Increased Aortic Stiffness With Acute Exercise in Heart Failure: Assessment by Cardiovascular Magnetic Resonance.

This study aimed to investigate the acute changes in proximal aortic distensibility, a measure of aortic stiffness, induced by acute exercise in participants with and without heart failure (HF). Participants with HF (n = 24) and without HF (n = 26) underwent cardiovascular magnetic resonance (CMR) (1.5 T) imaging at rest and after submaximal supine bicycle ergometry. The participants were further categorized into HF with reduced ejection fraction (HFrEF) (n = 14) and HF with preserved ejection fraction (n = 10) based on the left ventricular ejection fraction. At rest and immediately after exercise, cine CMR images of the cross-sectional ascending and descending aorta at the pulmonary artery bifurcation level were obtained to determine aortic distensibility (AoD), with lower AoD indicating greater aortic stiffness. Differences in means of values at rest and before and after exercise were compared using the nonparametric Wilcoxon sign test. There was no significant difference in AoD at rest between subjects with HF and controls. However, immediately after exercise, participants with HF but not controls exhibited a significant reduction in AoD, indicating higher aortic stiffness related to exercise (median [interquartile range] for the ascending aorta: 3.16 (1.26) × 10-3 mm Hg-1 to 2.39 (1.57) × 10-3 mm Hg-1 and the descending aorta: 4.19 (2.58) × 10-3 mm Hg-1 to 2.96 (1.79) × 10-3 mm Hg-1) (both p = 0.023). This decrease was particularly observed in participants with HFrEF but not in those with HF with preserved ejection fraction. Exercise-induced aortic stiffness, detectable by noninvasive CMR, may contribute to unfavorable ventricular-vascular interactions during exercise in participants with HF, especially HFrEF.

Cardiovascular magnetic resonance feature tracking strain analysis for discrimination between hypertensive heart disease and hypertrophic cardiomyopathy.

BACKGROUND: Hypertensive heart disease (HHD) and hypertrophic cardiomyopathy (HCM) are both associated with an increased left ventricular (LV) wall thickness. Whilst LV ejection fraction is frequently normal in both, LV strain assessment could differentiate between the diseases. We sought to establish if cardiovascular magnetic resonance myocardial feature tracking (CMR-FT), an emerging method allowing accurate assessment of myocardial deformation, differentiates between both diseases. Additionally, CMR assessment of fibrosis and LV hypertrophy allowed association analyses and comparison of diagnostic capacities. METHODS: Two-hundred twenty-four consecutive subjects (53 HHD, 107 HCM, and 64 controls) underwent 1.5T CMR including native myocardial T1 mapping and late gadolinium enhancement (LGE). Global longitudinal strain (GLS) was assessed by CMR-FT (CVi42, Circle Cardiovascular Imaging Inc.). RESULTS: GLS was significantly higher in HCM patients (-14.7±3.8 vs. -16.5±3.3% [HHD], P = 0.004; or vs. -17.2±2.0% [controls], P<0.001). GLS was associated with LV mass index (HHD, R = 0.419, P = 0.002; HCM, R = 0.429, P<0.001), and LV ejection fraction (HHD, R = -0.493, P = 0.002; HCM, R = -0.329, P<0.001). In HCM patients, GLS was also associated with global native T1 (R = 0.282, P = 0.003), and LGE volume (ρ = 0.380, P<0.001). Discrimination between HHD and HCM by GLS (c = 0.639, 95% confidence interval [CI] 0.550-0.729) was similar to LV mass index (c = 0.643, 95% CI 0.556-0.731), global myocardial native T1 (c = 0.718, 95% CI 0.638-0.799), and LGE volume (c = 0.680, 95% CI 0.585-0.775). CONCLUSION: CMR-FT GLS differentiates between HHD and HCM. In HCM patients GLS is associated with myocardial fibrosis. The discriminatory capacity of CMR-FT GLS is similar to LV hypertrophy and fibrosis imaging markers.