Key result
Chronic ventricular volume deprivation in sheep raises end-diastolic pressure to ~8 mmHg and reduces compliance.
Why the study?
Little is known about hemodynamic changes following chronic ventricular volume deprivation, which impacts understanding of disease course and treatment results.
Does chronic ventricular volume deprivation and subsequent acute reloading alter ventricular compliance and hemodynamics in an ovine model?
Does chronic ventricular volume deprivation and subsequent acute reloading alter ventricular compliance and hemodynamics in an ovine model?
Chronic ventricular volume deprivation leads to decreased ventricular compliance and elevated filling pressures, which acutely worsen upon volume reloading, highlighting the pathophysiological risk of flash pulmonary edema when relieving right-sided obstructions.
May raise flash pulmonary edema risk on acute reloading after chronic deprivation; leaves open translation to human ventricular disease.
OBJECTIVES: Little is known of the haemodynamic changes following chronic ventricular volume deprivation, which impact understanding the disease course and treatment results. An animal model was created to study the effects of chronic ventricular volume deprivation and acute reloading. METHODS: In 13 lambs, a polytetrafluoroethylene strip was placed around the inferior and superior caval vein through thoracotomy resulting in progressive ventricular volume deprivation during growth. After 10 months, the polytetrafluoroethylene bands were relieved. Magnetic resonance imaging and haemodynamic measurements including pressure-volume loops were performed before and after debanding and compared to age and weight-matched controls (n = 6). RESULTS: The end-diastolic pressure was elevated compared to healthy animals (median [interquartile range] 8.1 [7.2-9.1] vs 1.0 [1.0-2.7] mmHg, P 0.030). The end-diastolic pressure after debanding increased to 11.1 (10.4-17.2) mmHg, P 0.038. The end-diastolic volume and end-systolic volume of the intervention group were also significantly less than the healthy controls (71.5 [66.7-74.7] vs 81.5 [74.3-86.3] ml, P 0.004 and 34.5 [27.5-37.6] vs 42.7 [35.0-50.5] ml P 0.001). The end-diastolic pressure-volume relationship was significantly shifted upwards and to the left compared to controls, indicative of a decreased compliance of the chronically deprived left ventricle. Histologic assessment revealed no significant differences in fibrosis between the ventricles of the intervention group and healthy animals. CONCLUSIONS: When a healthy ventricle is chronically deprived of an adequate preload, it becomes less compliant with elevated filling pressures. Acute reloading does not lead to ventricular systolic dysfunction, but in the early phase, diastolic pressure may rise. A better understanding of this phenomenon might help to recognition and treatment of impaired ventricular compliance.
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Cools et al. (2025) studied Chronic ventricular volume deprivation (n=17). Bi-caval banding (PTFE strip around SVC and IVC) vs. Age and weight-matched healthy controls was evaluated on End-diastolic pressure (mmHg) (p=0.030). Chronic ventricular volume deprivation in an ovine model significantly increased end-diastolic pressure compared to healthy controls (8.1 vs 1.0 mmHg) and decreased ventricular compliance.
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