Oral Abstract Session
SCMR 22nd Annual Scientific Sessions
Background: Cardiac allograft vasculopathy (CAV) is a primary cause of allograft failure beyond the first year post heart transplantation (HTx). IVUS and coronary angiography are the gold standards for screening; however, these invasive procedures have limited ability to detect early onset CAV because epicardial vessels and microcirculation are affected independently and vary between patients[3-5]. Therefore, CMR has potential as a non-invasive alternative for graft assessment. CMR tissue phase mapping (CMR-TPM) allows for the measurement of 3-directional (long-axis, radial, circumferential) myocardial velocities of both the left (LV) and right ventricle (RV)[6-8]. Our hypothesis is that CMR-TPM can detect altered biventricular myocardial velocities in CAV patients.
Methods: 30 HTx patients greater than one year post-transplant (49±18 years,19 males, time after HTx=9±6years) and 18 age-matched controls (49±15 years, 12 males) underwent CMR-TPM at 3 short-axis locations (base, mid, apex). Demographics are reported in Table 1. Patient CAV status was graded 0 to 3 based on the ISHLT CAV grading scale . TPM data analysis included quantification of global and regional (extended 16+10 AHA model) LV and RV systolic and diastolic radial and long-axis peak velocities. Ventricular twisting motions were quantified as the difference between circumferential velocities between the base and apex.
Results: Most segments in HTx patients demonstrated significantly reduced long-axis peak velocities for the LV (5.2±2.1cm/s vs 3.5±0.8cm/s, p<0.001) and RV (4.2±1.3 cm/s vs 2.6±0.9cm/s, p<0.001) in systole and for RV in diastole (-3.9±1.3cm/s vs -2.1±0.9cm/s, p<0.001) when compared to controls(Fig.1).Patients also demonstrated reduced RV peak radial systolic velocities (4.1±0.9cm/s vs 3.4±0.6cm/s,p<0.001),systolic twisting(2.8±1.5cm/s 1.7±1.2cm/s, p<0.05)and diastolic untwisting(-3.1±1.6cm/s vs -1.8±0.9cm/s, p<0.001) compared to controls. Box plots (Fig.2) summarize differences in global RV and LV velocities by CAV severity subgroups. All CAV subgroups had impaired biventricular velocities compared to controls. Differences between CAV subgroups were less pronounced, although significant changes (p<0.05) were found for systolic LV and RV velocities between CAV grade 2&3, CAV grade 1, and patients without CAV (grade 0).
Conclusion: We demonstrated impaired global and segmental RV and LV velocities in HTx patients with and without signs of CAV in comparison to controls. Increased CAV severity grade was associated with altered systolic RV and LV velocities. Higher velocities in the CAV 2&3 group may be due to the small cohort size or related to higher stroke volume and ejection fraction in those patients. Further studies with larger cohorts are warranted to further characterize the diagnostic value of myocardial velocities in CAV detection.