Left ventricular hypertrophy revisited. cell and matrix expansion have disease-specific relationships

Left ventricular hypertrophy (LVH), a common pathway in health and disease, occurs because of cellular hypertrophy and expansion of extracellular matrix. Cardiovascular magnetic resonance (CMR) using T1 mapping can split LVMinto cellular and matrix components by measuring the extracellular volume fraction (ECV). Thisapproach was used to explore the biology of LVH. 190 subjects underwent CMR, including healthy volunteers (HV; n=30), and 160 subjects with LVH, defined as increased indexed LVM: athletes (AT; n=50), severe aortic stenosis awaiting valvereplacement (AS; n=30) Fabry disease (FD; n=20), hypertrophic cardiomyopathy (HCM; n=30), and cardiac amyloidosis (CA; n=30).We concluded that, for most causes of LVH, on average there is a proportional increase in cellular andmatrix components with 2 exceptions: physiological cell hypertrophy in AT (mainly cellular) and amyloidosis (almost exclusively matrix). Thus, ECV-derived volumes provide pathophysiological insights beyond quantifyingthe degree of hypertrophy.