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Heart Failure

December 29, 2016

 

With the recent deaths of Carrie Fisher and her mother Debbie Reynolds, both from heart disease, (a heart attack and a stroke respectively), I want to again focus on heart disease and how it can be truly monitored and prevented.

 

Life Extension my favorite go to site authored by doctors, discussed heart failure in depth. Let's take a look. 

 

Heart failure is a general term that describes a variety of pathologic causes and contributing factors that result in the inability of the heart to pump sufficient oxygenated blood throughout the body to meet demands. Heart failure may develop rapidly or gradually as a as a consequence of a variety of pathological disease states including structural heart muscle defects, cardiac valve disease, pulmonary disease (e.g., right-sided heart failure), coronary artery disease due to atherosclerosis, thyroid disease, and low red blood cells (anemia) to name a few.

 

Heart failure incidence is increasing. While 5.8 million people in the United States were affected by heart failure in 2009, the American Heart Association expects this number to balloon to more than 8 million individuals by 2030. Likewise, healthcare costs associated with heart failure care are projected to more than double in this time frame, from $31 billion in 2012 to $70 billion by 2030.

 

 

These grim statistics parallel the largely unimpressive conventional medical treatment options for heart failure patients. A prospective 19-year study involving over 13 000 volunteers showed that in men and women without heart failure at baseline, more than 60% of those who subsequently went on to suffer from heart failure later in life did so as a result of atherosclerotic heart disease. To this point, Life Extension® has identified at least 17 independent risk factors that must be actively managed if heart attack risk is to be managed optimally, which is of significant importance since prior heart attack due to atherosclerotic coronary artery disease is a major cause for subsequent heart failure.  Unfortunately, mainstream medicine frequently addresses only one or two contributing factors for heart attack risk, such as high blood pressure and elevated cholesterol. This leaves aging individuals exposed to the ravages of unchecked heart attack risk factors such as excess homocysteine, insufficient vitamin D, and hormone imbalance & deficiency. This deadly oversight is a fundamental reason cardiovascular disease continues to plague so many Americans.

 

 

For example, a major gap in conventional heart failure care is neglect for the critical role that testosterone plays in cardiovascular health and the potential for testosterone replacement therapy to improve symptoms in heart failure patients. An estimated 25–30% of men with heart failure have low testosterone levels, but this easily correctable risk factor is overlooked by many mainstream physicians. A comprehensive review of published studies revealed that testosterone replacement therapy for up to 52 weeks in men with heart failure resulted in a significant improvement in functional capacity compared to placebo. These results led the researchers to remark “Given the unmet clinical needs, testosterone appears to be a promising therapy to improve functional capacity in patients with [heart failure].”

 

In contrast to the relatively unimpressive conventional treatment options for heart failure patients, a major breakthrough in heart failure research came in 2013 with the presentation of early results of the Q-SYMBIO coenzyme Q10 (CoQ10) trial. This groundbreaking ten-year study provides strong support for a recommendation made by Life Extension many years prior in the context of heart failure. This exciting trial showed that CoQ10 supplementation significantly improves survival even for patients with severe Class III or IV heart failure while dramatically reducing incidence of hospitalization. Specifically, heart failure patients who took 100 mg of CoQ10 three times daily were significantly less likely to have a major cardiovascular event and significantly less likely to die from any cause during the study period compared to control subjects.

 

As shown by in several studies conducted by Life Extension Scientific Advisory Board Member Peter H. Langsjoen, MD, FACC, CoQ10 supplementation is especially important for individuals on cholesterol-lowering statin therapy (HMG CoA reductase inhibitors). Statin medications block the biosynthesis of both cholesterol and CoQ10, and these drugs have been shown to worsen heart muscle dysfunction in heart failure patients. In one study, diastolic dysfunction (heart muscle weakness) occurred in 70% of previously normal patients treated with 20 mg a day of Lipitor® for six months. This heart muscle dysfunction was reversible with 100 mg of CoQ10 three times daily.

 

 

Understanding the Heart and Heart Failure

 

The human heart consists of left and right halves, which behave as two parallel “pumps” with distinct roles in circulation. Both the left and right side of the heart contain two chambers: a smaller atrium, at the top, receives blood into the heart and transfers it to a larger, more muscular ventricle, which is situated at the bottom and pumps blood from the heart into circulation.

 

The right atrium receives low-oxygen blood from vessels throughout the body (systemic circulation), and the right ventricle then pumps it to the lungs to become oxygenated. The left atrium of the heart receives high-oxygen blood from vessels of the lungs (pulmonary circulation), and the left ventricle then pumps it into systemic circulation. Thus, the two sides of the heart work in parallel to collect oxygen-poor blood from peripheral tissues, send it to the lungs for gas exchange (to pick up oxygen and remove carbon dioxide), and redistribute the newly oxygenated blood to tissues and organs to meet metabolic demands.

 

As the heart begins to fail, compensatory mechanisms throughout the body are initiated to ensure that adequate oxygen is delivered to tissues. During compensated heart failure, signals from the brain and kidneys result in fluid retention (to increase blood pressure in an attempt to better distribute oxygenated blood), increased heart rate and contractile force, dilatation (expansion) of the ventricle to hold more blood, and growth of new heart muscle to increase the force of ejection. Increases in blood volume and ventricular filling pressures cause blood to “back up” in systemic or pulmonary circulation and leak fluid into peripheral tissues, causing edema (swelling) in the lungs, abdomen, and extremities. This is termed “congestive” heart failure. Since not all patients have fluid accumulation at the time of initial evaluation, the term “heart failure” is preferred over the older term “congestive heart failure”.

As heart failure progresses, compensatory reactions are increased to keep up with tissue oxygen demands. However, the compensatory mechanisms of the heart are not without their limits; the heart is restricted in how much it can expand to hold more blood or increase its contractile force and rate, and the kidneys can only retain so much water before fluid begins to infiltrate other organs and tissues. Once the limits of compensation are reached, the cardiovascular system is no longer able to satisfy tissue oxygen demands. This is called decompensated heart failure and requires aggressive medical intervention or death will occur.

 

Dietary and Lifestyle Risk Factors

 

Dietary and lifestyle factors associated with increased risk of heart failure include excessive alcohol consumption and nutritional deficiencies (eg, B vitamins). Smoking represents a major risk factor for developing heart failure, and quitting smoking was shown to have a significant effect on lowering morbidity and the risk of death in people with left ventricular dysfunction, an effect that was comparable to currently approved drugs. Physical inactivity, which is known to be a risk factor for many cardiovascular diseases, was shown to worsen the survival of patients with heart failure; a study reported that 2.5 years after being admitted to the hospital, only 25% of patients with a sedentary lifestyle were alive as compared to 75% of patients who were physically active. Insufficient intake of fruits and vegetables is another risk factor associated with heart failure. In a study that assessed fruit and vegetable intake by way of serum beta-carotene level measurement, men with the lowest beta-carotene blood levels had an almost 3-fold increased risk of heart failure compared to those with the highest intake.

 

Clinical Conditions Associated with Heart Failure

 

Heart disease. Atrial fibrillation, valve disease (eg, mitral regurgitation), ischemic heart disease due to coronary artery atherosclerosis,  and prior heart attack are associated with an increased risk of heart failure.

Hypertension. Hypertension (high blood pressure) increases heart failure risk 2- to 3-fold. Half of patients with acute heart failure have systolic blood pressure (the “top” number) over 140 mmHg and 70% have a history of high blood pressure. Life Extension’s assessment of the existing medical evidence suggests that for optimal cardiovascular health, most individuals should strive for a target blood pressure of 115/75 mmHg.

Diabetes. Diabetes increases heart failure risk up to five-fold, and 40% of patients with acute heart failure have a history of diabetes. Life Extension has identified an optimal fasting glucose level of no more than 85 mg/dL, which is in stark contrast to the acceptance of “normal” fasting glucose readings up to 110 mg/dl. Remember that normal is not the same as optimal.

Chronic obstructive pulmonary disease (COPD). Long-standing obstructive pulmonary disease, often associated with tobacco abuse, is associated with heart failure, and when the two conditions occur simultaneously, prognosis is worse than with either alone.

Renal insufficiency/kidney disease. Evidence suggests that 30% of patients with acute heart failure have severe renal dysfunction.

Overweight/obesity. High body mass index (BMI) is a risk factor for developing heart failure.

 

Other diseases less well-recognized to be linked with increased heart failure risk include hemochromatosis (iron overload), sarcoidosis, amyloidosis, infection (eg, HIV, pulmonary infection), endocrine disorders (eg, pheochromocytoma), collagen vascular diseases, and sleep apnea.

 

I have a list of tests you should have when you have your blood drawn. Please have these tests run so you know your homocysteine, C-reactive protein and fibrinogen numbers. These are the true bio-markers of heart disease!

 

Next time we will talk about how to circumvent heart attack risks.

 

I am with you and in your corner!

Christina :)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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