Neurocardiology: An Integrative Approach to the Prevention Of CAD and AMI

by Decker Weiss, NMD FASA

On a snowy Manhattan day in 1949, 14 cardiovascular physicians met to form a revolutionary new society they called the American College of Cardiology. This formation paved the way for the new subspecialty called cardiology and its new pioneering specialists, now called cardiologists.¹

Since that time, heart attack survival has improved dramatically. For example, 35 years ago, fully half of all patients with acute myocardial infarction (AMI) died. Today, two-thirds survive. Still, heart attacks are relatively prevalent, with 1.5 million people each year experiencing some size of AMI.²

In 2010, an estimated 2.66 million people experienced atrial fibrillation, and this number is trending upwards. If projections hold true, by 2050 as many as 12 million people will have A-fib.³ In 2005, A-fib’s estimated cost – including hospitalizations, in- and out-patient physician care, and medications – was a staggering $6.65 billion per year.⁴

Congestive heart failure (CHF) is also on the rise, with 550,000 new cases diagnosed annually.⁵ Nearly 5 million Americans are currently living with CHF.⁶ It’s the first-listed diagnosis in more than 875,000 hospitalizations, and is the most common diagnosis in hospital patients aged 65 years and older.⁷

• Naturopathy

At a meeting a few years ago, I had an interesting encounter with three interventional cardiologists. During a discussion about the alarming increase in heart failure, the cardiologists expressed concern about whether using stents and bypasses actually saved their patients’ lives, or simply “traded a fast death for a slow one.”

My background as a naturopathic cardiologist compelled me to share a deep-rooted tenet of natural medicine – that is, suppressing one disease often only allows it to manifest in another way. To my astonishment, the interventional cardiologists heartily agreed. For me, it was a rare, fascinating moment. It was a time when – at least briefly – the views of natural and allopathic medicine actually aligned.

But how can that golden moment be extended? If there’s general consensus that the allopathic model of cardiac disease suppression is not working as well as it should, how can the strengths of naturopathy be incorporated?

The key, I believe, is simple. We must shift our focus from the heart as a stand-alone organ, to one that honors its interconnection with all the other major systems of the body. In other words, we must “despecialize” and view the heart as a vital, integrated component of the body’s all-inclusive “super-system.”

Neuro-Endo-Immuno-Inflam Cardiology

The concept of the body as a “super-system” was pioneered by Dr. Gottfried Kellermann, president and CEO of NeuroScience Inc. Dr. Kellermann’s extensive research on neurotransmitter-related health concerns led him to the conclusion that the nervous system is not a separate entity, but tied closely to the neural and endocrine systems. Under this model, the nervous system “runs the show,” and neurosignaling processes play a key role in regulation and maintenance throughout the body. And this, of course, includes the heart.

NeuroCardio: Coronary Artery Disease

According to most experts, inflammation and oxidation are the two top underlying causes of heart disease. However, there are few laboratory tests that accurately diagnose inflammation and oxidation. CRP-HS has been a good start, but it is far from providing a clear avenue for preventive treatment.

Recently, a new test for oxidative LDL has come to market, which is a huge step in the right direction. But what about inflammation? The risk of developing heart disease has traditionally been assessed using a standard lipid panel. However, about half of all heart attacks and strokes occur in people with “normal” cholesterol. Thus, there are many individuals at risk who are presumed healthy.

While it’s essential to know a patient’s cholesterol levels, what actually causes adverse cardiac events is inflammation – specifically vulnerable plaque related to increased inflammation.

Currently there is definitive research demonstrating that pro-inflammatory cytokines can lead to predictable imbalances in both cortisol and neurotransmitter levels.⁸ Testing cellular cytokines and neurotransmitter levels can help diagnose the unique, underlying inflammatory mechanisms of individual patients. An individual’s risk for heart disease progression and mortality coincides with biomarker elevations along the inflammation continuum. Once discovered, these neurotransmitters and cytokines can be balanced through a variety of modalities, including nutrition stress management and nutritional supplementation.

It’s interesting to note that depressed patients have been found to have higher levels of pro-inflammatory cytokines, acute phase proteins, chemokines and cellular adhesion molecules.⁹ Pro-inflammatory cytokines have been definitively linked to lower GABA and serotonin expression resulting in depression.^10,11 Of course, depression is recognized as one of the leading risk factors for developing CAD.¹² Simply put, a happy patient is a happy heart. Balancing to the correct levels of serotonin and GABA may not only improve patients’ quality of life, but add years to it as well.

A truly integrative approach to prevention of CAD and AMI incorporates urine neurotransmitter testing, along with cellular cytokine analysis (looking for abnormal pro-inflammatory markers), while establishing appropriate cortisol levels throughout the day and night.

NeuroCardio: Congestive Heart Failure

There is currently much debate in CHF circles regarding the adequacy of ejection fraction, considered the “hallmark” of diagnosis.¹³ Markers such as BNP and others are becoming more prominent for risk stratification and prognosis.

As both a clinician and a professor, I teach my students about the neurohormonal responses created by the body in response to a lower EF. This includes activation of the sympathetic system (including epinephrine and norepinephrine) and the renin-angiotensin aldosterone system.¹⁴ Pro-inflammatory cytokines, in particular tumor necrosis factor-a, have tremendous regulatory effects on energy metabolism, immune and hormonal function, and the function of the neuroendocrine system.¹⁵ These inflammatory cytokines are known to contribute to the progression of heart failure, and have been related to patients’ prognosis.¹⁶

Advanced heart failure can be considered a state of chronic, low-grade inflammation.¹⁷ In the “NeuroCardio” world, the “low grade inflammation” component of a patient’s CHF would be diagnosed through urine neurotransmitter and stimulated cellular cytokine testing in order to risk stratify and create a prognosis. For example, if catecholamines such as norepinephrine and epinephrine are found to be elevated, and the inhibitory neurotransmitter taurine is found to be depressed, that may lead to a poor patient prognosis. Similarly, a poor prognosis would be made if a patient’s interleukins, cytokines, and TNF numbers demonstrate low-grade inflammation.

By linking the “super-system” of neurology, endocrinology, and immunology to inflammation, treatments can be devised that calm the body’s neurohormonal response to heart failure. This may lead to fewer medications and an improved prognosis. While most individual heart failure patients receive cookie-cutter treatment plans, accurate neurotransmitter and cellular cytokine analysis can help individualize treatment to optimize each individual patient’s prognosis and quality of life.

NeuroCardio: Atrial Fibrillation

Managing heart rate involves both intrinsic and extrinsic controls. Intrinsic regulation of heart rate is the result of the unique nature of cardiac tissue – it is self-regulating and maintains its own rhythm without direction.

Extrinsic controls, on the other hand, are those that emanate from hormonal responses, as well as from the commands of the nervous system (both the central and the autonomic nervous systems).¹⁸ The SA node displays intrinsic automaticity at a rate of 100 to 110 action potentials (“beats”) per minute. This “vagal tone” reduces the resting heart rate down to 60 to 80 beats/min.¹⁹

Neurotransmitters play a role in the mechanisms of both intrinsic and extrinsic heart rate control. At present, research on the causes of A-fib focus on risk factors such as hypertension, alcohol use, viral infections, pulmonary issues, and others.²⁰ But what is the underlying mechanism? What effects are these risk factors having on the neurotransmitters?

Research indicates that epinephrine, norepinephrine, and vagal tone are all implicated in the genesis of atrial fibrillation.²¹ One interesting fact is that in a patient who has prolonged atrial fibrillation, the vagal tone and possibly the neurotransmitters normalize, which may be one reason why atrial fibrillation is stubborn to resolve.²²

In clinical practice, practitioners often note warning signs of atrial fibrillation, such as episodes of palpitations, CAD, and high stress. In the “NeuroCardio” world, these signs would prompt immediate screening for “super-system” imbalances in cortisol and neurotransmitters. In addition, a variety of modalities may be utilized, such as balancing the physical parts of the body through spinal manipulation, allowing for unimpeded vagal nerve tone through visceral manipulation of the stomach and thoracic vertabrae, and incorporating relaxation techniques. In addition, amino acid therapies may be used to help “nudge” the neurotransmitters back into alignment.

Are Cardiologists Good for Cardiology?

This question has been debated since the advent of medical specialization. On the surface, the idea of focusing on a specific part or system of the human body seems to be a good idea, but results are mixed. It appears we may be reducing morbidity and mortality on the one hand, while creating other morbidity mortalities on the other.

Introducing the integrated “NeuroCardio” approach may be what’s needed. Utilizing the modern tools of valid urine neurotransmitter testing, cellular cytokine analysis, and saliva adrenal testing may be the “diagnostic connection” required to validate new approaches to addressing devastating heart conditions. The “NeuroCardio” approach offers immense opportunity to lessen health care costs, reduce our patients’ suffering, and extend their quality of life.

Decker Weiss, NMD, FASA, is the first naturopathic physician to complete a conventional internship, residency, and fellowship in a conventional medical system. Dr. Weiss trained in the Columbia Hospital system, the Arizona Heart Hospital, and the Arizona Heart Institute. Founder of the Scottsdale Heart Institute and the Center for Neuro-Endo-Immunological Cardiovascular Studies, Dr. Weiss consults with NeuroScience Inc. on practitioner medical education.

Notes

1. American College of Cardiology. History [Web page]. 2013. http://www.cardiosource.org/en/ACC/About-ACC/Who-We-Are/History.aspx.

2. Heart attack statistics by age [online article]. Buzzle. February 2013. http://www.buzzle.com/articles/heart-attack-statistics-by-age.html.

3. These are figures from a variety of sources, all compiled in Lloyd-Jones D, Adams RJ, Brown TM, et al. Heart disease and stroke statistics – 2010 update: a report from the American Heart Association. Circulation. 2010;121:e91.

4. Coyne KS, Paramore C, Grandy S, Mercader M, Reynolds M, Zimetbaum P. Assessing the direct costs of treating nonvalvular atrial fibrillation in the United States. Value Health. 2006 Sep–Oct;9(5):348–356.

5. Heart failure statistics [Web page]. Emory Healthcare. February 2010. http://www.emoryhealthcare.org/heart-failure/learn-about-heart-failure/statistics.html.

6. Ibid.

7. Ibid.

8. Kunz-Ebrecht SR, Mohamed-Ali V, Feldman PJ, Kirschbaum C, Steptoe A. Cortisol responses to mild psychological stress are inversely associated with proinflammatory cytokines. Brain Behav Immun. 2003 Oct;17(5):373–383.

9. Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression. Trends Immunol. 2006 Jan;27(1):24–31. Epub 2005 Nov 28.

10. Stellwagen D, Beattie EC, Seo JY, Malenka RC. Differential regulation of AMPA Receptor and GABA receptor trafficking by tumor necrosis factor α. J Neurosci. 23 March 2005;25(12):3219–3228; doi:10.1523/JNEUROSCI.4486-04.2005.

11. Zhu C-B, Randy D Blakely RD, Hewlett WA. The proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha activate serotonin transporters. Neuropsychopharmacology. 2006;31:2121–2131. doi:10.1038/sj.npp.1301029. Epub 1 February 2006.

12. Litchman JH et al. Depression and coronary heart disease: Recommendations for screening, referral and treatment. A science advisory from the American Heart Association Prevention Committee of the Council on Cardiovascular Nursing, Council on Clinical Cardiology, Council on Epidemiology and Prevention, and Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Psychiatric Association. Circulation. Oct 21 2008;118(17):1768–1775.

13. Cleve Clin J Med.March 2002;69(3).

14. Chatterjee K. Neurohormonal activation in congestive heart failure and the role of vasopressin. Am J Cardiol. 2005 May 2;95(9A):8B–13B.

15. Sharma R, Anker SD. Immune and neurohormonal pathways in chronic heart failure. Congest Heart Fail. 2002 Jan–Feb;8(1):23–28,48.

16. Ibid.

17. Ibid.

18. What affects the heart rate? [Web page]. HeartMonitors.com. February 2013. http://www.heartmonitors.com/exercisetips/changing_heartrate.htm.

19. Weiss, SA Decker. Anticoagulant therapy and antiarrhythmics. CNDA presentation; 2012.

20. Atrial fibrillation: causes [Web page]. Mayo Clinic. http://www.mayoclinic.com/health/atrial-fibrillation/DS00291/DSECTION=causes.

21. Van den Berg MP, Hassink RJ, Baljé-Volkers C, Crijns HJGM. Role of the autonomic nervous system in vagal atrial fibrillation. Heart. 2003 March;89(3):333–335.

22. Ibid.