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Effects of Pirfenidone on Echocardiographic Parameters of Left Ventricular Structure and Function in Patients with Idiopathic Pulmonary Fibrosis
Journal article   Peer reviewed

Effects of Pirfenidone on Echocardiographic Parameters of Left Ventricular Structure and Function in Patients with Idiopathic Pulmonary Fibrosis

Shehab Al-Ansari, Allen Borowski, Ali Fuad, Omar Alawadhi, Haris Riaz, Vikram Sharma, Nauman Khan, Brian D. Southern and W.H. Wilson Tang
Journal of Interdisciplinary Medicine, Vol.5(2), pp.35-42
06/01/2020
DOI: 10.2478/jim-2020-0009

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Abstract

Pirfenidone is a novel anti-fibrotic agent utilized in the treatment of idiopathic pulmonary fibrosis (IPF). It has been implicated in mitigating myocardial fibrosis and left ventricular (LV) systolic and diastolic dysfunction in animal models. However, its impact on LV mechanics in humans remains unknown. The aim of this study was to retrospectively evaluate the effects of pirfenidone on echocardiographic parameters of LV function and structure in patients with IPF. A total of 124 patients with IPF were included in this study: 64 patients treated with pirfenidone (treatment group) and 60 patients not taking pirfenidone (control group), who had serial pretreatment/baseline and posttreatment/follow-up echocardiograms done within a time frame of four years. Changes in the means of parameters of LV function (systolic, diastolic, and global longitudinal strain) and LV structure (mass and volume indices) were compared between the treatment and control groups. This was followed by a subgroup analysis that included only 88 patients (47 treated, 41 controls) with echocardiographic evidence of myocardial dysfunction at baseline (defined as an ejection fraction of ≤45, or diastolic dysfunction stage 1 or more) in addition to a known clinical diagnosis of congestive heart failure. To account for potential confounders, a secondary adjusted analysis by way of 1:1 propensity score matching (PSM) was carried out. This yielded a sample consisting of 62 patients with 56 patients in the subgroup cohort. Patients in the treatment group were significantly younger (69.4 vs. 77 years, p<0.001) and had relatively lower forced vital capacity (69.9% vs. 80.6%, p = 0.005) in comparison to the control group. However, after PSM, the age demographics were comparable between both groups (72.18 vs. 72.15, p = 0.9). In the primary unadjusted analysis, there was no statistically significant change in any of the mean parameters of LV function and structure after pirfenidone administration when compared to the control group. Furthermore, no significant differences were noted in the subgroup cohort. Such findings were re-demonstrated after a secondary analysis with PSM. From an echocardiographic perspective, pirfenidone had no significant effects on LV structure and function in patients with IPF, even in patients with more overt cardiac dysfunction.
 heart failure idiopathic pulmonary fibrosis myocardial dysfunction pirfenidone

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