The Heart of The Matter: Cardiovascular Effects of Parkinson’s disease

The heart of the matter: cardiovascular effects of Parkinson’s disease

It has long been understood that Parkinson’s disease (PD) does not just cause movement symptoms, but also causes a litany of non-motor symptoms with effects throughout the body. One of the organ systems that is affected is the cardiac system, encompassing the heart, as well as the major and minor blood vessels. I received this topic as a suggestion from a blog reader and we will be discussing this important issue today. Please feel free to suggest your own blog topic.

Understanding the neurologic control of the cardiac system

Before we explore this issue, let’s first learn a bit about the autonomic nervous system (ANS) and about the cardiac system’s place within it. The ANS is part of the peripheral nervous system, a network of nerves throughout the body. The ANS exerts control over functions that are not under conscious direction such as respiration, heart function, blood pressure, digestion, urination, sexual function, pupillary response, and much more.  The ANS is further subdivided into the parasympathetic nervous system and the sympathetic nervous system. Both the parasympathetic and sympathetic nervous systems regulate most major organs. Often, they have opposite effects, with the sympathetic nervous system activating a system and the parasympathetic system calming it down.

One of the systems controlled by the ANS is cardiac regulation. Blood pressure sensors, known as baroreceptors, reside in the heart as well as in the carotid artery, the major artery in the neck. If the baroreceptors sense a change in the blood pressure, a signal is sent to particular areas in the brain. From there, the autonomic nervous system sends signals to the heart to control heart rate and cardiac output. Signals are also sent to the blood vessels to change the size of their diameter, thereby regulating blood pressure.

How Parkinson’s disease affects the autonomic nervous system and the heart

In PD, there are two major reasons why the automatic control of the cardiac system is impaired. First, areas of the brain that control this system often contain Lewy bodies and have undergone neurodegeneration. In addition, the autonomic nervous system itself is directly affected by Lewy body-like accumulations and neurodegeneration. This means, when the baroreceptors in the heart and carotid artery sense a drop in blood pressure and try to generate a signal to the heart and blood vessels to increase the blood pressure, the message may not get through. This results in neurogenic orthostatic hypotension (nOH), or drops in blood pressure upon standing due to autonomic nervous system dysfunction. There are no medications that can cure nOH by restoring the autonomic nervous system in PD. nOH however, can be treated. Read more about nOH and its treatments here.

Typically, when discussing the cardiac effects of PD, the focus is on nOH. Another cardiac effect in PD however, is changes in heart rate. Heart rate variability, which is a measure of the variation in the time interval between heart beats, was found to be more pronounced in patients who eventually developed PD than those who did not, suggesting that cardiac autonomic dysfunction can be an early non-motor symptom of Parkinson’s disease. Other studies have shown that people with PD tend to have certain features on their electrocardiogram. These features include a prolonged PR interval and possibly a prolonged QTc interval, referring to longer than normal segments of the tracing of the heart. It remains unclear what the clinical consequences of these changes are, although they are not thought to commonly lead to cardiac rhythm abnormalities.

Structural problems of the heart such as coronary artery disease or cardiomyopathy are not thought to be part of the pathology of PD, although of course, could co-exist with PD.

Research is underway to further understand the cardiac effects of Parkinson’s

It is possible to image the sympathetic nervous system of the human heart by injecting a radioactive tracer, [123I]meta-iodo-benzyl-guanidine, (MIBG). Development of this technique, known as MIBG cardiac imaging, holds much promise as a test to confirm the diagnosis of PD (a state in which MIBG detection in the heart is diminished or absent), to identify those who are at risk of developing PD in the future, and to distinguish PD from related disorders. MIBG cardiac imaging is still considered an experimental procedure for detection of PD and is not yet in use as a clinical tool for this purpose.

A recent research study was conducted in monkeys in which the destruction of the sympathetic nerves of the heart was chemically induced to mimic the changes that are seen in PD. The cardiac system was then imaged using a number of new-generation radioactive tracers, which bind to markers of inflammation and oxidative stress. This model system may help to shed light on the molecular changes that accompany the loss of the sympathetic nerves of the heart and can also be used to track the response of the cardiac system to therapeutic agents.

Tips and takeaways

  • Lewy body pathology and neurodegeneration in both the brain and the autonomic nervous system can have early and profound effects on the cardiac system in people with PD.
  • The most well-understood effect of this is neurogenic orthostatic hypotension (nOH), or drops in blood pressure upon standing.
  • Although there are medications that can help the symptoms of nOH, there are no medications that directly improve the degeneration of the autonomic nervous system in PD. A new model system however, can be used to study potential therapies.
  • Routine cardiologic care makes sense for patients with PD. A cardiologist can help manage nOH and ensure that the heart rhythm is normal. He or she can also screen for additional cardiologic problems that are not linked to PD but are common in the general population, such as coronary artery disease.

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Dr. Rebecca Gilbert

APDA Vice President and Chief Scientific Officer

Dr. Gilbert received her MD degree at Weill Medical College of Cornell University in New York and her PhD in Cell Biology and Genetics at the Weill Graduate School of Medical Sciences. She then pursued Neurology Residency training as well as Movement Disorders Fellowship training at Columbia Presbyterian Medical Center. Prior to coming to APDA, she was an Associate Professor of Neurology at NYU Langone Medical Center. In this role, she saw movement disorder patients, initiated and directed the NYU Movement Disorders Fellowship, participated in clinical trials and other research initiatives for PD and lectured widely on the disease.

A Closer Look ArticlePosted in Parkinson's Disease Symptoms

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