LV reverse remodeling imparted by aortic valve replacement for severe aortic stenosis; is it durable? A cardiovascular MRI study sponsored by the American Heart Association.

BACKGROUND: In patients with severe aortic stenosis (AS), long-term data tracking surgically induced effects of afterload reduction on reverse LV remodeling are not available. Echocardiographic data is available short term, but in limited fashion beyond one year. Cardiovascular MRI (CMR) offers the ability to serially track changes in LV metrics with small numbers due to its inherent high spatial resolution and low variability. HYPOTHESIS: We hypothesize that changes in LV structure and function following aortic valve replacement (AVR) are detectable by CMR and once triggered by AVR, continue for an extended period. METHODS: Twenty-four patients of which ten (67 ± 12 years, 6 female) with severe, but compensated AS underwent CMR pre-AVR, 6 months, 1 year and up to 4 years post-AVR. 3D LV mass index, volumetrics, LV geometry, and EF were measured. RESULTS: All patients survived AVR and underwent CMR 4 serial CMR's. LVMI markedly decreased by 6 months (157 ± 42 to 134 ± 32 g/m2, p < 0.005) and continued trending downwards through 4 years (127 ± 32 g/m2). Similarly, EF increased pre to post-AVR (55 ± 22 to 65 ± 11%,(p < 0.05)) and continued trending upwards, remaining stable through years 1-4 (66 ± 11 vs. 65 ± 9%). LVEDVI, initially high pre-AVR, decreased post-AVR (83 ± 30 to 68 ± 11 ml/m2, p < 0.05) trending even lower by year 4 (66 ± 10 ml/m2). LV stroke volume increased rapidly from pre to post-AVR (40 ± 11 to 44 ± 7 ml, p < 0.05) continuing to increase non-significantly through 4 years (49 ± 14 ml) with these LV metrics paralleling improvements in NYHA. However, LVmass/volume, a 3D measure of LV geometry, remained unchanged over 4 years. CONCLUSION: After initial beneficial effects imparted by AVR in severe AS patients, there are, as expected, marked improvements in LV reverse remodeling. Via CMR, surgically induced benefits to LV structure and function are durable and, unexpectedly express continued, albeit markedly incomplete improvement through 4 years post-AVR concordant with sustained improved clinical status. This supports down-regulation of both mRNA and MMP activity acutely with robust suppression long term.

Routine evaluation of left ventricular diastolic function by cardiovascular magnetic resonance: a practical approach.

BACKGROUND: Cardiovascular magnetic resonance (CMR) has excellent capabilities to assess ventricular systolic function. Current clinical scenarios warrant routine evaluation of ventricular diastolic function for complete evaluation, especially in congestive heart failure patients. To our knowledge, no systematic assessment of diastolic function over a range of lusitropy has been performed using CMR. METHODS AND RESULTS: Left ventricular diastolic function was assessed in 31 subjects (10 controls) who underwent CMR and compared with Transthoracic echocardiogram (TTE) evaluation of mitral valve (MV) and pulmonary vein (PV) blood flow. Blood flow in the MV and PV were successfully imaged by CMR for all cases (31/31,100%) while TTE evaluated flow in all MV (31/31,100%) but only 21/31 PV (68%) cases. Velocities of MV flow (E and A) measured by CMR correlated well with TTE (r = 0.81, p < 0.001), but demonstrated a systematic underestimation by CMR compared to TTE (slope = 0.77). Bland-Altman analysis of the E:A ratio and deceleration time (DT) calculated from each modality showed excellent agreement (bias -0.29, and -10.3 ms for E:A and DT, respectively). When assessing morphology using TTE, CMR correctly identified patients as having normal or abnormal inflow conditions. CONCLUSION: We have shown that there is homology between CMR and TTE for the assessment of diastolic inflow over a wide range of conditions, including normal, impaired relaxation and restrictive. There is excellent agreement of quantitative velocity measurements between CMR and TTE. Diastolic blood flow assessment by CMR can be performed in a single scan, with times ranging from 20 sec to 3 min, and we show that there is good indication for applying CMR to assess diastolic conditions, either as an adjunctive test when evaluating systolic function, or even as a primary test when TTE data cannot be obtained.

Physiologic compensation is supranormal in compensated aortic stenosis: does it return to normal after aortic valve replacement or is it blunted by coexistent coronary artery disease? An intramyocardial magnetic resonance imaging study.

BACKGROUND: In compensated aortic stenosis (AS), cardiac performance measured at the ventricular chamber is typically supranormal, whereas measurements at the myocardium are often impaired. We investigated intramyocardial mechanics after aortic valve replacement (AVR) and the effects relative to the presence or absence of coronary artery disease (CAD+ or CAD-), respectively. METHODS AND RESULTS: Twenty-nine patients (46 to 91 years, 10 female) with late but not decompensated AS underwent cardiovascular MRI before AVR (PRE), with follow-up at 6+/-1 (EARLY) and 13+/-2 months (LATE) to determine radiofrequency tissue-tagged left ventricle (LV) transmural circumferential strain, torsion, structure, and function. At the myocardial level, concentric LV hypertrophy regressed 18% LATE (93+/-22 versus 77+/-17 g/m2; P<0.0001), whereas at the LV chamber level, ejection fraction was supranormal PRE, 67+/-6% (ranging as high as 83%) decreasing to 59+/-6% LATE (P<0.05), representing not dysfunction but a return to more normal LV physiology. Between the CAD+ and CAD- groups, intramyocardial strain was similar PRE (19+/-10 versus 20+/-10) but different LATE, with dichotomization specifically related to the CAD state. In the CAD- patients, strain increased to 23+/-10% (+20%), whereas in CAD+ patients it fell to 16+/-11% (-26%), representing a nearly 50% decline after AVR (P<0.05). This was particularly evident at the apex, where CAD- strain LATE improved 17%, whereas for CAD+ it decreased 2.5-fold. Transmural strain and myocardial torsion followed a similar pattern, critically dependent on CAD. AVR impacted LV geometry and mitral apparatus, resulting in decreased mitral regurgitation, negating the double valve consideration. CONCLUSIONS: In AS patients after AVR, reverse remodeling of the supranormal systolic function parallels improvement in cardiovascular MRI-derived regression of LV hypertrophy and LV intramyocardial strain. However, discordant effects are evident after AVR, driven by CAD status, suggesting that the typical AVR benefits are experienced disproportionately by those without CAD and not by those obliged to undergo concomitant coronary artery bypass grafting/AVR.