Protecting the Heart: A Role for Vitamin D

Last revision: 08-13-22

 

By Eugene L. Heyden, RN    

Vitamin D protects against Cancer.  Vitamin D protects against autoimmune disease.  Vitamin D protects against Alzheimer’s disease, against Parkinson’s disease, and against multiple sclerosis.  It protects against so many diseases.  So, why would it not protect against heart disease?  The answer is “it does.”

“In the Health Professionals Follow-up Study, men with a high circulating level of vitamin D had half the risk of myocardial infarction as men with vitamin D insufficiency.”  (Kilkkinen et al., 2009, emphasis added)

Heart disease, more formally referred to as cardiac disease, falls under the umbrella term cardiovascular disease (CVD).  Cardiac disease just happens to be our No. 1 killer.  Astonishingly, this killer will destroy approximately one out of three of us living here on planet Earth (Aleksova et al., 2015).  And yes, I’ve seen this killer in action.

In my nursing career, I have spent nearly a quarter of a century in the trenches battling this killer—taking care of acute heart attack victims, patients with various degrees of heart failure, individuals recovering from open heart surgery, and those recovering from heart transplantation.  So unexpectedly, this killer preys on those who are vitamin D deficient, which is why I am writing to warn you of the danger.  It is quite likely you are among those who are at great risk. Listen up!

“In the United States and Europe, > 40% of the adult population has low vitamin D levels.”  (Milazzo et al., 2017)

Surprisingly (but not to me), one study “found a high (96%) prevalence of vitamin D deficiency in patients with acute myocardial infarction.”  (De Metrio et al, 2015)  Apparently, vitamin D deficiency is something to avoid if you want to live a healthier life and a longer life, a life not inviting an early death to sweep you away.

A myocardial infarction (MI) is a fancy word for heart attack.  A heart attack is typically caused by a blood clot that forms in a narrowing in an artery, in this case a coronary artery, one that feeds a significant portion of the heart.  Given time, given circumstances, a blood clot will form in the narrowing and create a sudden blockage of blood flow, initiating the MI.  Unless resolved, death of the affected portion of the heart will occur.  And often the death of an entire person will occur.  Nearly 50% of MI sufferers die before they arrive at the hospital to receive life-saving care—all due to a coronary artery narrowing and the formation of a little blood clot.  One can see a narrowed coronary artery, as well as the occlusion, when coronary angiography is performed.  So now that you know the basics, as well as a medical term or two, you should readily appreciate the following:

“In more than 3000 subjects undergoing coronary angiography, severe vitamin D deficiency (25(OH)D <10 ng/mL) had 3 to 5 times risk of dying from sudden cardiac death or heart failure during a 7-year follow-up period compared with optimal levels of vitamin D (25(OH)D >30 ng/mL).”  (Judd and Tangpricha, 2009, emphasis added)

Unfortunately, there are so many individuals with vitamin D deficiency, even severe vitamin D deficiency, that given enough time, the commonplace yet the unthinkable will occur.  According to the Center for Disease Control and Prevention (CDC) (2015), coronary artery disease kills 370,000 Americans each year.  It looks like we could substantially reduce the number, perhaps by half, simply by solving the problem of vitamin D deficiency in our population.  But we’re not even close to thinking about doing this.  Instead, we think about other things, and allow vitamin D deficiency to persist.

At this point in our conversation, I should probably tell you how vitamin D protects against heart disease.

To begin with, vitamin D restrains both systemic and vascular inflammation, protecting against the development of vascular disease.  Conversely, “Vitamin D deficiency stimulates systemic and vascular inflammation, enabling atherogenesis.”  (Mozos and Marginean, 2015)  Things just don’t happen out of the blue.  Apparently, inflammation occurring in coronary arteries is a pivotal step that leads to atherogenesis.  Atherogenesis is the disease process that damages the coronary artery, allows the damaged portion to narrow, and sets the stage for coronary artery occlusion.  And should an occlusion occur, the result is an MI . . . and people die.  Vitamin D acts to prevent all this, at the very beginning and at several key steps along the way.  But to do so it must be in adequate supply.

In the disease process that leads to an MI, an abnormal uptake of both calcium and cholesterol progressively occurs within the wall of an injured, diseased portion of a coronary artery.  Vitamin D acts to prevent both calcification of a coronary artery and the accumulation of cholesterol within a compromised portion of a coronary artery (Mozos and Marginean, 2015).  Perhaps surprising to you (but not to me), cholesterol can accumulate in a coronary artery even when blood cholesterol levels are normal, as approximately 75% of heart attack victims have normal cholesterol levels (Champeau, 2015).  On the other hand, studies have shown that almost everyone who has a heart attack has a low vitamin D level.  So, it sounds like more attention should be paid to vitamin D levels than to cholesterol levels in our battle against coronary artery disease.  And why not? Vitamin D has so much to offer!

Among other things, vitamin D helps prevent abnormal clotting from occurring in a narrowed coronary artery.  (see Mozos and Marginean, 2015)  So, at the very least, vitamin D may postpone (perhaps forever) what may have become an inevitable MI.  But there is more to the story.

One response the heart mounts when experiencing a progressive narrowing of a coronary artery is to create what are called collaterals.  A collateral is a new vessel, created by the heart to perform a little bypass operation on itself.  A collateral will allow blood to flow around the narrowing in a coronary artery to supply blood to a threatened portion of the heart.  A network of collateral arteries can save you in the event of a sudden coronary occlusion.  Guess what?  Vitamin D stimulates the formation of collateral circulation!  It does so by stimulating growth factors and the like (Lima Jr. and Kunadian, 2015).  Importantly, less collateral circulation develops in the context of vitamin D deficiency.  Hence, “vitamin D levels were found to be an independent predictor of coronary collaterals development.”  (Lima Jr. and Kunadian, 2015)  Which is probably why one study found “vitamin D deficiency was more common among patients in the poor-collateralization group compared to patients in the well-collateralization group.”  (Hossein-Nezhad et al., 2015)  So, it should be of no surprise that the authors reporting on this study make the following statement:

“Maintaining a normal vitamin D status should be a high priority in the general population. Likewise, vitamin D supplementation may be beneficial in the prevention of CAD [coronary artery disease] in patients with an increased risk for CAD.”  (Hossein-Nezhad et al., 2015)

Since the subject was brought up, perhaps now would be a great time to discuss vitamin D supplementation.  Simply put, we need to supplement because diet won’t cut it.  We know this because all those individuals with those low vitamin D levels, those who have the MI’s, are eaters.  Diet offered them little to no protection against vitamin D deficiency and little to no protection from coronary artery disease.  Of course, anyone can generate thousands of units of vitamin D each day by relevant sunlight exposure—but only during late-morning to mid-afternoon, and between March through September, leaving approximately 5 months of the year when no vitamin D can be made (no matter how hard you try).

So, as you can see, vitamin D supplementation is the answer, but not the only answer.  Vitamin D testing is in order.  “Zittermann et al. found a vitamin D level of 30–35 ng/L. as the best choice for risk reduction in cardiovascular mortality.”  (Mozos and Marginean, 2015)  Combining testing to see where you are at, supplementing with vitamin D as indicated, and repeat testing to determine if a therapeutic goal has been achieved and is maintained, is clearly the best approach to substantially reduce the risk of drawing the attention of our No. 1 killer.

On, no!  You’ve gone and done it.  You have had an MI.  Since you are reading this, it is safe to say you did not die.  But be aware, those who do not die from their MI, have a list of threats lying in wait, problems also related to an individual’s vitamin D status.

“Vitamin D status is prognostic for major postinfarction adverse events, such as heart failure hospitalizations, recurrent acute myocardial infarction, death, or restenosis [reocclusion] after percutaneous coronary intervention. A significant, moderate association was found between circulating vitamin D concentration and the risk of all-cause mortality, especially deaths due to coronary disease.”  (Mozos and Mardinean, 2015, emphasis added)

I think I’ve made things abundantly clear.  Vitamin D can help protect you from experiencing an MI, death from an MI, and experiencing the adverse consequences of an MI.  But you can ignore all this if you want to (at your peril).

 

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References

Aleksova A, Belfiore R, Carriere C, Kassem S, La Carrubba S, Barbati G, Sinagra G 2015 Vitamin D Deficiency in Patients with Acute Myocardial Infarction: An Italian Single-Center Study. Int J Vitam Nutr Res. Jan 1; 85:23–30

Centers for Disease Control and Prevention 2015 Heart Disease Facts. Retrieved from https://www.cdc.gov/heartdisease/facts.htm

De Metrio M, Milazzo V, Rubino M, Cabiati A, Moltrasio M, Marana I, Campodonico J, Cosentino N, Veglia F, Bonomi A, Camera M 2015 Vitamin D Plasma Levels and In-Hospital and 1-Year Outcomes in Acute Coronary Syndromes: A Prospective Study. Medicine. May 1; 94(19):e857

Dogan Y, Sarli B, Baktir AO, Kurtul S, Akpek M, Sahin O, Odabas H, Dondurmacı E, Ugurlu M, Ozkan E 2015 25-Hydroxy-Vitamin D Level May Predict Presence of Coronary Collaterals in Patients with Chronic Coronary Total Occlusion. Postępy w Kardiologii Interwencyjnej= Advances in Interventional Cardiology. 11(3):191

Judd SE, Tangpricha V 2009 Vitamin D Deficiency and Risk for Cardiovascular Disease. The American Journal of the Medical Sciences. Jul; 338(1):40–44

Hossein-Nezhad A, Eshaghi SM, Maghbooli Z, Mirzaei K, Shirzad M, Curletto B, Chen TC 2014 The Role of Vitamin D Deficiency and Vitamin D Receptor Genotypes on the Degree of Collateralization in Patients with Suspected Coronary Artery Disease. BioMed Research International. Mar 6;2014

Kilkkinen A, Knekt P, Aro A, Rissanen H, Marniemi J, Heliövaara M, Impivaara O, Reunanen A 2009 Vitamin D Status and the Risk of Cardiovascular Disease Death. American Journal of Epidemiology. Oct 15; 170(8):1032–9

Milazzo V, De Metrio M, Cosentino N, Marenzi G, Tremoli E 2017 Vitamin D and Acute Myocardial Infarction. World Journal of Cardiology. Jan 26; 9(1):14

Mozos I, Marginean O 2015 Links between Vitamin D Deficiency and Cardiovascular Diseases. BioMed Research International. Apr 27; 2015

Lima Jr J, Kunadian V 2015 Vitamin D: Evidence for an Association with Coronary Collateral Circulation Development? Postępy w Kardiologii Interwencyjnej= Advances in Interventional Cardiology. 11(3):174

Champeau R 2009 Most Heart Attack Patients’ Cholesterol Levels Did Not Indicate Cardiac Risk [Press release]. http://newsroom.ucla.edu/releases/majority-of-hospitalized-heart-75668

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and not to be substituted for professional judgment and guidance or to provide a reason to neglect or delay appropriate medical care. It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein. The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy. This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician. The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the resources that are herein recommended.

 

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