T1 Mapping in Discrimination of Hypertrophic Phenotypes: Hypertensive Heart Disease and Hypertrophic Cardiomyopathy

Rocío Hinojar(Goethe University Frankfurt), Niharika Varma(Goethe University Frankfurt), Nick Child(Goethe University Frankfurt), Benjamin Goodman(Goethe University Frankfurt), Andrew Jabbour(Goethe University Frankfurt), Chung-Yao Yu(Goethe University Frankfurt), Rolf Gebker(Goethe University Frankfurt), Adelina Doltra(Goethe University Frankfurt), Sebastian Kelle(Goethe University Frankfurt), Sitara Khan(Goethe University Frankfurt), Toby Rogers(Goethe University Frankfurt), Eduardo Arroyo(Goethe University Frankfurt), Ciara Cummins(Goethe University Frankfurt), Gerald Carr‐White(Goethe University Frankfurt), Eike Nagel(Goethe University Frankfurt), Valentina O. Püntmann(Goethe University Frankfurt)
Circulation Cardiovascular Imaging
December 1, 2015
Cited by 249

Abstract

BACKGROUND: The differential diagnosis of left ventricular (LV) hypertrophy remains challenging in clinical practice, in particular, between hypertrophic cardiomyopathy (HCM) and increased LV wall thickness because of systemic hypertension. Diffuse myocardial disease is a characteristic feature in HCM, and an early manifestation of sarcomere-gene mutations in subexpressed family members (G+P- subjects). This study aimed to investigate whether detecting diffuse myocardial disease by T1 mapping can discriminate between HCM versus hypertensive heart disease as well as to detect genetically driven interstitial changes in the G+P- subjects. METHODS AND RESULTS: Patients with diagnoses of HCM or hypertension (HCM, n=95; hypertension, n=69) and G+P- subjects (n=23) underwent a clinical cardiovascular magnetic resonance protocol (3 tesla) for cardiac volumes, function, and scar imaging. T1 mapping was performed before and >20 minutes after administration of 0.2 mmol/kg of gadobutrol. Native T1 and extracellular volume fraction were significantly higher in HCM compared with patients with hypertension (P<0.0001), including in subgroup comparisons of HCM subjects without evidence of late gadolinium enhancement, as well as of hypertensive patients LV wall thickness of >15 mm (P<0.0001). Compared with controls, native T1 was significantly higher in G+P- subjects (P<0.0001) and 65% of G+P- subjects had a native T1 value >2 SD above the mean of the normal range. Native T1 was an independent discriminator between HCM and hypertension, over and above extracellular volume fraction, LV wall thickness and indexed LV mass. Native T1 was also useful in separating G+P- subjects from controls. CONCLUSIONS: Native T1 may be applied to discriminate between HCM and hypertensive heart disease and detect early changes in G+P- subjects.


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