So do these drugs increase the danger from COVID-19? If you use one of these agents to control your blood pressure, should you stop taking it?

“There is no data,” says Cleveland Clinic preventive cardiologist Leslie Cho, MD. “This is a theory. There is no clinical or experimental evidence of a connection between these drugs and increased harm from COVID-19 exposure.”

Major heart groups agree. On March 17, the American Heart Association, American College of Cardiology and Heart Rhythm Society issued a joint statement advising patients not to stop taking their ACE inhibitor or ARB.  European medical societies released similar statements a few days prior.

Where’s the Proof?

There is no doubt that patients with hypertension and heart disease who contract the virus are at increased risk for a serious outcome. Many of these patients take ACE inhibitors and ARBs. This means there is an association between the use of these drugs and complications, but it does not mean the drugs are responsible for causing worse problems.  People with chronic obstructive pulmonary disease and cancer are at increased risk of complications and death from the COVID 19 as well.

The inability to overcome COVID-19 is more likely to occur in people who are weakened by another condition. “We see this with other viruses as well. This is why we tell patients with underlying medical conditions to get immunized against flu and pneumonia,” says Dr. Cho.

Why Not Stop Anyway?

The potential danger posed by this novel virus has everyone looking for ways to protect themselves and the ones they love. Making the decision to discontinue a medication without your doctor’s permission is never wise. In the case of ACE inhibitors and ARBs, it may have unintended consequences.

“We understand everyone feels vulnerable right now, but try to act rationally,” Dr. Cho pleads. “If you stop taking your blood pressure medications, and your blood pressure gets out of control, we can say with great certainty that there will be true harm.”

 How to Protect Yourself

Until researchers are able to explore the potential impact of ACE inhibitors, ARBs and other common drugs on people exposed to the coronavirus, Dr. Cho suggests following the steps known to decrease the likelihood of becoming infected:

• Stay at home.
• Wash your hands with soap and water thoroughly and often.
• Avoid unnecessary contact with others.
• Cover your cough.
• Resist touching your face.

Fever is the primary symptoms of COVID-19. If you develop a fever, call your primary care physician immediately. Do not call your cardiologist.

“In some states, the HIPAA laws protecting patients’ privacy have been relaxed, so your provider can talk with you on the phone or do a virtual visit over Facetime,” says Dr. Cho.

Do not go to your doctor’s office or the Emergency Department. “If you do have the virus, you will put many other people, including doctors and nurses, at risk and if you don’t, you will put yourself at risk by exposing yourself” she says.  Call first.

The post Don’t Stop Taking Your Blood Pressure Meds, Cardiologists Say appeared first on University Health News.

Almost every person with COPD will be prescribed a short-acting bronchodilator (either a beta-agonist, an anticholinergic, or a combination of both) to use as needed to relieve shortness of breath, coughing, wheezing, and other symptoms. Some people also will need long-acting bronchodilators and/or an anti-inflammatory drug. Your doctor will work with you to figure out the right drugs and combinations of drugs to relieve your symptoms, and you also should get immunized against influenza and pneumonia.

One thing you should avoid using is over-the-counter cough medications, such as guaifenesin (Robitussin, Mucinex), since there is little evidence to show that these are helpful for people with COPD. Although coughing can be bothersome, it has the important function of helping to clear mucus. This means that suppressing a cough may increase the risk of lung infection.

Mild COPD Treatment

For a person with mild COPD who has occasional symptoms, a short-acting bronchodilator alone may be sufficient to manage the condition. Two short-acting bronchodilators—a beta-agonist plus an anticholinergic—also may be prescribed. To simplify this regimen, a combination of a short-acting beta-agonist plus a short-acting anticholinergic is available in a single inhaler. If more symptoms develop over time, additional medications will likely be necessary.

Moderate-to-Severe COPD Treatment

For people with moderate-to-severe COPD who tend to experience symptoms more frequently, one or more long-acting bronchodilators will be added to the regimen. These drugs will be taken regularly every 12 or 24 hours. If acute episodes of breathlessness or coughing occur while taking these medications, a short-acting bronchodilator such as albuterol can be used to quell the episodes.

Inhaled corticosteroids are recommended for people with moderate-to- severe COPD who do not get sufficient relief from bronchodilators alone, or who experience frequent exacerbations of symptoms. Inhaled corticosteroids have been shown to reduce flare-ups. However, some studies have found that using inhaled corticosteroids, with or without a bronchodilator, increases the risk of developing pneumonia. Nevertheless, because inhaled corticosteroids may decrease the risk of dying, they often are added when bronchodilators alone are insufficient. Hopefully further research will clarify the role of inhaled steroids in COPD. Patients should discuss any concerns they have with their physician.

For people prescribed long-term use of both a long-acting bronchodilator and a corticosteroid, combinations of both in a single inhaler are available.

Severe COPD Treatment

For patients with more severe COPD, combinations of two long-acting bronchodilators are generally used. These often are combined in a single inhaler.

Immunizations

For people with obstructive airway diseases, flu or pneumonia can be very serious and even life threatening. Fortunately, vaccines are available to protect against influenza and some forms of pneumonia. It is extremely important that everyone with obstructive airway disease follow the recommended vaccination schedule, or their doctor’s advice.

Flu Vaccine

People with COPD or other lung problems should receive an influenza vaccination once a year. The ideal time to get a flu shot is in October or November, as flu season runs from November to March.

Pneumococcal Vaccine

The pneumococcal vaccine protects against the bacteria that is the most common cause of pneumonia, Streptococcus pneumoniae. There are now two forms of pneumococcal vaccine, the Pneumovax and the Prevnar 13. It is recommended that all adults over age 65 receive a pneumococcal vaccination. Unlike the flu shot, which must be given every year in the fall, pneumococcal vaccination provides protection for at least five years. It can be given at any time of the year.

The pneumococcal vaccine is advised for all people with COPD age 65 and older. It also may be given to people with COPD who are younger than age 65 and have severe or very severe disease (FEV1 less than 40 percent of predicted), and recommended for people with asthma who are younger than age 65.

Treating COPD Exacerbations

The most common cause of an exacerbation is a lung infection that may increase mucus production. In these cases, antibiotics may be used. Before prescribing an antibiotic, the doctor may send a sample of the sputum for analysis to determine whether the infection is bacterial or viral, since antibiotics are only effective against bacteria. Studies have shown that a short course (five days) of antibiotics is just as effective as taking antibiotics for longer than five days.

In 2017, the American Thoracic Society and European Respiratory Society issued joined guidelines on the management of COPD exacerbations. Their recommendations included:

• For ambulatory patients with an exacerbation of COPD, a short course of oral corticosteroids plus antibiotics.
• For patients hospitalized with an exacerbation, oral corticosteroids rather than intravenous corticosteroids, if possible.
• For patients hospitalized with an exacerbation causing respiratory failure, noninvasive mechanical ventilation.
• After being discharged for an exacerbation, pulmonary rehabilitation should begin within three weeks. It should not be started during hospitalization.

A recent study found that engaging in any amount of regular exercise following hospitalization for a COPD exacerbation actually reduces the risk of dying.

To learn about other COPD treatment regimens, purchase COPD, Asthma and Other Lung Disorders at UniversityHealthNews.com.

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A diet that is rich in fiber (from whole grains, whole fruits, vegetables, beans, brown rice, and nuts), and low in red meat, refined grains, and sugar may help keep the lungs healthy and reduce the chances of getting COPD for both smokers and nonsmokers. However, it is unknown whether changing fiber intake improves lung function in patients who already have COPD.

COPD most often affects people age 40 and older who have smoked a pack of cigarettes per day for 10 or more years. Pipe and cigar smoking also can decrease lung function and increase the chance of COPD, even in people who have never smoked cigarettes—so can smoking water pipes or marijuana.

Smokers who have a family history of COPD are at particularly high risk. For some people, exposure to secondhand smoke can cause respiratory symptoms and possibly COPD. Exposure to secondhand smoke in childhood appears to increase the risk for developing COPD in adulthood. In a 2016 study, middle-aged people whose mothers were heavy smokers (more than 20 cigarettes a day) were more than twice as likely to have lung impairment indicative of COPD than people whose mothers had not smoked.

People who quit smoking are still at increased risk of eventually being diagnosed with COPD. However, stopping smoking significantly reduces the chances of getting COPD, as well as other lung and heart diseases, and smokers with COPD who stop smoking slow the progression of their COPD. Smoking also increases the risk for lung cancer, but this risk declines when a person stops smoking, and continues to decline the longer they go without smoking.

The Risk of COPD for Marijuana and E-Cigarette Smokers

In recent years, there has been interest in understanding the possible lung effects of marijuana smoke inhalation, due to its increased use recreationally and medicinally. To date, there have been no conclusive studies. It seems unlikely that we will know for many years, given that the permanent effects of smoke inhalation take time to manifest. There is, however, some concern that marijuana smoking may increase the risk of cancer as well as COPD.

E-cigarettes were introduced in the United States in 2006 as a supposedly safe alternative to tobacco cigarettes. Despite the lack of long-term research, some studies suggest these products may not be as benign as first thought. E-cigarettes typically contain nicotine, a flavoring, and a solvent. The nicotine encourages addiction, while the flavoring is for appeal. As of 2017, a whopping 7,700 flavors of vaping liquid were available. Although these flavorings are widely used in the food industry and are safe to eat, their safety when inhaled is unknown. Additionally, some vaping liquids contain impurities such as anabasine, which is principally used as an insecticide.

More studies are underway to assess whether e-cigarettes and other electronic nicotine delivery systems (ENDS) help with smoking cessation. To date, the results of randomized, controlled clinical trials is mixed. As far as safety goes, studies have linked the use of ENDS to changes in airflow that precede COPD, daytime cough, phlegm production, headache, dry mouth, vertigo, and nausea.

The U.S. Food & Drug Administration (FDA) regulates the manufacture, packaging, labeling, advertising, sale, and distribution of ENDS. All ENDS products must carry a warning that the product contains nicotine, and that nicotine is addictive. They are not required to say what other chemicals are contained in the product.

To learn about other causes of COPD, purchase COPD, Asthma and Other Lung Disorders at UniversityHealthNews.com.

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1. Pollen 

Outdoor allergens include pollen and mold. Allergy season, when pollen counts are highest, varies depending on where you live. To limit your exposure to pollen and outdoor mold during allergy season, keep windows closed as much as possible and try to stay indoors around midday, when pollen and some mold spore counts are highest. It may be necessary to increase your medication dose just before and during allergy season if you are sensitive to pollen and outdoor mold.

2. Mold

Indoor mold can grow wherever there is dampness or wetness. To keep the house as dry as possible, make sure faucets, pipes, and other sources of water are not leaking. Clean any surfaces that have mold. Basements, which can be damp, should be dehumidified if possible.

3. Pets

For people who have an allergic response to cats, dogs, or other animals with fur, it is the animals’ flakes of skin (dander) or dried saliva that cause the reaction. The best option for people with asthma triggered by animal dander is not to have a pet, or to have a hypoallergenic pet. For those who do not wish to deprive themselves of pet ownership, some precautions may help. The pet may be kept outdoors, or at minimum, out of the bedroom. Carpets can attract animal hair, dander, and dried saliva, so replace them with wood or tile floors, or keep the pet out of carpeted rooms.

4. Insects

Some people with asthma are allergic to the dried droppings and remains of cockroaches. To make your home as unappealing as possible to cockroaches, never leave food out, keep garbage in a closed container, and fix plumbing leaks. Use poison baits, powders, gels, or pastes to kill cockroaches if you see them.

Dust mites also are a common culprit. Dust mites are microscopic bugs that can live in carpets, furniture, mattresses, and bedding. The mites are harmless to humans, but can trigger allergies and asthma attacks.

5. Smoke 

Smoke from cigarettes, cigars, pipes, or a wood-burning stove or fireplace can trigger an asthma attack in some people. It is best to stay away from people who are smoking, and to keep your home smoke-free. A person with asthma who smokes should quit, and should encourage other people living in the home who smoke to stop as well. Smoking increases the risk for numerous diseases, including cancer and heart disease, as well as COPD.

6 & 7. Strong Odors, and Sprays

Strong odors and sprays, such as perfume, aftershave, scented body lotions, hair spray, talcum powder, paint, new carpet, and others also can be problematic for some people with asthma. Exposure to these irritants should be limited as much as possible.

8. Exercise

To minimize the chance of experiencing symptoms while exercising or engaging in sports, be sure to spend about 10 minutes warming up before engaging in vigorous exercise. Check the air quality and pollen levels if you are allergic to pollen, and try to exercise during times when air quality is good and pollen levels are low.

Many people with asthma also use their rescue inhaler 10 minutes prior to exercising, which decreases the chances of an attack during exercise and also improves exercise performance for many.

9. Medications

Some people with asthma are sensitive to certain medications. Drugs that can trigger asthma symptoms include beta-blockers (used to treat high blood pressure), aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are used for pain relief and include common over-the-counter drugs such as ibuprofen (Advil, Motrin) and naproxen (Aleve). Aspirin and NSAIDs trigger asthma symptoms in about 3 to 5 percent of adults with asthma.

For people who are bothered by any of these medications there are alternatives. Your physician can make specific recommendations.

10. Sulfites in Foods

Some foods and drinks contain sulfite compounds. These compounds work as a preservative to prevent discoloration, and can be found in beer, wine, processed potatoes, dried fruit, sauerkraut, and shrimp. About 5 percent of people with asthma have a worsening of symptoms when they eat foods containing sulfites. The only remedy for these individuals is to avoid sulfite-containing foods. Foods and beverages that contain sulfites must indicate this on the label.

Other Asthma Triggers

Some people find that viral infections, changes in weather, strong emotions, or their menstrual cycle worsen asthma symptoms, or even trigger an attack.

For more information on the prevention and treatment of asthma, purchase COPD, Asthma and Other Lung Disorders at www.UniversityHealthNews.com.

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1. A blood vessel can become blocked.
2. Blood pressure can suddenly drop.
3. A blood vessel in the brain can burst.

The way blood flow to the brain is interrupted defines the two major types of stroke: ischemic and hemorrhagic.

What Is an Ischemic Stroke?

About 87 percent of all strokes are ischemic. These strokes most often occur when an artery bringing blood to the brain becomes blocked, stopping blood flow. Less frequently, a severe drop in blood pressure causes an ischemic stroke.

Brain cells (neurons) rely on a constant stream of blood supplying oxygen and nutrients to operate normally. When blood flow is interrupted for more than a few seconds, the neurons begin to malfunction. If blood flow is not restored quickly, the neurons begin to die. This is why immediate medical evaluation and treatment is absolutely essential for people who are experiencing symptoms of a stroke.

There are two types of ischemic strokes:

Embolic Stroke

Many people wonder, “What is an embolism?” Sometimes a clot that develops elsewhere in the body—typically the heart, aorta, or carotid arteries in the neck—breaks off and travels in the bloodstream to the brain. This type of clot is called an embolus. When an embolus lodges in a brain artery, stopping blood flow, it produces an embolism that causes an embolic stroke. In addition to a blood clot, an embolus can be an air bubble or piece of debris.

Thrombotic Stroke

When a clot (thrombus) develops in a narrowed part of an artery—typically from fatty buildup in the arteries (atherosclerosis) of the brain or neck—the result is a thrombotic stroke. This type of stroke comprises about 50 percent of all strokes. A thrombotic stroke is further differentiated as a large-vessel or small-vessel thrombosis, depending on the size of the artery in which the thrombus occurs. A small-vessel thrombotic stroke deep within the brain is also called a lacunar stroke.

How Ischemic Strokes Are Categorized

Ischemic strokes are categorized according to the severity and duration of symptoms:

• Transient ischemic attack (TIA). A TIA is a sudden, transient episode of neurological dysfunction caused by lack of blood flow to part of the brain. A TIA is sometimes called a mini stroke, but it is actually a transient stroke, because it passes without causing permanent damage to the brain. TIAs typically last no more than 20 minutes or so. Since it is difficult to tell the difference between a stroke and a TIA until the TIA resolves, it’s wisest to treat a TIA as a medical emergency by calling 911.
• Progressing or evolving stroke. This is a stroke in the process of occurring. The sooner you get to an emergency department for stabilization and treatment, the better your outcome will be. If the stroke is treated quickly, you may have no lasting deficit or disability.
• Completed stroke. This is a cerebral infarction, and it means the stroke was severe enough and lasted long enough to kill a portion of brain tissue. Irreversible deficit, disability or death is likely.

What Is a Hemorrhagic Stroke

When a weakened artery in the brain ruptures, the result is a hemorrhagic stroke. Blood flowing into the brain compresses the tissue and kills brain cells.

About 75 percent of hemorrhagic strokes (13 percent of all strokes) occur within the brain itself. These are called intracerebral hemorrhages.

In the other 25 percent, the bleeding occurs in the space between the brain and the skull. These are known as subarachnoid hemorrhages.

The most common cause of a spontaneous subarachnoid hemorrhage is a ruptured aneurysm, a balloon-like outpouching from the wall of an artery,

Brain Attack Prognosis

The extent of your disability (if any) will be determined after the brain attack has ended and your condition has been stabilized. The length of time you will need to recover from a brain attack will depend on its severity. Fortunately, about 50 to 70 percent of stroke survivors are able to regain functional independence. Others are permanently disabled to various degrees.

The risk of death varies with the type of stroke and increases with age. About 40 percent of intracerebral hemorrhages cause death. About 10 to 15 percent of people who suffer a subarachnoid hemorrhage die before reaching the hospital; 40 percent die within the first week; and 50 percent die within the first six months.

With ischemic stroke, about 9 percent of patients aged 65 to 74, 13 percent of patients aged 74 to 84, and 23 percent of patients age 84 and older die within 30 days.

The post Brain Attack: Stroke Symptoms, Causes, and Treatment appeared first on University Health News.

Knowing a patient’s vital signs, and armed with the results of a CT scan, ECG, blood tests, and history of stroke symptoms including time of onset, a physician can make a diagnosis. If the diagnosis is ischemic stroke, and only a short time has passed since symptoms began, tPA may be used.

Standard Treatment: tPA to Dissolve the Blood Clot

The technique for treating blood clots causing stroke is called intravenous thrombolysis—in lay terms, “clot-busting.” Thrombolysis is the combination of two Greek words, “thrombus,” meaning blood clot, and “lysis,” meaning to dissolve or break apart. The body has a natural mechanism for doing this through proteins that circulate in the blood. One of these is plasminogen, an inactive protein that the body converts to plasmin, an enzyme that breaks apart and dissolves blood clots. To make this conversion, another enzyme called tissue plasminogen activator (tPA) is required.

Blood clotting is a dynamic process. Fibrin filaments act like nets to trap red blood cells and stop the bleeding. As fibrin filaments form, tPA in the serum of the trapped blood begins to adhere to the fibrin, converting plasminogen to plasmin. Plasmin attacks the fibrin filaments, dissolving the net and breaking up the blood clot.

Blood clots are broken apart by plasmin as they form. So long as there is sufficient stimulus for blood to clot, clots will form faster than plasmin can break them apart. When the stimulus vanishes, the blood clot eventually breaks apart and disappears. The objective of thrombolytic therapy is to accelerate the removal of a blood clot by enhancing the conversion of inactive plasminogen to clot-busting plasmin.

Emergency Medical Treatment for Stroke

The use of tPA is so effective in treating acute ischemic stroke that it is used in emergency departments throughout the country. Unfortunately, only about five percent of patients who qualify for the treatment receive it. One reason is failure to arrive at the hospital within the recommended treatment window of 4.5 hours.

While several tPA drugs can be used to break up heart attack-causing blood clots in the coronary arteries, only one is approved for the treatment of ischemic stroke: alteplase (Activase). It is given by intravenous infusion. About 10 percent of the entire dose is given at one time (bolus), with the remaining 90 percent infused over an hour.

Initially, it was thought alteplase had to be administered within three hours of stroke onset. But when clinical trials showed the drug was safe and effective for a longer period of time, the American Heart Association/American Stroke Association (AHA/ASA) endorsed expanding the treatment window to 4.5 hours. The drug label says that risks are increased when the drug is used in patients over age 75, and its effectiveness in those over age 80 has not been established. But in 2015, the AHA/ASA gave a positive recommendation to tPA use in older patients, acknowledging that risk may be increased, but that it does not outweigh the potential benefit in increasing the likelihood of remaining independent three months after a stroke.

The AHA/ASA continues to emphasize that results are better when patients are treated earlier. Patients who receive the therapy within 90 minutes have a better outcome than those who receive it later, even if within the allowed time period. For every 30 minutes that pass before blood flow is restored through a blocked artery, the probability of a good recovery drops by about 10 percent.

Know the Risks

A danger of thrombolytic therapy is the possibility of unwanted bleeding. Clot-busting drugs cannot tell the difference between a “bad” clot that prevents blood flow to the brain cells and a “good” clot that has been formed to stop blood flow from a ruptured intracranial artery. If the drug breaks down a good clot, a hemorrhagic stroke can occur. Despite careful dosing, intracranial hemorrhage occurs in some patients who receive alteplase. Nevertheless, in appropriately selected patients, the benefits far outweigh this potential complication.

When It’s Too Late for tPA

For patients diagnosed with ischemic stroke after the treatment window has passed, no medication to restore blood flow has been proven effective. However, some of these patients may benefit from mechanical removal of the clot with a catheter-based device up to six hours after stroke onset.

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Your circulatory system delivers blood to all organs and tissues of your body. Your heart is the pump, and your blood vessels are the plumbing. It’s a closed system: Blood pumped from the heart eventually returns to the heart, where it is sent to the lungs for oxygen and back to the heart to be pumped through the system again. The blood vessels that deliver oxygenated blood from the heart to your tissues and organs are called arteries; those that return oxygen-depleted blood to your heart are called veins. Veins are not usually involved in a common cerebrovascular disease.

Cerebrovascular Disease Caused by a Blood Clot

About 87 percent of all strokes are ischemic. These strokes most often occur when an artery bringing blood to the brain becomes blocked, stopping blood flow. Less frequently, a severe drop in blood pressure causes an ischemic stroke.

Brain cells (neurons) rely on a constant stream of blood supplying oxygen and nutrients to operate normally. When blood flow is interrupted for more than a few seconds, the neurons begin to malfunction. If blood flow is not restored quickly, the neurons begin to die. This is why immediate medical evaluation and treatment is absolutely essential for people who are experiencing symptoms of a stroke.

There are two types of ischemic strokes:

Embolic Stroke

Many people wonder, “What is an embolism?” Sometimes a clot that develops elsewhere in the body—typically the heart, aorta, or carotid arteries in the neck—breaks off and travels in the bloodstream to the brain. This type of clot is called an embolus. When an embolus lodges in a brain artery, stopping blood flow, it produces an embolism that causes an embolic stroke. In addition to a blood clot, an embolus can be an air bubble or piece of debris.

Thrombotic Stroke

When a clot (thrombus) develops in a narrowed part of an artery—typically from fatty buildup in the arteries (atherosclerosis) of the brain or neck—the result is a thrombotic stroke. This type of stroke comprises about 50 percent of all strokes. A thrombotic stroke is further differentiated as a large-vessel or small-vessel thrombosis, depending on the size of the artery in which the thrombus occurs. A small-vessel thrombotic stroke deep within the brain is also called a lacunar stroke.

Cerebrovascular Disease Caused by Bleeding in the Brain

When a weakened artery in the brain ruptures, the result is a hemorrhagic stroke. Blood flowing into the brain compresses the tissue and kills brain cells.

About 75 percent of hemorrhagic strokes (13 percent of all strokes) occur within the brain itself. These are called intracerebral hemorrhages.

In the other 25 percent, the bleeding occurs in the space between the brain and the skull. These are known as subarachnoid hemorrhages.

 The most common cause of a spontaneous subarachnoid hemorrhage is a ruptured aneurysm. An aneurysm is a balloon-like outpouching from a weakened area in the wall of an artery, typically at the base of the brain. Aneurysms are present at birth. Cerebral aneurysms are more likely to rupture in patients with a family history of ruptured aneurysms, and in those who currently smoke, have a large aneurysm, or suffer from high blood pressure.

The Heart-Brain Connection

People with cerebrovascular disease caused by atherosclerosis are at risk of having atherosclerosis elsewhere in the body. When atherosclerosis affects arteries supplying blood to the brain or inside the brain, the result is a stroke. When atherosclerosis affects the arteries supplying blood to the heart muscle (coronary artery disease, or CAD), the result is a heart attack. The same disease process can affect the arms and legs (peripheral arterial disease, or PAD) or the kidneys (renovascular disease).

If you have had an ischemic stroke, or have experienced symptoms of a transient ischemic attack (TIA) that indicate increased risk for stroke, you have a 20 to 40 percent chance of having CAD. In fact, two to five percent of ischemic stroke survivors have a fatal heart attack less than 90 days after their stroke. If you are under the age of 60 and have a TIA, your risk of having a heart attack is 15 times that of a healthy person your age.

Similarly, CAD is a risk factor for stroke, since patients with CAD may also have cerebrovascular disease. In addition, they are at increased risk for strokes caused by blood clots forming in the heart and traveling to the brain. While about 47 percent of all deaths from cardiovascular disease are due to CAD, about 16 percent are due to stroke.

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Your cardiologist will begin by taking a thorough medical history, discussing your symptoms, and conducting an extensive physical examination. Using a stethoscope, your cardiologist will listen for abnormal sounds (such as murmurs) that reveal problems with your heart’s function. A stethoscope will also allow the doctor to hear crackling sounds (called rales) that indicate fluid in the lungs). The cardiologist will check your neck for distended neck veins, feel your abdomen for signs of fluid retention and liver enlargement, evaluate your skin color, take your blood pressure, and check your pulse for a rapid or irregular heart rate. Blood and urine tests will likely be ordered.

Some tests will enable your doctor to view and measure your heart’s shape, size, function, and capacity to respond to stress and exercise. The most common tests you are likely to have during the evaluation are discussed below. These tests are noninvasive, which means that nothing punctures your skin.

Metabolic Stress Test

The metabolic stress test, also called a cardiopulmonary exercise test, is done on a treadmill or bicycle. This test is used to measure your functional capacity, and how well you utilize oxygen during exercise.

During the test, you will wear nose clips so that only mouth breathing is possible. A mouthpiece will measure how much oxygen you inhale and how much carbon dioxide you exhale. Your peak oxygen consumption will be calculated and compared with what is normal for someone of your age, size, and physique.

This provides an objective measure of functional impairment.

Radionuclide Nuclear Stress Test

When a stress test is combined with the use of a radioactive isotope (usually thallium and/or sestamibi) injected into a vein, it is called a nuclear stress test, myocardial perfusion scan, or SPECT scan. SPECT stands for single-photon emission computed tomography—“single-photon,” because the radioisotopes emit only a single type of radiation (gamma rays). A special camera that sees only gamma rays is used to collect the gamma rays that a computer uses to construct an image—hence, the test is “computed.” Tomography is a method of reconstructing images in sections or planes. This enables a physician to look at a specific section of the heart to see how much blood it is receiving.

When the isotope is injected, the blood carries it to the heart, where it accumulates in areas with adequate blood flow. If a coronary artery is blocked, the isotope can’t get through. The test is usually performed when your heart is at rest and again after exercise.

In larger individuals, sestamibi may work better than thallium. In some centers, thallium and sestamibi are combined for dual-isotope SPECT imaging.

MUGA Scan

A variation of the radionuclide test is the multiple-gated acquisition (MUGA) scan, which captures the heart in motion. A small amount of thallium or technetium is injected into a vein, and as the isotope flows through the heart, the size and shape of the ventricles and their pumping ability can be seen. This test helps assess how well the heart contracts, and measures the ejection fraction of both the left and right ventricles. The test may be done at rest or while exercising.

The post Nuclear Stress Test, MUGA Scan Effective Ways to Evaluate Heart Failure appeared first on University Health News.

What Are Beta Blockers?

By the mid-1980s, physicians had learned that people with heart failure and high levels of norepinephrine in their blood had an increased risk of dying from their condition. Beta blockers modulate the activity of the sympathetic nervous system that produces norepinephrine.

In several major clinical trials, adding beta blockers to other heart failure drugs improved survival by 34 percent. By the late 1990s, the overwhelmingly positive data prompted new guidelines calling for the addition of beta blockers to the standard treatment of diuretics and ACE inhibitors for heart failure patients.

In addition to increasing survival, beta blockers slow the progression of heart failure, improve NYHA functional class, and reduce the risk of hospitalization and arrhythmias. They also may prevent many of the harmful effects of ventricular remodeling by increasing the ejection fraction and decreasing the size of the heart. These biologic effects appear to reverse remodeling and return the heart to normal size. Beta blockers also lessen the symptoms of heart failure, and make patients feel better.

ACC/AHA heart failure guidelines recommend beta blockers for patients with left ventricular systolic dysfunction but no symptoms, patients with stable NYHA class II-IV heart failure, and all patients who have had a heart attack, regardless of whether they have heart failure. The Joint Commission, an independent body that accredits and certifies healthcare organizations, requires that heart failure patients be given a prescription for beta blockers when they are discharged from the hospital.

Beta Blockers: Dosing and Side Effects

Finding the proper dose of a beta blocker is extremely important, because the drug can slow heart rate or lower blood pressure, further limiting the heart’s ability to pump efficiently. Different beta blockers come in a variety of strengths and are taken once or twice a day. The dose of these beta blockers may be doubled every two weeks until the maximum tolerated dose is reached.

The most common side effects of beta blockers are dizziness, slow heartbeat (bradycardia), shortness of breath, and fatigue. These effects can usually be managed by adjusting the dose. However, it is important that you never adjust the dose on your own.

Other side effects may include cold hands and feet, headache, nightmares, difficulty sleeping, wheezing, difficulty breathing, skin rash, swelling of the feet and legs, and sudden weight gain.

Patients with acutely decompensated heart failure should not use beta blockers. Patients with very severe diabetes, asthma, or peripheral vascular disease may not be able to tolerate beta blockers. An experienced heart failure specialist may decide to use beta blockers in these situations, but you will need to be carefully monitored.

Unfortunately, some patients do not do well on beta blockers. In April 2015, the FDA approved the use of ivabradine (Corlanor) for symptomatic heart failure patients who cannot take beta blockers or tolerate the recommended doses. Ivabradine slows the heart rate like beta blockers do, enabling it to pump more effectively.

There are three main types of diuretics: thiazide, loop, and potassium-sparing. They work differently to achieve the same effect. Thiazide diuretics are most commonly used to treat high blood pressure, while the more powerful loop diuretics are often used in kidney and heart failure. Potassium-sparing diuretics are weaker and are mostly used in combination with thiazide or loop diuretics to prevent the loss of potassium that occurs with diuretic use.

In the past, standard medical therapy for heart failure consisted of three main classes of drugs:

• Digoxin to increase the heart’s pumping ability.
• A diuretic to eliminate excess fluid.
• An ACE inhibitor to increase blood flow.

With the advent of beta-blockers, and compelling evidence of their effectiveness, recommendations changed. In general, patients are now treated with an ACE inhibitor or angiotensin receptor blocker (ARB), plus a diuretic and a beta-blocker, to which an aldosterone antagonist or digoxin can be added.

Diuretic definition

Heart failure specialists prescribe diuretics for approximately 90 percent of patients, and strive to use the lowest effective dose. You may be allowed to adjust your own diuretics based on your symptoms, following specific instructions from your doctor. You will monitor your weight daily, and if you gain more than three pounds above your normal, baseline weight, you may increase the diuretic dose as instructed.

Some people with mild or moderate heart failure who take an ACE inhibitor and beta-blocker do not need a daily diuretic. As heart failure becomes more severe, diuretic requirements increase. Not complying with your sodium and fluid restrictions will also lead to greater fluid retention and a heavier reliance on diuretics.

Diuretic Dosing and Side Effects

The diuretic your doctor prescribes will depend on your individual situation. The vast majority of heart failure patients are started on a loop diuretic such as furosemide (Lasix), bumetanide (Bumex), or torsemide (Demadex). Those who need a stronger diuretic effect may require a combination of loop and thiazide diuretics. Spironolactone (Aldactone) is a potassium-sparing diuretic and neurohormonal modulator that improves survival in patients with severe heart failure when added to therapy with an ACE inhibitor, beta-blocker, digoxin, and diuretics.

For patients with acute decompensated heart failure who no longer benefit from traditional diuretics, intravenous treatment with a synthetic natriuretic peptide such as ularitide may help.

Diuretic doses are based on the severity of heart failure, as well as on diet, salt and fluid intake, activity level, and kidney function. Doses are adjusted as needed to relieve swelling and congestion. High doses can cause fluid and electrolyte imbalances from loss of sodium and water. Loss of too much sodium can cause hypotension, dehydration, and worsening kidney function. Overly aggressive use of diuretics can also cause imbalances in other minerals and electrolytes in the body, including potassium, magnesium, calcium, and chloride. Elderly or debilitated patients are more susceptible to these adverse effects than younger patients. Sometimes, a high dose of diuretics will be given intravenously or in bolus form (a large amount given at one time).

If you take diuretics, it is important to keep your blood potassium level normal to prevent an abnormal heart rhythm from occurring. Potassium-sparing diuretics raise blood potassium levels. Thiazide and loop diuretics lower blood potassium levels. Either way, severe imbalances produce the same symptoms: weakness, numbness, confusion, and heaviness in the legs. If you take a thiazide or loop diuretic, and are not on a potassium-sparing diuretic it is important to eat potassium-rich foods, such as baked potatoes, dried fruit, white beans, cantaloupe, and spinach. You may also need a potassium supplement. However, never take a potassium supplement or a salt substitute containing potassium unless instructed by your doctor, no matter which type of diuretic you are taking.

A few people who use diuretics find they sunburn more easily, and some may get a rash. A common effect of diuretic use is dry mouth—if this happens to you, use sugar-free hard candy to stimulate the flow of saliva. People who take diuretics are more susceptible to attacks of gout, a type of arthritis that causes painful joint inflammation. Diuretics may also cause nausea, confusion, drowsiness, weakness (due to low blood pressure), and muscle or leg cramps. If you experience any of these side effects, tell your doctor.

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