Magnetic susceptibility weighted cardiovascular MR (CMR) is an emerging (pre)clinical application in myocardial tissue characterization [1,2]. T₂^* weighted CMR is usually limited to single phase end diastolic acquisitions. Dynamic mapping of myocardial T₂^* allows probing the myocardium in different physiological states and holds the promise to facilitate distinction of healthy and pathologic tissue. High spatially and temporally resolved T₂^* mapping has been demonstrated in the in vivo human heart at 7.0T [3]. Myocardial BOLD contrast or T₂^* are commonly regarded as a surrogate for myocardial tissue oxygenation [2], but the factors influencing effective transversal relaxation times are numerous [4-6]. For meaningful interpretation of myocardial T₂^*, it is essential to identify influential factors and their contributions to T₂^*. This study examines the relationship of cardiac morphology and T₂*, and demonstrates that T₂^* in the ventricular septum correlates with septal wall thickness across the cardiac cycle in healthy volunteers at 7.0T.Ten healthy volunteers (7 male,age=40.8±15.6,BMI=22.8±3.2kg/m²) were examined using a 7.0T whole body MR system (Siemens Healthcare,Erlangen,Germany). A 16 channel transceiver array tailored for CMR at 7.0T was used for signal excitation/reception [7]. For CINE T₂^* mapping a cardiac triggered interleaved multi-echo gradient-echo technique (TE=(2.04-10.20)ms,spatial resolution=(1.1x1.1x4.0)mm³) was employed. Midventricular short axis views were acquired. Acoustic triggering (MRI.TOOLS GmbH,Berlin,Germany) was applied for detecting the onset of the cardiac cycle. T₂^* sensitized images were de-noised [8] and co-registered. The left ventricular myocardium was manually segmented for each cardiac phase and wall thickness was measured. T₂^* mapping was conducted using a mono-exponential signal decay model. R² and T₂^* fit standard deviation (T₂^*-STD, [9]) were used as goodness of fit measures. Fitting results with R²<0.7,T₂^*-STD>3ms or (0ms>T₂^*>50ms) were excluded from further analysis to account for image artifacts. Only septal segments (segment 8,9 [10]) were evaluated since they have been shown to provide most reliable T₂^* [11]. Cardiac phases were unified to allow for averaging between subjects. Correlation of mean septal T₂^* and wall thickness was assessed employing Pearson correlation coefficient. To investigate macroscopic magnetic field fluctuations, temporally resolved field maps were calculated from phase images obtained by the pulse sequence used for T₂^* mapping for three volunteers in short axis and 4 chamber views.Figure 1 illustrates T₂^* maps of a mid-ventricular short axis view of one volunteer overlaid onto anatomical FLASH images over the cardiac cycle. Septal T₂^* was found to change across the cardiac cycle increasing in systole and decreasing in diastole. Mean septal wall thickness was found to be 7.4±1.6mm, mean T₂^* was 14.2±1.4ms. Mean end-systolic septal wall thickness and T₂^* were 9.1±1.3mm and 14.7±1.5ms. Mean end diastolic values were 6.1±1.0mm and T₂^*=13.7±1.3ms. The mean T₂^* variation over the cardiac cycle was 3.5±1.0ms. Figure 2a shows the time course of mean septal T₂^* and wall thickness averaged per cardiac phase for all volunteers. Figure 2b shows the same values in a scatter plot. A significant positive correlation was found between mean septal T₂^* and wall thickness (R=0.92,p<0.001). The mean temporal variation of the macroscopic intra-voxel magnetic field gradient in the septum was found to be 1.9±0.5Hz/voxel.This study investigated ventricular septal T₂^* and wall thickness at 7.0T with high spatio-temporal resolution in healthy volunteers. Cyclic changes of mean T₂^* were found over the cardiac cycle with an increase in systole and a decrease in diastole. This is in line with previous reports about myocardial BOLD signal intensity changes reporting increased BOLD signal in systole [12,13]. The found macroscopic magnetic field fluctuations can be considered minor and excluded as source of the observed T₂^* changes. While T₂^* is often regarded as surrogate for tissue oxygenation, the found systolic increase of T₂^* cannot be explained by increased oxygenation. Instead it is potentially dominated by changes in relative myocardial blood volume. When the ventricular muscle contracts in systole, ventricular myocardial wall stress is massively increased. This temporarily ceases blood influx into the left ventricular myocardium [14]. At the same time blood is squeezed out of it [14] thereby decreasing the blood volume fraction and the amount of deoxygenized blood per voxel, which induces a T₂^* increase. Another possible confounder could be mesoscopic variations in magnetic field homogeneity induced by changes of myocardial morphology during contraction and relaxation.Ventricular septal T₂^* changes periodically during the cardiac cycle in healthy volunteers at 7.0T; increasing in systole and decreasing in diastole. Septal T₂^* correlates with septal wall thickness. Our findings suggest that blood volume fraction plays an important role in myocardial T₂^*. Temporally resolved MR relaxation mapping could be beneficial for understanding cardiac (patho)physiology in vivo.