Heart Failure (HF) is a complex clinical syndrome characterised by high levels of morbidity and mortality. Half of the 1 million people in the UK (1) with heart failure have normal, or near normal systolic fraction. These patients are classified as Heart Failure with preserved Ejection Fraction (HFpEF). The prevalence of HFpEF is expected to increase by 25% by 2030 (2).

There are challenges in diagnosing HFpEF due to the heterogeneous aetiologies and pathophysiologies that underlie this condition. Pressure volume loop studies are the diagnostic gold standard (3) however it is not appropriate for all patients to have invasive investigations. Practically echocardiography is widely used to detect diastolic dysfunction although only provides an indirect assessment of LV filling with no characterisation of myocardial tissue and in trials, poor correlation with invasive measurements (4).

There is an unmet clinical need in accurately detecting myocardial stiffness in vivo and diagnosing HFpEF. Magnetic Resonance Elastography (MRE) has been shown to detect stiffness in many organs and so we have applied this concept to measure myocardial stiffness.

This technique quantifies myocardial stiffness in vivo using transient MRE (tMRE). Aortic valve closure results in a shear wave that propagates through the myocardium. The speed of this wave can be measured if the sequence is timed to the exact valve closure time. Individual sequences are ECG and navigator gated and take approximately 90 seconds, the complete scan including planning takes approximately 40 minutes, making the scan very 'patient friendly'. Our study has three parts: sequence development and implementation on a clinical 3T MR scanner (Philips Medical Systems), a volunteer study (n=5) to assess cardiac and respiratory motion compensation strategies and the sensitivity of the motion encoding gradients; and a patient study (n=6) (Figure 1) to compare tMRE with conventional imaging markers of diastolic dysfunction (left ventricular hypertrophy (LVH) and left atrial (LA) dilatation and E/E’ from echocardiography). One patient had correlation with invasive pressure volume loop studies. The tMRE sequence was successfully developed and implemented. Motion-encoded images (motion sensitized gradient at 165Hz) demonstrated myocardial wall shear waves generated from the aortic valve closure at 329ms (range 270-420ms) after the R wave. tMRE successfully showed a difference in speed of propagation between volunteers and patients (speed volunteers 12.6m/s ± 3.0m/s, speed patients 20.8m/s ±4.4m/s, p<0.05, Figure 2). When compared to the volunteers, 5 out of the 6 patients had significant LVH and LA dilatation that supports the clinical diagnosis of HFpEF. One patient who had invasive pressure volume loop studies was found to have increased left ventricular end diastolic pressure (LVEDP) and prolonged tau (represents the exponential decay of the ventricular pressure during isovolumic relaxation) – this patient had a faster speed of sheer wave propagation in tMRE. However, there was no clear correlation shown between the speed of propagation in patients and the degree of diastolic dysfunction (measured by degree of LVH, LA dilatation and E/E’). Discussion We noted a statistical significant difference in speed of propagation between patients and volunteers that reflects a difference in myocardial stiffness. This was expected as they are clinical patients, 5 out of 6 had other imaging results supportive of diastolic impairment (LVH, LA dilatation) and one patient had invasive markers of diastolic impairment. An increased tau means delayed relaxation that results in a stiffer myocardium: this correlates with the tMRE results (increased speed). The technique of non-invasively measuring myocardial stiffness has the potential to have an enormous clinical impact. The current AHA guidelines for diagnosing HFpEF no longer include imaging measures of diastolic dysfunction such as LVH, LA dilatation and raised E/E’ (5). In our small cohort no clear correlation was noted between LVH, LA dilatation and E/E’: this accurately reflects current imaging challenges in diagnosis of HFpEF. We intend to continue this work by correlating tMRE in vivo myocardial stiffness measures in more patients with the accepted gold standard diagnostic techniques, invasive pressure volume loop studies and histopathology. We have successfully developed and applied a new technique to quantify myocardial stiffness in vivo from shear waves generated by aortic valve closure. tMRE is a patient friendly sequence and does not require a transducer. We have shown that tMRE has potential to be an important diagnostic tool for the early detection of myocardial stiffness.