Does MS Affect the Heart? A Deeper Look at Cardiac Impact
Explore how multiple sclerosis can influence heart function, from autonomic regulation to cardiac rhythm, and what this means for overall health.
Explore how multiple sclerosis can influence heart function, from autonomic regulation to cardiac rhythm, and what this means for overall health.
Multiple sclerosis (MS) is primarily known for affecting the central nervous system, leading to issues with movement, sensation, and cognition. However, research indicates it may also impact heart health, raising concerns about cardiovascular risks in people with MS. While not classified as a cardiac condition, MS can influence heart function in ways still being explored.
Understanding this interaction is essential for managing overall health in affected individuals.
The autonomic nervous system (ANS) regulates heart rate, blood pressure, and vascular tone without conscious effort. In MS, central nervous system damage can disrupt autonomic control, affecting cardiovascular stability. Heart rate variability (HRV) studies show that MS patients often exhibit reduced parasympathetic activity and heightened sympathetic dominance. This imbalance can lead to an increased resting heart rate, reduced heart rate adaptability, and a higher likelihood of orthostatic intolerance, where blood pressure fails to adjust properly upon standing.
Autonomic dysfunction varies among patients, depending on lesion location and disease progression. Research in Autonomic Neuroscience: Basic & Clinical indicates that individuals with greater spinal cord involvement experience more pronounced autonomic impairment, leading to symptoms such as dizziness, excessive sweating, and abnormal blood pressure fluctuations. Some studies also link autonomic dysfunction in MS to nocturnal hypertension, where blood pressure remains elevated during sleep, potentially increasing cardiovascular strain.
MS-related autonomic dysfunction can also affect baroreceptor sensitivity, which helps regulate blood pressure. A study in Clinical Autonomic Research found that MS patients often have blunted baroreflex responses, making it harder for their bodies to stabilize blood pressure. This can result in episodes of hypotension or hypertension, raising the risk of cardiovascular complications. Additionally, impaired vagal tone—indicating reduced parasympathetic influence—has been associated with a higher likelihood of arrhythmias, further underscoring the impact of autonomic dysfunction on heart function.
Structural and functional changes in the myocardium suggest MS may influence cardiac muscle integrity. Cardiac magnetic resonance (CMR) and echocardiography studies have detected myocardial abnormalities in some MS patients, even without traditional cardiovascular risk factors. Chronic inflammation, oxidative stress, and microvascular dysfunction may contribute to these changes.
One notable finding is increased myocardial fibrosis, or excessive collagen deposition in heart tissue. Research in JACC: Cardiovascular Imaging shows that MS patients exhibit elevated late gadolinium enhancement (LGE) on CMR scans, a marker of myocardial scarring. This fibrosis can impair the heart’s ability to contract and relax efficiently, leading to diastolic dysfunction, where the heart struggles to fill properly between beats. Some researchers suggest recurrent autonomic dysregulation may alter myocardial perfusion, fostering fibrosis.
Subtle impairments in myocardial strain—an echocardiographic measure of heart muscle deformation—have also been observed. A study in The International Journal of Cardiology found that MS patients had reduced global longitudinal strain (GLS), an indicator of subclinical myocardial dysfunction. Lower GLS values are linked to an increased risk of heart failure and adverse cardiovascular events, even in those without overt symptoms. These findings suggest MS may gradually affect myocardial performance, increasing the likelihood of long-term cardiac complications.
Heart rhythm disturbances have been observed in MS patients, suggesting the disease may influence cardiac electrophysiology. While arrhythmias are common in cardiovascular conditions, MS-related neurological disruptions appear to contribute to conduction abnormalities. MS patients show a higher prevalence of bradyarrhythmias, such as sinus node dysfunction, and tachyarrhythmias, including supraventricular tachycardia (SVT) and atrial fibrillation. These irregularities may cause palpitations, dizziness, or syncope, complicating disease management.
Lesions in brainstem and spinal cord pathways that regulate cardiac autonomic control may underlie these rhythm disturbances. Damage to medullary cardiovascular centers can disrupt vagal and sympathetic inputs, causing unpredictable heart rate fluctuations. A case series in Neurology documented MS patients experiencing transient asystole—brief pauses in heart activity—highlighting the potential severity of autonomic dysfunction. Additionally, prolonged QT intervals, a marker of delayed ventricular repolarization, have been noted in some MS patients, increasing the risk of life-threatening arrhythmias such as torsades de pointes.
Exercise is crucial for cardiovascular and muscular health, but MS patients often face limitations in sustained physical activity. Fatigue, a common MS symptom, reduces endurance, while muscle weakness and spasticity further hinder exertion. Cardiopulmonary exercise testing (CPET) shows that MS patients typically have lower peak oxygen uptake (VO₂ max), indicating diminished aerobic capacity. This can restrict participation in moderate-to-vigorous activities essential for heart health.
Beyond muscular limitations, some MS patients experience an attenuated heart rate response to exertion, known as chronotropic incompetence, which affects cardiovascular output during exercise. An exaggerated perception of effort has also been reported, where individuals feel more exhausted than expected for their workload. This discourages consistent exercise, leading to deconditioning and further reducing cardiovascular efficiency.