The relationship between myocardial microstructure and strain in chronic infarction using cardiovascular magnetic resonance diffusion tensor imaging and feature tracking.

BACKGROUND: Cardiac diffusion tensor imaging (cDTI) using cardiovascular magnetic resonance (CMR) is a novel technique for the non-invasive assessment of myocardial microstructure. Previous studies have shown myocardial infarction to result in loss of sheetlet angularity, derived by reduced secondary eigenvector (E2A) and reduction in subendocardial cardiomyocytes, evidenced by loss of myocytes with right-handed orientation (RHM) on helix angle (HA) maps. Myocardial strain assessed using feature tracking-CMR (FT-CMR) is a sensitive marker of sub-clinical myocardial dysfunction. We sought to explore the relationship between these two techniques (strain and cDTI) in patients at 3 months following ST-elevation MI (STEMI). METHODS: 32 patients (F = 28, 60 ± 10 years) underwent 3T CMR three months after STEMI (mean interval 105 ± 17 days) with second order motion compensated (M2), free-breathing spin echo cDTI, cine gradient echo and late gadolinium enhancement (LGE) imaging. HA maps divided into left-handed HA (LHM, - 90 < HA < - 30), circumferential HA (CM, - 30° < HA < 30°), and right-handed HA (RHM, 30° < HA < 90°) were reported as relative proportions. Global and segmental analysis was undertaken. RESULTS: Mean left ventricular ejection fraction (LVEF) was 44 ± 10% with a mean infarct size of 18 ± 12 g and a mean infarct segment LGE enhancement of 66 ± 21%. Mean global radial strain was 19 ± 6, mean global circumferential strain was - 13 ± - 3 and mean global longitudinal strain was - 10 ± - 3. Global and segmental radial strain correlated significantly with E2A in infarcted segments (p = 0.002, p = 0.011). Both global and segmental longitudinal strain correlated with RHM of infarcted segments on HA maps (p < 0.001, p = 0.003). Mean Diffusivity (MD) correlated significantly with the global infarct size (p < 0.008). When patients were categorised according to LVEF (reduced, mid-range and preserved), all cDTI parameters differed significantly between the three groups. CONCLUSION: Change in sheetlet orientation assessed using E2A from cDTI correlates with impaired radial strain. Segments with fewer subendocardial cardiomyocytes, evidenced by a lower proportion of myocytes with right-handed orientation on HA maps, show impaired longitudinal strain. Infarct segment enhancement correlates significantly with E2A and RHM. Our data has demonstrated a link between myocardial microstructure and contractility following myocardial infarction, suggesting a potential role for CMR cDTI to clinically relevant functional impact.

Cardiovascular MRI evidence of reduced systolic function and reduced LV mass in rheumatoid arthritis: impact of disease phenotype.

The accelerated risk of cardiovascular disease (CVD) in Rheumatoid Arthritis (RA) requires further study of the underlying pathophysiology and determination of the at-risk RA phenotype. Our objectives were to describe the cardiac structure and function and arterial stiffness, and association with disease phenotype in patients with established) RA, in comparison to healthy controls, as measured by cardiovascular magnetic resonance imaging (CMR). 76 patients with established RA and no history of CVD/diabetes mellitus were assessed for RA and cardiovascular profile and underwent a non-contrast 3T-CMR, and compared to 26 healthy controls. A univariable analysis and multivariable linear regression model determined associations between baseline variables and CMR-measures. Ten-year cardiovascular risk scores were increased in RA compared with controls. Adjusting for age, sex and traditional cardiovascular risk factors, patients with RA had reduced left ventricular ejection fraction (mean difference - 2.86% (- 5.17, - 0.55) p = 0.016), reduced absolute values of mid systolic strain rate (p < 0.001) and lower late/active diastolic strain rate (p < 0.001) compared to controls. There was evidence of reduced LV mass index (LVMI) (- 4.56 g/m2 (- 8.92, - 0.20), p = 0.041). CMR-measures predominantly associated with traditional cardiovascular risk factors; male sex and systolic blood pressure independently with increasing LVMI. Patients with established RA and no history of CVD have evidence of reduced LV systolic function and LVMI after adjustment for traditional cardiovascular risk factors; the latter suggesting cardiac pathology other than atherosclerosis in RA. Traditional cardiovascular risk factors, rather than RA disease phenotype, appear to be key determinants of subclinical CVD in RA potentially warranting more effective cardiovascular risk reduction programs.

Effects of hyperaemia on left ventricular longitudinal strain in patients with suspected coronary artery disease : A first-pass stress perfusion cardiovascular magnetic resonance imaging study.

AIMS: Myocardial perfusion imaging during hyperaemic stress is commonly used to detect coronary artery disease. The aim of this study was to investigate the relationship between left ventricular global longitudinal strain (GLS), strain rate (GLSR), myocardial early (E') and late diastolic velocities (A') with adenosine stress first-pass perfusion cardiovascular magnetic resonance (CMR) imaging. METHODS AND RESULTS: 44 patients met the inclusion criteria and underwent CMR imaging. The CMR imaging protocol included: rest/stress horizontal long-axis (HLA) cine, rest/stress first-pass adenosine perfusion and late gadolinium enhancement imaging. Rest and stress HLA cine CMR images were analysed using feature-tracking software for the assessment of myocardial deformation. The presence of perfusion defects was scored on a binomial scale. In patients with hyperaemia-induced perfusion defects, rest global longitudinal strain GLS (-16.9 ± 3.7 vs. -19.6 ± 3.4; p-value = 0.02), E' (-86 ± 22 vs. -109 ± 38; p-value = 0.02), GLSR (69 ± 31 vs. 93 ± 38; p-value = 0.01) and stress GLS (-16.5 ± 4 vs. -21 ± 3.1; p < 0.001) were significantly reduced when compared with patients with no perfusion defects. Stress GLS was the strongest independent predictor of perfusion defects (odds ratio 1.43 95% confidence interval 1.14-1.78, p-value <0.001). A threshold of -19.8% for stress GLS demonstrated 78% sensitivity and 73% specificity for the presence of hyperaemia-induced perfusion defects. CONCLUSIONS: At peak myocardial hyperaemic stress, GLS is reduced in the presence of a perfusion defect in patients with suspected coronary artery disease. This reduction is most likely caused by reduced endocardial blood flow at maximal hyperaemia because of transmural redistribution of blood flow in the presence of significant coronary stenosis.