Does CMR improve aetiological sub-phenotyping beyond echocardiography in patients with elevated LV filling pressure? A prospective registry study (PREFER-CMR)

Figures

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  Figure 1. Echocardiographic diagnoses in patients with high CMR LVFP. Normal findings, LVH and HFpEF were most common, followed by IHD, cardiomyopathy and valvular disease. Less frequent diagnoses included structural and infiltrative conditions. CMR, cardiovascular magnetic resonance; LVFP, left ventricular filling pressure.

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  Figure 2. CMR sub-phenotyping in patients with normal or non-diagnostic echocardiography. HFpEF, IHD and myocarditis were the most frequent findings, with additional diagnoses spanning cardiomyopathies and inflammatory conditions. CMR, cardiovascular magnetic resonance; DCM, dilated cardiomyopathy; HCM, hypertrophic cardiomyopathy; HFpEF, heart failure with preserved ejection fraction; ICM, ischaemic cardiomyopathy; IHD, ischaemic heart disease; MINOCA, myocardial infarction with non-obstructive coronary arteries; NICM, non-ischaemic cardiomyopathy; PPCM, peripartum cardiomyopathy.

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  Figure 3. Funnel plot: CMR sub-phenotyping in patients with non-specific LVH and cardiomyopathy. HFpEF was universal, with HCM, myocarditis, IHD and other cardiomyopathies as additional findings. CMR, cardiovascular magnetic resonance; CHD, congenital heart disease; DCM, dilated cardiomyopathy; HFpEF, heart failure with preserved ejection fraction; HCM, hypertrophic cardiomyopathy; IHD, ischaemic heart disease; LVH, left ventricular hypertrophy; MINOCA, myocardial infarction with non-obstructive coronary arteries; NICM, non-ischaemic cardiomyopathy; VHD, valvular heart disease.

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  Figure 4. CMR sub-phenotyping in patients with IHD and HCM. CMR confirmed the echocardiographic diagnosis, with additional findings including HFpEF, myocarditis and other cardiomyopathies. ARVC, arrhythmogenic right ventricular cardiomyopathy; CMR, cardiovascular magnetic resonance; HCM, hypertrophic cardiomyopathy; HFpEF, heart failure with preserved ejection fraction; IHD, ischaemic heart disease; MINOCA, myocardial infarction with non-obstructive coronary arteries; NICM, non-ischaemic cardiomyopathy; VHD, valvular heart disease.

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  Figure 5. Multimodal cardiac assessment of a 39-year-old female with SOB and palpitations. (a–d) TTE shows an indexed LA volume of 30 mL/m², E velocity of 1.1 m/sec, E/e’ of 11.6, and TR peak velocity of 2.2 m/sec, indicating an overall normal study. (e–g) CMR cine images demonstrate LVH (LV mass: 70 g/m²) with preserved LVEF (51%). (h–i) Native T1 reveals islets of global changes in the myocardium, whereas ECV mapping reveals more focal fibrosis in lateral wall. (g, j) LGE imaging highlights mesocardial fibrosis in the lateral wall (white arrows), consistent with NICM. CMR, cardiac magnetic resonance; ECV, extracellular volume; LA, left atrium; LV, left ventricle; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; LVFP, left ventricular filling pressure; LGE, late gadolinium enhancement; NICM, non-ischaemic cardiomyopathy; SOB, shortness of breath; TTE, transthoracic echocardiography; TR, tricuspid regurgitation.