Table 1 Summary of studies correlating global deformation parameters with tissue characteristics
From: Myocardial tissue characterisation using echocardiographic deformation imaging
Study | Patients and Pathology | Assessed global measures | Assessed Segmental measures | Tissue correlates | Correlations between global measures and tissue correlates | Correlations between segmental measures and tissue correlates |
|---|---|---|---|---|---|---|
Almaas et al. 2013 (18). | 63 patients. 24 patients had septal myectomy samples analysed. HCM with/without ventricular arrhythmia. | GLS (n = 63); HCM without ventricular arrhythmias (mean(SD)) -14.7 (3.4), with ventricular arrhythmias −12.2 (3.7). | SSL (n = 63); HCM without ventricular arrhythmia (mean(SD)) -13.6 (5.6), with ventricular arrhythmia - 9.0 (4.0). | Fibrosis (perivascular, interstitial, subendocardial, replacement). | – | SSL (n = 24); total fibrosis (R2 0.31, P < 0.05), interstitial fibrosis (R2 0.36, P < 0.05), replacement fibrosis (R2 0.03, NS). |
Almaas et al. 2014 (19). | HCM (n = 32). | (Total fibrosis> = 15%) GLS (OR 1.27, NS), GCS (OR 1.08, NS). | (Total fibrosis> = 15%) Septal LS (OR 1.38, P < 0.05), (Multivariate OR 1.79, P < 0.05). Septal CS (OR 1.06, NS). | Fibrosis (Total, interstitial, replacement). | – | SSL with fibrosis: total (r = 0.50, P < 0.05), interstitial (r = 0.40 P < 0.05), replacement fibrosis (r = 0.28, NS). |
Kobayashi et al. 2013 (13). | HCM (n = 171). | 3 subgroups: HCM without hypertension, HCM with hypertension, and hypertensive heart disease without HCM. GLSR (mean(SD)) (−1.05 (0.3), − 1.01 (0.3), and − 1.14 (0.3), NS respectively) and SRe (1.03 (0.4), 0.96 (0.4), and 1.09 (0.3), NS, respectively). | 3 subgroups: HCM without hypertension, HCM with hypertension, and hypertensive heart disease without HCM. Basal SSRs (mean(SD)) (− 0.87 (0.5), − 0.95 (0.5), and − 0.98 (0.4), NS, respectively) and SSRe (0.76 (0.5), 0.86 (0.5), and 0.82 (0.5), NS, respectively). | Myocyte hypertrophy, myocyte disarray, SICAD, interstitial fibrosis. | – | SSRe, myocyte disarray −0.19, P < 0.05. SSRs, myocyte hypertrophy 0.21, P < 0.05, myocyte disarray 0.23 P < 0.05. |
Witjas-Paalberends, et al. 2014 (11). | HCM (n = 46). | GLS (mean(SD)) was reduced in both HCMMUT (− 16.0 (3.2)%) and HCMSMN (− 15.1 (3.1)%) compared with controls (− 21.0 ( 3.2)%, P < 0.001 and P < 0.05 respectively). | SSL (mean(SD)) (%) HCMMUT (−7.0 (4.3) P < 0.001, SSRs(1/s) -0.64 (0.58), P < 0.05, SSRe (1/s) 0.47 (0.33) P < 0.001 versus controls). | Cardiomyocyte maximal developed tension. | – | Basal SSL: maximal tension (Spearman’s ρ 0.46, P < 0.05). |
Park et al. 2019 (23). | Severe AS (n = 71) | GLS (mean(SD)) (fibrosis, mild − 16.30 (2.97), moderate − 14.76 (3.95), severe −12.65 (3.07), P < 0.05) | – | Fibrosis. | GLS, r = 0.421, P < 0.001. Multivariate regression (R2 0.35, P < 0.05). | – |
Ávila-Vanzzini et al. 2016 (21). | Severe AS (n = 18). | Patients with more than 50% of PIELV and PIEF had (GLS (mean(SD)): −11.7 (3.3)% vs. -17.1 (1.7)%, P < 0.05). Patients with more than 50% fibrosis had significantly lower GLS. | – | Myocardial interstitial fibrosis, Fatty infiltration. | GLS: Fibrosis (R2 0.661, P < 0.05). | – |
Fabiani et al. 2016 (22). | Severe AS (n = 36, Histological analysis; n = 23). | GLS % (n = 36) (mean(SD)) −14.0 (3.88). | SSRs (1/s) (mean(SD)) −0.58 (0.17), SSRe (1/s) 0.62 (0.32), SSL (%) − 9.63 (2.97). | Fibrosis, interstitial miRNA-21, plasmatic miRNA-21. | GLS, fibrosis: R2 = 0.30 and P < 0.05. Interstitial miRNA-21, GLS: R2 = 0.34 and P < 0.05. | SSL, Fibrosis: R2 = 0.36 and P < 0.05; SSRs: R2 = 0.39 and P < 0.001; SSRe: R2 = 0.35 and P < 0.05. Interstitial miRNA-21, SSL: R2 = 0.32 and P < 0.05 Plasmatic miRNA-21, SSL: R2 = 0.35; P < 0.05. |
Cameli et al. 2016 (20). | DCM, ICM (n = 47). | Patients with extensive fibrosis (> 50%) versus fibrosis(≤50%); GLS, GCS and torsion (mean(SD)) (− 5.4 (2.2) vs − 15.2 (9.1)%, P < .0001; − 10.9 (3.1) vs − 16.2 (9.8)%, P < 0.05 and 4.2 (1.3) vs 6.6 (2.5)°, respectively). | – | Myocardial fibrosis. | GLS (r = 0.75, P < 0.001). GCS and LV torsion (r = 0.61, P < 0.05 and r = 0.52, P < 0.05, respectively). | – |
Escher et al. 2013 (24). | Myocarditis (n = 25). | In the acute phase all patients showed a reduction in GLSR (mean(SD)) (0.53 (0.29) 1/s) and GLS (− 8.36 (3.47)%) At follow-up GLS and GLSR were significantly lower in patients with inflammation, in contrast to the patients without inflammation (− 9.4 (1.4) versus − 16.8 (2.0)%, P < 0.0001; 0.78 (0.4) versus 1.3 (0.3) 1/s, respectively). | – | Lymphocytic infiltrates, monocytes/macrophages (Mac-1). | GLS; lymphocytic infiltrates (for CD3 r = 0.7, P < 0.0001, and LFA-1 r = 0.8, P < 0.0001) but not with monocytes/macrophages (Mac-1). | |
Kasner et al. 2013 (25). | Acute myocarditis (n = 34). | GLS (mean(SD)) (No myocarditis vs acute myocarditis − 17.86 (3.86) vs − 10.24 (4.12), P < 0.05) GLSR (No myocarditis vs acute myocarditis 1.24 (0.26) vs 0.79 (0.27), P < 0.05). | – | – | – | – |
Mehta et al. 2019 [28]. | Cardiac Amyloidosis (n = 59) | GLS (mean (SD)) in patients with low-to-moderate amyloid burden versus patients with high amyloid burden − 10.7 (4.9) vs − 6.4 (3.7), P < 0.05. | – | – | – | – |