Impact of interstitial lung disease on left ventricular myocardial function

Background Interstitial lung disease (ILD) comprises a wide variety of pulmonary parenchymal disorders within which progressive fibrosing ILD (PF-ILD) constitutes a phenotypic subset. By use of speckle tracking -based strain analysis we aimed to evaluate the degree of left ventricular (LV) dysfunction in progressive vs. non -progressive fibrosing ILD (non-PF-ILD). Methods A total of 99 ILD patients (mean age 63.7 +/- 13.5 years, 37.4% female), composed of 50 PFILD and 49 non-PF-ILD patients, and 33 controls were prospectively enrolled and underwent conventional and speckle tracking echocardiography. Additional laboratory and pulmonary function testing, as well as six -minute walk test were performed. Results As compared to the non-PF-ILD cohort, PF-ILD patients exhibited a significantly impaired forced vital capacity (2.4 +/- 1.0l vs. 3.1 +/- 0.9l, p = 0.002), diffusion capacity for carbon monoxide (DLCO, 25.6 +/- 16.3% predicted vs. 43.6 +/- 16.67% predicted, p <0.001) and exercise capacity response as measured by the six -minute walk test distance (268.1 +/- 178.2m vs. 432.6 +/- 94.2m, p <0.001). Contrary to conventional echocardiographic LV parameters, both regional and global longitudinal LV strain measurements were significantly altered in ILD patients as compared to controls. No differences in LV strain were found between both patient groups. Significant correlations were observed between global longitudinal strain, on the one hand, and systemic inflammation markers, total lung capacity (TLC) and DLCO, on the other hand (high -sensitivity C -reactive protein: Pearsons r = -0.30, p< 0.001; interleukin-6: Pearsons r = -0.26, p = 0.007; TLC % predicted: Pearsons r = 0.22, p = 0.02; DLCO % predicted: Pearsons r = 0.21, p = 0.02). Conclusions ILD is accompanied by LV dysfunction. LV functionality inversely correlates with the severity of the restrictive ventilatory defect and inflammation marker levels. These observations support the assumption of persistent low-grade systemic inflammation that may link systemic cardiovascular function to ILD status.