Vascular Targeting in ME/CFS

In the last lecture of the conference, Prof. Wirth addressed the disturbed vascular function in ME/CFS. According to his hypothesis, expansion and contraction of the blood vessels are out of balance. Energy deficit in the skeletal muscles and in the brain is triggered by a combination of hypoperfusion and mitochondrial dysfunction. Prof. Wirth presented the hypothesis that the metabolism-related release of vascular mediators is transferred from the muscle to the blood. The resulting cycle could be disrupted by vasoactive drugs. For example, vasodilating drugs in low doses could be suitable for this, so that the supply of oxygen to the muscles and the brain is improved. However, there are currently no drugs that selectively dilate the vessels in the muscles and brain. Yet simultaneous dilatation of the vessels in the abdominal cavity should be avoided. While some drugs can increase blood flow to the brain, this cannot yet be done specifically for the muscles. For patients with OI, nicotine patches and acetylcholine esterase inhibition may help. The choice of drugs depends on the nature of the circulatory problems: OI and POTS or orthostatic hypotension.