Dr Burkhoff began by stating that the Acute Cardiac Unloading and REcovery symposium is focused on ventricular unloading using mechanical circulatory support devices to improve or maintain myocardial function. Laboratories around the world are investigating other novel methods for ventricular unloading and improving the haemodynamic status of other end-organs. He stated that congestion plays an important role in acute decompensated heart failure (ADHF) and is an important target of therapy.1 It is characterised by elevated filling pressures, clinical signs of dyspnoea, peripheral oedema, ascites and end-organ dysfunction resulting in poor prognosis. Studies suggest that venous congestion reduces glomerular filtration and limits urine output, thereby attenuating the effects of diuretics and promoting HF.2,3
Existing approaches to reduce congestion are limited. Hence, there exists a need for rapid and effective cardiac decongestion in patients with ADHF. Dr Burkhoff highlighted a recent significant effort aimed at decreasing congestion: decrease central venous pressure and pulmonary capillary wedge pressure (DRIPPS). One of the components of DRIPPS includes a class of devices/drugs nicknamed ‘pullers’, whose mechanism of action is to decrease the central venous pressure or pulmonary capillary wedge pressure by ‘pulling’ volume out of the venous system. This effect of pullers should decongest the patient and promote increased end-organ perfusion by increasing the arterial-to-venous pressure gradient. Pullers also include devices that can transiently occlude the superior vena cava (SVC), leading to reduced cardiac filling pressures without reducing cardiac output (CO) or systemic blood pressure. Because SVC accounts for only about 30% of venous return, it was postulated that the SVC could be totally occluded, potentially with less impact on CO or systemic blood pressure, with a subsequent reduction in end-organ venous pressure.
The recent pre-clinical publication from Kapur et al. showed that while the inferior vena cava occlusion reduced CO, left ventricular end-systolic pressure (LVESP) and left ventricular end-diastolic pressure (LVEDP), SVC occlusion on the other hand led to a reduction in only LVEDP with no effect on CO or LVESP.4
The encouraging results of the pre-clinical studies led to the clinical proof-of-concept study to provide initial evidence of safety and feasibility of transient SVC occlusion in patients with ADHF and reduced ejection fraction (<40%), who were referred for cardiac catheterisation.4 SVC occlusion was performed using a commercially available occlusion balloon in eight patients with systolic heart failure. Five minutes of SVC occlusion reduced biventricular filling pressures without decreasing systemic blood pressure or total cardiac output in five of the eight patients. In three of the eight patients, a second 10-minute occlusion period had similar haemodynamic effects. SVC occlusion was well-tolerated without the development of new symptoms, new neurological deficits or any adverse events, including stroke, heart attack or reported SVC injury or thrombosis at 7 days of follow-up. The favourable results of this proof-of-concept study have led to the prospective, multicentre early feasibility and safety study of the preCARDIA system in the SVC Occlusion in Subjects With Acute Decompensated Heart Failure (VENUS-HF) study.
In conclusion, venous congestion is an important prognostic indicator of ADHF and CS and contributes to impaired end-organ function. In an early clinical study testing transient SVC occlusion, this approach appears to be a safe therapeutic approach to rapidly reduce cardiac filling pressures in HF, while preserving blood pressure and CO and increasing urine output.