Key result
Device-driven cyclic compression of the superior vena cava at 85% increased cardiac output by 27.3% (from 3.83 to 4.88 L/min) compared to baseline in a porcine model of heart failure.
Why the study?
To evaluate the physiological efficacy and safety of a novel device-based preload reduction strategy applying external cyclic compression to the SVC in a preclinical heart failure model.
Does device-driven cyclic compression of the superior vena cava improve hemodynamic parameters in a preclinical pig model of heart failure?
Does device-driven cyclic compression of the superior vena cava improve hemodynamic parameters in a preclinical pig model of heart failure?
Effect estimate: +27.3%
Absolute Event Rate: 4.88% vs 3.83%
p-value: p=0.125
Device-driven external cyclic compression of the superior vena cava effectively reduces preload and augments cardiac performance in a preclinical heart failure model, providing proof-of-concept for its potential utility in acute decompensated heart failure.
Hypothesis-generating for device-based SVC compression in acute HF; leaves open translation to human efficacy and safety.
We evaluated the physiological efficacy and safety of a novel device-based preload reduction strategy that applies external cyclic compression to the superior vena cava (SVC) in a preclinical heart failure model. Heart failure was induced in eleven pigs using ischemia–reperfusion injury, and a 3D-printed SVC compression device was tested under varying compression ratios (70%, 85%, and 100%) and protocols. Hemodynamic responses were monitored using right-heart catheterization and pressure–volume loop analysis. Among the tested conditions, cyclic compression at 85% with 20/5-minute compression–release cycles resulted in marked within-group improvements in key hemodynamic parameters. Cardiac output increased by 27.3% (3.83 to 4.88 L/min, Wilcoxon signed-rank test, p = 0.125) and stroke volume by 19.5% (38.6 to 46.1 mL, p = 0.125), while mean arterial and pulmonary pressures remained stable. Systemic vascular resistance decreased by 29.0% (from 1,200 to 852 dyn·s·cm− 5, p = 0.125), accompanied by reductions in left ventricular end-diastolic pressure and a trend suggestive of improved contractility. These results demonstrate that externally applied cyclic SVC compression effectively reduces preload and augments cardiac performance without compromising hemodynamic stability. Our study provides a proof-of-concept for the clinical utility of device-driven external cyclic compression of the SVC as an adjunctive therapy for acute decompensated heart failure, especially in perioperative or critical care settings, and supports further development toward an implantable clinical system. These findings are preliminary, based on small subgroup sizes (n = 1, n = 2, n = 4, and n = 4), and require confirmation in larger, adequately powered studies. Future development of a fully implantable and autonomous version of the device could enable real-time, closed-loop preload modulation in advanced heart failure care.
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Kim et al. (2026) studied Heart failure (n=11). Device-driven cyclic compression of the superior vena cava vs. Baseline was evaluated on Cardiac output (+27.3%, p=0.125). Device-driven cyclic compression of the superior vena cava at 85% increased cardiac output by 27.3% (from 3.83 to 4.88 L/min) compared to baseline in a porcine model of heart failure.
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