Portal Pressure in Heart Failure PoP-HF: a pilot study

Heart failure (HF) is a complex clinical syndrome due to a structural and/or
functional abnormality of the heart that results in elevated intracardiac
pressures and/or inadequate cardiac output at rest or during exercise. The
pathophysiology of HF progression is complex and consists of hypoperfusion and
unrestrained neurohormonal up-regulation, sympathetic activation and systemic
congestion. Abdominal congestion manifests in a substantial proportion of HF
patients and there is increasing evidence for its role of the disease
progression and derangement.

The abdominal, *splanchic*, venous system is the largest reservoir in the human
body. Splanchnic veins are extremely compliant and responsive to sympathetic
and angiotensin modulation and thus capable of buffering changes in circulating
blood volume. In HF, due to longstanding congestion and neurohormonal
activation, this system becomes maladaptive, resulting in redistribution of
effective circulatory volume and increased cardiac filling pressures,
aggravating decompensated (acute) HF.

The splanchnic circulation drains into the portal system, entailing that, in
the absence of (cirrhotic) liver disease, portal pressures are directly related
to venous pressure in the abdominal compartment and vice versa. To our
knowledge, no studies evaluating portal pressure in a HF population without
(suspected) hepatopathy exist. This is striking given the increasing emphasis
on abdominal congestion in HF and the clinical deterioration (inflammation,
electrophysiological abnormalities, and malnutrition) associated with portal
hypertension. Additionally, right sided pressures are the most significant
predictor of cardiac cachexia (8) and (independently) related to dysfunction of
abdominal organs such as the kidney, intestine and pancreas. This leads us to
believe portal hypertension, perhaps more than central venous hypertension, is
capable of driving organ dysfunction in HF.

Data concerning the association between splanchnic and systemic hemodynamics
and clinical status/organ dysfunction would provide new insight into the role
of the abdominal compartment in (congestive) HF. The aim of this study is to
provide hemodynamic measurements of portal pressure in HF and to relate this to
clinical surrogates and organ (dys)function. We are specifically interested in
the impact of portal pressure on the kidney and pancreas. *

Primary Objective:
1. To provide data on portal pressure in a heart failure (HF) cohort without
substantiated hepatopathy

Secondary Objective(s):
1. To provide data on the hepatic venous pressure gradient in a HF cohort
without substantiated hepatopathy
2. To relate portal pressure to renal functioning in a HF cohort without
substantiated hepatopathy
3. To relate portal pressure to exocrine pancreatic function in a HF cohort
without substantiated hepatopathy
4. To relate portal pressures to central right/left sided hemodynamic
parameters

This concerns a cross-sectional, single center, pilot study. Patients
undergoing right cardiac catheterization for the evaluation of HF will be
included and for this study additional measurements of portal pressure are
performed. In the UMCG this includes patients with advanced HF who are screened
for mechanical circulatory support or transplantation, patients with
(suspected) heart failure with preserved ejection fraction (HFpEF) in whom
cardiac (filling) pressure are evaluated and patients with congenital cardiac
disease for hemodynamic evaluation.
Right heart catheterization in the UMCG is performed by introduction of a
sheath and Swan-Ganz catheter through the femoral or jugular vein under local
anesthesia. For this study additional measurements of portal pressure are
performed by advancing the (abovementioned) small balloon catheter under X-ray
guidance into the hepatic vein. The wedged hepatic venous pressure (WHVP) is
obtained by inflating a balloon, thereby blocking blood flow. This pressure
represents the transmission pressure from the portal vein. Afterwards the
balloon is deflated and free hepatic venous pressure (FHVP) is measured. The
gradient between the FHVP and WHVP is equal to the portal pressure gradient
(HPVG). A total of 30 subjects will be included in this pilot study. A total of
30 subjects will be included in this pilot study.

A benefit is that subjects will be provided additional information concerning
portal pressure and pancreas/renal function.
No additional risks are associated with the measurements required for this
study. The disadvantage is that the catheterization could take more time
(approximately 5 minutes) that this could be associated with slight additional
radiation, and that fecal sampling is required.