Association of Right Ventricular Myocardial Blood Flow With Pulmonary Pressures and Outcome in Cardiac Amyloidosis.

Background: Cardiac amyloidosis (CA) is a restrictive and infiltrative cardiomyopathy, characterized by increased biventricular filling pressures and low output. Symptoms are predominantly of right heart origin. The role of right ventricular (RV) myocardial blood flow (MBF) in CA has not been studied.
Objectives: This study aimed to first associate RV MBF measured by using positron emission tomography (PET) with reference standards of RV pressures and then to explore its prognostic value in CA.
Methods: Cardiac PET was performed at rest in 52 patients with CA and 9 healthy control subjects. MBF was quantified from the right and left ventricles by using ¹¹ C-acetate, ¹⁵ O-water, or both (n = 25). RV pressure was measured invasively or by echocardiography. Associations between biventricular MBF toward symptoms, RV function, and outcome (death or acute heart failure) were studied in patients with CA.
Results: MBF of the right ventricle (MBF _RV ) and the ratio of MBF _RV and MBF of the left ventricle (MBF _RV/LV ) for the 2 tracers were significantly correlated (r > 0.92). MBF _RV was directly correlated with RV systolic pressures with both tracers (P ≤ 0.005). MBF _LV was inversely correlated with wall thickness (P < 0.0001). MBF _RV/LV was significantly associated with N-terminal pro-B-type natriuretic peptide levels, NYHA functional class, RV pressures, and RV systolic function (all; P < 0.001). Twenty-six cardiac events (25 deaths) occurred during follow-up (median 44 months). MBF _RV/LV higher than 56% was associated with a diagnosis of pulmonary hypertension (AUC: 0.96 [95% CI: 0.91-1.00]; P < 0.0001); and predicted outcome with HR: 9.0 (95% CI: 4.2-14.5), P < 0.0001).
Conclusions: Measurements of MBF _RV using PET are feasible, as confirmed with 2 different tracers. Imbalance between RV and LV myocardial perfusion is associated with increased RV load and adverse events in cardiac amyloidosis.
Competing Interests: Funding Support and Author Disclosures This study was supported by grants from Lundbeck foundation (grant number R192-2015-966, awarded to Dr Harms) and Swedish Heart-Lung Foundation (grant numbers 20160746 and 20190593 awarded to Dr Sorensen). Drs Harms, Tolbod, and Sorensen are co-founders and co-owners of MedTrace Pharma A/S. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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