy and the management of complications. However, cardiac allograft vasculopathy (CAV) and allograft failure continue to be frequent causes of late morbidity, death, and retransplantation (1).
In recent years, assessment of myocardial mechanics using echocardiographic strain imaging has shown promise in the prediction of clinical outcomes in heart transplant recipients (2–7). Cardiovascular magnetic resonance imaging (CMR) is increasingly used in heart transplant recipients because of its ability to characterize myocardial tissue, particularly the detection of myocardial fibrosis using late gadolinium enhancement (LGE). Recent developments in CMR feature tracking (CMR-FT) techniques now allow the assessment of strain using standard cine CMR images with no specialized pulse sequences or complex post-processing (8). CMR-FT-derived global longitudinal strain (GLS) has been shown to have prognostic value in patients with ischemic and non-ischemic cardiomyopathies incremental to left ventricular ejection fraction (LVEF) and LGE (9,10).
Whether CMR-FT GLS is independently associated with long-term adverse cardiac outcomes in heart transplant recipients has not been studied. We, therefore, sought to determine the independent prognostic significance of CMR-FT GLS in a large consecutive cohort of heart transplant recipients with long-term follow-up. We hypothesized that CMR-FT GLS is associated with a higher risk of long-term cardiovascular events after heart transplantation.
METHODS
Patients
We included consecutive adult heart transplant recipients who had CMR performed for surveillance between January 2004 and December 2017 at the University of Minnesota, Minneapolis, Minnesota, USA. To identify the study patients, the institutional heart transplant database was cross-matched with the University of Minnesota Cardiovascular Magnetic Resonance Registry (11–15). For recipients with multiple CMRs, the earliest one was included. This retrospective cohort study was approved by the University of Minnesota’s Institutional Review Board with a waiver of informed consent.
Baseline Measures
We collected demographic data, medical history, co-morbidities, and outcomes data blinded to CMR data. CAV and rejection were defined according to the International Society for Heart and Lung Transplantation (ISHLT)’s recommended nomenclature (16,17).
CMR Protocol
CMR was performed on clinical 1.5T Siemens scanners (Avanto or Aera) using phased-array receiver coils, according to standard recommendations. A typical protocol included steady-state free precession cine CMR images acquired in the short-axis (every 10 mm to cover the entire left ventricle (LV) from the mitral valve plane through the apex) and three long-axis views (two-, three-, and four-chamber). Typical cine CMR parameters were repetition time of 3.0–3.5 ms, echo time of 1.2–1.5 ms, in-plane spatial resolution of 1.8 x 1.4 mm, temporal resolution of 35–40 ms. Standard LGE CMR imaging was performed 10-15 minutes after administration of gadolinium contrast (0.15 mmol/kg), using a two-dimensional segmented inversion-recovery gradient-echo sequence in identical views as cine CMR imaging. Typical LGE CMR parameters were inversion time set to null viable myocardium, typically 280–360 ms, in-plane spatial resolution of 1.8 x 1.5 mm, temporal resolution of 180–200 ms, and slice thickness of 6 mm. The same CMR protocol was used during the entire study period.
CMR Analyses
CMRs were re-interpreted and analyzed for this study, blinded to all other patient data. LV and right ventricular (RV) ejection fractions (LVEF and RVEF) were determined by quantitative analysis according to standard recommendations(18). For CMR-FT analysis, a single expert physician blinded to all other patient data manually traced the LV endo- and epicardial borders at end-diastole in all three long-axis cine-views (two-chamber, three-chamber, and four-chamber) to derive GLS using Segment CMR software (Medviso AB, Lund, Sweden) (Figure 1). The GLS value was provided by the software by integrating data from all three long-axis views in every patient (19). End-diastole was identified as the frame just before the closure of the mitral valve. For LGE analysis, the investigators first identified the presence or absence of focal myocardial fibrosis based on visual assessment. For those with myocardial fibrosis, the extent was quantified using the full-width-at-half-maximum method and expressed as a percentage of the LV myocardial mass (18,20).
Figure 1. Measurement of CMR-FT GLS.
Endo- and epicardial LV contours were manually traced in all three long-axis cine views to derive GLS. GLS in this recipient was −15.3%.
Clinical Follow-up and Outcomes
Follow-up data were collected through a review of electronic medical records blinded to CMR data. The pre-specified primary endpoint was a composite of all-cause death or major adverse cardiac events (MACE) – retransplantation, non-fatal myocardial infarction, coronary revascularization, or heart failure hospitalization – during follow-up. Myocardial infarction was defined according to the Fourth Universal Definition of Myocardial Infarction (21). Mortality status and death dates were cross-checked with the Minnesota Department of Health’s Office of Vital Records.
Statistical Analysis
Normally distributed continuous variables were expressed as mean ± standard deviation (SD), and non-normally distributed continuous variables were presented as medians with interquartile range (IQR). Categorical variables were expressed as counts with percentages. Comparison between groups was performed with a 2-sample Student t test for continuous, normal variables, and Mann-Whitney rank-sum test for continuous, non-normal data. Pearson chi-square tests were used to compare discrete data between groups; in those cases where the expected cell count was <5, Fisher exact test was used. Intra-observer variability for GLS was assessed in a random sample of 30 patients. Kaplan–Meier analyses and unadjusted and adjusted Cox proportional hazards regression analyses were used to assess relationships between clinical and imaging variables, and all-cause death or MACE. The assumption of proportional hazards was assessed by plotting the scaled Schoenfeld residuals for each independent variable against time; these correlations were nonsignificant for all variables included in the multivariable models. To test the incremental prognostic value of GLS, the final model was compared with a model in which GLS was not included, using the likelihood ratio test. All tests were two-tailed. A p value of <0.05 was used to denote statistical significance. Analyses were performed using R version 3.4 (R Foundation for Statistical Computing).
RESULTS
Overall Patient Characteristics
Table 1 lists the patient characteristics at the time of the index CMR. One hundred and fifty-two heart transplant recipients were included in the study. The mean time from cardiac transplant to CMR was 5.0 years, and the median was 3.1 years. Comorbidities were common (62% hypertension, 35% diabetes mellitus, and 42% chronic kidney disease [glomerular filtration rate <60 mL/min per 1.73 m2]). Thirty-two percent had CAV, and 32% had a history of either ISHLT grade 2R or 3R cellular, or antibody-mediated rejection. Mycophenolate mofetil and tacrolimus were commonly used among the varied immunosuppression regimens. Aspirin and statins were also frequently used.
Table 1.
Patient characteristics at the time of CMR for all recipients, and stratified using median GLS
| All recipients (n = 152) | GLS worse than median (n = 76) | GLS better than median (n = 76) | p value | |
|---|---|---|---|---|
| Demographics | ||||
| Age, years (SD) | 54.2 (15.2) | 53.2 (14.8) | 55.3 (15.7) | 0.39 |
| Women, n (%) | 44 (28.9) | 18 (23.7) | 26 (34.2) | 0.15 |
| Time since transplantation, years (SD) | 5.0 (5.4) | 5.3 (5.2) | 4.8 (5.5) | 0.58 |
| Transplantation indication | ||||
| Ischemic cardiomyopathy, n (%) | 53 (34.9) | 32 (42.1) | 21 (27.6) | 0.06 |
| Comorbidities | ||||
| Body mass index, kg/m2 (IQR) | 26.6 (23.5, 30.2) | 26.5 (23.8, 29.6) | 26.7 (23.4, 30.9) | 0.97 |
| Hypertension, n (%) | 95 (62.5) | 52 (68.4) | 43 (56.6) | 0.13 |
| Diabetes mellitus, n (%) | 54 (35.5) | 30 (39.5) | 24 (31.6) | 0.31 |
| Chronic kidney disease (eGFR <60 mL/min per 1.73 m2), n (%) | 65 (42.8) | 34 (44.7) | 31 (40.8) | 0.62 |
| Ischemic time, minutes (SD) | 224.0 (61.5) | 231.2 (63.5) | 217.0 (59.0) | 0.16 |
| Cardiac allograft vasculopathy, n (%) | 48 (31.6) | 24 (31.6) | 24 (31.6) | 1.00 |
| History of ISHLT grade 2R or 3R cellular rejection or antibody-mediated rejection, n (%) | 48 (31.6) | 31 (40.8) | 17 (22.4) | 0.015 |
| Immunosuppressant medications | ||||
| Tacrolimus, n (%) | 114 (75.0) | 55 (72.4) | 59 (77.6) | 0.46 |
| Sirolimus/everolimus, n (%) | 28 (18.4) | 13 (17.1) | 15 (19.7) | 0.68 |
| Cyclosporine, n (%) | 26 (17.1) | 13 (17.1) | 13 (17.1) | 1.00 |
| Mycophenolate mofetil, n (%) | 123 (80.9) | 61 (80.3) | 62 (81.6) | 0.84 |
| Azathioprine, n (%) | 9 (5.9) | 4 (5.3) | 5 (6.6) | 0.73 |
| Prednisone, n (%) | 44 (28.9) | 23 (30.3) | 21 (27.6) | 0.72 |
| Other cardiac medications | ||||
| Aspirin, n (%) | 132 (86.8) | 67 (88.2) | 65 (85.5) | 0.63 |
| Statin, n (%) | 129 (84.9) | 62 (81.6) | 67 (88.2) | 0.26 |
| ACE-Inhibitor/ARB, n (%) | 69 (45.4) | 37 (48.7) | 32 (42.1) | 0.42 |
| Beta blocker, n (%) | 26 (17.1) | 18 (23.7) | 8 (10.5) | 0.032 |
| Calcium channel blocker, n (%) | 46 (30.3) | 22 (28.9) | 24 (31.6) | 0.72 |
| CMR findings | ||||
| LVEDVI, ml/m2 (IQR) | 53.8 (44.4, 61.8) | 52.2 (42.5, 59.3) | 56.1 (47.2, 62.8) | 0.020 |
| LVESVI, ml/m2 (IQR) | 22.3 (17.7, 27.8) | 23.4 (18.0, 30.6) | 22.0 (17.8, 26.1) | 0.30 |
| LVEF, % (IQR) | 56.4 (50.1, 62.2) | 53.0 (44.4, 58.9) | 59.0 (56.1, 63.3) | <0.001 |
| RVEDVI, ml/m2 (IQR) | 50.6 (44.3, 59.8) | 47.4 (39.6, 60.1) | 52.4 (46.5, 59.7) | 0.010 |
| RVESVI, ml/m2 (IQR) | 23.0 (18.2, 28.4) | 23.5 (17.6, 32.2) | 22.5 (18.8, 26.8) | 0.53 |
| RVEF, % (IQR) | 55.6 (47.0, 60.5) | 48.9 (41.9, 57.7) | 58.1 (53.8, 62.2) | <0.001 |
| Myocardial fibrosis presence, n% | 27 (17.8) | 19 (25.0) | 8 (10.5) | 0.020 |
| Myocardial fibrosis extent, % (SD) | 2.2 (6.2) | 3.6 (8.0) | 0.7 (3.0) | 0.004 |
ACE = angiotensin converting enzyme; ARB = angiotensin receptor blocker; CI = confidence interval; EDVI = end-diastolic volume index; eGFR = estimated glomerular filtration rate; EF = ejection fraction; ESVI = end-systolic volume index; ISHLT = International Society for Heart and Lung Transplantation; IQR = interquartile range; LV = left ventricle; RV = right ventricle; SD = standard deviation
CMR Findings
The median LVEFs and RVEFs were >55% (Table 1). The median GLS was −11.6% (IQR −13.6%, −9.2%). Bland-Altman analysis of intra-observer variability for GLS showed a bias of 0.05%. The 95% limits of agreement were −0.44 to 0.53%.
Recipients with GLS worse than the median were more likely to have a history of rejection, and use beta-blockers, compared with recipients with GLS better than the median. On CMR, recipients with GLS worse than the median were more likely to have lower LVEFs, lower RVEFs, and a higher prevalence of myocardial fibrosis, compared with recipients with GLS better than the median.
Myocardial fibrosis was detected in 27 (18%) recipients: infarct pattern (subendocardial or transmural) in 10 (37%), non-infarct pattern (mid-myocardial or subepicardial) in 11 (41%), and both in 6 (22%). The mean extent of the myocardial fibrosis was 12.2% and the median was 9.7%.
Association of GLS with All-cause Death or MACE
Follow-up data were available for all recipients. Fifty-nine (38.8%) recipients experienced all-cause death or MACE over a median follow-up of 2.6 years (IQR 1.3 to 5.2 years). The individual outcomes were death in 36 (23.7%), retransplantation in 7 (4.6%), non-fatal MI in 1 (0.7%), coronary revascularization in 17 (11.2%), and heart failure hospitalization in 28 (18.4%). Kaplan-Meier analyses stratified by the median GLS showed a significantly higher estimated cumulative incidence of all-cause death or MACE in recipients with GLS worse than the median, compared with recipients with GLS better than the median (log-rank p = 0.002; Figure 2).
Central Illustration. Kaplan-Meier cumulative incidence curves for all-cause death or MACE stratified by median GLS.
Cumulative incidence curves comparing all-cause death or MACE between heart transplant recipients with GLS worse than the median (orange) and GLS better than the median (green). The log-rank p was 0.002. Each vertical tick on the curves displays a censored patient.
In multivariable analyses (Table 2) including CAV, history of rejection, LVEF, RVEF, GLS as a continuous variable, and either myocardial fibrosis presence (Model 1) or myocardial fibrosis extent (Model 2), GLS was independently associated with all-cause death or MACE in both models. The hazard ratios were 1.15 (95% CI 1.06-1.24; p<0.001) and 1.14 (95% CI 1.05-1.24; p = 0.002) respectively, showing that the risk of all-cause death or MACE increased by 14-15% for every 1% worsening in GLS.
Table 2.
Cox multivariable proportional hazards modeling for death or MACE in all recipients (n = 152)
| Model 1* | Model 2† | |||
|---|---|---|---|---|
| Hazard Ratio (95% CI) | P value | Hazard Ratio (95% CI) | P value | |
| Cardiac allograft vasculopathy | 1.46 (0.80-2.65) | 0.22 | 1.59 (0.87-2.92) | 0.13 |
| History of ISHLT grade 2R or 3R cellular rejection or antibody-mediated rejection | 0.79 (0.44-1.42) | 0.43 | 0.75 (0.41-1.38) | 0.36 |
| LVEF, per 1% decrease | 0.98 (0.95-1.01) | 0.10 | 0.97 (0.94-1.00) | 0.07 |
| RVEF, per 1% decrease | 1.04 (1.01-1.08) | 0.007 | 1.04 (1.01-1.07) | 0.011 |
| Myocardial fibrosis presence | 2.15 (1.15-4.05) | 0.017 | - | - |
| Myocardial fibrosis extent, per 1% increase | - | - | 1.03 (0.99-1.06) | 0.13 |
| GLS worsening, per 1% worsening | 1.15 (1.06-1.24) | <0.001 | 1.14 (1.05-1.24) | 0.002 |
Model 1 included myocardial fibrosis presence as a binary variable.
Model 2 included myocardial fibrosis extent as a continuous variable.
Abbreviations as in Table 1.
Incremental Prognostic Value
The addition of GLS to a Cox model that included CAV, history of rejection, LVEF, RVEF, and either myocardial fibrosis presence or myocardial fibrosis extent resulted in a significantly improved model fit as assessed with the likelihood ratio test (p<0.001 for both comparisons).
Subgroup Analyses
In a subgroup analysis of recipients with LVEF>50% (n = 114) (Table 3), GLS was independently associated with all-cause death or MACE after adjustment for CAV, history of rejection, RVEF, and either myocardial fibrosis presence (Model 3) or myocardial fibrosis extent (Model 4) with hazard ratios of 1.20 (95% CI 1.09-1.31; p<0.001) and 1.19 (95% CI 1.07-1.33; p = 0.001) respectively.
Table 3.
Cox multivariable proportional hazards modeling for death or MACE in recipients with LVEF>50% (n = 114)
| Model 3* | Model 4† | |||
|---|---|---|---|---|
| Hazard Ratio (95% CI) | P value | Hazard Ratio (95% CI) | P value | |
| Cardiac allograft vasculopathy | 1.19 (0.54-2.65) | 0.67 | 1.35 (0.60-3.05) | 0.47 |
| History of ISHLT grade 2R or 3R cellular rejection or antibody-mediated rejection | 0.48 (0.22-1.06) | 0.07 | 0.46 (0.21-1.03) | 0.06 |
| RVEF, per 1% decrease | 1.07 (1.02-1.11) | 0.003 | 1.06 (1.02-1.11) | 0.005 |
| Myocardial fibrosis presence | 1.95 (0.84-4.53) | 0.12 | ||
| Myocardial fibrosis extent, per 1% increase | 1.02 (0.96-1.07) | 0.58 | ||
| GLS worsening, per 1% worsening | 1.20 (1.09-1.31) | <0.001 | 1.19 (1.07-1.33) | 0.001 |
Model 3 included myocardial fibrosis presence as a binary variable.
Model 4 included myocardial fibrosis extent as a continuous variable.
Abbreviations as in Table 1.
In a second subgroup analysis of recipients without myocardial fibrosis (n = 125) (Table 4), GLS was again independently associated with all-cause death or MACE after adjustment for CAV, history of rejection, LVEF, and RVEF, with a hazard ratio of 1.22 (95% CI 1.10-1.34; p<0.001).
Table 4.
Cox multivariable proportional hazards modeling for death or MACE in recipients with no myocardial fibrosis (n = 125)
| Hazard Ratio (95% CI) | P value | |
|---|---|---|
| Cardiac allograft vasculopathy | 1.46 (0.66-3.25) | 0.35 |
| History of ISHLT grade 2R or 3R cellular rejection or antibody-mediated rejection | 0.63 (0.30-1.31) | 0.22 |
| LVEF, per 1% decrease | 1.00 (0.97-1.04) | 0.83 |
| RVEF, per 1% decrease | 1.04 (1.00-1.08) | 0.07 |
| GLS worsening, per 1% worsening | 1.22 (1.10-1.34) | <0.001 |
Abbreviations as in Table 1.
DISCUSSION
In a large cohort study of 152 heart transplant recipients, CMR-FT GLS was independently associated with long-term death or MACE after adjustment for known clinical and imaging predictors. There was an incremental prognostic value for GLS over known clinical and imaging predictors of long-term clinical outcomes after heart transplantation. The association was also noted in subgroups of recipients with LVEF>50% and no myocardial fibrosis, showing that GLS has prognostic value even in recipients without functional or structural abnormalities by well-established criteria. These findings suggest a role for CMR-FT GLS in the risk stratification of heart transplant recipients.
Other markers with prognostic significance included myocardial fibrosis presence and RVEF. RV dysfunction has been described after heart transplantation using echocardiography measures (22–24), however, the mechanisms of RV dysfunction after heart transplantation are poorly understood.
Echocardiography derived GLS in Heart Transplant Recipients
Prior studies have suggested an association between echocardiography derived GLS and various adverse clinical outcomes in heart transplant recipients(3,4,6). Our findings of an independent prognostic value for CMR-FT GLS are consistent with these prior echocardiographic studies. Besides, we show the prognostic value of CMR-FT GLS incremental to myocardial fibrosis and quantitative LVEF as assessed by the gold standard technique of CMR. To our knowledge, there have been no prior studies investigating the prognostic association of CMR-derived GLS on clinical outcomes in heart transplant recipients.
Myocardial Mechanics in Heart Transplant Recipients
LV ejection fraction is a global measure reflecting the combined function of both longitudinal and circumferential fibers, without the ability to distinguish between these components. Possibly because of their subendocardial location, longitudinal myocardial fibers seem to be exquisitely sensitive to disturbance by various pathologies (25–29). Thus, in the early stages of many myocardial diseases, longitudinal impairment appears to precede reduction in circumferential contraction, resulting in subclinical impairment of LV function despite a normal ejection fraction. Some suggest that early compensatory increase in circumferential function helps maintain the LVEF despite impaired longitudinal function (30).
In heart transplant recipients, an abnormal GLS may represent an early integrated biomarker of clinical and subclinical pathologies that affect the subendocardium, such as CAV and allograft failure. These processes could adversely affect the subendocardium in various ways – perfusion abnormalities, wall stress abnormalities, myocardial fibrosis, and myocardial edema – and result in myocardial contractile dysfunction manifesting as an abnormal GLS.
Clinical Implications
Assessment of echocardiography derived GLS is recommended by the European Association of Cardiovascular Imaging during routine surveillance in heart transplant recipients for the diagnosis of subclinical allograft dysfunction, and with endomyocardial biopsy to characterize and monitor an acute rejection or “global dysfunction episode” (31). Our data provide evidence to support a role for CMR-FT GLS in determining the long-term prognosis of transplant recipients. We have previously shown a prognostic role for myocardial fibrosis in heart transplant recipients (15). Here we showed an independent and incremental prognostic value for CMR-FT GLS over myocardial fibrosis presence and extent, and an independent prognostic value in a subgroup without LGE. An abnormal GLS could be an early trigger for further investigation and changes in therapy. However, prospective studies are warranted first to investigate whether such a GLS-guided strategy is associated with improved long-term outcomes. The prognostic value of CMR-FT GLS combined with data from cine, perfusion, LGE, T1 mapping, and T2 mapping needs to be established.
Chronic kidney disease is not uncommon among heart transplant recipients and may preclude the use of LGE CMR to detect myocardial fibrosis in some recipients due to the perceived risk of nephrogenic systemic fibrosis. CMR-FT GLS does not require contrast administration and could help obtain prognostic information even in recipients with chronic kidney disease.
Limitations
This is a single-center retrospective study and is, therefore, subject to referral bias and all the limitations inherent to the study design. The long (14 years) study period results in heterogeneity in the referral of recipients for CMRs, and in the clinical care they received. Newer CMR techniques such as T1 and T2 mapping were not clinically available during the entire study period and may add prognostic information incremental to GLS. Similar to echocardiography derived GLS, there are algorithmic differences between various CMR-FT strain software programs, which may lead to differing values (32). Thus, our findings would benefit from replication using other CMR-FT strain software programs. Studies comparing echocardiography derived GLS and CMR-FT GLS are also warranted. We did not measure less-validated strain measures such as global circumferential strain and global radial strain in this first study of the prognostic value of CMR-FT in heart transplant recipients. Finally, we did not investigate longitudinal changes in CMR-FT GLS in this study.
CONCLUSIONS
In a large cohort of heart transplant recipients, CMR-FT GLS was associated with the long-term risk of death or MACE after adjustment for clinical and CMR risk factors. Each 1% worsening in GLS was independently associated with a 15% increased risk of events. Importantly, CMR-FT GLS was independently associated with the long-term risk of death or MACE even in the subgroups of recipients with LVEF>50%, and no myocardial fibrosis. Future studies are needed to explore the role of CMR-FT GLS-guided strategies for clinical decision-making in heart transplant recipients.
PERSPECTIVES.
COMPETENCY IN MEDICAL KNOWLEDGE:
In heart transplant recipients, CMR-FT GLS is associated with the long-term risk of death or MACE incremental to clinical and CMR risk factors. This is true even in the subgroups of recipients with LVEF>50%, and no myocardial fibrosis.
TRANSLATIONAL OUTLOOK:
Future studies are needed to explore the role of CMR-FT GLS-guided strategies for clinical decision-making in heart transplant recipients.
Acknowledgements:
Sources of Funding: Mehmet Akçakaya was supported by NIH grant R00HL111410. Chetan Shenoy was supported by NIH grant K23HL132011, University of Minnesota Clinical and Translational Science Institute KL2 Scholars Career Development Program Award (NIH grant KL2TR000113-05) and NIH grant UL1TR000114.
ABBREVIATIONS:
- CAV
cardiac allograft vasculopathy
- CI
confidence interval
- CMR
cardiovascular magnetic resonance imaging
- EDVI
end-diastolic volume index
- ESVI
end-systolic volume index
- FT
feature tracking
- GLS
global longitudinal strain
- IQR
interquartile range
- LGE
late gadolinium enhancement
- LV
left ventricular
- LVEF
left ventricular ejection fraction
- MACE
major adverse cardiovascular events
- RV
right ventricular
- RVEF
right ventricular ejection fraction
- SD
standard deviation
Footnotes
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Disclosures: None
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