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Abstract Background Coronary artery bypass grafting surgery is an effective treatment modality for patients with severe coronary artery disease. The conduits used during the surgery include both the arterial and venous conduits. Long- term graft patency rate for the internal mammary arterial graft is superior, but the same is not true for the saphenous vein grafts. At 10 years, more than 50% of the vein grafts would have occluded and many of them are diseased. Why do the saphenous vein grafts fail the test of time? Many causes have been proposed for saphenous graft failure. Some are non-modifiable and the rest are modifiable. Non-modifiable causes include different histological structure of the vein compared to artery, size disparity between coronary artery and saphenous vein. However, researches are more interested in the modifiable causes, such as graft flow dynamics and wall shear stress distribution at the anastomotic sites. Formation of intimal hyperplasia at the anastomotic junction has been implicated as the root cause of long- term graft failure. Many researchers have analyzed the complex flow patterns in the distal sapheno-coronary anastomotic region, using various simulated model in an attempt to explain the site of preferential intimal hyperplasia based on the flow disturbances and differential wall stress distribution. In this paper, the geometrical bypass models (aorto-left coronary bypass graft model and aorto-right coronary bypass graft model) are based on real-life situations. In our models, the dimensions of the aorta, saphenous vein and the coronary artery simulate the actual dimensions at surgery. Both the proximal and distal anastomoses are considered at the same time, and we also take into the consideration the cross-sectional shape change of the venous conduit from circular to elliptical. Contrary to previous works, we have carried out computational fluid dynamics (CFD) study in the entire aorta-graft-perfused artery domain. The results reported here focus on (i) the complex flow patterns both at the proximal and distal anastomotic sites, and (ii) the wall shear stress distribution, which is an important factor that contributes to graft patency. Methods The three-dimensional coronary bypass models of the aorto-right coronary bypass and the aorto-left coronary bypass systems are constructed using computational fluid-dynamics software (Fluent 6.0.1). To have a better understanding of the flow dynamics at specific time instants of the cardiac cycle, quasi-steady flow simulations are performed, using a finite-volume approach. The data input to the models are the physiological measurements of flow-rates at (i) the aortic entrance, (ii) the ascending aorta, (iii) the left coronary artery, and (iv) the right coronary artery. Results The flow field and the wall shear stress are calculated throughout the cycle, but reported in this paper at two different instants of the cardiac cycle, one at the onset of ejection and the other during mid-diastole for both the right and left aorto-coronary bypass graft models. Plots of velocity-vector and the wall shear stress distributions are displayed in the aorto-graft-coronary arterial flow-field domain. We have shown (i) how the blocked coronary artery is being perfused in systole and diastole, (ii) the flow patterns at the two anastomotic junctions, proximal and distal anastomotic sites, and (iii) the shear stress distributions and their associations with arterial disease. Conclusion The computed results have revealed that (i) maximum perfusion of the occluded artery occurs during mid-diastole, and (ii) the maximum wall shear-stress variation is observed around the distal anastomotic region. These results can enable the clinicians to have a better understanding of vein graft disease, and hopefully we can offer a solution to alleviate or delay the occurrence of vein graft disease.

There has been much characterization of the heart as a pump by means of models based on elastance and compliance. The present paper puts forward the new concept of time-varying passive and active elastance. The biomechanical basis of cyclic elastances of the left ventricle (LV) is presented. Elastance is defined in terms of the relationship between ventricular pressure and volume as d P = E d V + V d E , where E includes passive elastance, E p , and active elastance, E a . By incorporating this concept in LV models to simulate diastolic (filling) and systolic phases, a time-varying expression has been obtained for E a , and an LV volume dependent expression has been obtained for E p . It is proposed to use these two elastances E a and E p to represent the intrinsic LV properties. The active elastance, E a , can be used to characterize the LV contractile state and represents LV pressure variation due to LV volume variation (such as during the filling and ejection phases). The passive elastance, E p , can serve as a measure of LV resistance to filling. Furthermore, it has been demonstrated how the LV pressure dynamics (and LV pressure response to LV volume) can be explained in terms of E a and E p . [ABSTRACT FROM AUTHOR]

Background: In this paper, the left ventricle (LV) is modeled as a cylinder with myocardial fibers located helically within its wall. A fiber is modeled into myocardial structural units (MSUs); the core entity of each MSU is the sarcomeric contractile element. The relationship between the sarcomere unit's contractile force and shortening velocity is expressed in terms of the LV model's wall stress and deformation, and hence in terms of the monitored LV pressure and volume. Then, the LV systolic performance is investigated in terms of a mechatronic (excitation-contraction) model of the sarcomere unit located within the LV cylindrical model wall., Methods: The governing equation of dynamics of the LV myocardial structural unit (MSU) is developed, involving the parameters of the series-elastic element (SE), the viscous element (VE) and the contractile element (CE). We then relate the MSU's force and displacement variables (in terms of SE, VE and CE parameters) to the LV pressure and volume, using the patient's catheterization-ventriculogram data. We thereby evaluate the MSU elements' parameters., Results: We then determine the sarcomere (CE) 'force vs. shortening-velocity' characteristics as well as the power generated by the sarcomere (or CE) element. These are deemed to be important LV functional indices. When our computed sarcomeric peak-power is compared against the traditional LV contractility indices (by linear regression), a high degree of correlation is obtained., Conclusions: We have provided herein, a LV systolic-phase (cylindrical geometry) model whose wall contains the myocardial fibers having sarcomere units. We have expressed the LV myocardial sarcomere's CE (force vs. shortening-velocity) characteristics in terms of the LV pressure-volume data. These CE properties express the intrinsic performance capacity of the LV. Hence, indices containing these properties are deemed to reflect LV performance. In this regard, our new LV contractility index correlates very well with the traditional LV contractility index dP/dt(max).