A high-salt diet in Dahl salt-sensitive rats progressively deteriorated longitudinal strain compared to control (-17% vs -27%; P<0.001), which correlated with subendocardial layer fibrosis.
Does a high-salt diet-induced hypertensive heart disease model show correlation between left ventricular wall strain and transmural structural remodeling?
Longitudinal strain measured by speckle tracking echocardiography correlates with subendocardial fibrotic changes and may serve as a surrogate marker for risk stratification in hypertensive heart failure.
Absolute Event Rate: -17% vs -27%
p-value: p=<0.001
Left ventricular (LV) systolic wall strain is a new candidate for prognostic indicator of hypertensive heart failure. It remains unclear how underlying transmural structural remodeling corresponds to LV wall systolic deformation as hypertensive hypertrophy progresses. We fed 68 Dahl salt-sensitive rats a high-salt (hypertensive group) or low-salt diet (control group) from 6 weeks old. At 10, 14, and 18 weeks, pressure-volume relation, transmural distribution of LV fibrosis, and myocyte hypertrophy were evaluated. LV global longitudinal and circumferential strain was measured with speckle tracking echocardiography. Emax was preserved throughout the study period, whereas τ and end-diastolic pressure-volume relation progressively deteriorated from 14 weeks (diastolic dysfunction stage). Lung weight increased significantly at 18 weeks (decompensated stage). Histological percentage area fibrosis and collagen type I/III, myocyte hypertrophy, and α-myosin heavy chain isoform increased in the subendocardial layer at 14 weeks and progressed into the midlayer at 18 weeks. Longitudinal strain progressively deteriorated in the hypertensive group versus control group at 14 weeks (hypertensive group: -17±3%, control: -27±4%; P<0.001), and circumferential strain decreased at 18 weeks (hypertensive group: -17±2%, control: -27±3%; P=0.002). After adjustment for systolic wall stress, subendocardial percentage area fibrosis was selected as the independent determinant of longitudinal strain. This study showed that LV wall strain alternations were accompanied by fibrosis and myocyte hypertrophy from subendocardium to epicardium, and longitudinal strain related significantly to subendocardial layer fibrosis. Longitudinal strain could be a surrogate of subendocardial fibrotic changes and may be useful for risk stratification of hypertensive heart failure.
Ishizu et al. (2014) studied Hypertensive heart disease (n=68). High-salt diet vs. Low-salt diet was evaluated on Longitudinal strain at 14 weeks (p=<0.001). A high-salt diet in Dahl salt-sensitive rats progressively deteriorated longitudinal strain compared to control (-17% vs -27%; P<0.001), which correlated with subendocardial layer fibrosis.