It is known that a hyper flow state, such as a coronary fistula, can be a cause of accelerated atherosclerotic changing in the feeding coronary artery.
The internal thoracic artery is known to display the ability to adapt its flow to required flow; yet, it is unknown whether this demanded supplementary flow, such as in the composite grafting CABG, can be a degenerative accelerating factor to atherosclerosis in the mid and long run.
There is a natural model of increased flow in the internal thoracic artery such as the aortic coarctation; whereby, the intra-thoracic artery flow is dramatically increased without any reported accelerated atherosclerotic degeneration.
You are assuming that increased flow during the cardiac cycle translates into accelerated degeneration. Grafted left internal thoracic arteries (GLITA) do indeed experience some modifications that could be defined as preatherosclerotic, such as intimal thickening.
This has been demonstrated by Italo Porto , who measured differences in the intima-media ratio using OCT in vivo between the GLITA and the in situ RITA (ISRITA). The intima-media ratio was greater in the GLITA compared to the ISRITA, but I argue that this is not due to increased total flow experienced by the GLITA.
For a detailed analysis of flow velocities in arterial grafts see:
https://www.annalsthoracicsurgery.org/article/0003-4975(94)00795-9/pdf
Briefly, the velocity-time integral (VTI), and therefore the area under the velocity-time curve (roughly flow), is generally greater for grafted thoracic arteries compared to in situ thoracic arteries. This is due to the increased blood flow demand in the grafted state, particularly when the graft is used to bypass a significantly stenosed or occluded coronary artery.
The flow profile is also different, with greater velocities measured in the diastolic phase of the cardiac cycle for the GLITA, as opposed to the in situ left internal thoracic artery (ISLITA), and a higher diastolic/systolic flow ratio.
In the human circulatory system, blood pressure and flow velocity are intricately linked during the phases of the cardiac cycle—systole and diastole.
Consider two scenarios:
Using Bernoulli's principle, we understand that in a flowing fluid, an increase in flow velocity leads to a decrease in pressure exerted by the fluid on the vessel walls, and vice versa. For the ISLITA, the high flow velocity during systole means that a significant portion of the systolic pressure is converted into kinetic energy. As a result, the actual hydrostatic pressure exerted on the vessel walls is lower, despite the high systolic pressure of 160 mmHg. Conversely, in the GLITA, with higher flow during diastole, the flow velocity during systole is lower. Consequently, less of the systolic pressure is converted into kinetic energy, leaving more of it as hydrostatic pressure exerted on the vessel walls. Therefore, the GLITA, with its lower flow velocity during systole, experiences higher hydrostatic pressure on the vessel's walls.
Poiseuille's Law, which describes the flow of incompressible fluids through a cylindrical vessel, further supports this argument. According to Poiseuille's Law, the flow rate is directly related to the pressure difference, vessel radius, fluid viscosity, and vessel length. In the ISLITA, the high flow velocity during systole indicates that the pressure difference (160 mmHg) is effectively driving the flow, resulting in a lower hydrostatic pressure on the vessel walls due to the conversion of pressure energy into kinetic energy.
In contrast, in the GLITA, during diastole, the pressure is lower (80 mmHg) but the flow velocity is higher. When systolic pressure (160 mmHg) is applied, the flow velocity is lower, meaning less of the pressure energy is converted into kinetic energy, leaving more of it as hydrostatic pressure on the vessel walls.
Integrating both Bernoulli's principle and Poiseuille's Law, it becomes clear that the GLITA, with lower flow velocity during systole, experiences higher hydrostatic pressure.
This elevated pressure results in significant stretching of the vessel wall, increased circumferential strain, and ultimately, vessel wall remodeling characterized by intimal thickening.
thanks
an alternative explanation as to effectively treat the systemic arterial hypertension , specially in regards to RITA grafted to RCA
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