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Carnitine in Coronary Insufficiency

We have previously demonstrated that cardiac carnitine depletion occurs as a result of myocardial ischemia (insufficient oxygen supply to the heart) and that myocardial energy failure, compromised ATP production, is more likely to occur when carnitine levels are low.  It therefore stands to reason that carnitine supplementation would be of value to the patient with coronary artery disease.  Carnitine supplementation should allow you to engage in more exercise before you need to stop due to ischemic symptoms (heart pain due to ATP deficiency).

Four studies of carnitine supplementation during temporary atrial pacing have been carried out.  Here a temporary pacemaker is placed within the heart (in the catheterization lab), and used to control the patient's heart rate.  As the heart rate increases, cardiac work increases, and the requirement for oxygenated blood will rise.  If coronary disease is present, the supply of oxygen cannot keep up with demand, ATP production will stop, and you will experience chest pain and demonstrate ST depression on your EKG.  In these studies, it was shown that following carnitine administration:
            · At a given paced heart rate, there was less ST depression and less angina with carnitine on board, and
            · The pacing rate at which ischemia was brought out was higher with carnitine supplementation

In other words, at the same workload, with carnitine on board, there was less ATP deficiency, and more cardiac work could be done before ischemic phenomena (ATP deficiency, angina, or ST depression) were brought out.

In a treadmill study, patients with coronary disease received either placebo or carnitine 900 mg/day over 12 weeks.  Nothing happened with placebo therapy, while in the carnitine group treadmill walking time increased by 12%, from 11.4 to 12.8 minutes, and time to ST depression was prolonged by 37%, from 6.4 to 8.8 minutes.

Another study assessed the effect of two week's supplementation with 1500 mg/day of propionylcarnitne (carnitine bound to propionic acid, another molecule that participates in ATP production) in stable coronary patients.  Total work capacity increased by 17%, from 514 to 600 watts (a unit of energy expenditure).  Exercise time increased by 10%, from 515 to 565 secs., and time to ST depression increased by 14%, from 375 to 425 secs.

Claudication, effort related calf muscle pain due to ATP deficiency, in turn due to lower extremity vascular disease, is really angina of the leg muscles.  In this study patients with stable claudication received 4,000 mg/day of carnitine.  The researchers found that aerobic metabolism was prolonged.  That is, at the same exercise level, the carnitine patients remained able to utilize oxygen while the placebo patients had switched over to low yield, oxygen independent, anaerobic metabolism.  Carnitine supplementation increased effort capacity by 75%. 

Carnitine does play a role in the prevention of atherosclerotic vascular disease.  Carnitine promotes fat metabolism, and thus has beneficial effects on cholesterol. triglyceride, and Lp(a) levels, but carnitine's major role in integrative cardiology is in the treatment of coronary insufficiency and CHF.  By enhancing ATP production, particularly in the oxygen deficient or strained myocardial cell, carnitine improves the functional performance of the heart and helps neutralize the effect of oxygen deficiency.  Like CoQ10, carnitine gives you more ATP per molecule of oxygen present.