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Introduction: Dobutamine and exercise stress echo are routinely performed on patients with advanced cirrhosis though have low sensitivity in this patient population, even when target heart rate is achieved. This is in part due to their unique cardiovascular physiology which is frequently marked by reduced peripheral vascular resistance with low blood pressure, impaired chronotropic response to stress, hyperdynamic left ventricular systolic function and elevated cardiac output. In the general population, achieving a rate pressure product (RPP), defined as peak systolic blood pressure multiplied by peak heart rate, > 25,000 is typically considered a high level of stress and is an adequate workload to detect ischemia, however this has not been validated in patients with advanced cirrhosis. We aimed to assess the impact of achieving a RPP > 25,000 on the ability of stress echo to detect obstructive coronary artery disease (CAD) in patients with advanced cirrhosis. Methods: We performed a case-control study on patients with advanced cirrhosis where 88 had and 97 did not have CAD based on invasive coronary angiography. A total of 159 patients (85.9%, 77 with CAD and 82 without) had dobutamine and 26 (14.1%, 11 with CAD and 15 without) had exercise as their stress modality. Continuous variables were compared by means of Wilcoxon Rank Sum test. Categorical variables were expressed as numbers and percentages and compared by means of chi-square and Fisher exact tests. Results: The average maximum RPP was 19,999 ± 4,969.4 with 32 patients (17.3%) achieving a RPP > 25,000 (14 with and 18 without CAD, P = 0.63). The average percent of maximum predicted HR (MPHR) achieved was 86.7 ± 9.2% with 136 patients (73.5%) achieving > 85% of MPHR. Achieving a maximum RPP > 25,000 (OR 0.83, 95% CI 0.39 - 1.79, P = 0.63) or a MPHR > 85% (OR 1.04, 95% CI 0.54 - 1.99, P = 0.92) did not improve the ability of stress echo to detect obstructive CAD. Conclusions: Achieving a maximum RPP > 25,000 did not improve the ability of stress echo to detect obstructive CAD in patients with advanced cirrhosis.

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Introduction: There is currently no published data studying the effect that cirrhosis may have on the rate of progression of aortic stenosis (AS). We hypothesize that AS may have accelerated progression in patients with cirrhosis compared with the general population due to high stroke volumes, hyperdynamic left ventricular function, and a pro-inflammatory state. The aim of this study is to determine the rate of progression of AS in patients with cirrhosis, elucidate risk factors, and assess progression based on the severity of cirrhosis as determined by Model for End Stage Liver Disease (MELD-Na) scores. Methods: This single center retrospective study included 48 patients with the diagnosis of cirrhosis and at least mild AS confirmed by two or more transthoracic echocardiograms (TTEs) taken ≥ 6 months apart. Historical data describing rates of AS progression in non-cirrhotic patients were used for comparison. Results: There was not a significant difference in the rate of AS progression between patients with cirrhosis and those without (table). Using univariate regression analysis, the yearly rate of aortic valve area (AVA) decline was positively correlated with the diagnosis of hyperlipidemia (HLD) (r=.228, P=0.047, B=0.116), initial AVA (r=0.504, P<0.001, B=0.224), initial left ventricular outflow track to aortic valve velocity time integral ratio (LVOT:AV VTI) (r=0.519, P<0.001, B=0.75) and initial left-ventricular stroke volume index (LV-SVI) (r=0.385, P=0.0070, B=0.0070). The yearly decrease of the LVOT:AV peak velocity ratio was inversely correlated with beta-blocker use (r=0.313, P=0.030, B=-0.047). There was not a significant relationship between MELD-Na scores and the rate of AS progression. Conclusion: Patients with cirrhosis can expect a similar rate of AS progression compared with those without cirrhosis. A higher initial LV-SVI and a history of HLD were both associated with faster AS progression in our study cohort.

Background:Early myocardial dysfunction is a known complication following liver transplant. Although hepatic ischemia/reperfusion injury (hIRI) has been shown to cause myocardial injury in rat and porcine models, the clinical association between hIRI and early myocardial dysfunction in humans has not yet been established. We sought to define this relationship through cardiac evaluation via transthoracic echocardiography (TTE) on postoperative day (POD) 1 in adult liver transplant recipients. Material/Methods:TTE was performed on POD1 in all liver transplant patients transplanted between January 2020 and April 2021. Hepatic IRI was stratified by serum AST levels on POD1 (none: <200; mild: 200-2000; moderate: 2000-5000; severe: >5000). All patients had pre-transplant TTE as part of the transplant evaluation. Results:A total of 173 patients underwent liver transplant (LT) between 2020 and 2021 and had a TTE on POD 1 (median time to echo: 1 day). hIRI was present in 142 (82%) patients (69% mild, 8.6% moderate, 4% severe). Paired analysis between pre-LT and post-LT left ventricular ejection fraction (LVEF) of the entire study population demonstrated no significant decrease following LT (mean difference: -1.376%, P=0.08). There were no significant differences in post-LT LVEF when patients were stratified by severity of hIRI. Three patients (1.7%) had significant post-transplant impairment of LVEF (<35%). None of these patients had significant hIRI. Conclusions:hIRI after liver transplantation is not associated with immediate reduction in LVEF. The pathophysiology of post-LT cardiomyopathy may be driven by extra-hepatic triggers.