Naturopathic Care of the Cardiovascular System


Fraser Smith, MATD, ND

In a previous edition of the Townsend e-Letter, we examined what a naturopathic model of care can be. In this update, we apply that model to care of the cardiovascular system. Specific cardiovascular disease presentations in particular patients will always demand individualized therapy. In this discussion, we consider some of the more important issues in this system as a whole. This discussion is based on a portion of Chapter 8 of the 2022 Textbook, Naturopathic Medicine, A Comprehensive Guide (Springer).1

In a model of naturopathic care, we look at the progression of dysfunction. One way to consider this progression is the levels of hypofunction, impaired circulation and communication, inflammation (early and deeper with more immune system intrusion), fibrosis and degeneration of the extracellular matrix, decline of function, and in some cases, neoplasm.

Hypofunction

An early occurring state of hypofunction in the cardiovascular system is in the endothelium itself. Oxidative stress can damage the endothelium, leading to changes in endothelial interaction with lipoproteins. This sets the stage for lipid accumulation and the progression of atheromas. It also damages the ability to produce nitric oxide from the amino acid L-arginine. Nitric oxide is needed to reduce inflammation, strengthen the junctions between endothelial cells, and relax blood vessels.2-4 So while this is a reversible situation, it definitely increases long term disease risk.

Impaired Communication and Circulation

The capillaries and smaller arterioles of the heart are vital for heart muscle function. If these microcirculatory vessels become inflamed and constricted, the heart muscle will not be evenly and adequately supplied with blood.6,7 This limits the work that the heart can do, and if severe enough, can cause ischemia in stressful situations. As endothelial degradation proceeds, the way in which it interacts with lipoprotein particles begins to change. There is more intrusion of cholesterol and free fatty acids from lipoprotein particles, particularly LDL, through the endothelial and into the underlying arterial intima. This is more likely with oxidized LDL, and in particular oxidized polyunsaturated fatty acids within the LDL particular, such as linoleic acid.8

Inflammation

Once the endothelium is damaged, and an atheroma is established, an ongoing inflammatory process is underway. This is evidenced by elevated hsCRP levels, and appearance of indicators of poor nitric oxide status, including asymmetric dimethyl arginine.9,10 This inflammation is the primary driver of the pathology. Increased LDL levels, high insulin levels, appearance of linoleic acid in the lipoprotein in excessively high amounts, lack of antioxidants, and lack of HDL (or dysfunctional HDL) will certainly promote the disease process. The heart muscle itself is not immune to this degeneration. Macro and microvascular impairment can damage the heart, both its myocytes and the electrical system that coordinates their actions.7

Deeper Damage and More Aggressive Intrusion by the Immune System

There are many forms of deep inflammation in the cardiovascular system, some triggered by pathogens and some of it accelerated by ongoing damage to the system. Constriction of blood flow can happen because of the narrowing of the arteries due to atherosclerosis. It can also occur due to increased vessel muscular tone, at least in arteries. This is under the control of the autonomic nervous system.

An injured endothelium is less able to control the intrusion of LDL into the intima. Much of the LDL, under conditions of high oxidative stress and inflammation, became oxidized. This makes it less likely to be returned to the liver (due to dysfunction apo proteins in the LDL particle) and more likely to interact with and enter the intima. This leads to macrophage involvement, and as many macrophages die attempting to remove oxidized fats and cholesterol, they heap up as foam cells and expand the plaque. The liver makes pentameric C Reactive protein in response to TNF and IL-6 (which are elevated as white blood cells detect damage). Monomeric C-reactive protein activates innate defenses, which leads to accelerated inflammation.11-13

As atherosclerotic plaques progress, they can become more inflamed and unstable. White blood cells such as neutrophils release myeloperoxidase, “as if” the lesion were a foreign body. But it is not enough to remove it. The plaque grows and as its core expands, the collagen cap, which no longer has normal endothelium on it, becomes more friable.The day arrives when they rupture, and this activates platelets, leading to a thrombus. While this is a normal reaction to acute injury, it can be disastrous for the body. If the thrombus obstructs blood flow, then any tissue downstream that depends on flow of blood from that area for oxygen, will undergo ischemia. 

Fibrosis and Breakdown of the Extracellular Matrix

Arteriosclerosis is a more advanced, degenerative, disease that is almost always following on atherosclerotic lesions within the artery. (Table 8.1) In arteriosclerosis, the artery is calcified.14-16 This, of course, increases the pressure of blood and reduces the flexibility and distension of these vessels–they are stiff instead of elastic. The calcification may also have a beneficial effect of stabilizing intimal atherosclerotic plaques, preventing their rupture. As in many situations of the body, calcium deposition on top of fibrotic tissue has a scarring, but stabilizing effect.

The myocardium begins to remodel in later stages of atherosclerosis and cardiomyopathy. The extracellular matrix begins to lose some of its elasticity, with excessive collagen formation. This creates a situation of ventricular and arterial stiffness.17 This negatively impacts filling of these chambers and can decrease ejection fraction. Sodium retention induced by renal renin secretion will somewhat offset this due to volume overload, as will cardiac dilatation (where possible) but this is only a short-term compensation. 

Decline of Function 

As the compensations in this system fail, the ischemia experienced by remote tissues such as the extremities, the kidneys, and brain, due to lack of cardiac output, will be found in the heart muscle itself. (Table 8.1) Mitochondria begin to display decreased autophagy, and the lack of protein maintenance takes its toll in mitochondrial fission or fusion.  The remaining mitochondria begin to uncouple and decrease in numbers.18,19 Death of electrical fibers in the heart, or even prominent conduction nodes, will lead to arrhythmias. Destabilization events such as an infarction or even excessive exertion can provoke fibrillation of atria or ventricles. The sodium retaining aspects of renin will lead to pulmonary edema, and the right ventricle will struggle to move enough blood through the pulmonary vasculature in order to stave off hypoxia.  

Table 8.1
Levels of dysfunction in the cardiovascular system (adapted from Smith, F. Naturopathic Medicine, A Comprehensive Guide. Cham, Switzerland: Springer, 2022.)

Levels of dysfunction Tests to consider 
Hypofunction: oxidative stress, early endothelial dysfunction F2 isoprostane Lipid panel  Stress test
Impaired circulation and communication: Vessel constriction, early plaque formationOxidized LDL Asymmetric dimethyl arginine Nuclear stress test  
Inflammation: establishment of atheroma and change to intima High sensitivity C reactive protein  
Deeper inflammation and intrusion of the immune system: Rapid plaque progression, Cardiac output decline Myeloperoxidase Angiogram (for higher risk score patients) Coronary nuclear scan Coronary artery CT scan Carotid artery ultrasound Doppler echocardiogram 
Fibrosis and extreme compensations: Left ventricular dilatation, plaque thickening, plaque instability Doppler echocardiogram Lipoprotein associated phospholipase A2 Angiogram
Deterioration of function: Cardiomyopathy, rigid heart muscle Doppler echocardiogram (including measurement of pre-load) CT scan of heart PO2 and oxygen saturation 

Moving to Therapy

Once we have established what levels of dysfunction exist in the cardiovascular system, we have needed information to make therapeutic decisions. Perhaps medical/allopathic treatments are needed to stabilize the situation. Lower levels of dysfunction often indicate that focusing on the determinants of health and using nutritive treatments will allow the system to rectify itself. Deeper inflammation and the beginning of fibrosis suggest that a lot of more direct biochemical and whole person support will be part of the treatment plan. In the next installment in this series, we’ll dive right into a treatment model that balances therapies to increase adaptive responses and those that decrease maladaptive responses.

References

  1. Smith, F. Naturopathic Medicine, A Comprehensive Guide. Cham, Switzerland: Springer, 2022.
  2. Steven S, Frenis K, Oelze M, Kalinovic S, Kuntic M, Bayo Jimenez MT, et al. Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular  Disease. Oxid Med Cell Longev. 2019;2019:7092151.
  3. Bachschmid MM, Schildknecht S, Matsui R, Zee R, Haeussler D, Cohen RA, et al. Vascular aging: chronic oxidative stress and impairment of redox  signaling-consequences for vascular homeostasis and disease. Ann Med. 2013 Feb;45(1):17–36.  
  4. Daiber A, Hahad O, Andreadou I, Steven S, Daub S, Münzel T. Redox-related biomarkers in human cardiovascular disease – classical footprints and beyond. Redox Biol [Internet]. 2021/01/23. 2021 Jun;42:101875. Available from: https://pubmed.ncbi.nlm.nih.gov/33541847
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  8. Guijarro C, Cosín-Sales J. LDL cholesterol and atherosclerosis: The evidence. Clin e Investig en Arterioscler  Publ Of la Soc  Esp Arterioscler. 2021 May;33 Suppl 1:25–32. 
  9. Kvietys PR, Granger DN. Role of reactive oxygen and nitrogen species in the vascular responses to  inflammation. Free Radic Biol Med. 2012 Feb;52(3):556–92.
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  11. Fioranelli M, Bottaccioli AG, Bottaccioli F, Bianchi M, Rovesti M, Roccia MG. Stress and Inflammation in Coronary Artery Disease: A Review  Psychoneuroendocrineimmunology-Based. Front Immunol. 2018;9:2031.
  12. Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat Rev Cardiol. 2018 Sep;15(9):505–22.
  13. Zhu Y, Xian X, Wang Z, Bi Y, Chen Q, Han X, et al. Research Progress on the Relationship between Atherosclerosis and Inflammation. Biomolecules. 2018 Aug;8(3). 
  14. Rosin NL, Sopel MJ, Falkenham A, Lee TDG, Légaré J-F. Disruption of collagen homeostasis can reverse established age-related myocardial  fibrosis. Am J Pathol. 2015 Mar;185(3):631–42.
  15. Jin H-Y, Weir-McCall JR, Leipsic JA, Son J-W, Sellers SL, Shao M, et al. The Relationship Between Coronary Calcification and the Natural History of  Coronary Artery Disease. JACC Cardiovasc Imaging. 2021 Jan;14(1):233–42. 
  16. Frangogiannis NG, Kovacic JC. Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar. J Am Coll Cardiol. 2020 May;75(17):2219–35.
  17. Díez J, González A, Kovacic JC. Myocardial Interstitial Fibrosis in Nonischemic Heart Disease, Part ¾: JACC Focus  Seminar. J Am Coll Cardiol. 2020 May;75(17):2204–18.
  18. Martín-Fernández B, Gredilla R. Mitochondria and oxidative stress in heart aging. Age (Dordr). 2016 Aug;38(4):225–38. 
  19. Oka T, Hikoso S, Yamaguchi O, Taneike M, Takeda T, Tamai T, et al. Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure. Nature. 2012 May;485(7397):251–5.

Published January 27, 2024

About the Author

Fraser Smith, MATD, ND, is Assistant Dean of Naturopathic Medicine and an associate professor at National University of Health Sciences (NUHS; Lombard, Illinois).

Dr. Smith was the founding academic leader of the ND program at NUHS, which joined NUHS’ family of programs in 2006. He is the author of several books on wellness and nutrition for the public and author of the textbook Introduction to the Principles and Practice of Naturopathic Medicine. In addition to being an educator and licensed naturopathic physician, Dr. Smith is a licensed dietician nutritionist and cardiovascular health researcher.