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Master Thesis

Évaluation par IRM cardiaque de l’atteinte cardiaque de l’HTA maligne, données de la cohorte du CHU de Bordeaux

Abstract : Context: cardiac damage is now recognized as part of the definition of malignant hypertension. It can manifest itself as troponin elevation, systolic dysfunction or disproportionate left ventricular hypertrophy. However, its pathogenesis remains uncertain. Cardiac MRI seems to be an ideal tool to progress in the understanding of its pathophysiology. Method: we retrospectively included patients from the Bordeaux cohort of malignant hypertension who received cardiac MRI between January 2009 and January 2020. MRIs were considered acute if the post-diagnosis delay was less than or equal to 40 days. We collected telediastolic, telestolic, LVEF, left ventricular mass, segmental kinetics from SSFP sequences, and the presence or absence of pathological late enhancement 10 minutes after injection of gadolinium chelate by a PSIR sequence (± HR). The most recent cardiac MRIs included T2-weighted and T1 mapping sequences. Results: we included 39 patients out of the 202 present in the Bordeaux cohort. The mean time to complete cardiac MRI was 20.9 days (±17.8). 33 patients received an acute MRI, performed with a mean time of 14.8 days (±10.3). MRI data in this subgroup showed a mean indexed LVM of 127.1 g/m2 (±41.8). There were no significant anomalies on the T2-weighted sequences. The mean VEC was 24.4 (± 2.6%). Late enhancement abnormalities were found in 34.4% of patients, mostly of mesomyocardial location. Only two patients had subendocardial elevation without a context suggestive of acute coronary syndrome. Follow-up MRI was performed in 18 of these patients with a significant decrease in indexed LVM (92.8 ± 20.1gr/m2 (p < 0.05)) and a significant increase in ECV (26.7 ± 2.6% (p = 0.049)). Conclusion: these data suggest that the disproportionate LVH sometimes observed in the acute phase of malignant hypertension appears to be secondary to a mixed mechanism. The latter would associate myocyte hyperplasia and excessive fibrotic damage, probably due to over activation of the ARAS. The absence of ischemic sequelae on the late enhancement sequences suggests a diffuse microvascular cause explaining myocardial ischemia, a hypothesis consistent with the pathophysiology of the disease.
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Submitted on : Thursday, June 11, 2020 - 10:02:15 AM
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Julien Doublet. Évaluation par IRM cardiaque de l’atteinte cardiaque de l’HTA maligne, données de la cohorte du CHU de Bordeaux. Sciences du Vivant [q-bio]. 2020. ⟨dumas-02864458⟩

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