Pulmonary Vascular Disease |

Investigation of a Relationship Between Portopulmonary Hypertension and Hepatorenal Syndrome Type II FREE TO VIEW

Andrea Ling*, MD; Richard Shaw, MD; Todd Frederick, MD; Tze-Ming Chen, MD
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California Pacific Medical Center, San Francisco, CA

Chest. 2012;142(4_MeetingAbstracts):822A. doi:10.1378/chest.1375361
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SESSION TYPE: DVT/PE/Pulmonary Hypertension Posters I

PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: Patients with cirrhosis exhibit complications involving pulmonary and renal systems. Portopulmonary hypertension (POPH) and Type II hepatorenal syndrome (HRS II) involve intense vasoconstriction. Increase of vasoactive substances such as endothelin 1 (ET-1) and nitric oxide (NO) have been implicated in the pathophysiology. This study aims to determine if a correlation exists between POPH and HRS II thereby raising the question of a shared pathophysiology.

METHODS: Using a retrospective observational cohort study design, we identified adult patients with cirrhosis undergoing right heart catheterization (RHC) for orthotopic liver transplant (OLT) evaluation between 2007-2009. This population was screened for POPH and HRS II. POPH was defined as a mean pulmonary artery pressure > 25mmHg, and pulmonary capillary wedge pressure (PCWP) <15mmHg. If the PCWP was not < 15mmHg, we used a pulmonary vascular resistance > 3 woods units. HRS II was defined by the International Ascites Club Criteria and physician diagnosis.

RESULTS: 112 patients with ESLD underwent RHC. 12.5% of patients met criteria for POPH. 19.6% met criteria for HRS II. 2.7% of study subjects met criteria for both. Using chi-square analysis of proportions resulted in a p value of 0.114 suggesting no correlation between the incidence of POPH and HRS II.

CONCLUSIONS: Our results did not show a correlation between POPH and HRS II. Although there are common mediators (NO, ET-1) implicated in POPH and HRS II, our findings suggest different vasoactive pathophysiologies for these diseases. Our incidence for POPH and HRS II are higher than seen in the literature. This is likely due to our screening of patients with cirrhosis who underwent RHC, who had abnormal right ventricular function on transthoracic echocardiograms. To our knowledge this is the first study to demonstrate no correlation in the incidence of POPH and HRS II in patients without refractory ascites.

CLINICAL IMPLICATIONS: Our findings suggest alternate pathophysiological disturbances resulting in POPH and HRS II in patients with cirrhosis without refractory ascites.

DISCLOSURE: The following authors have nothing to disclose: Andrea Ling, Richard Shaw, Todd Frederick, Tze-Ming Chen

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California Pacific Medical Center, San Francisco, CA




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