logoJadeHouse Lab
Background Image

ItmtSVCOccl

Intermittent Occlusion of the Superior Vena Cava Reduces Cardiac Filling Pressures in Preclinical Models of Heart Failure

19 June 2024

Summary

Research Objective

  • Investigate the acute hemodynamic effects of occlusion of the superior (SVC) versus the inferior vena cava (IVC).
  • Test a novel SVC occlusion system in swine models of heart failure (HF).

Results

  • IVC occlusion acutely reduced left ventricular (LV) systolic and diastolic pressures, LV volumes, cardiac output (CO), and mean arterial pressure (MAP).
  • SVC occlusion reduced LV diastolic pressure and volumes without affecting CO or MAP.
  • SVC therapy with the preCARDIA system provided a sustained reduction in cardiac filling pressures with stable CO and MAP.

Methods

Research Design

Myocardial Infarction

  • 3.0 × 8 mm angioplasty balloon deployed in the mid-LAD (left anterior descending artery).
  • 120 min occlusion, followed by LAD balloon deflation for reperfusion.

Comparison of Acute IVC and SVC Occlusion

  • 32-cc endovascular balloon deployed via right internal jugular vein.
  • Balloon inflated to occlude IVC for up to 5 min, followed by a 15-min recovery period.
  • Balloon repositioned to occlude SVC for up to 5 min, with LV pressure and volume recorded.

Intermittent SVC Occlusion in a Model of Volume Overload Heart Failure

  • 120 min LAD occlusion, followed by 120 min right and left renal artery occlusion.
  • Right and left renal arteries occluded in alternating fashion for 30 min in each artery for an additional 6 h.
  • PreCARDIA catheter introduced.
  • Occlusion phase:
    • 5 min SVC occlusion.
    • 10 sec volume removal (reperfusion).
    • Duty cycle performed up to 18 h of continuous pumping.

Tools

  • LV pressure and volume: 5Fr conductance catheter system deployed via left carotid.
  • SVC occlusion: PreCARDIA catheter introduced via right internal jugular vein with a distal tip positioned in the right or left pulmonary artery and a proximal occlusion balloon positioned in the SVC.
    • Semi-compliant, atraumatic balloon occlusion catheter with tubing set and a pump console.
    • Enables controlled delivery and removal of fluid into the occlusion balloon.

Results

Occlusion of IVC and SVC

IVC

IVC occlusion rapidly reduced cardiac filling pressures but severely reduced total cardiac output and systemic blood pressure:

  • Reduced left ventricular (LV) systolic and diastolic pressures.
  • Reduced LV volumes.
  • Reduced cardiac output.
  • Reduced systemic blood pressure.
  • Created a gradient of high pressure in the abdomen and low pressure in the left atrium, leading to:
    • Increased renal, hepatic, and intestinal vein pressures.
    • Impaired urine output, hepatic function, and drug absorption.
    • Exacerbated congestive heart failure.

SVC

SVC occlusion rapidly decreased cardiac filling pressures without affecting cardiac output or systemic blood pressure:

  • Reduced LV diastolic pressure and volume.
  • No effect on cardiac output.
  • No effect on systemic blood pressure.

Intermittent SVC Occlusion (up to 18 hrs)

Measurements

Intermittent SVC occlusion provided sustained reduction in cardiac filling pressure without significant harm or adverse effects:

  • Increased right internal jugular (IJ) venous pressure.
  • Decreased right atrial (RA) pressure.
  • Decreased pulmonary capillary wedge pressure (PCWP).
  • Decreased mean pulmonary artery (PA) pressure.
  • No effect on cardiac output (CO).
  • Mean arterial pressure (MAP) remained above 60 mmHg.
  • No evidence of increased cerebral edema, pulmonary emboli, or cardiac damage.
  • No evidence of SVC damage or thrombosis due to the preCARDIA device.

Discussion

Concerns and Limitations

  • Impact of elevated jugular vein pressure on cerebral function.
  • Small sample size.
  • Lack of awareness regarding the effects of prolonged SVC therapy.

Future Studies

  • Test on patients with other preload-dependent conditions, such as:
    • Heart failure with preserved ejection fraction (HFpEF).
    • Pulmonary hypertension with right heart congestion.
    • Valvular regurgitation.
    • Congestive heart failure.
    • Patients without evidence of cardiogenic shock.
  • Increase the number of test subjects.
  • Prolong SVC therapy to study its effects over an extended period.