Left ventricular hypertrophy, wall thickness, and histological myocyte alteration in end-stage heart failure: a call for a standard definition

Abstract Objective This study aimed to examine the relationship between different left ventricular hypertrophy (LVH) classification criteria according to the American Society of Echocardiography (ASE), and anatomical measurement of LV wall thickness (LVWT) and histological evidence of myocyte hypertrophy. Methods Data from 146 consecutive patients (47 years; 75% were male) who have undergone heart transplantation were analysed. Fixed ventricles were dissected and measured in weight after both atria, great vessels, and epicardial fat were removed. The fixed biventricular weight was calculated as 87% of total weight (the effect of fixed formalin reduced the total weight by 3%). Anatomical LVWT was measured with a ruler at LV free wall where maximal thickness is located. A comprehensive echocardiogram was performed in all patients before heart transplantation. LVM and relative wall thickness (RWT) (2 PWT/LVEDD) were measured by M-mode echocardiography in parasternal long-axis view. Patients were considered to have LVH when the LVM index exceeds 95 g/m2 in women and exceeds 115 g/m2 in men. Patients were considered to have concentric LVH when RWT > 0.42. LVWT was measured using 2D echocardiography perpendicular to the LV long axis. Results Of 146 explanted hearts, dilated cardiomyopathy (CM), cardiac amyloid, and hypertrophic CM were diagnosed in 53 (47%), 1 (1%), and 8 (5%) patients, respectively. Anatomic ventricular mass correlated with echocardiographic LVM (r=0.5, p < 0.01). Anatomic LVWT modestly correlated with echocardiographic LVWT (r=0.2, p=0.01). Of 146 patients, echocardiographic normal LV geometry, concentric LV remodelling, concentric LVH, and eccentric LVH were present in 22 (15%), 6 (4%), 14 (10%), and 104 (71%), respectively. Increased LVWT (≥ 13 mm) assessed by 2-D echocardiography was present in normal LV geometry (5%), concentric LV remodelling (5%), concentric LVH (57%), and eccentric LVH (33%) (p <0.001) in those classified by ASE guidelines. Anatomic LVWT (≥ 13 mm) was present in normal LV geometry (14%), concentric LV remodelling 5%), concentric LVH (14%), and eccentric LVH (80%) (p <0.001) in those classified by ASE guidelines. Histological myocyte hypertrophy was present in normal LV geometry (12%), concentric LV remodelling (2%), concentric LVH (11%), and eccentric LVH (70%) (p <0.001) in those classified by ASE guidelines. Conclusions 2D-derived echocardiographic increased LVWT in patients with LVH defined by increased LVM index was present in approximately 30-50%. Furthermore, anatomical increased LVWT in those with LVH classified by ASE guidelines was present in a varying range of 10-70%. Patients with concentric LVH had a low prevalence of histological myocyte hypertrophy (approximately 10%). Inconsistencies in classification methods reveal the need for more robust LVH terminologies and definition that is consistent across cardiac imaging and anatomico-pathological examination, particularly in patients with CM.