Heart Failure In-Depth Report
To understand what occurs in heart failure, it helps to be familiar with the anatomy of the heart and how it works. The heart is composed of two independent pumping systems, one on the right side, and the other on the left. Each has two chambers, an atrium and a ventricle. The ventricles are the major pumps in the heart.
The external structures of the heart include the ventricles, atria, arteries, and veins. Arteries carry blood away from the heart while veins carry blood into the heart. The vessels colored blue indicate the transport of blood with relatively low content of oxygen and high content of carbon dioxide. The vessels colored red indicate the transport of blood with relatively high content of oxygen and low content of carbon dioxide.
The Right Side of the Heart. The right system receives blood from the veins of the whole body. This is “used” blood, which is poor in oxygen and rich in carbon dioxide.
The Left Side of the Heart. The left system receives blood from the lungs. This blood is now rich in oxygen.
The Valves. Valves are muscular flaps that open and close so blood will flow in the right direction. There are four valves in the heart:
The Heart’s Electrical System. The heartbeats are triggered and regulated by the conducting system, a network of specialized muscle cells that form an independent electrical system in the heart muscles. These cells are connected by channels that pass chemically-triggered electrical impulses.
DESCRIPTION OF HEART FAILURE
Heart failure is not a disease. It is a condition or process in which the heart is unable to pump enough blood to meet the needs of the body’s tissues. The heart doesn’t “fail” in the sense of ceasing to beat (as occurs during cardiac arrest). Rather, it weakens, usually over the course of months or years, so that it is unable to pump out all the blood that enters its chambers. As a result, fluids tend to build up in the lungs and tissues, causing congestion. This condition used to be called “congestive heart failure,” but the name was officially changed to heart failure in 2005.
Ways the Heart Can Fail. Heart failure can occur in several ways:
The specific effects of heart failure on the body depend on whether it occurs on the left or right sides of the heart. Over time, however, in either form of heart failure, the organs in the body do not receive enough oxygen and nutrients, and the body’s wastes are removed slowly. Eventually, vital systems break down.
Failure on the Left Side (Left-Ventricular Heart Failure). Failure on the left side of the heart is more common than failure on the right side. The failure can be a result of abnormal systolic (contraction) or diastolic (relaxation) action:
Failure on the Right Side (Right-Ventricular Heart Failure). Failure on the right side of the heart is most often a result of failure on the left. Because the right ventricle receives blood from the veins, failure here causes the blood to back up. As a result, the veins in the body and tissues surrounding the heart to swell. This causes swelling in the feet, ankles, legs, and abdomen. Pulmonary hypertension (increase in pressure in the lung’s pulmonary artery) and lung disease may also cause right-sided heart failure.
Ejection Fraction. To help determine the severity of left-sided heart failure, doctors use an ejection fraction (EF) calculation, also called a left-ventricular ejection fraction (LVEF). This is the percentage of the blood pumped out from the left ventricle during each heartbeat. An ejection fraction of 50 – 75% is considered normal. Patients with left-ventricular heart failure are classified as either having a preserved ejection fraction (greater than 50%) or a reduced ejection fraction (less than 50%).
Patients with preserved LVEF heart failure are more likely to be female and older, and have a history of high blood pressure and atrial fibrillation (a disturbance in heart rhythm).
Heart failure has many causes and can evolve in different ways.
In all cases, the weaker pumping action of the heart means that less blood is sent to the kidneys. The kidneys respond by retaining water and salt. This in turn increases edema (fluid buildup) in the body, which causes widespread damage.
HIGH BLOOD PRESSURE
Uncontrolled high blood pressure (hypertension) is a major cause of heart failure even in the absence of a heart attack. In fact, about 75% of cases of heart failure start with hypertension. It generally develops as follows:
Hypertension is a disorder characterized by consistently high blood pressure. Generally, high blood pressure consists of systolic blood pressure (the “top” number, which represents the pressure generated when the heart beats) higher than 140, or diastolic blood pressure (the “bottom” number, which represents the pressure in the vessels when the heart is at rest) over 90.
CORONARY ARTERY DISEASE AND HEART ATTACK
Coronary artery disease is the end result of a complex process called atherosclerosis (commonly called “hardening of the arteries”). It is the most common cause of heart attack and involves the build-up of unhealthy cholesterol in the arteries, with inflammation and injury in the cells of the blood vessels. The arteries narrow and become brittle. Heart failure in such cases most often results from a pumping defect in the left side of the heart.
People now often survive heart attacks, but eventually many develop heart failure from the physical damage the attack does to the heart muscles. Ironically, heart attack recovery is probably one of the major factors in the dramatic increase in heart failure cases over the past decade.
VALVULAR HEART DISEASE
The valves of the heart control the flow of blood leaving and entering the heart. Abnormalities can cause blood to back up or leak back into the heart.
In the past, rheumatic fever, which scars the heart valves and prevents them from closing, was a major cause of death from heart failure. Fortunately, antibiotics have relegated this disease to a minor cause of heart failure. Birth defects may also cause abnormal valvular development. Although more children born with heart defects are now living to adulthood, they still face a higher than average risk for heart failure as they age.
Cardiomyopathy is disease that damages the heart muscles and leads to heart failure. There are several different types. Injury to the heart muscles may cause the heart muscles to thin out (dilate) or become too thick (become hypertrophic). In either case, the heart doesn’t pump correctly. Viral myocarditis is a rare viral infection that involves the heart muscle and can produce either temporary or permanent heart muscle damage.
Dilated Cardiomyopathy. Dilated cardiomyopathy involves an enlarged heart ventricle. The muscles thin out, reducing the pumping action, usually on the left side. Although this condition is associated with genetic factors, the direct cause often is not known. (This is called idiopathic dilated cardiomyopathy.) Research strongly indicates that viruses, such as Coxsackie virus, or other infections may be at the base of this condition. Researchers think that an autoimmune response occurs in which infection-fighting antibodies attack a person’s own proteins in the heart, mistaking them for foreign substances.
Chronic alcohol abuse can damage the heart muscles, can cause hypertension, and may be one cause of idiopathic dilated cardiomyopathy. Moderate alcohol consumption, on the other hand (generally defined as 2 drinks a day for men and 1 drink for women), may protect against heart failure. Non-drinkers, though, are not advised to begin drinking.
Hypertrophic Cardiomyopathy. In hypertrophic cardiomyopathy, the heart muscles become thick and contract with difficulty. Some research indicates that this occurs because of a genetic defect that causes a loss of power in heart muscle cells and, subsequently, lower pumping strength. To compensate for this power loss, the heart muscle cells grow. This condition, rare in the general population, is often the cause of sudden death in young athletes.
Restrictive Cardiomyopathy. Restrictive cardiomyopathy refers to a group of disorders in which the heart chambers are unable to properly fill with blood because of stiffness in the heart. The heart is of normal size or only slightly enlarged. However, it cannot relax normally during the time between heartbeats when the blood returns from the body to the heart (diastole). The most common causes of restrictive cardiomyopathy are amyloidosis and scarring of the heart from an unknown cause (idiopathic myocardial fibrosis). It frequently occurs after a heart transplant.
SEVERE LUNG DISEASES
Chronic obstructive pulmonary disease (severe emphysema) and other major lung diseases are risk factors for right-side heart failure.
Pulmonary hypertension is increased pressure in the pulmonary arteries that carry blood from the heart to the lungs. The increased pressure makes the heart work harder to pump blood, which can cause heart failure. The development of right-sided heart failure in patients with pulmonary hypertension is a strong predictor of death within 6 – 12 months.
An overactive thyroid (hyperthyroidism) or underactive thyroid (hypothyroidism) can have severe effects on the heart and increase the risk for heart failure.
Many symptoms of heart failure result from the congestion that develops as fluid backs up into the lungs and leaks into the tissues. Other symptoms result from inadequate delivery of oxygen-rich blood to the body’s tissues. Since heart failure can progress rapidly, it is essential to consult a doctor immediately if any of the following symptoms are detected:
Fatigue. Patients may feel unusually tired.
Shortness of Breath (Dyspnea).
Fluid Retention (Edema) and Weight Gain. Patients may complain of foot, ankle, leg or abdominal swelling. In rare cases, swelling can occur in the veins of the neck. Fluid retention can cause sudden weight gain and frequent urination.
Wheezing or Cough. Patients may have asthma-like wheezing, or a dry hacking cough that occurs a few hours after lying down but then stops after sitting up.
Loss of Muscle Mass. Over time, patients may lose muscle weight due to low cardiac output and a significant reduction in physical activity.
Gastrointestinal Symptoms. Patients experience loss of appetite or a sense of feeling full after eating small amounts. They may also have abdominal pain.
Pulmonary Edema. When fluid in the lungs builds up, it is called pulmonary edema. When this happens, symptoms become more severe. These episodes may happen suddenly, or gradually build up over a matter of days:
Abnormal Heart Rhythms. Patients may have episodes of abnormally fast or slow heart rate.
Central Sleep Apnea. This sleep disorder results when the brain fails to signal the muscles to breathe during sleep. It occurs in up to half of people with heart failure. Sleep apnea causes disordered breathing at night. If heart failure progresses, the apnea may be so acute that a person, unable to breathe, may awaken from sleep in panic.
Nearly 5 million Americans suffer from heart failure. About 550,000 new cases of heart failure are diagnosed each year. In 1970, there were only 250,000 new cases, so the annual numbers have risen dramatically. Such numbers represent an increasingly older population. Although there has been a dramatic increase over the last several decades in the number of people who suffer from heart failure, survival rates have greatly improved.
Coronary artery disease, heart attack, and high blood pressure are the main causes and risk factors of heart failure. Other diseases that damage or weaken the heart muscle or heart valves can also cause heart failure. Heart failure is most common in people over age 65, African-Americans, and women.
Heart failure risk increases with advancing age. Heart failure is the most common reason for hospitalization in people age 65 years and older.
Men are at higher risk for heart failure than women. However, women are more likely than men to develop diastolic heart failure, (a failure of the heart muscle to relax normally), which is often a precursor to systolic heart failure (impaired ability to pump blood).
African-Americans are more likely than Caucasians to develop heart failure before age 50 and to die from the condition.
FAMILY HISTORY AND GENETICS
People with a family history of cardiomyopathies (diseases that damage the heart muscle) are at increased risk of developing heart failure. Researchers are investigating specific genetic variants that increase heart failure risk.
People with a family history of cardiomyopathies (diseases that damage the heart muscle) are at increased risk of developing heart failure. Researchers are investigating specific genetic variants that increase heart failure risk.
Obesity is associated with both hypertension and type 2 diabetes, conditions that place people at risk for heart failure. Evidence strongly suggests that obesity itself is a major risk factor for heart failure, particularly in women.
Smoking, sedentary lifestyle, and alcohol and drug abuse can increase the risk for developing heart failure.
MEDICATIONS ASSOCIATED WITH HEART FAILURE
Long-term use of anabolic steroids (male hormones used to build muscle mass) increases the risk for heart failure. The drug itraconazole (Sporanox), used to treat skin, nail, or other fungal infections, has occasionally been linked to heart failure. The cancer drug imatinib (Gleevec) has been associated with heart failure cases and other chemotherapy drugs, such as doxorubicin, can increase the risk for later developing heart failure years after cancer treatment. (Cancer radiation therapy to the chest can also damage the heart muscle.)
For people over age 65, heart failure is the number one cause of death, with nearly 290,000 people dying from this disease each year. Nevertheless, although heart failure produces very high mortality rates, treatment advances in hypertension, heart surgeries, and heart pacemakers are improving survival rates.
Cardiac Cachexia. If patients with heart failure are overweight to begin with, their condition tends to be more severe. Once heart failure develops, however, an important indicator of a worsening condition is the occurrence of cardiac cachexia, which is unintentional rapid weight loss (a loss of at least 7.5% of normal weight within 6 months).
Impaired Kidney Function. Heart failure weakens the heart’s ability to pump blood. This can affect other parts of the body including the kidneys (which in turn can lead to fluid build-up). Decreased kidney function is common in patients with heart failure, both as a complication of heart failure and as a complication of other diseases associated with heart failure (such as diabetes). Studies suggest that in patients with heart failure, impaired kidney function increases the risks for heart complications including hospitalization and death.
Congestion (Fluid Buildup). In left-sided heart failure, fluid builds up first in the lungs. Later, as right-sided heart failure develops, fluid builds up in the legs, feet, and abdomen. Fluid buildup is treated with lifestyle measures, such as reducing salt in the diet, as well as drugs, such as diuretics.
Arrhythmias (Irregular Beatings of the Heart)
Depression. The presence of depression indicates a poorer outlook for the heart. Studies indicate that depression may have adverse biologic effects on the immune and nervous systems, blood clotting, blood pressure, blood vessels, and heart rhythms. People who are depressed may fail to follow medical instructions and may not take good care of themselves.
Angina and Heart Attacks. While coronary artery disease is a major cause of heart failure, patients with heart failure are at continued risk for angina and heart attacks. Special care should be taken with sudden and strenuous exertion, particularly snow-shoveling, during colder months.
Doctors can often make a preliminary diagnosis of heart failure by medical history and careful physical examination.
A thorough medical history may identify risks for heart failure that include:
The following physical signs, along with medical history, strongly suggest heart failure:
Both blood and urine tests are used to check for problems with the liver and kidneys and to detect signs of diabetes. Lab tests can measure:
An electrocardiogram (ECG) cannot diagnose heart failure, but it can indicate underlying heart problems. It is also called an EKG. The test is simple and painless to perform. It may be used to diagnose:
If a patient has a completely normal ECG they are unlikely to have heart failure.
The best diagnostic test for heart failure is echocardiography. Echocardiography is a noninvasive, entirely safe test that uses ultrasound to image the heart as it is beating. Cardiac ultrasounds provide the following information:
Doctors use information from the echocardiogram for calculating the ejection fraction (how much blood is pumped out during each heartbeat), which is important for determining the severity of heart failure. Stress echocardiography may be needed if coronary artery disease is suspected.
Doctors may recommend angiography if they suspect that blockage of the arteries is contributing to heart failure. This procedure is invasive.
OTHER IMAGING TESTS
X-Rays. Chest x-rays can show whether the heart is enlarged. Computed tomography (CT) and magnetic resonance imaging (MRI) may also be used to evaluate the heart valves and arteries.
Radionuclide Ventriculography. Radionuclide ventriculography is an imaging technique that uses a tiny amount of radioactive material (called a trace element). It is very sensitive in revealing heart enlargement or evidence of fluid accumulation around the heart and lungs. It is may be done at the same time as coronary artery angiography. It can help diagnose or exclude the presence of coronary artery disease and helps demonstrate how the heart works during exercise.
Magnetic Resonance Imaging. Magnetic resonance imaging (MRI) scans that use contrast dyes to improve resolution may help identify whether there is any heart muscle that can be helped by opening up the arteries feeding it. Damage appears as very bright areas on the scan.
EXERCISE STRESS TEST
The exercise stress test measures heart rate, blood pressure, electrocardiographic changes, and oxygen consumption while a patient is performing physically, usually walking on a treadmill. Can help determine heart failure symptoms. Doctors also use exercise tests to gauge long-term outlook and the effects of particular treatments. A stress test may be done using echocardiography or may be done as a nuclear stress test.
Heart failure is classified into four stages (Stage A through Stage D) that reflect the development and progression of the condition. Treatment depends on the stage of heart failure.
The first two stages (Stage A and Stage B) are technically not heart failure, but indicate that a patient is at high risk for developing it.
MANAGEMENT OF RISK FACTORS AND CAUSES
Stage A. In Stage A, patients are at high risk for heart failure but do not show any symptoms or have structural damage of the heart. The first step in managing or preventing heart failure is to treat the primary conditions that cause or complicate heart failure. Risk factors include high blood pressure, heart diseases, diabetes, obesity, metabolic syndrome, and previous use of medications that damage the heart (such as some chemotherapy).
Important risk factors to manage include:
TREATMENT BASED ON HEART FAILURE
Stage B. Patients have a structural heart abnormality seen on echorcardiogram or other imaging tests but no symptoms of heart failure. Abnormalities include left ventricular hypertrophy and low ejection fraction, asymptomatic valvular heart disease, and a previous heart attack. In addition to the treatment guidelines for Stage A, the following types of drugs and devices may be recommended for some patients:
Stage C. Patients have a structural abnormality and current or previous symptoms of heart failure, including shortness of breath, fatigue, and difficulty exercising. Treatment includes those for Stage A and B plus:
Stage D. Patients have end-stage symptoms that do not respond to standard treatments. Treatment includes appropriate measures used for Stages A, B, and C plus:
MANAGEMENT OF PRECIPITATING FACTORS
Whenever heart failure worsens, whether quickly or chronically over time, various factors must be considered as the cause:
Many different medications are used in the treatment of heart failure. They include:
Angiotensin-converting enzyme (ACE) inhibitors are among the most important drugs for treating patients with heart failure. ACE inhibitors open blood vessels and decrease the workload of the heart. They are used to treat high blood pressure but can also help improve heart and lung muscle function. ACE inhibitors are particularly important for patients with diabetes, because they also help slow progression of kidney disease.
Brands and Indications. ACE inhibitors treat Stage A high-risk conditions such as high blood pressure, heart disease, and diabetic nerve disorders (neuropathy). They also treat Stage B patients who have had a heart attack or who have left ventricular systolic disorder, and Stage C patients with heart failure. Specific brands of ACE inhibitors include:
Side Effects of ACE Inhibitors:
Patients who have difficulty tolerating ACE inhibitor side effects are usually switched to an angiotensin-receptor blocker (ARB).
ANGIOTENSIN-RECEPTOR BLOCKERS (ARBS)
ARBs, also known as angiotensin II receptor antagonists, are similar to ACE inhibitors in their ability to open blood vessels and lower blood pressure. They may have fewer or less-severe side effects than ACE inhibitors, especially coughing, and are sometimes prescribed as an alternative to ACE inhibitors. Some patients with heart failure take an ACE inhibitor along with an ARB.
Brands and Indications. ARBs are used to treat Stage A high-risk conditions such as high blood pressure and diabetic nerve disorders (neuropathy). They are also used to treat Stage B patients who have had a heart attack or who have left ventricular systolic disorder, and Stage C patients with heart failure. Specific brand include:
Common Side Effects
Beta blockers are almost always used in combination with other drugs, such as ACE inhibitors and diuretics. They help slow heart rate and lower blood pressure. When used properly, beta blockers can reduce the risk of death or rehospitalization.
Brands and Indications. Beta blockers treat Stage A high blood pressure. They also treat Stage B patients (both those who have had a heart attack and those who have not had a heart attack but who have heart damage). Patients with heart failure receiving beta blockers should probably be under the care of a specialist. Recent guidelines identify three drugs best for treating Stage C patients with heart failure:
Beta Blocker Concerns
Common Side Effects
Check with your doctor about any side effects. Do not stop taking these drugs on your own.
Diuretics cause the kidneys to rid the body of excess salt and water. Fluid retention is a major symptom of heart failure. Aggressive use of diuretics can help eliminate excess body fluids, while reducing hospitalizations and improving exercise capacity. These drugs are also important to help prevent heart failure in patients with high blood pressure. In addition, certain diuretics, notably spironolactone (Aldactone), block aldosterone, a hormone involved in heart failure. This drug class is beneficial for patients with more severe heart failure (Stages C and D).
Patients taking diuretics usually take a daily dose. Under the directions and care of a doctor or nurse, some patients may be taught to adjust the amount and timing of the diuretic when they notice swelling or weight gain.
Diuretics come in many brands and are generally inexpensive. Some need to be taken once a day, some twice a day. Treatment is usually started at a low dose and gradually increased. Diuretics are virtually always used in combination with other drugs, especially ACE inhibitors and beta blockers. There are three main types of diuretics:
Thiazide diuretics. These include chlorothiazide (Diuril), chlorthalidone (Hygroton), indapamide (Lozol), hydrochlorothiazide (Esidrix, HydroDiuril), and metolazone (Mykrox, Zaroxolyn).
Loop diuretics. These are considered the preferred diuretic type for most patients with heart failure.
Common Side Effects
Aldosterone is a hormone that is critical in controlling the body’s balance of salt and water. Excessive levels may play important roles in hypertension and heart failure. Drugs that block aldosterone are prescribed for some patients with symptomatic heart failure. They have been found to reduce mortality or death rates for patients with heart failure and coronary artery disease, especially after a heart attack. These blockers pose some risk for high potassium levels. Brands include:
Elevated levels of potassium in the blood are also a concern with these drugs. Patients should not take potassium supplements at the same time as this drug without their doctor’s knowledge and may need to avoid foods with high potassium content.
Digitalis is derived from the foxglove plant. It has been used to treat heart disease since the 1700s. Digoxin (Lanoxin) is the most commonly prescribed digitalis preparation. Digoxin decreases heart size and reduces certain heart rhythm disturbances (arrhythmias).
Unfortunately, digitalis does not reduce mortality rates, although it does reduce hospitalizations and worsening of heart failure. Controversy has been ongoing for more than 100 years over whether the benefits of digitalis outweigh its risks and adverse effects.
Digitalis may be useful for select patients with left-ventricular systolic dysfunction who do not respond to other drugs (diuretics, ACE inhibitors). It may also be used for patients who have atrial fibrillation.
Side Effects and Problems. While digitalis is generally a safe drug, it can have toxic side effects due to overdose or other accompanying conditions. The most serious side effects are arrhythmias (abnormal heart rhythms that can be life threatening). Early signs of toxicity may be irregular heartbeat, nausea and vomiting, stomach pain, fatigue, visual disturbances (such as yellow vision, seeing halos around lights, flickering or flashing of lights), and emotional and mental disturbances.
Many factors increase the chance for side effects.
Digitalis also interacts with many other drugs, including quinidine, amiodarone, verapamil, flecainide, amiloride, and propafenone.
A blood test that monitors drug levels in patients taking the drug can limit the rate of toxicity to about 2%. For most patients with mild-to-moderate heart failure, low-dose digoxin may be as effective as higher doses. If side effects are mild, patients should still consider continuing with digitalis if they experience other benefits.
HYDRALAZINE AND NITRATES
Hydralazine and nitrates are two older drugs that help relax arteries and veins, thereby reducing the heart’s workload and allowing more blood to reach the tissues. They are used primarily for patients who are unable to tolerate ACE inhibitors and angiotensin receptor blockers. In 2005, the FDA approved BiDil, a drug that combines isosorbide dinitrate and hydralazine. BiDil is approved to specifically treat heart failure in African-American patients.
Statins are important drugs used to lower cholesterol and to prevent heart disease leading to heart failure. These drugs include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor). In 2007, the Food and Drug Administration (FDA) approved atorvastatin to reduce the risks for hospitalization for heart failure in patients with heart disease.
ANTI-PLATELET AND ANTICOAGULATION DRUGS
Aspirin. Aspirin is a type of non-steroid anti-inflammatory (NSAID). Aspirin is recommended for preventing death in patients with heart disease, and can safely be used with ACE inhibitors, particularly when it is taken in lower dosages (75 – 81 mg).
Warfarin (Coumadin). Warfarin is recommended only for patients with heart failure who also have:
Nesiritide (Natrecor). Nesiritide treats patients who have arrived at a hospital with decompensated heart failure. Decompensated heart failure is a life-threatening condition in which the heart fails over the course of minutes or a few days, often as the result of a heart attack or sudden and severe heart valve problems. However, nesiritide may cause serious kidney damage. This drug should only be used in a hospital setting to treat patients with decompensated heart failure who have shortness of breath (dyspnea) and trouble breathing. It should not be a replacement for diuretics.
Erythropoietin. Many patients with chronic heart failure are also anemic. Treatment of these patients with erythropoietin has been shown to provide some benefit for heart failure control and hospitalization risk. However, erythropoietin therapy can also increase the risk of blood clots. The exact role of this drug for the treatment of anemia in patients with heart failure is not yet decided.
Tolvaptan. Tolvaptan is an investigational drug that is being studied in combination with standard therapy for treatment of heart failure. It is especially being investigated for acute decompensated heart failure, a type of heart failure categorized by fluid build-up in the lungs (pulmonary edema) for which there are few available treatments. In patients hospitalized with heart failure, tolvaptan plus standard drugs has been shown to improve breathing problems (dyspnea) and reduce fluid accumulation (edema) and body weight. However, the drug does not appear to reduce the risk of re-hospitalization or death.
Levosimendan. Levosimendan is an experimental inotropic drug that is being investigated as a treatment for severely ill patients with heart failure. It belongs to a new class of drugs called calcium sensitizers that may help improve heart contractions and blood flow. Clinical trials suggest that levosimendan may improve survival in patients hospitalized for heart failure. The drug also appears to reduce levels of BNP (brain natriuretic peptide), a chemical marker for heart failure severity.
Surgery and Devices
Revascularization surgery helps to restore blood flow to the heart. It can treat blocked arteries in patients with coronary artery disease and may help selected patients with heart failure. Surgery types include coronary artery bypass graft (CABG) and angioplasty (also called percutaneous coronary intervention [PCI]). CABG is a traditional type of open heart surgery. Angioplasty uses a catheter to inflate a balloon inside the artery. A metal stent may also be inserted during an angioplasty procedure.
Pacemakers, also called pacers, help regulate the heart’s beating action, especially when the heart beats too slowly. Biventricular pacers (BVPs) are a special type of pacemaker used for patients with heart failure. Because BVPs help the heart’s left and right chambers beat together, this treatment is called cardiac resynchronization therapy (CST).
BVPs are recommended for patients with moderate-to-severe heart failure that is not controlled with medication therapy and who have evidence of left-bundle branch block on their EKG. Left-bundle branch block is a condition in which the electrical impulses in the heart do not follow their normal pattern, causing the heart to pump inefficiently.
IMPLANTABLE CARDIOVERTER DEFIBRILLATORS (ICDS)
Patients with enlarged hearts are at risk for having serious cardiac arrhythmias that are associated with sudden death. Implantable cardioverter defibrillators (ICDs) have been shown to reduce the incidence of sudden-death in patients with symptomatic heart failure and an ejection fraction less than 30%. Generally, patients should also be on full medical therapy. Studies have also found ICDs effective in preventing sudden death from severe rhythm disturbances in patients with a history of these serious arrhythmias and in patients with genetic hypertrophic cardiomyopathy.
In recent years, certain ICD models and biventricular pacemaker-defibrillators have been recalled by the manufacturers because of circuitry flaws. However, doctors stress that the chance of an ICD or pacemaker saving a person’s life far outweigh the possible risks of these devices failing.
VENTRICULAR ASSIST DEVICES
A growing array of heart devices and machines are being used in heart failure treatment. Ventricular assist devices are machines that help improve pumping actions. They have gained widespread acceptance for use as a bridge to transplant in patients who are on medications but still have severe symptoms and are awaiting a donor heart. Increasingly, though, doctors are exploring the possibility that such devices may be satisfactory treatments themselves, forestalling the need for a transplant altogether in some patients. Therefore they may be used as short-term (less than 1 week) or longer term support.
Ventricular assist devices include:
Short-term support may be provided for patients who have reached end-stage disease in order to “bridge” them until an appropriate heart for transplantation is available. Some patients may require short-term support while the heart muscle recovers after a serious cardiac event. Permanent use to chronically support a patient is also increasing.
Complications after implantation of these devices are not insignificant, as are some of the long-term complications in patients who make it through after surgery. The risks involved with many of these devices include bleeding, blood clots, and right-side heart failure. Infections are a particular hazard.
Patients who suffer from severe heart failure and whose symptoms do not improve with drug therapy or mechanical assistance may be candidates for heart transplantation. Some 3,600 people are awaiting a transplant, although only about 2,000 operations are performed each year.
The most important factor for heart transplant eligibility is overall health. Chronological age is less important. Most heart transplant candidates are ages 50 – 64 years.
While the risks of this procedure are high, the 1-year survival rate is about 86% for men and 84% for women. Five years after a heart transplant, about 71% of men and 67% of women remain alive. In general, the highest risk factors for death 3 or more years after a transplant operation are coronary artery disease and the adverse effects (infection and certain cancers) of immunosuppressive drugs used in the procedure. The rejection rates in older people appear to be similar to those of younger patients.
IMPLANTABLE ARTIFICIAL HEART
In 2004, the FDA approved a temporary artificial heart (Syncardia) intended to keep patients alive in the hospital while they waited for a heart transplant. In 2006, the FDA approved the first permanent implantable artificial heart (AbiCor). The AbiCor is available only for patients who are not eligible for a heart transplant and who are not expected to live more than a month without medical treatment. The device requires a large chest cavity, which means that most women will not be eligible for it. Of the 14 men who have received the AbiCor, the average survival was less than 5 months after surgery. Only one patient was discharged from the hospital. The device’s manufacturer is working on a new model that it hopes will extend survival.
Up to half of patients hospitalized for heart failure are back in the hospital within 6 months. Many people return because of lifestyle factors, such as poor diet, failure to comply with medications, and social isolation.
Programs that offer intensive follow-up to ensure that the patient complies with lifestyle changes and medication regimens at home can reduce rehospitalization and improve survival. Patients without available rehabilitation programs should seek support from local and national heart associations and groups. A strong emotional support network is also important.
MONITORING WEIGHT CHANGES
Patients should weigh themselves each morning and keep a record. Any changes are important:
Salt Restriction. All patients with heart failure should limit their salt intake to less than 1,500 mg a day, and in severe cases, very stringent salt restriction may be necessary. Patients should not add salt to their cooking and their meals. They should also avoid foods high in sodium. These salty foods include ham, bacon, hot dogs, lunch meats, prepared snack foods, dry cereal, cheese, canned soups, soy sauce, and condiments. Some patients may need to reduce the amount of water they consume. People with high cholesterol levels or diabetes require additional dietary precautions.
Here are some tips to lower your salt and sodium intake:
People with heart failure used to be discouraged from exercising. Now, doctors think that exercise, when performed under medical supervision, is extremely important for stable patients with stable conditions. Studies have reported that patients with stable conditions who engage in regular moderate exercise (three times a week) have a better quality of life and lower mortality rates than those who do not exercise. However:
Studies report benefits from specific exercises:
Some people with severe heart failure may need bed rest. To reduce congestion in the lungs, the patient’s upper body should be elevated. For most patients, resting in an armchair is better than lying in bed. Relaxing and contracting leg muscles is important to prevent clots. As the patient improves, a doctor will progressively recommend more activity.
Stress reduction techniques, such as meditation and relaxation response methods, may have direct physical benefits. Anxiety can cause the heart to work harder and beat faster.
HERBS AND SUPPLEMENTS
Patients with heart failure may resort to alternative remedies. Such remedies are often ineffective and may have severe or toxic effects. Of particular note for patients with heart failure is an interaction between St. John’s wort (an herbal medicine used for depression) and digoxin (a heart drug). St. John’s wort can significantly interfere with this drug.
Fish Oil Supplements. Some research shows that a daily capsule of fish oil may help improve survival in patients with heart failure. Fish oil contains omega-3 polyunsaturated fatty acids, a healthy kind of fat. However, while evidence is not conclusive, some studies have suggested that fish oil supplements may not be safe for patients with implanted cardiac defibrillators.
Coenzyme Q10 and Vitamin E. Small studies have suggested that coenzyme Q10 (CoQ10) may help patients with heart failure, particularly when combined with vitamin E. CoQ10 is a vitamin-like substance found in organ meats and soybean oil. More recent studies, however, have found that CoQ10 and vitamin E do not help the heart or prevent heart disease. In fact, vitamin E supplements may actually increase the risk of heart failure, especially for patients with diabetes or vascular diseases.
Other Vitamins and Supplements. A wide variety of other vitamins (thiamin, B6, and C), minerals (calcium, magnesium, zinc, manganese, copper, selenium), nutritional supplements (carnitine, creatine), and herbal remedies (hawthorn) have been proposed as treatments for heart failure. None have been adequately tested. There is no evidence that a particular vitamin or supplement can cure heart failure. In any case, vitamins are best consumed through the food sources contained in a healthy diet.
Generally, manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body’s chemistry, and therefore have the potential to produce side effects that may be harmful. There have been several reported cases of serious and even lethal side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.
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Phil Kennedy no longer saw any other way to get the data. That was how one day he came to lie blissfully unconscious on an operating table in Belize while a neurosurgeon sawed off the top of his skull.
Last year, Kennedy, a 67-year-old neurologist and inventor, did something unprecedented in the annals of self-experimentation. He paid a surgeon in Central America $25,000 to implant electrodes into his brain in order to establish a connection between his motor cortex and a computer.
Along with a small group of pioneers, Kennedy, who was born in Ireland, had in the late 1980s developed “invasive” human brain-computer interfaces—literally wires inside the brain attached to a computer, and he is widely credited as the first to allow a severely paralyzed “locked-in” patient to move a computer cursor using her brain. “The father of cyborgs,” one magazine called him.
Kennedy’s scientific aim has been to build a speech decoder—software that can translate the neuronal signals produced by imagined speech into words coming out of a speech synthesizer. But this work, carried out by his small Georgia company Neural Signals, had stalled, Kennedy says. He could no longer find research subjects, had little funding, and had lost the support of the U.S. Food and Drug Administration.
That is why in June 2014, he found himself sitting in a distant hospital contemplating the image of his own shaved scalp in a mirror. “This whole research effort of 29 years so far was going to die if I didn’t do something,” he says. “I didn’t want it to die on the vine. That is why I took the risk.”
This fall, Kennedy presented studies of his own brain at the Society for Neuroscience in Chicago, where his actions provoked both awe and concern among colleagues. By arranging for surgery on a healthy person—even himself, even in the name of science—he’d likely violated his doctor’s oath. “I’m glad he’s fine now,” says Eddie Chang, a University of California, San Francisco, neurosurgeon whose recent work mapping the areas of the motor cortex that control speech helped guide Kennedy’s calculations. “I hope he gets some precious, precious data.”
Kennedy says his self-experiment was driven by frustration and by scientific questions. As a young physician, Kennedy was so intrigued by the brain that he returned to school to earn a Ph.D. in neuroscience. While running a lab at the Georgia Institute of Technology in the 1980s, he developed and patented an innovative type of electrode consisting of a pair of gold wires encased in a tiny glass cone. Filled with a proprietary blend of growth factors, the electrode induced nearby neurons to grow into the device.
In 1996, after tests in animals, the FDA agreed to allow Kennedy to implant his electrodes into locked-in patients with paralysis so severe they could no longer speak or move. His first volunteer was a special education teacher and mother of two named Marjory, or “MH,” who agreed to undergo the procedure at the very end of her life. Marjory had ALS but demonstrated she could turn a switch on and off just by thinking. But she was so sick that only 76 days later, she died. Next, in 1998, came Johnny Ray, a 53-year-old Vietnam veteran and drywall contractor who awoke from a coma with his mind fully intact but unable to move anything except his eyelids.
Kennedy personally oversaw the implantation of the electrodes in at least five subjects, and his team began showing that if it recorded from just a few neurons, patients could move a cursor on a computer screen and communicate by picking words or letters from a menu.
By 2004, Kennedy had implanted his electrodes in the brain of Erik Ramsey, a volunteer who suffered a catastrophic brain stem stroke in a car accident that left him locked in at the age of 16. Thanks to the data collected from Ramsey, Kennedy and his collaborators continued to publish high-profile papers on the results in journals like PLOS One and Frontiers in Neuroscience as recently as 2009 and 2011. One paper described how software could pick out the sounds Ramsey was imagining and allow him to very roughly pronounce a few simple words. Eventually, Ramsey became too ill to keep participating in the research.
By then, the FDA had also withdrawn permission to use the devices in any more patients. Kennedy says the agency began asking him for more safety data, including on the neurotrophic factors he was using to induce neuronal growth. When Kennedy couldn’t provide the data, the FDA refused to approve any more implants.
Kennedy never fully accepted the FDA decision (he took at least one other patient to Belize for an implant). There were also scientific frustrations working with disabled people. Locked-in people can’t communicate, except at times with grunts or their eyes, something that added a confounding variable to his experiments. When a given neuron fired off, he could never be sure what the patient had been thinking.
Kennedy became convinced that the way to take his research to the next level was to find a volunteer who could still speak. For almost a year he searched for a volunteer with ALS who still retained some vocal abilities, hoping to take the patient offshore for surgery. “I couldn’t get one. So after much thinking and pondering I decided to do it on myself,” he says. “I tried to talk myself out of it for years.”
The surgery took place in June 2014 at a 13-bed Belize City hospital a thousand miles south of his Georgia-based neurology practice and also far from the reach of the FDA. Prior to boarding his flight, Kennedy did all he could to prepare. At his small company, Neural Signals, he fabricated the electrodes the neurosurgeon would implant into his motor cortex—even chose the spot where he wanted them buried. He put aside enough money to support himself for a few months if the surgery went wrong. He had made sure his living will was in order and that his older son knew where he was.
Walking the walk
Down in Belize, the procedure did not go smoothly, pointing to the dangers of brain-computer interface science to volunteers. There is a small but real chance of death anytime the skull is opened. After waking up from his first surgery, Kennedy says, he could not reply when the surgeons spoke to him. He had lost the ability to speak. The doctors later explained that his blood pressure had spiked during the 12-hour surgery, causing the brain to swell and leading to temporary paralysis. “I wasn’t the least bit scared,” says Kennedy. “I knew what was going on. I invented the surgery.”
The side effects were very serious, but Kennedy says he recovered and returned for a second 10-hour procedure in Belize City several months later so the surgeon could implant electronics that would let him collect signals from his own brain.
Kennedy’s heroics impress some of his former patients. “Talk about walking the walk!” David Jayne, an ALS patient implanted by Kennedy’s team in the early 2000s, said in an e-mail. “I admire the hell out of Phil.”
To some researchers, Kennedy’s decisions could be seen as unwise, even unethical. Yet there are cases where self-experiments have paid off. In 1984, an Australian doctor named Barry Marshall drank a beaker filled with viruses in order to prove they caused stomach ulcers. He later won the Nobel Prize. “There’s been a long tradition of medical scientists experimenting on themselves, sometimes with good results and sometimes without such good results,” says Jonathan Wolpaw, a brain-computer interface researcher at the Wadsworth Center in New York. “It’s in that tradition. That’s probably all I should say.”
After returning home to Duluth, Georgia, Kennedy began to toil largely alone in his speech lab, recording his neurons as he repeated 29 phonemes (such as e, eh, a, o, u, and consonants like ch and j) out loud, and then silently imagined saying them. He did the same with about 290 short words such as “Dale” and “plum.” There were also phrases to speak: “Hello, world,” “Which private firm,” and “The joy of a jog makes a boy say wow.”
Kennedy says his early findings are “extremely encouraging.” He says he determined that different combinations of the 65 neurons he was recording from consistently fired every time he spoke certain sounds aloud, and also fired when he imagined speaking them—a relationship that is potentially key to developing a thought decoder for speech. At UCSF, Chang says that Kennedy may have learned something new. His own research uses different electrodes placed outside the brain, which he says are able to collect only a “relatively rough” signal (see “A Speech Synthesizer Direct to the Brain”). “I think what he might have access to there is something a lot more detailed,” says Chang.
There was one major disappointment. Kennedy had hoped to live with the implants in his brain for years, collecting data, improving his control, and publishing papers. But the incision in his skull never closed entirely, creating a dangerous situation. After a few weeks of collecting data, last January Kennedy was forced to ask doctors at a local Georgia hospital to remove the implants. The bill came to $94,000. Kennedy submitted the claim to his insurance company (he says it paid $15,000).
Kennedy attributes this setback to his decision to build the electrodes extra large and install them at an unusual angle so they would be easier to work with—a decision he now believes was a mistake. “But I got away with it, so I’m happy,” he says. “I had a few bumps and bruises after the surgery, but I did get four weeks of good data. I will be working on these data for a long time.”
by Joe DiBuduo
Can Zelda sacrifice her son to save humanity?
Pastors in Africa beat children in exorcism rituals. Christian and “traditional healers” charge a fortune for their services. Zelda’s goal is to end the abuse of children accused of witchcraft. Zelda battles her enemies alone by using her growing paranormal powers. Do they descend from the God, Mithras, an alien, or the devil? Or are they the result of a genetic mutation that allows her to see into other dimensions? Can she break the code in ancient documents or will they remain hidden? Read more
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A Penis Manologue has been out since 2009, yet it holds a pretty good rank .Though almost 3 million overall, one has to consider there are over 42 million books for sale on Amazon. But it’s in the 4000’s in medical books, psychology and sexuality, and in the 5000’s in health fitness and dieting, psychology & counselling > Sexuality.
Paperback: 142 pages
Publisher: CreateSpace Independent Publishing Platform (November 25, 2009)…