Effects of chronic volume deprivation on the ventricle

TL;DR

Chronic ventricular volume deprivation in lambs leads to reduced ventricular compliance and elevated filling pressures, with no significant fibrosis observed.

Contribution

The study introduces a novel animal model to investigate chronic ventricular volume deprivation and its effects on ventricular compliance and hemodynamics.

Findings

Chronic volume deprivation caused elevated end-diastolic pressure and reduced ventricular volumes compared to controls.

Acute reloading after debanding increased end-diastolic pressure further, indicating impaired compliance.

Histologic analysis showed no significant fibrosis in the deprived ventricles.

Abstract

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.

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).

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.

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.

Extensive research has been conducted to evaluate the adaption of the ventricle when it becomes overstretched and dilated due to chronic volume or pressure overload, both clinical conditions commonly encountered in cardiologic practice.

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