Abstract

BackgroundBoth ischemic and non-ischemic heart disease can cause disturbances in the myocardial blood volume (MBV), myocardial perfusion and the myocardial extracellular volume fraction (ECV). Recent studies suggest that native myocardial T1 mapping can detect changes in MBV during adenosine stress without the use of contrast agents. Furthermore, native T2 mapping could also potentially be used to quantify changes in myocardial perfusion and/or MBV. Therefore, the aim of this study was to explore the relative contributions of myocardial perfusion, MBV and ECV to native T1 and native T2 at rest and during adenosine stress in normal physiology.MethodsHealthy subjects (n = 41, 26 ± 5 years, 51% females) underwent 1.5 T cardiovascular magnetic resonance (CMR) scanning. Quantitative myocardial perfusion [ml/min/g] and MBV [%] maps were computed from first pass perfusion imaging at adenosine stress (140 microg/kg/min infusion) and rest following an intravenous contrast bolus (0.05 mmol/kg, gadobutrol). Native T1 and T2 maps were acquired before and during adenosine stress. T1 maps at rest and stress were also acquired following a 0.2 mmol/kg cumulative intravenous contrast dose, rendering rest and stress ECV maps [%]. Myocardial T1, T2, perfusion, MBV and ECV values were measured by delineating a region of interest in the midmural third of the myocardium.ResultsDuring adenosine stress, there was an increase in myocardial native T1, native T2, perfusion, MBV, and ECV (p ≤ 0.001 for all). Myocardial perfusion, MBV and ECV all correlated with both native T1 and native T2, respectively (R2 = 0.35 to 0.61, p < 0.001 for all).Multivariate linear regression revealed that ECV and perfusion together best explained the change in native T2 (ECV beta 0.21, p = 0.02, perfusion beta 0.66, p < 0.001, model R2 = 0.64, p < 0.001), and native T1 (ECV beta 0.50, p < 0.001, perfusion beta 0.43, p < 0.001, model R2 = 0.69, p < 0.001).ConclusionsMyocardial native T1, native T2, perfusion, MBV, and ECV all increase during adenosine stress. Changes in myocardial native T1 and T2 during adenosine stress in normal physiology can largely be explained by the combined changes in myocardial perfusion and ECV.Trial registrationClinicaltrials.gov identifier NCT02723747. Registered March 16, 2016.

Highlights

  • Both ischemic and non-ischemic heart disease can cause disturbances in the myocardial blood volume (MBV), myocardial perfusion and the myocardial extracellular volume fraction (ECV)

  • Stress ECV images could not be processed in 4 cases because pre and post T1 maps were mistakenly acquired with different field of view (FOV), and these cases were excluded from analysis of ECV

  • We demonstrate that native myocardial T1, native myocardial T2, myocardial perfusion, MBV, and ECV all increase in response to adenosine stress in healthy subjects

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Summary

Introduction

Both ischemic and non-ischemic heart disease can cause disturbances in the myocardial blood volume (MBV), myocardial perfusion and the myocardial extracellular volume fraction (ECV). Recent studies suggest that native myocardial T1 mapping can detect changes in MBV during adenosine stress without the use of contrast agents. The aim of this study was to explore the relative contributions of myocardial perfusion, MBV and ECV to native T1 and native T2 at rest and during adenosine stress in normal physiology. Global and focal reduction in myocardial blood flow (MBF) [ml/min] during adenosine stress first pass imaging with cardiovascular magnetic resonance (CMR) has a high diagnostic accuracy for detecting significant coronary stenosis [2,3,4,5,6]. Significant coronary artery stenosis induces an increase in MBV by capillary recruitment and dilatation to supply the demanded oxygen to the cardiac myocytes. Disturbances in MBV can detect and determine the functional relevance of a significant coronary stenosis [12]

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