Delayed hyperenhancement in magnetic resonance imaging of left ventricular hypertrophy caused by aortic stenosis and hypertrophic cardiomyopathy: visualisation of focal fibrosis

Abstract

Objective: To compare the extent and distribution of focal fibrosis by gadolinium contrast-enhanced magnetic resonance imaging (MRI; delayed hyperenhancement) in severe left ventricular (LV) hypertrophy in patients with pressure overload caused by aortic stenosis (AS) and with genetically determined hypertrophic cardiomyopathy (HCM). Methods: 44 patients with symptomatic valvular AS (n = 22) and HCM (n = 22) were studied. Cine images were acquired with fast imaging with steady-state precession (trueFISP) on a 1.5 T scanner (Sonata, Siemens Medical Solutions). Gadolinium contrast-enhanced MRI was performed with a segmented inversion-recovery sequence. The location, extent and enhancement pattern of hyperenhanced myocardium was analysed in a 12-segment model. Results: Mean LV mass was 238.6 (SD 75.3) g in AS and 205.4 (SD 80.5) g in HCM (p = 0.17). Hyperenhancement was observed in 27% of patients with AS and in 73% of patients with HCM (p , 0.01). In AS, hyperenhancement was observed in 60% of patients with a maximum diastolic wall thickness > 18 mm, whereas no patient with a maximum diastolic wall thickness , 18 mm had hyperenhancement (p , 0.05). Patients with hyperenhancement had more severe AS than patients without hyperenhancement (aortic valve area 0.80 (0.09) cm 2 v 0.99 (0.3) cm 2 , p , 0.05; maximum gradient 98 (22) mm Hg v 74 (24) mm Hg, p , 0.05). In HCM, hyperenhancement was predominant in the anteroseptal regions and patients with hyperenhancement had higher end diastolic (125.4 (36.9) ml v 98.8 (16.9) ml, p , 0.05) and end systolic volumes (38.9 (18.2) ml v 25.2 (1.7) ml, p , 0.05). The volume of hyperenhancement (percentage of total LV myocardium), where present, was lower in AS than in HCM (4.3 (1.9)% v 8.6 (7.4)%, p, 0.05). Hyperenhancement was observed in 4.5 (3.1) and 4.6 (2.7) segments in AS and HCM, respectively (p = 0.93), and the enhancement pattern was mostly patchy with multiple foci. Conclusions: Focal scarring can be observed in severe LV hypertrophy caused by AS and HCM, and correlates with the severity of LV remodelling. However, focal scarring is significantly less prevalent in adaptive LV hypertrophy caused by AS than in genetically determined HCM. R emodelling in left ventricular (LV) hypertrophy is accompanied by several structural changes. Interstitial and replacement fibrosis are among the morphological alterations that have been observed in LV hypertrophy caused by pressure overload and in genetically determined hypertrophic cardiomyopathy (HCM).

Equilibrium Contrast Cardiovascular Magnetic Resonance for the Measurement of Diffuse Myocardial Fibrosis

“…This was an expected finding, as fibrosis in hypertrophic cardiomyopathy is thought to be less diffuse in nature than fibrosis in our primary disease model, aortic stenosis. 30,31 Other noninvasive measures of diffuse fibrosis have limitations: Blood biomarkers are relatively nonspecific because collagen degradation products may arise in other tissues, and levels are influenced by clearance variability. Echocardiog- Figure 3.…”

Impact of Myocardial Fibrosis in Patients With Symptomatic Severe Aortic Stenosis

“…14 In an initial clinical study, focal late enhancement could be observed in the hypertrophic myocardium of patients with aortic stenosis. 15 …”

Cardiovascular Magnetic Resonance Imaging for Valvular Heart Disease

“…19 Areas of delayed gadolinium enhancement of the left ventricular myocardium correlate histopathologically with infarction 20 but have also been described in patients with hypertrophic, dilated, and infiltrative cardiomyopathies. Several patterns of delayed gadolinium enhancement have been reported in adults with severe aortic stenosis, 21,22 although the clinical implications of these findings in terms of prognosis and timing of intervention have not been fully elucidated.…”