Assessing left ventricular hemodynamic forces in systemic sclerosis patients: pilot study

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Abstract Background Systemic sclerosis (SSc) is a connective tissue disease characterized by sustained inflammation, microvascular pathology changes and fibrosis. Cardiac comorbidities, particularly pulmonary arterial hypertension (PAH), are the leading cause of mortality among SSc patients. Early PAH diagnosis remains difficult. Cardiovascular magnetic resonance imaging (CMR) has emerged as a great noninvasive tool to assess cardiological impact in SSc. Hemodynamic forces (HDF) are a measurement of the global force exchanged between blood volume and myocardium assessed using CMR, based on the Navier-Stokes equation measuring the relationship between pressure gradient and velocity field. Purpose To assess diagnostic value of HDF measurement in SSc compared to healthy controls, as a potential early indicator of subclinical cardiac dysfunction. Methods In a single-center study, all patients with SSc who met the American college of rheumatology, and the European League against Rheumatism classification criteria were included and a CMR exam a 1.5T was performed. HDF were obtained using a post-processing software (Medis Suites, Netherlands). Patients with atrial fibrillation were excluded. To assess HDF, movements from deformation imaging of long axis cine were used for longitudinal (Figure 1) and transversal left ventricle (LV) HDF calculation after initial feature-tracking and measurements of mitral and aortic valve width. To compare different LV sizes, HDF are normalized to LV volume and blood specific weight, thus reported as percentage of gravity acceleration. Then, we performed age matching from an external cohort of healthy controls (1). Results Of the 11 SSc patients (age 46.27±15.2 years, 19% male) recruited, 5 (46%) patients had a diffuse form and 5 (46%) patients had PAH. Two (18%) patients exhibited LV systolic dysfunction with a mean LV ejection fraction (LVEF) of 59%. Regarding the right ventricle (RV), 5 (46%) patients had RV systolic dysfunction (mean RVEF of 50%). Biventricular volumes were normal (mean LV end-diastolic volume [EDV] of 80 ml/m2, respectively mean RV EDV of 77 ml/m2). To assess the diagnostic performance of HDF values we compared HDF in 11 SSc patients and in 11 age-matched healthy controls from an external cohort. SSc patients showed larger LV longitudinal HDF in systole (both RMS and peak, p=0.029, respectively p=0.047) (Figure 2), changes which could be explained by anatomical deformation caused by increased pressure in the RV. During diastole, only one parameter was significantly lower (diastolic deceleration, p=0.040), a finding that might indicate reduced LV compliance in the context of elevated LV filling pressures. Conclusion This pilot study is the first to describe the interest of HDF in SSc patients. HDF analysis has the potential to be a more sensitive marker of cardiac deterioration than traditional volumetric and functional parameters, as patients had higher systolic HDF despite having similar LVEF to controls.

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