Energetics and Heart Conditions:
Abnormal energy metabolism in diseased hearts is causing changes in basic function of the heart muscle and cells.
Studies reveal that both the level of restriction in blood flow and duration of oxygen deprivation, are important determinants for the extent of ATP (energy) degradation and loss of the total energy pool. These factors determine the extent to which the heart can recover following episodes of chest pain, heart attack, or even after surgery or angioplasty.
It has been shown that large loss of energy pool during procedures can impact the patient’s life. This is why I put my patients on Q10, carnitine, ribose, PQQ, Amino Acids, and magnesium before any surgical procedure. Any intervention that will slow the rate of ATP degradation or speed the recovery of ATP will minimize heart damage and improve cardiac function in chronically ill hearts.
Many heart diseases have abnormal energy metabolism at their core.
Coronary artery disease is caused by the buildup of plaque in the blood vessels feeding the heart. The plaque formation restricts blood flow to the heart muscle and deprives the heart cells of oxygen, forcing them to use energy supply faster than it can be restored. In heart disease, there is severe depression in the cardiac energy pool.
Patients with heart disease have a wide variety of symptoms, including chest pain, chest pressure, tightness, heaviness, shortness of breath, indigestion, and associated symptoms. They may have a cough or just feel tired. Even after surgery or stent placement, or angioplasty, blood flow may be restored, but the energy pool does not recover, or recovery is very slow. Importantly, patients who have a high energy prior to procedures such as surgery or angioplasty, have improved functional recovery after these procedures.
Therefore, it is important on focusing on the health of the energy pool in these patients.
Congestive heart failure or dilated cardiomyopathy
are progressive diseases in which the heart muscle becomes so weak that it cannot effectively pump blood to the various parts of the body. Patients with these conditions usually experience shortness of breath with minimal exercise and have pains in their legs or peripheral skeletal muscles, because the heart cannot pump enough blood to supply the oxygen needed by the rest of the body to make energy. Fluid builds up in the legs and lungs, and finally, the heart itself becomes congested with blood because it is no longer strong enough to move it forward out of the circulation.
Hearts in congestive heart failure are energy-starved.
There is dysfunction of the cardiac energy recycling in these hearts, and the cardiac energy pool is depleted. Patients in congestive heart failure are deficient in co-enzyme Q10 and carnitine, restricting mitochondrial functions and exacerbating the metabolic dysfunction.
Cardiomyopathy is the state in which the muscle tissue of the heart has become damaged, diseased, or enlarged, or stretched and thin.
This most often happens as the result of heart attacks or longstanding, untreated high blood pressure. Cardiomyopathy can also be caused by genetic modification associated with energy production. There may also be a result of nutritional deficiencies or longstanding excessive alcohol consumption, infection, or severe inflammation such as a viral assault on the heart. Cardiomyopathic hearts just do not metabolize enough energy. No matter the cause, the patient with cardiomyopathy and congestive heart failure are unable to generate enough energy, or to allow sufficient relaxation for refilling of the heart. Studies have shown improvement in cardiac energy metabolism with Q10, carnitine, and d-ribose therapy.
Heart palpitations or cardiac arrhythmias
are a common complaint that bring people to the cardiologist. Fortunately, irregular heartbeats are rarely a cause for concern, in about one-third of normal hearts. One of the more common arrhythmias is premature ventricular contractions. The patient may experience a “skipped heartbeat.” There are many causes for premature ventricular contractions such as stimulants like caffeine, chocolate, low-potassium states, alcohol, and age and conduction systems, anti-arrhythmics, street drugs, lack of oxygen at high altitudes, mitral valve prolapse, and so on–the list is long. Initial interventions include eliminating the cause if possible, or normalizing electrolytes such as potassium.
Most cardiologists do not treat premature ventricular contractions (PVC’s) unless they are happening frequently and on a regular basis, like more than six times a minute in couplets, triplets, or in short runs. Co-enzyme Q10 is a good treatment for bothersome arrhythmias. By stabilizing the membrane of the electrical conduction system, Q10 can make it harder for arrhythmias to occur in the first place.
The complexity of the cardiac energy system is clear. The bottom line is that patients need to be aware of the vital importance of energy metabolism in cardiac disease, both from the standpoint of accelerating adequate ATP turnover, as well as reserve, and maintaining the size of the energy pool itself.
The triad of cardiac supplements, including Q10, L-carnitine, d-ribose, and PQQ are critical for establishing the energy health of the heart and to assist the ailing heart in its quest to supply the energy it needs.
In summary, metabolic cardiology is a fascinating new concept.
Attention is given to the energy demands of the diseased heart, and it is often missed in conventional cardiology practice. Disease states such as heart disease, heart failure, or cardiomyopathy are associated with low cardiac energy production. Optimal cardiovascular function is dependent on maintaining adequate levels and energy reserves. Metabolic cardiology highlights the importance of sustaining key enzymatic and biochemical reactions that revitalize the energy charge in failing hearts.
Efforts to support the metabolic needs of the heart have been well documented, yet are not known to most cardiologists. These therapies have an excellent safety profile, and are a key factor in light of the finding that the fourth leading cause of death in the United States is properly-prescribed medications. The importance of supporting energy production in the heart cells and preservation of the mitochondria is essential. The heart contains more energy per gram than any other organ, and the chemical energy that fuels the heart comes primarily from ATP; ATP reserves must be maintained.
In diastolic dysfunction, which is an early sign of heart failure, despite the presence of normal systolic function and preserved ejection fraction, high concentrations of ATP are needed and can reverse this early heart disease. In failing hearts, such as heart failure, these energetic changes become even more profound as the left ventricle proceeds from hypertrophy to dilatation. Cardiac energetics also provides important prognostic information in the patients for heart failure, in determining the heart contractility reserve. It is especially necessary prior to surgery and/or angioplasty to protect the patient.
Cardiovascular function depends on the operational capacity of the heart cell to generate energy, to expand and contract. Insufficient myocardial energy contributes significantly to congestive heart failure. Literally, heart failure is energy-starved heart. It is no longer enough that physicians focus on fluid retention aspects of pump failure, giving a diuretic. Diuretic therapies target the kidney indirectly, to relieve the heart failure without addressing the root cause. Metabolic solutions, on the other hand, treat the heart muscle directly.
Metabolic cardiology supports the biochemical interventions that can be employed to directly improve energy, and therefore energy metabolism in the heart cells; d-ribose, PQQ, co-enzyme Q10, carnitine, and magnesium all promote cardiac energy metabolism and help normalize myocardial energy reserve. All of these interventions positively impact the cardiac systolic and diastolic function. Acknowledging this metabolic support for the heart provides a missing link that offers great potential for the future treatment of cardiovascular disease.
DEAN R. SILVER, M.D.