scholarly journals Multi-parametric cardiovascular magnetic resonance with regadenoson stress perfusion is safe following pediatric heart transplantation and identifies history of rejection and cardiac allograft vasculopathy

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Nazia Husain ◽  
Kae Watanabe ◽  
Haben Berhane ◽  
Aditi Gupta ◽  
Michael Markl ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Left Ventricular ◽  
Stress Perfusion ◽  
Low Grade ◽  
Healthy Controls ◽  
Allograft Vasculopathy ◽  
Significant Relationships ◽  
Pediatric Heart Transplantation ◽  
History Of ◽  
Regadenoson Stress

Abstract Background The progressive risk of graft failure in pediatric heart transplantation (PHT) necessitates close surveillance for rejection and coronary allograft vasculopathy (CAV). The current gold standard of surveillance via invasive coronary angiography is costly, imperfect and associated with complications. Our goal was to assess the safety and feasibility of a comprehensive multi-parametric CMR protocol with regadenoson stress perfusion in PHT and evaluate for associations with clinical history of rejection and CAV. Methods We performed a retrospective review of 26 PHT recipients who underwent stress CMR with tissue characterization and compared with 18 age-matched healthy controls. CMR protocol included myocardial T2, T1 and extracellular volume (ECV) mapping, late gadolinium enhancement (LGE), qualitative and semi-quantitative stress perfusion (myocardial perfusion reserve index; MPRI) and strain imaging. Clinical, demographics, rejection score and CAV history were recorded and correlated with CMR parameters. Results Mean age at transplant was 9.3 ± 5.5 years and median duration since transplant was 5.1 years (IQR 7.5 years). One patient had active rejection at the time of CMR, 11/26 (42%) had CAV 1 and 1/26 (4%) had CAV 2. Biventricular volumes were smaller and cardiac output higher in PHT vs. healthy controls. Global T1 (1053 ± 42 ms vs 986 ± 42 ms; p < 0.001) and ECV (26.5 ± 4.0% vs 24.0 ± 2.7%; p = 0.017) were higher in PHT compared to helathy controls. Significant relationships between changes in myocardial tissue structure and function were noted in PHT: increased T2 correlated with reduced LVEF (r = − 0.57, p = 0.005), reduced global circumferential strain (r = − 0.73, p < 0.001) and reduced global longitudinal strain (r = − 0.49, p = 0.03). In addition, significant relationships were noted between higher rejection score and global T1 (r = 0.38, p = 0.05), T2 (r = 0.39, p = 0.058) and ECV (r = 0.68, p < 0.001). The presence of even low-grade CAV was associated with higher global T1, global ECV and maximum segmental T2. No major side effects were noted with stress testing. MPRI was analyzed with good interobserver reliability and was lower in PHT compared to healthy controls (0.69 ± − 0.21 vs 0.94 ± 0.22; p < 0.001). Conclusion In a PHT population with low incidence of rejection or high-grade CAV, CMR demonstrates important differences in myocardial structure, function and perfusion compared to age-matched healthy controls. Regadenoson stress perfusion CMR could be safely and reliably performed. Increasing T2 values were associated with worsening left ventricular function and increasing T1/ECV values were associated with rejection history and low-grade CAV. These findings warrant larger prospective studies to further define the role of CMR in PHT graft surveillance.

Proposed stages of Fabry disease: insights from multiparametric cardiac MRI and advanced ECG

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
JA Bicho Augusto ◽  
N Johner ◽  
D Shah ◽  
S Nordin ◽  
K Knott ◽  
...  
Keyword(s):  
Fabry Disease ◽  
Cardiac Mri ◽  
Cardiac Involvement ◽  
T2 Mapping ◽  
Left Ventricular ◽  
P Wave ◽  
Stress Perfusion ◽  
Healthy Controls ◽  
T Wave ◽  
Advanced Analysis

Abstract Funding Acknowledgements Type of funding sources: None. Background Staging of Fabry disease (FD) cardiomyopathy uses multiparametric cardiac MRI. Advanced disease is characterized by left ventricular hypertrophy (LVH), myocardial inflammation/oedema (high native T2 mapping) and/or fibrosis (late gadolinium enhancement, LGE). Pre-LVH involvement has been described and includes myocardial sphingolipid storage (low native T1 mapping), impaired LV global longitudinal strain (GLS) and microvascular disease/dysfunction (low stress myocardial blood flow, MBF, in perfusion mapping). We aimed to define (1) the early myocardial phenotype prior to T1 lowering/pre-storage and (2) the stages of cardiac involvement in FD.   Methods FD patients and age, sex and heart rate matched healthy controls underwent same-day ECG with advanced analysis and multiparametric CMR (cines, GLS, pre-contrast T1 and T2 mapping, adenosine stress perfusion mapping [for MBF] and LGE). Results 114 Fabry patients (46 ± 13 years, 61% female, 37% [n = 72] had LVH) and 76 controls (49 ± 15 years, 50% female) were included. FD with vs without LVH in brief and as expected, FD with LVH had significantly (p &lt; 0.05) lower MBF, GLS and T1, and higher T2 and %LGE. FD pre-LVH low T1 vs pre-LVH normal T1: low T1 patients (32/72, 44%) had higher LV mass index (67 ± 14 vs 59 ± 10g/m2, P = 0.011), maximum Q wave amplitude (2[1-2] vs 1[1-2]mm, P &lt; 0.001), Sokolow-Lyon index (22[16-28] vs 17[13-23]mm, P = 0.031) and more fractionated QRS complexes (44 vs 18%, P = 0.020). FD pre-LVH normal T1 vs healthy controls: normal T1 pre-LVH Fabry patients (40/72, 56%) had reduced GLS (-18 ± 2 vs -20 ± 2%, P &lt; 0.001), microvascular impairment (lower MBF 2.5 ± 0.7 vs 3.0 ± 0.8mL/g/min, P = 0.028), subtle T2 elevation (50 ± 4 vs 48 ± 2ms, p = 0.027) and limited LGE (%LGE 0.3 ± 1.1 vs 0%, P = 0.004) when compared to healthy controls; ECG abnormalities included shorter P wave duration (88 ± 12 vs 94 ± 15ms, P = 0.010) and T wave peak time (Tonset–Tpeak; 104 ± 28 vs 115 ± 20ms, P = 0.015), resulting in a more symmetric T wave with lower T wave time ratio (Tonset–Tpeak)/(Tpeak–Tend) (1.5 ± 0.4 vs 1.8 ± 0.4, P &lt; 0.001) compared to controls. Conclusion Prior staging of Fabry cardiomyopathy included a pre-LVH stage (accumulation/storage) and two LVH stages (hypertrophy and inflammation; fibrosis and impairment). Here we define an even earlier stage, pre-LVH pre-detectable storage, defined by microvascular dysfunction, impaired GLS and altered atrial depolarization and ventricular repolarization intervals (see Figure). Abstract Figure. Proposed stages of cardiac involvement

Reversal of severe late left ventricular failure after pediatric heart transplantation and possible role of plasmapheresis

2000 ◽  
Vol 85 (6) ◽  
pp. 735-739 ◽  
Author(s):  
Elfriede Pahl ◽  
Susan E Crawford ◽  
Richard A Cohn ◽  
Sherrie Rodgers ◽  
David Wax ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Ventricular Failure ◽  
Pediatric Heart Transplantation

scholarly journals P970 Significant differences in atrial structural and functional parameters leading to differing mechanisms of atrial fibrillation in athletes compared to non-athletes

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Trivedi ◽  
G Claessen ◽  
L Stefani ◽  
D Flannery ◽  
P Brown ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Longitudinal Strain ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Endurance Athletes ◽  
Healthy Controls ◽  
Age And Gender ◽  
History Of ◽  
And Gender

Abstract Background/Introduction: There is an increased incidence of atrial fibrillation (AF) in endurance athletes. We sought to evaluate the likely mechanistic basis for this phenomenon. Methods 36 endurance athletes in sinus rhythm, with a previous history of AF (ATH-AF) were compared to age and gender matched endurance athletes with no prior history of AF (ATH), non athletes with paroxysmal AF (NONATH-AF) and age and gender matched healthy controls (CONTROL). A detailed transthoracic echocardiogram was performed with all groups in sinus rhythm, with detailed left atrial (LA) and left ventricular (LV) measurements, including strain analysis. Results All athletes had increased LA and LV size when compared with healthy controls (Table 1). Non athletes with paroxysmal AF had increased LA size when compared with controls. However, indexed LA/LV ratio was preserved in athletes and similar to healthy individuals, whilst AF patients had significantly increased LA/LV ratio. Athletes with AF had higher e’ velocity and lower E/e’, whereas e’ was reduced and E/e’ elevated in non-athlete AF patients. Athletes had impaired LA reservoir and contractile strain, and reduced LV global longitudinal strain (GLS) compared with healthy controls. Conclusions Compared to healthy controls, athletes have reduced LA and LV strain, with preserved LV diastolic function and LA/LV ratio. In contrast, altered diastolic function with differential increase in LA volume was observed in AF patients. The increased risk of AF in athletes is likely mediated by different mechanistic processes other than an atrial myopathy consequent to diastolic dysfunction as observed in non-athletes with AF. Table 1. LA and LV parameters Parameter ATH-AF ATH NONATH-AF CONTROL P value LVEDV indexed (ml/m2) 84 ± 12 79 ± 14 57 ± 10 51 ± 13 &lt;0.001 LVESV indexed (ml/m2) 35 ± 6 34 ± 7 25 ± 8 27 ± 33 0.02 LV ejection fraction (%) 58 ± 4 56 ± 4 56 ± 10 58 ± 8 0.586 LV global longitudinal strain (%) 19.2 ± 1.7 18.9 ± 2.1 21 ± 3.1 21.7 ± 2.9 &lt;0.001 e’ vel (cm/s) 10 ± 2 10 ± 3 8 ± 2 9 ± 2 0.007 E/e’ 5.7 ± 1.3 5.9 ± 1.8 9.1 ± 3.3 7.5 ± 1.5 &lt;0.001 LAV max indexed (ml/m2) 45 ± 11 43 ± 12 38 ± 11 27 ± 8 &lt;0.001 Indexed LAV/LVEDV ratio 0.5 ± 0.1 0.6 ± 0.2 0.7 ± 0.2 0.5 ± 0.1 &lt;0.001 LA reservoir strain (%) 27.2 ± 4.8 28.2 ± 3.7 27.9 ± 8.4 33.2 ± 7.0 &lt;0.001 LA conduit strain (%) 14.2 ± 4.5 14.4 ± 4.0 14.9 ± 5.5 16.6 ± 6.3 0.182 LA contractile strain (%) 13.0 ± 3.1 13.8 ± 3.6 13.0 ± 5.1 16.6 ± 3.1 &lt;0.001 LV = left ventricular, LAV = left atrial volume, LA = left atrial

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