Quantitative assessment of paravalvular regurgitation following transcatheter aortic valve replacement.

BACKGROUND: Paravalvular aortic regurgitation (PAR) following transcatheter aortic valve implantation (TAVI) is well acknowledged. Despite improvements, echocardiographic measurement of PAR largely remains qualitative. Cardiovascular magnetic resonance (CMR) directly quantifies AR with accuracy and reproducibility. We compared CMR and transthoracic echocardiography (TTE) analysis of pre-operative and post-operative aortic regurgitation in patients undergoing both TAVI and surgical aortic valve replacement (AVR). METHODS: Eighty-seven patients with severe aortic stenosis undergoing TAVI (56 patients) or AVR were recruited. CMR (1.5 T) and transthoracic echocardiography (TTE) were carried out pre-operatively and a median of 6 days post-operatively. The CMR protocol included regurgitant aortic flows using through-plane phase-contrast velocity. None/trivial, mild, moderate and severe AR by CMR was defined as ≤8%, 9-20%, 21-39%, >40% regurgitant fractions respectively. RESULTS: Pre- and post-operative left ventricular ejection fraction (LVEF) was similar. Post-procedure aortic regurgitant fraction using CMR was higher in the TAVI group (TAVI 16 ± 13% vs. AVR 4 ± 4%, p < 0.01). Comparing CMR to TTE, 27 of 56 (48%) TAVI patients had PAR which was at least one grade more severe on CMR than TTE (Z = -4.56, p <0.001). Sensitivity analysis confirmed the difference in PAR grade between TTE and CMR in the TAVI group (Z = -4.49, p < 0.001). CONCLUSION: When compared to CMR based quantitative analysis, TTE underestimated the degree of paravalvular aortic regurgitation. This underestimation may in part explain the findings of increased mortality associated with mild or greater AR by TTE in the PARTNER trial. Paravalvular aortic regurgitation post TAVI assessed as mild by TTE may in fact be more severe.

Myocardial perfusion is impaired in asymptomatic renal and liver transplant recipients: a cardiovascular magnetic resonance study.

BACKGROUND: Myocardial ischemia is a major cause of death in chronic kidney disease (CKD) patients, which can be caused by either epicardial or microvascular coronary artery disease (CAD). Although renal transplantation improves survival, cardiovascular disease remains a major cause of mortality in post renal transplant recipients, including those with no significant epicardial CAD pre-transplant. We aim to utilize stress cardiovascular magnetic resonance (CMR) and MR coronary angiography (MRCA) to assess silent myocardial ischemia and epicardial CAD in renal transplant recipients. METHODS: Forty-five subjects: twenty renal transplant (RT) with no known CAD, fifteen liver transplant (LT) controls without prior CKD and no known CAD, and ten hypertensive (HT) controls underwent stress perfusion CMR and MRCA. RESULTS: A total of 1308 myocardial segments (576 of RT, 468 of LT, and 264 of HT) were compared using mixed linear modeling. Left ventricular mass index, septal diameter and presence of diabetes mellitus were similar between the groups. The mean transmural MPRI was significantly lower in the RT and LT groups compared to HT controls (1.19 ± 0.50 in RT versus 1.23 ± 0.36 in LT versus 2.04 ± 0.32 in HT controls, p < 0.0001), in the subepicardium (1.33 ± 0.57 in RT versus 1.30 ± 0.33 in LT versus 2.01 ± 0.30 in HT controls, p < 0.001), and in the subendocardium (1.19 ± 0.54 in RT versus 1.11 ± 0.31 in LT versus 1.85 ± 0.34 in HT controls, p < 0.0001). Seven (35%) RT and five (33%) LT had significant epicardial CAD compared to none in HT controls, p = 0.12. One RT and one LT had LGE suggesting sub-endocardial infarction. CONCLUSIONS: RT recipients have impaired myocardial perfusion independent of LVH or diabetes mellitus. The impaired myocardial perfusion in RT is similar to LT without prior renal disease, thus unlikely related to previous CKD. It is not fully explained by the presence of significant epicardial CAD, and therefore most likely represents microvascular CAD.

Changes of left ventricular mechanics after trans-catheter aortic valve implantation and surgical aortic valve replacement for severe aortic stenosis: A tissue-tracking cardiac magnetic resonance study.

BACKGROUND: Left ventricular (LV) mechanics are impaired in patients with severe aortic stenosis (AS). The aim of the present study was to assess their changes early and late after trans-catheter aortic valve implantation (TAVI) and surgical aortic valve replacement (AVR) using cardiac magnetic resonance (CMR) tissue-tracking imaging. METHODS: In 59 patients with severe AS undergoing either TAVI (n=35) or surgical AVR (n=24), CMR with late gadolinium enhancement (LGE) imaging was performed before and early post-procedure to evaluate LV function and mass, and presence/extent of LGE. A third CMR scan was performed in 29 patients after a mean follow-up of 15±4months. Tissue-tracking analysis was applied to cine CMR images, to assess LV global longitudinal (GLS), circumferential (GCS) and radial (GRS) strains. RESULTS: The TAVI and surgical AVR groups were similar with respect to baseline (p=0.14) and early post-procedure (p=0.16) LV ejection fraction. However, baseline LV GLS was significantly impaired in TAVI patients compared to surgical AVR patients (p=0.025). Early post-procedure, TAVI resulted in a significant improvement of LV GLS (p=0.003), while a significant worsening of LV GLS was observed early after surgical AVR (p=0.012). At longer term follow-up, both TAVI and surgical AVR groups experienced a significant reduction of LV mass and a significant improvement of LV myocardial mechanics in all the three directions. CONCLUSIONS: Treatment-specific differences in the changes of LV myocardial mechanics early after afterload release by TAVI and surgical AVR are present. Later, both interventions are associated with an improvement of LV myocardial deformation, alongside a regression of LV hypertrophy.

Early effects of transcatheter aortic valve implantation and aortic valve replacement on myocardial function and aortic valve hemodynamics: insights from cardiovascular magnetic resonance imaging.

OBJECTIVES: There remains a paucity of mechanistic data on the effect of transcatheter aortic valve implantation (TAVI) on early left and right ventricular function and quantitative aortic valve regurgitation. We sought to assess and compare the early effects on myocardial function and aortic valve hemodynamics of TAVI and aortic valve replacement (AVR) using serial cardiovascular magnetic resonance (CMR) imaging and echocardiography. METHODS: A prospective comparison study of 47 patients with severe aortic stenosis undergoing either TAVI (n = 26) or high-risk AVR (n = 21). CMR (for left ventricle/right ventricle function, left ventricular mass, left atrial volume, and aortic regurgitation) was carried out before the procedure and early postprocedure (<14 days). RESULTS: Groups were similar with respect to Society of Thoracic Surgeons score (TAVI, 7.7 vs AVR, 5.9; P = .11). Preoperative left ventricular (TAVI, 69% ± 13% vs AVR, 73% ± 10%; P = .10) and right ventricular (TAVI, 61% ± 11% vs AVR, 59% ± 8%; P = .5) ejection fractions were similar. Postoperative left ventricular ejection fraction was preserved in both groups. In contrast, decline in right ventricular ejection fraction was more significant in the TAVI group (61%-54% vs 59%-58%; P = .01). Postprocedure aortic regurgitant fraction was significantly greater in the TAVI group (16% vs 4%; P = .001), as was left atrial size (110 vs 84 mL; P = .02). Further analysis revealed a significant relationship between the increased aortic regurgitant fraction and greater left atrial size (P = .006), and a trend toward association between the decline in right ventricle dysfunction and increased postprocedure aortic regurgitation (P = .08). CONCLUSIONS: There was no significant difference in early left ventricular systolic function between techniques. Whereas right ventricle systolic function was preserved in the AVR group, it was significantly impaired early after TAVI, possibly reflecting a clinically important pathophysiologic consequence of paravalvular aortic regurgitation.