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    Unraveling the complex role of perfusion pressure in glaucoma progression

    Pressure rate under closer scrutiny since investigation began into the disease’s causes

     

    The mathematical model

    This has led to the exploration of mathematical models.

    “Basically, this model calculates stresses and strains in the lamina cribosa, which becomes deformed based on the action of the IOP and the retrolaminar pressure,” he said. “We look at fluid/structure interactions. The model describes the relationship between stresses and strains in the lamina cribosa and the blood flow in the vessels.”

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    Professors Harris and Giovanna Guidoboni of the Department of Mathematics at IUPUI are collaborators on the dynamic model, Dr. Harris added.

    Importantly, this model also considers blood pressure and it simulates a relationship between an increase in IOP and venous collapse, i.e., the Starling resistor effect. A final factor evaluated is autoregulation, which, Dr. Harris said, can turn on, off, or keep constant.

    He demonstrated an example of how this model works to interpret clinical data. In this example, three theoretical patients had three different blood pressure levels, low, high, and normal. Among the three patients, the IOPs were changed in the model from 15 mmHg up to 45 mmHg in correspondence with a mean arterial pressure and IOP level. With this information, the model predicts blood flow, of which perfusion pressure is a surrogate.  

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    “We saw that at an IOP of less than 26 mmHg, the blood flow plateaus for high blood pressure and normal blood pressure,” he explained. “There is no plateau in a patient with low blood pressure. At IOPs of 26 to 36 mmHg, the same decreasing slope is seen for all three patients.

    “Over 36 mmHg, a steeper slope is seen due to what we think is partial venous collapse, which begins earlier in patients with lower blood pressure,” he added.

    Next: Concluding thoughts

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