Ventricular strain is compromised outside of the coronary autoregulatory range – assessment by cardiovascular magnetic resonance

Abstract

Introduction Coronary autoregulation maintains near-constant myocardial blood flow in a range of approximately 60-140 mmHg of mean arterial pressure (MAP). Using oxygenation-sensitive (OS) cardiovascular magnetic resonance (CMR), we showed that myocardial oxygenation is compromised at MAP levels below the lower limit of this range. Above its upper limit we observed luxury perfusion and mild oxygen excess. There is a lack of data exploring the relationship between coronary autoregulation, myocardial oxygenation and ventricular function. CMR feature tracking software allows to quantify myocardial deformation and strain in OS images. Our aim was to explore our data from an animal study for associations between myocardial function, myocardial oxygenation and coronary blood flow (CBF) over a wide range of MAP levels. Methods In ten anaesthetized swine a flow probe was surgically attached to the proximal left anterior descending coronary artery before the animals were placed into a 3 Tesla MRI scanner. Starting from a baseline of 70 mmHg, MAP was varied in steps of 10-15 mmHg using phenylephrine and urapidil, respectively. At each MAP level, OS cine images and CBF readings of the anterior descending coronary artery were obtained, as well as arterial and coronary sinus blood gas samples to determine myocardial oxygen extraction ratio. Using feature tracking-software, strain data were acquired from images by tracing endo- and epicardial contours in end-diastole, from which peak global circumferential strain (GCS) was calculated for both ventricles. The relationships of peak GCS to MAP, CBF and myocardial oxygenation were established. Results We analysed 101 MAP levels, which ranged between 35 and 196 mmHg. Oxygenation as assessed by OS-CMR showed a curvi-linear relationship to MAP, with a steeper decrease below the lower limit of the autoregulatory range and an increase above its upper limit. Peak GCS of both ventricles became progressively impacted when MAP was forced from its baseline (70 mmHg) towards and beyond the lower and upper autoregulatory limit (dashed yellow lines in figure). There was no apparent association between changes of peak GCS and CBF. GCS of left ventricular myocardium decreased linearly with increasing myocardial oxygen extraction ratio (r=0.261, p=0.026), and in a non-linear fashion with decreasing myocardial tissue oxygenation. Discussion In a porcine model with non-diseased hearts, biventricular systolic function becomes compromised when MAP reaches levels either below or above coronary autoregulatory limits. Contractile dysfunction at pressures below the lower limit appears to be caused by myocardial deoxygenation. Conversely, hypertension-induced systolic dysfunction is associated with increased coronary flow and oxygen excess, which points to high afterload rather than O2 demand/supply imbalance as the most likely mechanism. We conclude that in hearts without coronary disease, global strain abnormalities elicited by hypotensive or hypertensive stress also differ in their underlying pathophysiological mechanisms.