Thursday, December 5, 2019

Is migraine medication hurting your heart?



The neuropeptide αCGRP is a strong vasodilator (Russell, F. A., King, R., Smillie, S.-J., Kodji, X., & Brain, S. D., 2014). Vasodilation can decrease blood pressure through the decrease of resistance in blood vessels. Recently a medication that stops αCGRP signaling has been approved for migraine prevention as it decreases the triggering of migraines through its affect near meninges in the brain (Skaria, T., Mitchell, K. J., Vogel, O., Wälchli, T., Gassmann, M., & Vogel, J., 2019). This is an example of the same signal having different affects throughout the body based on the receptor to which it binds. This dual signaling pathway is important because people with hypertension who are taking anti αCGRP medication for migraines could be increasing their risk of heart complications due to the decreased protective signaling of αCGRP. Without αCGRP signaling, blood pressure can remain high and can cause cardiac hypertrophy to compensate. This hypertrophy is beneficial for the short term, but can cause many complications in the long term and decreased heart efficiency. These detrimental off target effects of the drug are important to consider. It’s important for physicians to consider medical complications and possibly causing harm with medications which violates the ethical principle of non-maleficence. With the new research findings, persistent HTN should be a contraindication for this migraine treatment to better align with the ethical principle of non-maleficence.   
References: 
Russell, F. A., King, R., Smillie, S.-J., Kodji, X., & Brain, S. D. (2014). Calcitonin Gene-Related Peptide: Physiology and Pathophysiology. Physiological Reviews, 94(4), 1099–1142. doi: 10.1152/physrev.00034.2013

Skaria, T., Mitchell, K. J., Vogel, O., Wälchli, T., Gassmann, M., & Vogel, J. (2019). Blood Pressure Normalization–Independent Cardioprotective Effects of Endogenous, Physical Activity–Induced αCGRP (α Calcitonin Gene-Related Peptide) in Chronically Hypertensive Mice. Circulation Research, 125(12), 1124–1140. doi: 10.1161/circresaha.119.315429

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