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Table 1 Summary of studies correlating global deformation parameters with tissue characteristics

From: Myocardial tissue characterisation using echocardiographic deformation imaging

StudyPatients and PathologyAssessed global measuresAssessed Segmental measuresTissue correlatesCorrelations between global measures and tissue correlatesCorrelations 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 inboth 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 morethan 50% of PIELV and PIEF had (GLS (mean(SD)): −11.7 (3.3)%vs. -17.1 (1.7)%, P < 0.05).Patients with morethan 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 < 0.05Plasmatic 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.
  1. HCM Hypertrophic cardiomyopathy, GLS global longitudinal strain, SSL septal longitudinal strain, GCS global circumferential strain, NS not significant, AS aortic stenosis, PIELV percentage of infiltrating intra-endocardial lipid vacuoles, PIEF percentage of intra-endomyocardial fibrosis, GLSR global longitudinal systolic strain rate, SRe early systolic strain rate, SSRs septal systolic strain rate, SSRe septal early diastolic strain rate, SICAD small intramural coronary arteriole dysplasia, HCMMUT sarcomere mutation-positive HCM, HCMSMN sarcomere mutation-negative HCM, Mac-1 Macrophage 1 antigen, LFA-1 Lymphocyte function-associated antigen 1, MRI magnetic resonance imaging, FA-CM Friedreich ataxia cardiomyopathy