Cardiac Magnetic Resonance T1 mapping in pulmonary hypertension. Is Native T1 mapping an alternative to Late Gadolinium Enhancement?
Geeshath Jayasekera1, Colin Church1, Martin Johnson1, Andrew Peacock1, and Aleksandra Radjenovic2

1Scottish Pulmonary Vascular Unit, Golden Jubilee National Hospital, Glasgow, United Kingdom, 2Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom

Synopsis

Pulmonary hypertension is a rare progressive disorder characterised by elevated pulmonary artery pressure leading to right ventricular failure and death. Native T1 mapping is a CMR technique for myocardial tissue characterisation that does not require MRI contrast administration1. We investigated whether native T1 values relate to invasive pressure measurements and markers of RV dysfunction in patients with pulmonary hypertension.

Background

Pulmonary hypertension is a rare progressive disorder characterised by elevated pulmonary artery pressure leading to right ventricular (RV) failure and death. Cardiac MR (CMR) derived right and left ventricular functional variables were shown to be prognostic in pulmonary hypertension1. We showed that late gadolinium enhancement (LGE) occurs at the Right Ventricular insertion points in patients with pulmonary hypertension2. It is suggested that a predilection for fibrosis to develop at the inter-ventricular insertion regions is caused by mechanical stress due to the bowing of the inter-ventricular septum into the Left ventricle (LV). Native T1 mapping is a CMR technique for myocardial tissue characterisation that does not require MRI contrast administration3. We investigated whether native T1 values relate to invasive pressure measurements and markers of RV dysfunction in patients with pulmonary hypertension (PH). We hypothesized that native T1 mapping maybe used as an alternative to LGE for characterisation of the RV insertion points in patients with PH.

Methods

36 patients suspected of pulmonary hypertension underwent cardiac MR and right heart catheterisation (male = 19, mean age 62 ± 15.1). Ventricular volumes and ejection fraction were determined by CMR while pulmonary artery pressure measurements, cardiac output and pulmonary vascular resistance (PVR) were obtained during right heart catheterisation. T1 maps were acquired on a Siemens Avanto 1.5T scanner using a MOLLI sequence4 on a mid ventricular short axis plane with a trigger delay to coincide with systole. Native T1 values were determined using regions of interest (ROI) in the RV insertion points, Inter-ventricular septum (IVS) and left ventricle (LV). ROI size and placement ensured avoidance of partial volume effects.

Results

Six of the 36 patients did not have pulmonary hypertension on right heart catheterisation. The other 30 patients (male =18, mean pulmonary artery pressure 47 ± 14 mmHg) consisted of 21 WHO Group 1 patients ( 8 Idiopathic Pulmonary Arterial Hypertension, 4 Connective Tissue Disease PH, 3 porto-pulmonary PH, 2 Congenital Heart Disease PH, 4 Pulmonary Veno-Occlusive Disease), 2 patients with PH secondary to left heart disease, 2 patients with PH associated with hypoxaemia and 5 patients with chronic thromboembolic pulmonary hypertension. Raised native T1 values at the RV insertion points were visually identified in all but one patient (mPAP 26, PVR 3.4 Wood Units) with pulmonary hypertension. In patients with pulmonary hypertension RV insertion point T1 values (1079±70) were significantly higher (p<0.001) compared to LV (984±43) and the inter-ventricular septum (985±40). There was no significant difference in T1 values between LV free wall and IVS. In PH patients Native T1 values of the RV insertion points were significantly correlated to RV Ejection Fraction (p = 0.004 Pearson R =-0.524), RV End Diastolic Volume Index (p = 0.001 Pearson R = 0.579), RV End Systolic Volume Index (p < 0.001 Pearson R 0.660) but not to CMR derived Left ventricular indices and Cardiac output or PVR at right heart catheterisation.

Conclusions

The native T1 values of the RV insertion points are increased in patients with pulmonary hypertension and are associated with CMR markers of RV dysfunction. These may suggest myocardial histological changes occurring at the right ventricular insertion points. Native T1 imaging may become a potential biomarker in patients with pulmonary hypertension and may be an alternative to late gadolinium enhancement without the need for a contrast agent.

Acknowledgements

British Heart Foundation, Siemens Medical for provision of the prototype T1-mapping sequence

References

1. Peacock AJ, Vonk Noordegraaf A. Cardiac magnetic resonance imaging in pulmonary arterial hypertension. Eur Respir Rev. 2013;22(130):526-34.

2. Blyth KG, Groenning BA, Martin TN, Foster JE, Mark PB, Dargie HJ, et al. Contrast enhanced-cardiovascular magnetic resonance imaging in patients with pulmonary hypertension. Eur Heart J. 2005;26(19):1993-9.

3. Kellman P, Hansen MS. T1-mapping in the heart: accuracy and precision. J Cardiovasc Magn Reson. 2014;16:2.

4. Messroghli DR, Radjenovic A, Kozerke S, Higgins DM, Sivananthan MU, Ridgway JP. Modified Look-Locker inversion recovery (MOLLI) for high-resolution T1 mapping of the heart. Magn Reson Med. 2004;52(1):141-6.

Figures

CMR T1 map of a patient with pulmonary arterial hypertension showing higher T1 values at the RV insertion points

Summary of native T1 measurements (mean with SD) in three regions of interest (LV = left ventricle, Sep= inter-ventricular septum, IP = Insertion points) in 30 patients with pulmonary hypertension



Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)
3166