Migraine is a complex neurological disorder characterized by recurrent, severe headaches that are often accompanied by other symptoms like nausea or sensitivity to light and sound. The condition is traditionally viewed through a neurological lens, but research increasingly points to a strong, shared connection with cardiovascular health. This relationship suggests that the neurological and cardiovascular systems share common underlying biological vulnerabilities. Understanding this link is important for managing both conditions, as heart problems can influence migraine frequency and severity, and vice versa. This article explores the specific cardiac conditions and the physiological mechanisms that explain this relationship between the brain and the heart.
Specific Cardiac Conditions Associated with Migraines
One of the most frequently cited cardiac findings in migraine patients is the presence of a Patent Foramen Ovale (PFO). The PFO is a small flap-like opening between the upper two chambers of the heart, the atria. This opening is a normal structure during fetal development and typically seals shortly after birth; however, it remains open, or patent, in approximately 25% of the general adult population.
The statistical association between PFO and migraine is considerably higher, particularly for individuals who experience migraine with aura. Studies suggest that the prevalence of a PFO can range from 46% to as high as 88% in patients who suffer from migraine with aura, which involves transient visual, sensory, or speech disturbances. This increased rate is one of the clearest physical links established between a structural heart anomaly and a neurological disorder. The connection is less pronounced for those with migraine without aura.
Other cardiac conditions and risk factors also show an association with migraine, indicating a broader cardiovascular connection beyond the PFO. Migraineurs, particularly those with aura, have a higher risk of developing atrial fibrillation, an irregular and often rapid heart rhythm. There is also an increased prevalence of ischemic heart disease risk factors, such as endothelial dysfunction, in individuals who experience frequent migraines. These observations suggest that the underlying vascular health of a migraine sufferer may be compromised.
Shared Mechanisms Explaining the Connection
The physiological link between the heart and the brain in the context of migraine is explained by several overlapping mechanisms. One primary theory centers on the concept of paradoxical embolism, which is directly relevant to the PFO connection. In individuals with a PFO, small venous clots or biologically active substances that would normally be filtered by the lungs can pass through the opening and directly enter the arterial circulation.
If these unfiltered substances travel to the brain, they may trigger a neurological event known as Cortical Spreading Depression (CSD). CSD is a slow-moving wave of electrical activity across the brain’s cortex that is widely accepted as the underlying cause of the migraine aura. The paradoxical passage of an embolus is hypothesized to initiate this electrical disturbance, causing the transient symptoms of aura and the subsequent headache pain. This mechanism provides a direct pathway for a cardiac factor to initiate a neurological event.
Beyond the PFO, a common thread linking the two conditions is systemic vascular dysfunction, which involves the inner lining of blood vessels, known as the endothelium. Endothelial dysfunction can impair the blood vessels’ ability to dilate and constrict properly, leading to vascular vulnerability in both the heart and the brain. Migraineurs show an altered responsiveness to vasoactive substances, such as nitric oxide, which regulates blood vessel diameter. This shared vascular sensitivity contributes to both the blood flow changes seen in migraine and the increased risk for cardiovascular events.
Chronic, low-grade systemic inflammation is also a shared mechanism, as it plays a role in the pathology of both cardiovascular disease and migraine. Inflammatory markers in the blood are often elevated in both conditions, suggesting that a generalized inflammatory state may drive the progression or severity of both disorders. This systemic inflammation contributes to endothelial damage, further exacerbating the underlying vascular vulnerability. Furthermore, genetic studies have identified shared risk loci between migraine and coronary artery disease, such as a variant in the PHACTR1 gene, suggesting a common inherited predisposition.
The Direction of Risk
The relationship between migraine and heart health is complex and often described as bidirectional, meaning that each condition can influence the risk of the other. Migraine, particularly the type accompanied by an aura, is recognized as an independent risk factor for certain cardiovascular events. For example, women who experience migraine with aura have been found to have an approximately two- to four-fold increased risk of ischemic stroke compared to the general population.
Migraine is also associated with an increased risk for myocardial infarction (heart attack) and conditions like venous thromboembolism. This suggests that the underlying vascular pathology causing the migraine attacks may also predispose the person to arterial blockages and clotting issues. The frequency of migraine attacks also appears to correlate with the level of cardiovascular risk, indicating that more severe migraine may reflect a greater burden of vascular disease.
Conversely, the presence of a cardiac anomaly like a PFO can function as a direct trigger for migraine attacks in susceptible individuals. The mechanism of paradoxical embolism represents a pathway where the heart condition directly contributes to the neurological disorder. In many cases, the link is not direct causation but rather a manifestation of a shared risk profile. Both the heart and the brain are affected by the same genetic, inflammatory, and vascular factors.
Implications for Diagnosis and Treatment
The established link between heart problems and migraines has significant implications for diagnosis and clinical management. When a patient presents with severe, frequent, or refractory migraines, especially those with aura, a physician may recommend screening for underlying cardiac issues. Diagnostic tools like a transthoracic echocardiogram with a saline bubble test are used to detect the presence and size of a PFO.
For patients with a confirmed PFO and severe, medication-resistant migraines, a procedure known as PFO closure may be considered. This involves a minimally invasive, catheter-based procedure to permanently seal the opening between the heart chambers. While initial clinical trials on PFO closure for migraine were mixed, a pooled analysis showed that the procedure resulted in a significantly greater reduction in the number of monthly migraine days and attacks compared to medical therapy alone.
The decision to proceed with PFO closure is typically reserved for highly selected patients who have failed multiple preventive medications. This requires consultation between a neurologist and an interventional cardiologist. For the broader group of migraineurs with increased cardiovascular risk, treatment focuses on optimizing general heart health. This includes aggressive management of traditional cardiovascular risk factors, such as high blood pressure, cholesterol, and diabetes, to mitigate the shared vascular vulnerability.