Parkinson’s disease (PD) is a progressive neurological disorder primarily known for its effects on movement, such as tremor and rigidity. The disease extends far beyond the motor system, profoundly affecting the cardiovascular system and causing complex heart and blood pressure problems. These effects often appear as non-motor symptoms, sometimes occurring years before movement issues are diagnosed. Understanding this link is important for managing the condition.
Specific Cardiac Manifestations in Parkinson’s Disease
One of the most common heart-related issues in people with PD is orthostatic hypotension (OH). This is a sudden, sustained drop in blood pressure when moving from sitting or lying to standing. The drop is defined as a decrease of at least 20 mmHg in systolic pressure or 10 mmHg in diastolic pressure within three minutes. Symptoms include lightheadedness, dizziness, blurred vision, weakness, and fainting, which increases the risk of falls. OH affects 30% to 50% of individuals with PD.
The opposite problem, supine hypertension, occurs when blood pressure becomes abnormally high while the person is lying down, particularly at night. This condition is often seen alongside OH, creating a difficult cycle of high blood pressure when resting and low blood pressure upon standing. Reduced heart rate variability (HRV) is another measurable effect, representing the natural variation in time between heartbeats. A lower HRV indicates the heart has a reduced ability to adapt to changing body demands.
Less common, but more serious, manifestations include structural changes to the heart muscle, such as increased thickness of the left ventricle. PD is also associated with an increased risk for conditions like heart failure and certain arrhythmias, or irregular heart rhythms. These cardiac issues contribute to the overall burden of the disease and require specific attention.
Autonomic Dysfunction: The Neurological Link to the Heart
The underlying cause for many cardiac issues is the disruption of the Autonomic Nervous System (ANS). The ANS controls involuntary bodily functions like heart rate, blood pressure, and digestion. It is divided into the sympathetic system (action) and the parasympathetic system (rest and recovery). These two branches rapidly adjust blood pressure and heart rate in response to gravity or stress.
The pathological hallmark of PD is the accumulation of misfolded alpha-synuclein protein into clumps called Lewy bodies. These Lewy bodies accumulate in the brain and in peripheral nerves that regulate the heart and blood vessels. This leads to cardiac sympathetic denervation, the loss of sympathetic nerve fibers supplying the heart. This nerve loss can sometimes rival the nerve loss seen in brain areas responsible for motor symptoms.
Because the sympathetic nerves are damaged, the heart and blood vessels cannot receive signals to release norepinephrine. Norepinephrine is a chemical messenger that normally narrows blood vessels and increases heart rate to maintain blood pressure when standing. This poor signaling directly leads to neurogenic orthostatic hypotension, as the body cannot compensate for gravity. This autonomic dysfunction can appear early, indicating widespread nervous system damage.
Medication-Related Cardiovascular Side Effects
Not all cardiovascular issues in PD result directly from the disease; many arise as side effects from motor symptom medications. Levodopa, the primary treatment, can decrease blood pressure and worsen pre-existing orthostatic hypotension (OH). This effect is partly due to the drug’s impact on blood pressure regulation and its potential to lessen the heart’s contractility.
Dopamine agonists, another common drug class, also carry cardiovascular risks. These medications can cause peripheral edema, or swelling in the limbs. Older ergot-derived agonists have been associated with restrictive valvular heart disease, though newer non-ergot agonists are generally safer. Certain Monoamine Oxidase B (MAO-B) inhibitors, which prolong dopamine’s effect, can also worsen postural hypotension.
The goal of PD treatment is to balance effective motor symptom control with minimizing adverse effects on the heart and blood pressure. Combining Levodopa with certain MAO-B inhibitors may potentiate the hypotensive effect. This necessitates regular communication between the patient and their prescribing physician to maintain stable blood pressure.
Monitoring and Collaborative Care
Given the complex interplay between PD and the cardiovascular system, a proactive approach to monitoring and care is beneficial. Patients and caregivers should regularly monitor blood pressure and heart rate at home. Checking values while seated and immediately after standing provides valuable data regarding daily fluctuations associated with orthostatic hypotension.
Diagnostic tools assess cardiac involvement. These may include a tilt-table test, which precisely measures blood pressure changes while the patient is tilted upright. An electrocardiogram (EKG) evaluates the heart’s electrical activity for rhythm abnormalities. Specialized neuroimaging scans using tracers like MIBG can also visualize the extent of cardiac sympathetic denervation.
Successful management requires collaborative care involving both a neurologist and a cardiologist. The neurologist manages PD medications, while the cardiologist addresses heart and blood pressure issues. The neurologist can adjust PD drug timing or dosage to lessen blood pressure side effects. This integrated approach ensures simultaneous management of both neurological and cardiovascular aspects of the disease.