Reply: Liver, heart, and kidney crosstalk in cirrhosis: POCUS is the focus

To the editor, We read with interest the letter by Agrawal and Ariga, and we thank them for the comments in response to our paper on point-of-care ultrasound in cirrhosis with hepatorenal syndrome-acute kidney injury).1 First, they comment on the lack of systolic dysfunction noted in this cohort. We noted left ventricular diastolic dysfunction in 53 (38%) patients, with 19 (14%), 25 (18%), and 9 (6%) having grades 1, 2, and 3 left ventricular diastolic dysfunction, respectively. Thus, 24% met the criteria for cirrhotic cardiomyopathy as per the 2020 cirrhotic cardiomyopathy consortium criteria.2 The study was carried out in an intensive care unit equipped with a point-of-care ultrasound device capable of tissue Doppler imaging but not speckle-tracking echocardiography. However, due to a low reported prevalence of abnormal global longitudinal strain (~1.5%) and lack of a universal definition of 'blunted response to stress,' we don't expect the lack of strain assessment to have affected the results.2,3 Alternatively, we assessed serial changes in velocity time integral, stroke volume, and cardiac index(CI) as surrogates for systolic function. A reduction in CI was shown in patients who failed to respond to terlipressin.2 The second observation related to mean arterial pressure that was maintained > 65-70 mm Hg in our cohort by optimizing volume status and, in this case, by use of a pressor agent (terlipressin). Therefore, we are unlikely to observe a significant reduction in mean arterial pressure in this setting. However, we found despite preserved mean arterial pressure, the CI may decline, which makes it a better indicator of tissue perfusion.4 Moreover, the authors brought up a valid point about the intravascular volume status for the study participants upon enrolment. When we used the inferior vena cava collapsibility index as a surrogate of volume status, there was no difference between responders (to terlipressin) and nonresponders at baseline, 48 h or 72 h after enrolment, as demonstrated in Table 2 in our manuscript. We respectfully disagree with the postulation of 2 distinct profiles in patients with cirrhosis and acute kidney injury, where responders to terlipressin were termed as patients with hepatorenal syndrome-acute kidney injury and nonresponders were termed as patients with hepato-cardio-renal syndrome. What may argue against the hepato-cardio-renal syndrome hypothesis is that, in our study, 18/34 (53%) of patients with cirrhotic cardiomyopathy still responded to terlipressin, but the response rate was reduced with high grades of left ventricular diastolic dysfunction. We believe that cardiac dysfunction in cirrhosis is a continuum that pertains to changes in myocardial contractility, structure, response to stress, renal perfusion, and tolerance for albumin and/or pressors, and this fascinating interplay warrants further investigation.