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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.

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.

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