Much of this mitochondrial research has focused on defects in the electron transport chain (ETC) embedded in the membranes of the mitochondria. The ETC directly fuels the ATP synthase enzyme vital to the production of ATP at the end of that chain. The ETC has four main complexes, or steps, that work to optimally shuttle electrons to the terminal ATP-producing enzyme. [118,119]
Defects in the ETC have been specifically identified in heart failure and are always present. [123] In even the most advanced cases of heart failure, most affected hearts still have inflamed but viable heart cells that can be positively impacted with improved ATP production. Aside from the chelation therapies noted above, bolstering mitochondrial function has been a major physiological goal in the treatment of heart failure. [124]
Traditional medicine has no drugs which directly work to normalize mitochondrial dysfunction in heart failure patients. Instead, all the current prescription drugs work only to basically mobilize excess fluid accumulations and/or to lessen the workload (peripheral resistance) faced by the failing heart muscle. This is not to say that there is no place for these drugs, only that they should not be the only agents given to the patient. As with most prescription drugs, the therapeutic goal appears limited to symptom improvement while letting the underlying pathology continue to evolve. Traditional medicine is much better at diagnosing and naming medical conditions than at reversing or resolving them.
CoQ10 is the most researched of these ETC-targeted therapies for cardiomyopathy, and its enormous benefits on cardiac function have been well-documented. The especially vital role of CoQ10 in supporting ATP production in the heart is reflected in its concentrations in different tissues in the body. Far more CoQ10 is found in the heart than is found in any of 12 other human tissues examined. Furthermore, the heart contained roughly twice as much CoQ10 as the kidneys, the organ/tissue in the study with the second highest CoQ10 concentrations. Non-cardiac muscle had only one-third of the CoQ10 as the heart muscle. [126]
CoQ10 directly promotes the mitochondrial ETC by supporting the electron transfer in complexes I and II, as well as by its established role in complex III. Its impact in restoring heart function in cardiomyopathy has been significant and sometimes stunning, especially since this is a condition that is only given supportive care by traditional cardiologists while steady cardiac deterioration continues.
In a randomized, double-blind trial in 420 patients with severe heart failure and followed for two years, there was a 42% reduction in all-cause mortality and cardiac mortality in patients given 100 mg of CoQ10 three times daily. Fewer hospitalizations for heart failure occurred in the treated group as well. [127] The supplementation of selenium along with CoQ10 appears to be especially effective in reducing mortality in cardiomyopathy patients. [128]
The ejection fraction (EF), a measure of how effectively the heart contracts and empties on each beat, is the most direct objective and readily measurable parameter to evaluate cardiac function. EFs considered to be normal run roughly from 65 to 80%. EFs of 10% to 15% represent the greatest loss of cardiac function and are characteristic numbers for patients on heart transplant waiting lists. CoQ10 supplementation has rescued many patients considered to have terminal heart failure, and this has been accompanied by dramatic improvements in EF and functional capacity in most patients, with one study showing the mean EF going from 25 to 42%. [129-134] It should also be noted that increasing an EF from 15% to 25% can take a patient who has difficulty walking across the room without shortness of breath to one who can function normally as long as major physical stresses are avoided.
The initial pathology seen in the heart failure of hypertrophic cardiomyopathy with preserved EFs is also clearly improved with CoQ10 supplementation. [135,136]
Low CoQ10 levels, along with increased CRP (C-reactive protein, a marker of oxidative stress) levels have been documented in heart failure, whether due to coronary disease or of unknown cause. [137] Other studies have also shown that lower CoQ10 serum levels correlated with increased all-cause mortality in general, as well as in heart failure patients. [138,139]
As CoQ10 increases the energy production in all the cells in the body, it should not be surprising that studies have shown its benefits in a wide variety of diseases. Low levels have been documented in many medical conditions, along with evidence of its clear benefits when properly supplemented or administered. Such conditions include the following: