Atrial Fibrillation, Cardiac Disorders Linked with Mitochondria Dysfunction

Linda J. Dobberstein, Chiropractor, Board Certified in Clinical Nutrition

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Atrial Fibrillation, Cardiac Disorders Linked with Mitochondria Dysfunction
The door to understanding several heart-related conditions is opening up wider. Recent research shows that the heart is one of the most affected organs in the body with mitochondrial disorders. This may not come as a surprise because the heart is one of the most energy demanding organs in the body. However, those who have been keeping an eye on the new field of metabolic cardiology may be surprised at how many cardiac disorders are related to mitochondrial disorders.

Multiple Heart Disorders Related to Mitochondria Disorders



A recent review article from the International Journal of Cardiology showed numerous disorders of the heart were related to mitochondria dysfunction. Cardiac disorders that seemed to be physiologically different and classified into various groups are more related to mitochondria disorders than previously thought.

Mitochondria are the organelles or little factories found in cells. They produce energy after the burning of glucose and fat via the Kreb’s cycle through a process known as oxidative phosphorylation. They also make proteins for their own use to execute the transcription of DNA to RNA and then RNA to amino acids. Mitochondria are the powerhouse or the batteries of cells, essential to life energy. They are also central to apoptosis or programmed cell death. This is the routine housekeeping process used by cells to get rid of cellular trash. When mitochondria don’t do this well because they themselves are damaged, then the rest of the cell components fail to function in a healthy manner, like a city’s garbage and sewer systems broken down and on strike.

The cardiac disorders identified with mitochondrial problems are diverse. These include cardiomyopathy and heart failure, arrhythmias, pulmonary hypertension, dilation of the aortic artery, pericardial effusion, fluid around the heart, coronary heart disease, autonomic nervous system dysfunction (blood pressure, syncope, POTS, rhythm), congenital heart defects, and even sudden cardiac death. Children with congenital heart defects, rhythm problems, and metabolic cardiomyopathy are not immune to underlying mitochondrial problems. These concerns areoften associated with significant gene mutations negatively inferring with mitochondria early on in life.

Atrial Fibrillation



The most common cardiac rhythm problem is atrial fibrillation (A-fib). A-fib is now gaining recognition as related to mitochondrial dysfunction. A-fib is an irregular and often rapid heart rate that causes poor blood flow to the body. There may be shortness of breath, chest pain, palpitations, fatigue, and weakness or trouble exercising. The irregular rhythm may come and go; sometimes the disorder can worsen so that the atrial fibrillation does not go away. Cell apoptosis or cell death is a contributing factor to the start, relapse, and progression of A-fib. When A-fib fails to resolve and remains present for months and years, it can lead to heart failure from the chronic metabolic stress or stroke or heart attack from clots and disrupted blood flow. In response to the potential clot risk, A-fib patients are often put on lifelong Coumadin or other blood thinning medications to prevent blood clots from occurring. Coumadin has its own risks.

To get the heart back into rhythm, Mayo Clinic’s medical approach is to use electrical shock to stop the heart and the abnormal rhythm and hope that the heart restarts its normal rhythm. Powerful drugs may also be used to force the heart back to a regular rhythm as a medication conversion with subsequent long-term use of anti-arrhythmic meds to prevent future episodes. If the problem persists or medications fail, the long-term approach is to ablate or literally “surgically fry” the nerve tissue (pacemaker) in the heart that regulates rhythm and abnormal pacemaker firing. Another surgical treatment option is the use of the surgical maze procedure during open heart surgery. The surgeon intentionally creates incisions in the heart muscle during open heart surgery to create scar tissue. This is to interfere with stray electrical impulses that cause the A-fib. Mayo Clinic does admit that while the procedures have a high success rate, even with these extraordinary attempts A-fib can reoccur.

Hopefully the intentional destruction of cardiac nerve tissue becomes a barbaric thing of the past, in light of the mitochondria dysfunction research linked with cardiac rhythm disorders. It becomes alarming to think of scar tissue and dead pacemaker cells albeit “planned” within the “ticker” as these concerns are far from the essence of heart health.

Post-Operative Surgery, Mitochondrial Stress and A-fib


Patients who undergo surgery and then develop complications with A-fib may find themselves with an underlying mitochondrial problem induced by the oxidative stress of the surgery. Researchers studied 104 patients with metabolic syndrome, but in normal heart rhythm underwent coronary bypass surgery. This was a high risk group of patients. Following surgery, 44 percent of patients developed post-operative atrial fibrillation. The scientists identified that the patients who developed A-fib had significantly lower levels of carnitine. Carnitine is a critical amino acid for mitochondria function and the production of ATP. Its presence is also fundamental to burning glucose and fats for fuel. In the presence of metabolic syndrome with often increased need for carnitine, coupled with high levels of inflammation leading up to the surgery and further worsened after the surgery, it is no wonder that A-fib and mitochondria stress occurred.

Another recent study in the Journal of the American Heart Association on the topic of post-surgical A-fib found similar findings with mitochondrial stress. It was identified that high levels of reactive oxygen species caused by an enzyme called MAO (monoamine oxidase) led to a 10-fold breakdown in redox (antioxidant) balance and deficiencies in glutathione enzyme. This means that the delicate redox balance and glutathione levels that protect mitochondria and quench oxidative stress was terribly stressed from ROS and MAO.

One of the treatments for post-operative A-fib is cholesterol lowering statin drugs, Atorvastatin specifically. The attempt at using the statin was considered partially and temporarily effective in a sample of 130 patients who underwent cardiac surgery. The authors of this study described an up-regulation of inflammatory enzymes which occurred as a natural result following cardiac surgery and post-op A-fib development. The surgery affected the nitric-oxide redox balance (Rac 1 and NOX2-NADPH) and led to high levels of ROS. The rational was to use statins to decrease the Rac1 and NOX2-NADPH. Based on their description within their findings, the up-regulation of the NADPH enzyme is a natural, momentary response that triggers post-op A-fib and is transient. The more damaging ROS however remains and perpetuates A-fib. The study showed statins had zero effect on the most damaging ROS free radicals. It also had no effect on improving nitric oxide function or other enzymatic support needed for A-fib. Yet the authors viewed the statins effective in the early stages of A-fib. They did however acknowledge that statins were ineffective or worthless in A-fib management. Thankfully this was acknowledged given the connection identified with statins poisoning mitochondria and linked with heart failure.

De-Energizing Medications or Nutrients for Mitochondria


Research continues to remain very strong with certain nutrients and protecting mitochondria and the birth of new mitochondria. Individuals who struggle with cardiac disorders receive standard treatment with de-energizing medications and procedures as an attempt to improve metabolic cardiac fitness. Many cardiac medications are often toxic to the mitochondria further worsening the situation. These include anthracyclines (particularly doxorubicin), mitoxantrone, cyclophosphamide, cisplatin, fluorouracil, imatinib, bortezomib, trastuzumab, arsenic trioxide, cyclosporine-A, zidovudine, lamotrigine, glycosides, lidocain, isoproterenol, nitroprusside, pivalic acid, alcohol, cocaine, pesticides, cadmium, mycotoxins, cyanotoxins, meat meal, or carbon monoxide.

The nutrients that have time and time again stood out for mitochondrial support are resveratrol, curcumin, quercetin, PQQ, and coenzyme Q10. Other nutrients like carnitine, arginine, grape seed extract, B-vitamins, especially thiamin, riboflavin, and folate, vitamins C, D, and E, lipoic acid, glutathione precursors, magnesium, and more provide substantial nourishment and protection for heart and mitochondria health.

Friendly Dietary Fats and Mitochondria



Dietary fats are also part of protecting mitochondria. Research from July 2015 Journal of Nutritional Biochemistry showed that DHA was particularly important for cardiac mitochondria. The heart mitochondria have a special fat or phospholipid called cardiolipin that is essential to maintaining physiological function. The scientists compared DHA, EPA, and arachidonic acid and how it affected mitochondria cardiolipin in cellular studies. The results showed that DHA provided the best protection from free radical damage within the mitochondria and protecting the cardiolipin.

In the journal Mitochondrion, an animal study was done comparing oxidative stress of mitochondria and which types of oils offered the most protection. They compared coconut (saturated), olive (monounsaturated) and fish (polyunsaturated) oil. In this 16 week long study, the heart mitochondria taken from rodents fed with coconut oil showed the lowest concentration of oxidized proteins and fats compared to olive and fish oil. Fish oil decreased the total and LDL cholesterol levels, but did not have nearly as much protection for the heart mitochondria. In a separate study, when coenzyme Q10 was added to the fish oil and olive oil, significant benefit was achieved in protecting the mitochondria from oxidative stress with less cell damage, improved density and structure.

Physical Exercise and Calorie Restriction


When physical exercise is added with calorie restriction, the family of Sirtuins (Sirt1- Sirt7) become activated. Sirtuins control critical cellular functions in throughout the cell but especially with mitochondria. They protect against cellular damage and dampen inflammation, maintaining metabolic homeostasis or balance. Sirt1, Sirt3, Sirt 6 and Sirt7 are involved heavily with cardiovascular health. Most is known about Sirt1 protects against endothelial dysfunction, the one cell thick lining of blood vessels, hardening and narrowing of arteries with clot formation, diet-induced obesity, type 2 diabetes, fatty liver congestion, and myocardial infarction. Sirt3 provides beneficial effects in the context of left ventricular hypertrophy, cardiomyopathy, oxidative stress, metabolic homeostasis, and cholesterol imbalances. Sirt6 is implicated in ameliorating cholesterol imbalances, cellular aging, and left ventricular hypertrophy. Sirt7 plays a role in lipid metabolism and cardiomyopathies.

Anyone young or old dealing with minor or major cardiac concerns must take care of their heart’s mitochondria. While medications and surgeries may be somewhat helpful in acute or severe cardiac situations, the long-term concern is related to protecting the mitochondria from the disorder as well as the treatment. Physical exercise, quality healthy organic fats, richly colored organic vegetables and fruits provide basic stability and health benefits to the heart mitochondria. For those who need more intensive support, the 21st century provides wonderful options with nutritional supplements. Find a combination that helps you feel energized and combats the drug-induced stress responses. Health is all about aging well. Adding this dimension of support to any medical approach may just help bring about stability and quality of life that has been desperately missing for so many. How well are you and your heart aging?

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