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BMC Cardiovascular Disorders recently published the results of a small clinical trial evaluating CoQ10’s effect on cardiac function following a myocardial infarction (MI). One hundred forty-seven study participants had successful percutaneous coronary intervention (PCI) following MI, received standard acute coronary syndrome medications (e.g., aspirin, ticagrelor, clopidogrel, statins, etc.), and were then randomized to either 30mg of CoQ10 per day or to a control group. Cardiac function was assessed at 1 and 3 months, including left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), along with brain natriuretic peptide (BNP) levels. A small subset (11) of participants who recently experienced an MI also had their baseline plasma CoQ10 levels compared to healthy controls, and an experimental animal model of CoQ10 supplementation following MI was also reported in this publication.
Compared to the age and gender-matched controls, CoQ10 plasma levels following MI were found to be significantly lower, suggesting a “deficiency state.” Of the 120 study participants who completed the trial, people receiving CoQ10 had greater increases in their LVEF and LVFS at 1 and 3 months, suggesting a faster recovery of cardiac function. There was also a significantly greater drop in BNP levels at 3 months among people taking CoQ10, also suggesting improved cardiac function and a potentially reduced risk for heart failure.
The mouse model used in conjunction with the clinical trial indicated that the macrophages of mice treated with CoQ10 had a lower inflammatory state, mediated through suppression of the NLRP3/IL1β pathway, as well as a significantly reduced degree of cardiac remodeling following MI. Additionally, CoQ10 downregulated the expression of genes associated with macrophage activation, inflammatory cytokine expression, and those related to reactive oxygen species (ROS) generation. A number of experimental models suggest much of the adverse cardiac remodeling that takes place following an MI is mediated by a specific pro-inflammatory macrophage subtype. Additionally, activation of the NLRP3 inflammasome (and subsequent IL1β production) triggers direct and indirect myocardial damage, and blockade of this pathway may prevent recurrence and improve exercise capacity and cardiac function. The NLRP3 inflammasome is known to be activated by ROS, serving as “kindling” for subsequent highly inflammatory state. Thus, the experimental model may provide a basis by which CoQ10 inhibits cardiac damage following an MI, reducing ROS production and NLRP3 activation, thereby helping to preserve cardiac function.
Surprisingly, there are very few clinical trials evaluating CoQ10 use and recovery from myocardial infarction. In 2003, Molecular and Cellular Biochemistry published the results of a randomized and double-blind controlled trial (B vitamins served as the control) among participants who recently had an MI. This trial found a reduction in total cardiac events (24.6% versus 45%) among those receiving CoQ10 (120 mg/day), as well as significant reductions in fatal and non-fatal events. Furthermore, 41% of those receiving B vitamins experienced fatigue compared to only 7% receiving CoQ10. In 1998, Cardiovascular Drugs and Therapy published the results of a randomized and controlled trial among people with recent MI and found significant reductions in angina (9.5% vs. 28.1%), arrhythmias (9.5% vs. 25.3%), impaired left ventricular function (8.2% vs. 22.5%), and half the number of total cardiac events over a 28 day period among those receiving CoQ10 vs. placebo, as well as multiple indicators of reduced oxidative stress.
In addition to anti-inflammatory and antioxidant actions, CoQ10 was also shown to significantly reduce lipoprotein(a) levels compared to placebo in a 1998 study published in the International Journal of Cardiology. This is clinically relevant because lipoprotein(a) is also a known mediator of the residual risk following lipid-lowering therapy. While it is unclear if the level of reduction of lipoprotein(a) is meaningful (other therapies have been shown to reduce lipoprotein(a) without reducing its associated risk), a follow-up to the clinical trial published in 1998 might help to answer this question.
A 2022 review of clinical trials published in the Journal of the American College of Cardiology found that at a median dose of 50mg (range 33-100mg in 7 clinical trials) per day, CoQ10 reduced all-cause mortality among people with heart failure by 32%, ranking it among the top nutrients for supporting cardiovascular health and function. However, nearly all of the trials for CoQ10 are related to heart failure, limiting its clinical usage for other cardiovascular conditions. No other clinical trials evaluating CoQ10 use among people who have had an MI between 2003 and this recent trial appear to have been published, and it is difficult to understand why larger well-controlled (as well as dose-finding) studies have not been conducted, given the early promise shown in the two clinical trials just mentioned. As the authors of the recent paper point out, despite aggressive LDL-C lowering, considerable residual cardiovascular risk remains, and this appears to be mediated at least in part via pro-inflammatory mechanisms. CoQ10 is a therapy with no established adverse effects that may help preserve cardiac function, and should be a prime candidate for study, if not directly implemented into post-MI recovery protocols.
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