Abstract
BackgroundMyocardial T1 relaxation times have been reported to be markedly abnormal in diverse myocardial pathologies, ascribed to interstitial changes, evaluated by T1 mapping and calculation of extracellular volume (ECV). T1 mapping is sensitive to myocardial water content of both intra- and extracellular in origin, but the effect of intravascular compartment changes on T1 has been largely neglected. We aimed to assess the role of intravascular compartment on native (pre-contrast) T1 values by studying the effect of adenosine-induced vasodilatation in patients with severe aortic stenosis (AS) before and after aortic valve replacement (AVR).Methods42 subjects (26 patients with severe AS without obstructive coronary artery disease and 16 controls) underwent cardiovascular magnetic resonance at 3 T for native T1-mapping (ShMOLLI), first-pass perfusion (myocardial perfusion reserve index-MPRI) at rest and during adenosine stress, and late gadolinium enhancement (LGE).ResultsAS patients had increased resting myocardial T1 (1196 ± 47 ms vs. 1168 ± 27 ms, p = 0.037), reduced MPRI (0.92 ± 0.31 vs. 1.74 ± 0.32, p < 0.001), and increased left ventricular mass index (LVMI) and LGE volume compared to controls. During adenosine stress, T1 in AS was similar to controls (1240 ± 51 ms vs. 1238 ± 54 ms, p = 0.88), possibly reflecting a similar level of maximal coronary vasodilatation in both groups. Conversely, the T1 response to stress was blunted in AS (ΔT1 3.7 ± 2.7% vs. 6.0 ± 4.2% in controls, p = 0.013). Seven months after AVR (n = 16) myocardial T1 and response to adenosine stress recovered towards normal. Native T1 values correlated with reduced MPRI, aortic valve area, and increased LVMI.ConclusionsOur study suggests that native myocardial T1 values are not only influenced by interstitial and intracellular water changes, but also by changes in the intravascular compartment. Performing T1 mapping during or soon after vasodilator stress may affect ECV measurements given that hyperemia alone appears to substantially alter T1 values.
Highlights
Myocardial T1 relaxation times have been reported to be markedly abnormal in diverse myocardial pathologies, ascribed to interstitial changes, evaluated by T1 mapping and calculation of extracellular volume (ECV)
There were a small number of diabetics (15%) in the aortic stenosis (AS) patient group, but their blood glucose and lipid levels were similar to the controls
We confirm that resting myocardial T1 values are elevated in severe AS patients compared to normal controls and correlate with markers of disease severity, such as aortic valve area, Left ventricular hypertrophy (LVH) [8], and myocardial perfusion reserve
Summary
Myocardial T1 relaxation times have been reported to be markedly abnormal in diverse myocardial pathologies, ascribed to interstitial changes, evaluated by T1 mapping and calculation of extracellular volume (ECV). T1 mapping is sensitive to myocardial water content of both intra- and extracellular in origin, but the effect of intravascular compartment changes on T1 has been largely neglected. Native (pre-contrast) T1 values are elevated in conditions associated with increased myocardial water content such as acute myocardial infarction [2,3], oedema [4], acute myocarditis [5] and Takotsubo cardiomyopathy [6]. T1 values have been shown to be elevated in conditions associated with myocardial fibrosis and expanded interstitial space such as dilated cardiomyopathy, hypertrophic cardiomyopathy [7] and aortic stenosis [8]. The documented native T1 elevation in diffuse fibrosis cannot originate directly from collagen itself, which in large enough concentrations would tend to reduce T1 to other proteins [15]. The influence of intravascular water volume to the T1 values has never been investigated before, either in normal or pathological conditions
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