204 Chapter 9 elusive, although genetic analyses have hinted at the existence of common genetic factors influencing vascular structure and function in both migraine and cervical artery dissection.30 While our findings suggest a comparable annual incidence of 0.34% for ischemic stroke among patients with migraine, it is essential to acknowledge that we cannot definitively exclude the possibility that treatment with anti-CGRP(R)-mAbs might influence the risk of all CV events. Notably, our cohort consisted of healthy individuals with no cardiovascular risk factors at baseline. In contrast, the aforementioned population-based study reporting a one-year incidence of 1.64% included approximately 10% of subjects who were smokers, some had a history of diabetes, and the mean age was approximately 10 years higher compared to our cohort.27 Additionally, the other population-based study included individuals with diabetes (1.37%), hypercholesterolemia (0.73%), hypertension (3.03%), and even other comorbidities such as cancer or liver/renal disease.28 Given these differences, further studies are warranted, particularly those that include control groups matched for CV risk factors and migraine severity. For now, it remains crucial for practitioners to be vigilant, as anti-CGRP(R)-mAbs may potentially increase the severity or impact of such events if they do occur.6 During myocardial infarction (MI) or stroke, there is a release of CGRP, which possesses vasodilatory properties.31, 32 Vasodilation improves the blood flow and oxygen delivery to affected tissue and therefore plays a protective role. Consequently, CGRP may mitigate the extent of tissue damage. Inhibiting CGRP, either through blocking its receptors or capturing the released CGRP before it reaches the receptor, has the potential to exacerbate the deleterious effects of MI or TIA/stroke.5 The above is especially important since real-world data (RWD) studies revealed elevated BP after exposure to anti-CGRP(R)-mAbs, which was not previously observed in the pivotal randomized clinical trials.20, 21, 33 This discrepancy is most likely due to the dichotomization of the BP outcome variable used in the clinical trials, which focused solely on the occurrence of hypertension. This approach may mask the absolute impact of anti-CGRP(R)-mAbs on BP and potentially downplay the significance of the data.33 Treatment with anti-CGRP(R)-mAbs is associated with an average increase of 5.2 mmHg in systolic BP.21 While some clinicians may perceive this increase as mild, it is crucial to recognize the clinical significance. In fact, a mere 5 mmHg increase in systolic BP will raise the risk of non-fatal CV events by approximately 10%.34 Due to the possibility of many years of treatment, this relative risk increase is clinically important even in participants aged 55 years or younger, which is the age group most represented among patients with migraine.34 Hence, these seemingly modest elevations in BP associated with anti-CGRP(R)-mAbs warrant careful consideration
RkJQdWJsaXNoZXIy MjY0ODMw