Myocardial infarction (MI) is the most common form of acute cardiac injury and a leading cause of death in the Western world. Advances in treatment have led to a decline in mortality during the acute phase. On the other hand, there has been an increase in heart failure in patients surviving an MI due to significant heart damage.
The heart has little regenerative capacity and MI generates repair mechanisms that produce a cardiac scar. The development of heart failure after MI is determined by the size of the injured area, the wound healing response that occurs in the days after the event, and the healing of the scar.
The healing process of the heart after an infraction can be divided into three phases: the inflammatory phase, the proliferative phase, and wound scarring phase. Dying heart cells trigger an inflammatory reaction, signaled by inflammatory cytokines, such as IL-6, IL-8 and C-reactive protein (CRP). The higher the cytokine levels, the more severe the cardiac injury. (Anything that would lower cytokine levels after an MI should lessen chronic heart damage, in theory.)
The proliferative phase is triggered by adhesion molecules, such as VCAM-1 and E-selectin, which begins to form the scar. As with cytokines, anything that would lessen the levels of adhesion molecules should lessen the eventual cardiac scar.
Recently, Dr Yoav Arnson and colleagues of Tel Aviv University decided to see if vitamin D affected the cardiac scaring process.
They gave 25 MI patients standard care plus 4,000 IU/day of pure 25(OH)D or calcidiol (which is roughly equivalent to 40,000 IU/day of vitamin D3) for five days, comparing them to 25 MI patients treated with standard care alone. They measured cytokine and adhesion molecule levels before and after treatment.
Levels of the inflammatory cytokine IL-6 decreased by 31 % in the treated patients, compared to a 48.7 % increase in the untreated group (p=.05). Another inflammatory cytokine (IL-8) decreased by 25 % in the vitamin D treated patients, compared to a 76 % increase in the control group (p=.01). CRP concentrations increased by 108% in the treated patients, compared to an average 361% increase for the patients without vitamin D supplementation (p=.03).
The tests of the adhesion molecules, VCAM-1 and E-selectin, also showed a favorable result for vitamin D. For example, in the treated group, VCAM-1 levels decreased 3%, compared to a 23% increase in the control group (p=.03). E-selectin levels showed a favorable trend, decreasing by 8% among the treated patients, compared to a 0.4% decrease in the control group (p=0.15).
The authors concluded,
“Understanding the inflammatory response to ischemic myocardial injury and the role of cytokines after MI may allow us to promote improved healing and cardiac remodeling after MI. Low levels of 25(OH)D are known to be associated with increased atherosclerosis and higher risk of MI. The results of this study demonstrated that vitamin D can attenuate the inflammatory process following AMI. As vitamin D deficiency is widespread in many populations and is in theory amenable to potential interventions, clarification of its role in myocardial ischemia and infarction may be of great public health relevance.”
While calcidiol or pure 25(OH)D is no longer available in the USA, oral vitamin D3 is rapidly converted to 25(OH)D in the liver, roughly at a rate of 50,000 IU of D3 becoming 5,000 IU of 25(OH)D. Based on this study, I recommend that health care professionals prescribe patients with a heart attacks pharmacological doses of vitamin D, such as 50,000 to 100,000 IU/day for ten days, beginning immediately after presentation. This is safe and will result in less inflammation and scarring and should result in less heart failure after an MI.