|Ph.D Student||Shenhav Avshalom|
|Subject||The Performance of a Novel Physiological Assist Device that|
Works in Synchrony with the Failing Heart;
Experimental Data and Analysis Based on
Cellular Control Mechanisms
|Department||Department of Biomedical Engineering||Supervisor||Professor Amir Landesberg|
|Full Thesis text|
We present a novel Synchronized Pulsatile Assist Device (SPAD) that ejects blood into the left ventricle (LV) after the aortic valve opening on draws blood back from the LV during the diastole. It augments cardiac stroke-work and unloads the ventricle only during diastole, by utilizing a sort single cannula. The two main hypotheses were: (i) a pulsatile synchronized mode of assist is feasible and has hemodynamic advantages. (ii) The effects of the SPAD on cardiac function can be explained be relating to the sub-cellular Sarcomeric Control of Contraction (SCC).
An analytical model of the SCC was integrated with the model of the circulatory system. The predictions of this integrated SCC model were compared with the commonly used Elastance model and experimental data. Three animal models were tested: Pigs with acute cardiogenic shock, sheep with acute myocardial infarction and sheep with chronic heart failure induced by multiple injections of microspheres into the coronary circulation. Under general anesthesia the heart was exposed by left thoracotomy. The SPAD was inserted into the LV cavity through the apex. Cardiac mechanics and energetics were continuously monitored. The SPAD displaced volume was around 10 mL in all the experiments.
In pigs with cardiogenic shock the SPAD increased the cardiac-output by 57.8% and decreased the end diastolic pressure by 5.7?4.3 mmHg. In sheep with acute myocardial infarction it increased the cardiac-output by 11.1% (p<0.001) and decreased the cardiac oxygen consumption by 13.4?7.5% (p<0.001). In sheep with CHF it increased the cardiac-output by 20.8?15.4% although the device displaced value was only 6% of the LV end-diastolic volume! It only slightly elevated the systolic pressure (6.7?5.7%). The device significantly improved the diastolic function by decreasing the left atrial pressure and shifting the end-diastolic pressure-volume relationship downward.
The integrated SSC model predicts device efficiency (defined as the ratio between the added work to the circulatory system and the device external work) of 70%. It also predicts that the added work is dominated by the SPAD displaced volume. The Elastance model predicts a maximal device efficiency of only 39%.
The SPAD supports the circulation, improves systolic and the diastolic functions and decreases cardiac oxygen consumption. The observations are in congruent with the integrated SCC model and are incompatible with the Elastance concept. The results establish the feasibility of synchronized assist and have significant clinical implications. It sheds light on the regulation of cardiac function by relating to cellular mechanisms.