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Altered myocardial velocities and stress perfusion in heart transplant patients affected by coronary allograft vasculopathy
Roberto Sarnari1, Muhannad Abbasi 1, Arif Jivan 1, Rahim Gulamali1, Alexander Ruh1, Julie Anne Blaisdell1, Brandon Clifford Benefield1, Ryan Dolan1, Kambiz Ghafourian1, Jane Wilcox1, Sadiya Sana Khan1, Esther Vorovich1, Jonathan Rich1, Allen Anderson1, Clyde Yancy1, James Carr1, Daniel Lee1, and Michael Markl1

1Northwestern University, Chicago, IL, United States

Synopsis

Coronary allograft vasculopathy (CAV) is responsible for long term mortality after heart transplant (HTx). Myocardial perfusion impairment resulting from CAV can lead to early graft dysfunction. Our study aimed to quantify perfusion and 3-directional myocardial velocities by cardiac magnetic resonance perfusion and tissue phase mapping (TPM) sequences and describe the relationship at global and segmental level. Thirty two HTx patients affected by CAV were analyzed. Myocardial perfusion reserve was reduced in CAV patients and associated with reduced left ventricular twist during contraction. LV diastolic radial velocities and interventricular synchrony were associated as to rest and to stress myocardial perfusion variations

Purpose

Coronary allograft vasculopathy (CAV) is a leading cause of long term mortality in patients after heart transplantation (HTx). CAV alters myocardial perfusion, at rest or stress, which is a major cause of graft dysfunction in the long term1. Cardiovascular magnetic resonance (CMR) allows for myocardial perfusion and perfusion reserve (MPR) quantification2 using rest and stress first pass perfusion sequences. CAV severity is currently classified by epicardial coronary invasive study and global cardiac function analysis, which don’t allow for adequate assessment of the coronary microcirculation3. Discrepancies between left ventricular (LV) perfusion and LV function are reported in CAV patients. Moreover, global and segmental right ventricular (RV) function alterations in relation to LV perfusion abnormalities have not been clarified in HTx patients developing CAV. CMR has high potential to better characterize CAV4 due to its ability to quantify rest/stress blood flow, cardiac global and regional function, and myocardial velocities by tissue phase mapping (TPM)5,6. The aim of our study was to quantify RV and LV myocardial velocities and verify myocardial velocity/perfusion relationships in HTx patients affected by CAV by using TPM and myocardial perfusion CMR.

Methods

Thirty two patients affected by CAV were analyzed. All patients underwent coronary angiography and CMR. CAV severity was classified based on coronary angiography and global cardiac function, as previously recommended3. Five patients were classified as CAV grade 0, 23 patients as CAV grade 1, 4 patients as CAV grade 2-3. Patients had undergone first-pass stress perfusion CMR using Regadenoson7 (turbo fast low-angle single-shot gradient-echo sequence; Gadobuterol contrast agent), short axis CINE covering the RV and LV (steady state free precession sequence), and TPM5,6 (2D cine phase contrast with 3-directional velocity encoding) in 3 short axis locations (base, mid, apex). Global and segmental LV and RV myocardial velocities were calculated in long-axis (vz), radial (vr) and circumferential (všœ™) directions8. Data analysis included: CINE SFFP calculated parameters: LV and RV ejection fraction (EF%); First pass perfusion parameters: global and segmental rest and stress myocardial blood flow, MPR; TPM parameters: radial and long axis peak velocities in systole and diastole, myocardial twist (difference between average circumferential velocity time courses from base and apex), interventricular synchrony (cross correlation coefficient between slice-averaged LV and RV velocity time courses).

Results

There was no significant difference between CAV groups regarding age, time after HTx, heart rate, systolic and diastolic blood pressure and ejection fraction [Table 1]. CAV patients showed reduced myocardial perfusion reserve compared to values reported in healthy controls9 and reduction was inversely associated with increased CAV severity [Table 2]. In all cohort analysis [Fig.1] myocardial perfusion during stress and myocardial perfusion reserve correlated positively with LV systolic twist (both r=0.36, p<0.05). There was a positive significant relationship between rest and stress perfusion values with LV diastolic peak radial velocity (r=0.47, p<0.01 and r=0.41, p<0.05, respectively) and with interventricular synchrony in radial direction (r=0.37, p<0.05 and r=0.44, p<0.05, respectively). LV stress perfusion values also correlated positively with RV diastolic peak untwist (r=0.38, p<0.05) [Figure 1]. At segmental level [Fig.2], significant correlation between diastolic radial velocity and rest perfusion was found in all segments of the anterior wall (and in the antero-septal basal segment) and in apical and mid (and infero-lateral mid) segments of the inferior wall. Stress perfusion and diastolic peak radial velocity correlation was significant at basal and mid (and antero-lateral mid) level of the anterior wall and at basal inferior wall.

Discussion

Our study showed that global and segmental abnormalities of myocardial velocities and correspondence with perfusion parameters occur in different CAV classes, including patients with normal cardiac function. Specific parts of the cardiac cycle were affected by different type of perfusion alteration. LV perfusion variation also showed an impact on RV diastolic performance. Quantification of myocardial perfusion and relationships with myocardial velocities may add significant information to the current CAV classification, allowing for a more complete disease staging based on myocardial tissue blood flow and motion parameters. Cases of reported discrepancies between CAV grade and global cardiac function may also be addressed by this approach and possibly clarified.

Conclusion

Simultaneous quantification of myocardial blood flow and 3-directional velocities may lead to a different classification of CAV in HTx patients, focused on the pathophysiological effects exerted at myocardial level. Larger studies are needed to further explore how CAV classification could be optimized.

Acknowledgements

No acknowledgement found.

References

1.The registry of the International Society for Heart and Lung Transplantation: seventeenth official pediatric lung and heart-lung transplantation report--2014; focus theme: retransplantation.
Benden C, Goldfarb SB, Edwards LB, Kucheryavaya AY, Christie JD, Dipchand AI, Dobbels F, Levvey BJ, Lund LH, Meiser B, Yusen RD, Stehlik J; International Society for Heart and Lung Transplantation.
J Heart Lung Transplant. 2014 Oct;33(10):1025-33.

2. Quantification of absolute myocardial blood flow by magnetic resonance perfusion imaging. Lee DC, Johnson NP. JACC Cardiovasc Imaging. 2009;2(6):761-70.

3. International Society for Heart and Lung Transplantation working formulation of a standardized nomenclature for cardiac allograft vasculopathy-2010. Mehra MR, Crespo-Leiro MG, Dipchand A, Ensminger SM, Hiemann NE, Kobashigawa JA, Madsen J, Parameshwar J, Starling RC, Uber PA. J Heart Lung Transplant. 2010 Jul;29(7):717-27.

4. Multiparametric cardiovascular magnetic resonance assessment of cardiac allograft vasculopathy. Miller CA1, Sarma J, Naish JH, Yonan N, Williams SG, Shaw SM, Clark D, Pearce K, Stout M, Potluri R, Borg A, Coutts G, Chowdhary S, McCann GP, Parker GJ, Ray SG, Schmitt M. J Am Coll Cardiol. 2014 Mar 4;63(8):799-808.

5. Detailed Analysis of Myocardial Motion in Volunteers and Patients Using High-Temporal-Resolution. MR Tissue Phase Mapping. Jung B, Föll D, Böttler P, Petersen S, Hennig J, Markl M. J Magn Reson Imaging. 2006;24:1033–9

6. Cardiac Structure-Function MRI in Patients After Heart Transplantation. Dolan RS, Rahsepar AA, Blaisdell J, Lin K, Suwa K, Ghafourian K, et al. J Magn Reson Imaging. 2018. doi: 10.1002/jmri.26275

7. Risk stratification by regadenoson stress magnetic resonance imaging in patients with known or suspected coronary artery disease. Abbasi SA, Heydari B, Shah RV, Murthy VL, Zhang YY, Blankstein R, Steigner M, Jerosch-Herold M, Kwong RY. Am J Cardiol. 2014 Oct 15;114(8):1198-203.

8. Normal Pediatric and Adult Regional Biventricular Myocardial Motion by Tissue Phase Mapping. Ruh A, Sidoryk K, Lin K, Rose MJ, Robinson JD, Rigsby CK, et al. In: CMR 2018 - A Joint EUROCMR/SCMR Meeting. 2018. p. 624–6

9. A myocardial perfusion reserve index in humans using first-pass contrast-enhanced magnetic resonance imaging. Cullen JH1, Horsfield MA, Reek CR, Cherryman GR, Barnett DB, Samani NJ. J Am Coll Cardiol. 1999 Apr;33(5):1386-94.

Figures

Figure 1. Correlations between global myocardial blood flow (rest, stress and perfusion reserve) and global myocardial velocities. CC: cross-correlation coefficient indicating interventricular synchrony (cc=1 completely synchronous motion, reduced cc: increased dyssynchrony).

Figure 2. Segmental correlations between myocardial rest and stress blood flow (ml/min/g) and diastolic peak radial LV velocities during cardiac relaxation. Displayed are Pearson correlation coefficients (r) for each segment with significant results (p<0.05) marked by asteriks.

Table 1. Patients demographics. Number of patients for each group is reported between parentheses. CAV: coronary allograft vasculopathy. HTx: heart transplant. HR: heart rate. BP: blood pressure. EF: ejection fraction.

Table 2. Myocardial perfusion in patients affected by coronary allograft vasculopathy: rest, stress and reserve (stress/rest) values are reported. Number of patients are shown between parentheses. CAV: coronary allograft vasculopathy. MPR: myocardial perfusion reserve.

Proc. Intl. Soc. Mag. Reson. Med. 27 (2019)
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