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1 VOLUME 16 NUMBER 4 november 2011 Polymyalgia rheumatica It sounds like a new threat to health, but it was first diagnosed in 1888 as senile rheumatic gout. It sounds rare, even exotic, but it s actually quite common. It sounds serious, even ferocious, but it responds beautifully to proper treatment. It s polymyalgia rheumatica (PMR), a painful, sometimes disabling condition that can be associated with giant cell arteritis (GCA), a disease that is much less common but much more serious. You don t have to remember the unfamiliar name or even the simple initials, but you should understand the symptoms and treatments that can restore comfort in PMR and, in the case of GCA, preserve your vision. What is PMR? The disorder s name tells more about its symptoms than its underlying nature. PMR s characteristic clinical feature is muscle pain (the myalgia ) in several locations (the poly ). But the name does not do justice to the inflammation that s responsible for the pain. And although most patients with PMR complain of pain in their muscles, the inflammation is actually most intense in the synovium, the membrane surrounding the joints near the painful muscles, and in the bursa, the fluid-filled sacs that cushion these joints. Joint inflammation justifies the rheumatica designation, but unlike rheumatoid arthritis and other rheumatic disorders, PMR never produces joint damage and destruction. Despite these major differences, PMR and the classic rheumatic diseases do share a common feature: their cause is unknown, but doctors believe they are autoimmune disorders that develop when the body s powerful immune system turns against the body s own tissues, producing inflammation by friendly fire. In most cases, it s likely that the autoimmune process depends on a combination of a genetic predisposition and an environmental trigger. In the case of PMR, though, there is only a slight tendency for the disorder to run in families, and although several infections have been suspected as triggers, none has been firmly implicated. Who gets PMR? Anyone can get it, but almost all people with PMR are above age 50; risk increases with age, so the typical patient is just over 70. The disease is most common in Caucasians, especially those with Northern European ancestry, but no ethnic group is immune. Women are at higher risk than men, but many males are affected. In all, one of every 133 people above age 50 has PMR. A particular genetic type (HLA-DR4) indicates an enhanced susceptibility to both PMR and GCA; similar genes are linked to rheumatoid arthritis. Symptoms PMR usually begins fairly abruptly, gaining force over a few days. Because of the relatively acute start, many patients assume they have strained a muscle or sprained a joint even though they haven t had a recent injury. Despite the rapid onset and considerable distress, the typical patient is ill for over a month before he s diagnosed; PMR can fly under the radar of both doctors and patients. The two most common symptoms are pain and stiffness. The shoulders are affected most often, with the hips and neck next in line; the shoulder and hip discomfort is usually equally severe on both sides of the body. Stiffness is at its worst in the early morning, and it usually takes 45 to 60 minutes for patients to loosen up. But even though the stiffness wears off as the day wears on, the pain does not. In fact, the pain is usually increased by physical activity. In severe cases of PMR, pain and stiffness may prevent patients from rising from a bed or chair without INSIDE Atrial fibrillation It s a very common heart rhythm disorder, and it can be very serious. Fortunately, modern treatment can help. On call Penile shortening after prostate surgery On the long list of worries facing men with prostate cancer, this is a small one. What s New Food Allergy, Intolerance, and Sensitivity Better Bladder and Bowel Control Special Health Reports from Harvard Medical School To order, call (toll-free) or visit us online at The Perfectionist s Handbook: Take Risks, Invite Criticism, and Make the Most of Your Mistakes, a new book co-published with Harvard Health Publications. Receive Harvard Health Publications free newsletter Go to to subscribe to HEALTHbeat. This free, weekly newsletter brings you health tips, advice, and information on a wide range of topics. You can also join in discussion with experts from Harvard Health Publications and folks like you on various health topics, medical news, and views by reading the Harvard Health Blog ( CONTACT US Write to us at For customer service, write us at

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Its contents are not intended to provide personal medical advice, which should be obtained directly from a physician. We regret that we cannot respond to inquiries regarding personal health matters. PUBLICATIONS MAIL AGREEMENT NO RETURN UNDELIVERABLE CANADIAN ADDRESSES TO: CIRCULATION DEPT., 1415 JANETTE AVENUE, WINDSOR, ON N8X 1Z1 Polymyalgia rheumatica (continued) assistance. Activities that require raising the arms above shoulder height are particularly challenging. Even turning over in bed can be painful and difficult. On its own, PMR does not produce muscle weakness or restricted joint motion. But if untreated, pain and stiffness limit a patient s activity to the extent that muscles become wasted and weak, and joints become stiff from simple disuse. Pain and stiffness are bad enough, but there s even more to PMR. Without treatment, most patients develop fatigue and many lose their appetites, so weight loss is common. The combination of weakness and weight loss can trigger depression but since depression itself causes fatigue and saps energy and appetite, a blue mood can make the diagnosis even more difficult. In addition, many people with PMR complain of fever. The fever is usually low-grade, but it can sometimes be dramatic, especially when GCA is also present. If fever is prominent, especially if it develops before other symptoms, doctors often suspect infections or tumors. And since most people with PMR are anemic, doctors often suspect the worst. False leads Because there is no specific test to diagnose PMR, doctors may think of other illnesses before they consider the right diagnosis. Fever, weight loss, anemia, and weakness may tilt their thinking toward cancer or a serious infection such as tuberculosis or endocarditis (heart valve infection). Fatigue and weakness can suggest an endocrine disorder such as an underactive thyroid. Severe stiffness may mimic Parkinson s disease. More often, though, joint pain directs attention to ordinary osteoarthritis or inflammatory diseases of joints or muscles such as rheumatoid arthritis or polymyositis. If fever and other signs of inflammation are subtle or absent, doctors may think of fibromyalgia, particularly in women. Neck pain can be severe enough to mimic a pinched nerve, and shoulder pain may suggest rotator cuff problems. Adverse reactions to medications can also confuse things, particularly since many older people take several drugs; statininduced muscle pain is a prime example of a false lead. Zeroing in Despite all the things that can mimic PMR and the lack of a specific diagnostic test, PMR is usually not difficult to diagnose providing a doctor thinks of it. You can help him by remembering the three initials that can put his thinking on the right track. The key clinical features that make PMR likely include age over 50, particularly over 65 morning stiffness lasting at least 30 minutes; an hour is even more typical pain in both shoulders, usually symmetrically; hip and neck pain are also common symptoms that reach their peak within two weeks of their onset and persist for at least two months (unless treated) no evidence of cancer, infection, or inflammatory joint disease such as rheumatoid arthritis. Even though doctors don t have a specific laboratory test for PMR, they do have several tests that strongly support the diagnosis. The most important are two that reflect inflammation, the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Most patients with PMR have high ESRs (usually above 40 millimeters per hour) and CRPs (usually above 6 milligrams [mg] per liter). Some patients, particularly younger men with mild PMR, can have normal or nearly normal ESR levels, but even then, the CRP is usually high. Because many inflammatory conditions, ranging from appendicitis to tonsillitis, produce high ESR and CRP readings, these tests are not at all specific for PMR. The same is true for the other characteristic laboratory abnormalities. Most PMR patients have anemia, which is usually mild to moderate. In addition to low red blood cell counts, these people have low blood iron levels but since they also have normal or high levels of the blood protein ferritin, they are not actually iron deficient. Instead, they have a condition called the 2 Harvard Men s Health Watch November 2011

3 anemia of chronic disease, a common but nonspecific reflection of long-standing inflammation anywhere in the body. PMR does not produce any other abnormal blood tests. Imaging tests such as ultrasounds and MRIs often show inflammation in areas of pain, but these studies are not needed in most cases. Amidst so many nonspecific laboratory findings, perhaps the most characteristic feature of PMR is its prompt and dramatic response to therapy. Treatment PMR is unlikely to respond to the medications that relieve most joint and muscle pain; acetaminophen (Tylenol and many other brands) and nonsteroidal antiinflammatory drugs (NSAIDs) such as aspirin, ibuprofen (Motrin, Advil, and others), and naproxen (Aleve and others) are ineffective. But although NSAIDs generally flop, steroids produce dramatic benefits. Most doctors prescribe prednisone, a corticosteroid, for PMR. Although high doses are required for many inflammatory diseases, including GCA (see below), PMR responds to modest doses of 10 to 20 mg a day. A typical regimen starts with 15 mg once each morning; a typical patient feels dramatically better in just two or three days. Because long-term corticosteroid therapy can have serious side effects (including hypertension, diabetes, osteoporosis, cataracts, and infections) and because patients improve so rapidly, doctors may be tempted to reduce the steroid dosage rapidly. It s a mistake. To avoid relapses, PMR requires prolonged therapy, sometimes even as long as one to two years. That s why a 2009 study suggests a very slow dose reduction, amounting to a decrease of perhaps 1 mg of prednisone a month. Most patients do very well, but their doctors should keep an eye out to be sure benefits are sustained and the side effects are minimal. Patients who relapse may need slightly higher doses and an even slower dose reduction. A patient with PMR is likely to think of the doctor who gave him prednisone as a miracle worker. With such gratitude in store, it s tempting for doctors to start prednisone whenever PMR is a possibility. But before starting low-dose steroids, doctors should first ask a crucial question: does my patient also have GCA? What is GCA? Giant cell arteritis is also called temporal arteritis. By any name, it is a serious inflammatory condition of blood vessels so serious, in fact, that it can cause blindness and 10% to 30% of patients with PMR also have GCA. There are many types of blood vessel inflammation. GCA is distinctive because when a pathologist examines an artery biopsy through a microscope, he sees granulomatous inflammation, typically containing the giant cells that give the disease its name. The inflammation is most intense in the arteries of the head and neck, especially the arteries in the temples (hence the alternative name, temporal arteritis). Arteries in the arms and chest can also be affected. Like PMR, GCA almost always develops after age 50 and becomes more common with age. Like PMR, the cause of GCA is not known. Symptoms of GCA The symptoms of GCA usually begin more gradually than those of PMR. They fall into two groups, those related to the abnormal arteries themselves, and those reflecting the whole body s response to inflammation. The most important arterial symptom is headache. That s why doctors should ask every patient with PMR if they have recently developed new or unfamiliar headaches; if the answer is yes, GCA is a serious possibility. The head pain is often most prominent over the temples, but may be less localized. Other, less common arterial symptoms include jaw pain on chewing, tongue pain, and dental or sinus discomfort. If arterial inflammation reduces blood flow to the brain, GCA can produce neurological symptoms, even including strokes. But the most feared symptom is visual loss; it occurs in about 15% of GCA patients and it may involve one eye or both, be partial or complete, and be temporary or permanent. Because of the threat of blindness, doctors consider GCA a medical emergency. General inflammatory symptoms are often very prominent. Up to 40% of patients also have full-blown PMR. Even if they don t have PMR, many GCA patients have fever, loss of appetite and of weight, and weakness and fatigue. Diagnosing GCA Most patients with GCA have high ESR and CRP readings and anemia of chronic disease. PMR shares these features; in both cases, these abnormalities are not specific or diagnostic (though their absence argues against the diagnosis). But unlike PMR, GCA also features specific diagnostic findings. When doctors examine patients with GCA, they may find thickened, beaded, tender, or pulseless arteries in the temples. A patient who has these abnormalities along with a high ESR or CRP and a typical clinical history merits immediate therapy. But if the diagnosis is less clear, duplex ultrasound imaging may reveal characteristic abnormalities in the temporal arteries. Still, the most specific test of all is a temporal artery biopsy, which may be performed on one side or both. It is invasive, but it s done under local anesthesia and is extremely safe. Treating GCA Steroid therapy is very effective; it quiets inflammation and prevents vision loss. Prednisone is the usual drug of choice. It s the same medication used for PMR, but there are two important differences in the way the two diseases are treated. The first is speed: treatment for GCA should be started as soon as possible, because while prednisone can prevent visual loss, it cannot restore vision after it has been lost. In contrast, while treatment is important in PMR, there is no element of urgency. The second November 2011 Harvard Men s Health Watch 3

4 difference is dose; PMR responds well to modest doses of prednisone, typically about 15 mg a day, while GCA requires three or four times more. That increases the risk of side effects, but when vision hangs in the balance, it s a risk well worth taking. In general, doctors continue high-dose prednisone for two to four weeks and then begin to slowly reduce the dose over the next six months to two years, providing the disease remains well controlled. More research is needed to uncover the causes of GCA and PMR and to develop better diagnostic tests. New treatments will also be welcome, but even now, steroids can preserve vision for patients with GCA and restore comfort and function for patients with PMR. That makes six little initials worth a man s attention. Atrial fibrillation: Common, serious, treatable M en who are old enough to remember the sound of windup clocks often refer to their hearts as their tickers. It s an affectionate term that pays tribute to the regular, rhythmic beat of the healthy heart. In fact, though, the healthy heart is much more sophisticated than the most precise Swiss timepiece. Instead of maintaining a single, monotonous beat, the heart can speed up in response to exercise, strong emotions, and fever. Common chemicals can also jack up the heart rate; examples include caffeine, nicotine, and decongestants. And the healthy heart can also slow down when you rest, relax, or sleep. A clock keeps a steady rate of 60 beats per minute, while your heart rate may vary between 50 and 100 beats at rest and rev up to twice as fast during exercise. But sometimes the mechanisms that regulate the rate and rhythm go awry. Doctors call these disorders arrhythmias; they come in many varieties, but the most common sustained arrhythmia of all is atrial fibrillation (AF). An age-old problem AF is a new concept for many men, but it s plagued men s hearts for millennia. In fact, the first written description dates back to China some 4,000 years ago. An English physician named William Withering discovered the first useful treatment for AF in 1785 when he gave the leaf of the foxglove plant (Digitalis purpurea) to a patient whose pulse became more full and regular. Digitalis derivatives are still in use today, but modern understanding of AF was delayed until the invention of the electrocardiograph in the early 1900s. And more than a century later, the treatment of AF continues to evolve and improve, providing important benefits to many people, but introducing many complexities for both doctors and patients. What is AF? The human heart is divided into four pumping chambers (see figure, page 5). The two upper chambers are called the atria; they collect blood from the veins, then pump it into the two ventricles, larger and stronger chambers that propel the blood out from the heart to the rest of the body. To function best, the atria should contract first, with the ventricles close behind. The electrical messages that signal the heart muscle to contract begin in the atria (at the SA node), and then travel across the AV node into the ven tricles to trigger the contractions you feel as your pulse. The entire sequence can be recorded on an electrocardiogram (ECG), where the atrial contractions appear as P waves and the ventricular contractions that follow show up as QRS complexes (see figure, page 5). When the heart is in its normal rhythm, the atria contract at steady, regular intervals. But in AF, the atria s electrical signals occur much more rapidly, often 350 to 500 times per minute. At these rates, the muscle just can t contract in a coordinated fashion. Instead of producing an atrial beat, the muscles just quiver (fibrillate) ineffectively. The ventricles are bombarded by fast, irregularly spaced atrial impulses, but they are partially protected from breakneck speed by the AV node, which intercepts the atrial impulses and blocks many of them before conducting some to the ventricles. Still, the ventricular rate is usually much faster than normal, and the rhythm is irregular, as is your pulse. On the rise AF is an old problem, but it s becoming more common. At present, between 2.3 million and 5.1 million Americans are affected, and 150,000 new cases are diagnosed each year. The consequences are enormous, including almost 400,000 hospital admissions, 5 million office visits, and health care costs of over $6.5 billion a year. Even worse, AF increases the risk of stroke fivefold and almost doubles the risk of premature death. But there is good news, too: treatment can help. What causes AF? Scientists don t fully understand the basic problems behind AF, but they do know many of the factors that increase the risk of AF. Age is an important factor; AF is uncommon before age 50, but it affects nearly 8% of men between 65 and 74 and almost 12% between 75 and 84. Gender is also important; AF occurs about 50% more frequently in men than women. Since about a third of all patients with AF have a family history of the disorder, heredity also plays a role, and several specific genetic abnormalities have already been identified. Cardiovascular conditions are strongly linked to AF. The three most important are high blood pressure, heart valve disorders (particularly mitral valve problems), and coronary artery disease (with or without a heart attack). Heart 4 Harvard Men s Health Watch November 2011

5 failure, a debilitating problem that occurs when the weakened heart muscle is unable to pump blood effectively, is another risk factor for AF. Less often, inflammation in the membrane around the heart (pericarditis) triggers AF. Lung disorders also increase the risk of AF. Culprits include chronic obstructive lung disease (see Harvard Men s Health Watch, February 2010), blood clots in the lungs (pulmonary emboli; see HMHW, April 2009), and pneumonia. Chest surgery is another cause. A wide variety of medical conditions are associated with AF. An overactive thyroid gland (hyperthyroidism) is the best known; it s what sent President George H.W. Bush into AF (and into the Bethesda Naval Hospital) in 1991, and even high-normal thyroid activity predisposes one to AF. Diabetes and obesity increase risk, as do medications such as bronchodilators used for asthma and COPD, decongestants, steroids, and nonsteroidal anti-inflammatory drugs. Behavioral factors are also tied to AF. Always a villain, smoking is on the hit list. Moderate drinking does not lead to AF, but excessive alcohol consumption does, particularly in the setting of binge drinking. Anger and hostility boost the risk of AF in men. Surprisingly, perhaps, caffeine does not appear to be a risk factor. Although vigorous exercise sometimes triggers AF in young men, walking and other moderate physical activities provide long-term protection. Some studies suggest that taking statin drugs or eating fish may reduce the risk of AF over the long run, while others do not. Beta blockers, ACE inhibitors, and angiotensin-receptor blockers (ARBs) appear to reduce the risk of AF in patients with hypertension. Classification There are several ways to categorize AF. In one system, it s called primary AF when the problem originates in the heart itself, and secondary AF when it results from a noncardiac medical condition, in which case the AF often resolves when the underlying problem is corrected. AF: Up close and personal A. Normal sinus rhythm Coordinated activity in atria Sinus node Right atrium B. Atrial fibrillation Chaotic activity in atria 2011 Harriet Greenfield Right ventricle Left atrium Left ventricle When primary AF occurs in a structurally normal heart, it is called lone AF, which carries a relatively low risk of complications. Other types of primary AF, however, can be more troublesome. Another classification system for AF depends on the frequency and duration of the arrhythmia: paroxysmal AF recurrent episodes of AF that end within seven days without treatment. Most bouts of paroxysmal AF end in less than 24 hours, but even though episodes are brief, patients are still at risk of stroke. persistent AF episodes that last longer than seven days or require treatment to convert back to a normal heart rhythm. The longer an episode lasts, the harder it is to restore a normal rhythm. permanent AF AF that has lasted longer than a year. Normal sinus rhythm QRS Electrocardiogram (ECG) 25 squares = 1 second In normal sinus rhythm, the sinus node initiates the electrical activity that triggers each heartbeat. The electrical impulse travels through the atria, signaling the muscle to contract; each atrial contraction shows on the ECG as a p wave. The electrical activity then crosses into the ventricles, stimulating them to contract and pump blood to the body s tissues (shown in ECG as the QRS complex). Atrial fibrillation p In atrial fibrillation, the atria s electrical signals are very rapid and erratic; the atria don t contract and there is no p wave. Without a coordinated signal to guide them, the ventricles contract at a rapid rate in an irregular rhythm. Symptoms The symptoms of AF vary widely. They tend to be more severe in older people and in those who also have structural heart or lung disease. Men who are in good general health may not even be aware of the arrhythmia. Others notice a fluttering sensation in the chest or a rapid and/or irregular heartbeat. Fatigue, increased nighttime urination, shortness of breath, and exercise intolerance are common and can be severe in patients who had weakened hearts or diseased lungs even before AF hit. Lightheadedness, confusion, and sometimes even fainting may signal a substantial fall in blood pressure due to AF. Patients with coronary artery disease may suffer angina or a heart attack when they develop AF. Because AF reduces the heart s pumping capacity, fluid can build up November 2011 Harvard Men s Health Watch 5

6 in the legs or lungs, particularly if the patient had some degree of heart failure even before the onset of AF. Diagnosis Doctors suspect AF when they hear an irregular heartbeat or feel an irregular pulse; a standard electrocardiogram, or ECG (see figure, page 5), will confirm the diagnosis if the patient is tested during an episode of AF. But if the AF is paroxysmal, or intermittent, a doctor may ask his patient to wear a Holter monitor or event monitor at home; these are small devices that record ECG tracings continuously (Holter) or intermittently (event) to docu ment brief or episodic arrhythmias. Diagnosing AF is relatively easy, but testing doesn t stop there. In most cases, doctors will order an echocardiogram or cardiac ultrasound to evaluate the heart s valves and muscular contractions; an advanced type of ultrasound, the transesophageal echocardiogram, may be used to evaluate stroke risk. Blood tests to measure thyroid, kidney, and liver function and red blood cell levels are important. Many patients benefit from additional lung or heart studies. Diagnosing AF may be relatively easy, but deciding how to treat it can be quite difficult. To understand your therapeutic options, you should first understand why AF needs treatment. The hazards of AF Patients with AF are at risk for three major complications: heart failure, angina, and stroke. AF reduces the heart s pumping capacity. Although the atria are small chambers with relatively weak muscles, they still contribute a kick or boost to the larger, more powerful ventricles. In addition, the rapid heart rate of AF reduces the efficiency of each beat. In all, AF reduces the heart s pumping capacity by 10% to 30%. People whose hearts are otherwise healthy can compensate for this impairment, but those with damaged heart muscles or valves cannot. As a result, they experience the fatigue, breathlessness, exercise intolerance, and swelling of the feet and legs that are so characteristic of heart failure. AF can also trigger the chest pain of angina or a heart attack in patients with coronary artery disease. The other major complication of AF is stroke. Although doctors have studied AF for over 100 years, the risk of stroke was not fully appreciated until the 1980s, when the Framingham Heart Study reported that 24% of its stroke patients were also in AF, and that the abnormal heart rhythm developed within the six months preceding the stroke in about a third of these participants. AF quintuples the risk of stroke. It accounts for about 15% of all strokes and for nearly a quarter of all strokes in people ages 80 to 89. How does a cardiac abnormality cause brain damage? Since fibrillating atria don t contract, they contain relatively stagnant pools of blood. Clots (thrombi) form in these areas, then break off and travel to the brain, where they block small arteries, depriving the brain of its vital oxygen and causing tissue damage and death. It s a devastating sequence of events, but it can be prevented by anticoagulants, medications that fight blood clots. In fact, the use of anticoagulants is one of the key priorities in the management of patients with AF. The others are slowing the heart rate and, in some patients, restoring a normal heart rhythm. Slow or steady? Since the dangerous complications of AF result from its abnormal rhythm, logic dictates that restoring a normal rhythm would be the highest priority of therapy. Cardiologists understand that logic, but they also know that clinical trials are necessary to find out if theory translates into reality. Between 2000 and 2008, six independent, high-quality clinical trials randomly assigned patients with AF to one of two treatment groups. In one group, the goal of therapy was to control the heart rate while tolerating the irregular rhythm; in the other, the goal was to restore and maintain a normal rhythm when possible. A similar, very high percentage of patients in both groups received the recommended anticoagulant therapy to prevent strokes. A total of 6,615 patients volunteered for the six trials. Despite differences in the patient groups and the methods used to achieve rate or rhythm control, all the trials arrived at the same conclusion: rhythm control does not produce better results than rate control in terms of survival, cardiac complications, or relief of symptoms. In fact, the rhythm control strategy was associated with a higher rate of hospitalizations and greater expense. Why did rhythm control morph from no-brainer to no benefit? Restoring and maintaining normal rhythm is no small feat. It typically involves medications and may require additional procedures ranging from an electric shock to heart surgery (see page 7). Slowing a racing heart requires medications, too, but they are safer and produce fewer side effects than the specialized drugs used for rhythm control. And since most AF patients require anticlotting medication even after normal rhythm is restored, the rhythm control strategy does not even have the advantage of reducing the burden of anticoagulation. These important randomized clinical trials suggest that rate control may be the first choice for many, even most, patients with AF. Still, some may benefit from rhythm control. Likely candidates include individuals who are diagnosed promptly after the onset of AF, patients with a first episode of AF, patients with AF triggered by a medical problem that has been corrected, younger people, and those who continue to have troublesome symptoms despite rate control. And if these considerations are not complex enough, there are several ways to slow rapid AF and many, many options for rhythm control. Here s a brief rundown. Reining in rapid rates Medication can slow down the racing heartbeat in nearly all patients with AF. 6 Harvard Men s Health Watch November 2011

7 The most useful drugs are beta blockers (such as propranolol and metoprolol) and calcium-channel blockers (such as diltiazem and verapamil); even so, digoxin (the modern version of the foxglove plant first used for AF over 225 years ago) still has a role in select patients. Some patients with an abnormal electrical pathway in their hearts (the WPW syndrome) respond to amiodarone. Patients who have chest pain or shortness of breath can receive rate-controlling medications intravenously; most respond in minutes to hours. Oral medications take longer to kick in, but most patients with sustained AF require long-term oral medications to maintain heart rate control. Although precise heart rate targets have not been established, many doctors adjust medications to achieve a heart rate of about 60 to 80 beats per minute when the patient is at rest and about 90 to 115 during moderate exercise. However, a recent study found that lenient heart rate control with a target resting rate of up to 110 beats per minute is just as beneficial as stricter target heart rates. Restoring normal rhythm The fastest and most effective way to convert AF back to a normal heart rhythm is to jolt the heart with an electric shock. Electrical cardioversion sounds shocking, even drastic, but since it uses only a small, brief pulse of DC current, it is really quite safe and since patients are sedated, it s only mildly uncomfortable. Electrical cardioversion is most likely to succeed when used soon after the onset of AF. To prevent stroke, nearly all patients who have been in AF for more than 48 hours should have three to four weeks of anticoagulation (see below) prior to cardioversion, and nearly all benefit from at least four weeks of anticoagulation after the procedure. Anticoagulation should be continued indefinitely in patients at moderate to high risk of stroke, even if they maintain a normal rhythm. Drugs can also be used to convert patients from AF to a normal rhythm, and long-term medication may be needed to preserve a normal rhythm after successful electrical or pharmacological cardioversion; long-term anticoagulation is also generally necessary. The choice of medication is tricky, and antiarrhythmic medications can have severe side effects, even including serious arrhythmias. As a result, while primary care physicians often manage rate control, rhythm control is best guided by cardiologists. Amiodarone is frequently the drug of choice. Dronedarone is a similar but more expensive medication; although it once appeared safer, serious side effects have been reported recently. Other specialized drugs that may be useful include sotalol, flecainide, and propafenone. Some carefully selected patients with recurrent bouts of AF can take a single dose of flecainide or propafenone on their own (the pill-in-the-pocket approach) to convert AF as soon as they notice the irregular heartbeat of AF. Cardiologists don t give up easily, and they have developed a new treatment for patients who do not respond to electrical or pharmacologic cardioversion and continue to have symptoms from AF despite rate control. The idea is to destroy a tiny amount of tissue in or near the heart to stop it from sending out the abnormal electrical signals that trigger AF. First, patients undergo sophisticated testing to detect and map the offending tissue. Next, doctors thread a tiny catheter, or tube, through a blood vessel in the groin up into the heart. When the tip of the catheter is up against the offending tissue, which is usually in or near the pulmonary veins, a radiofrequency electrical current is passed through the catheter to destroy, or ablate, the target. Radiofrequency ablation is a relatively new and tricky procedure that is only available at specialized cardiac centers. Short-term results have been promising, but relapses of AF mount over the years; more research is needed. And doctors continue to develop additional treatments for patients who need more help; examples include approaches that involve pacemakers and even surgery (the Cox maze and mini-maze operations). These new developments offer help to the relatively small number of patients who need cutting-edge therapy. But for most patients with AF, the most important step of all is to use simple anticlotting medications to prevent stroke. Preventing stroke Most patients with AF feel fine once their heart rate is controlled. But their well-being is deceptive, since they are still at risk for stroke. The risk is particularly high in older patients, in patients with hypertension, and especially in patients with previous strokes or heart valve disease, particularly an artificial valve or narrowing of the mitral valve (mitral stenosis). Fortunately, anticoagulants ( blood thinners ) can help protect AF patients from stroke. Three choices are currently available. Aspirin is the simplest, safest, and least expensive, but it is also the least effective, reducing the risk of stroke by about 20%. Warfarin (Coumadin) reduces the risk of stroke by about 60%. It has been the mainstay of therapy for decades, but it requires careful attention to medications and dietary factors that affect therapy as well as frequent adjustments in dose, based on the results of blood tests performed every two or three weeks. Dabigatran (Pradaxa), a major new option, was approved for use in the U.S. in October Dabigatran is at least as effective and safe as warfarin, and it does not require the dietary restrictions and frequent blood tests that make warfarin therapy tricky and inconvenient. On the downside, dabigatran therapy requires two pills a day, and because it is new, long-term results are not known. Dabigatran is also much more expensive than warfarin and, unlike warfarin (which can be reversed by vitamin K), there is no way to rapidly counter its anticoagulant effect. Patients with severe liver or kidney disease, recent strokes, November 2011 Harvard Men s Health Watch 7

8 Atrial fibrillation (continued) or artificial or severely diseased heart valves should not use dabigatran. Rivaroxaban (Xarelto) is similar to dabigatran; it has already been approved in the U.S. to prevent blood clots after hip and knee surgery, and, based on successful trials, is up for FDA approval to prevent strokes due to AF. Apixaban (Eliquis) is an even newer member of the same drug class. It has been approved in Europe, and a major 2011 American trial reported that it was safer and better than warfarin for preventing strokes in patients with AF. Which program is best for a patient with AF? The so-called CHADS2 score can help estimate the risk of stroke and guide the choice (see chart). Risk factor Points Age 75 or above 1 Diabetes 1 Heart failure 1 Hypertension 1 Previous stroke or transient ischemic attack 2 (TIA, or mini-stroke ) Patients with a CHADS2 score of 0 do not need anticoagulants; those with a score of 1 may take aspirin, warfarin, or dabigatran (or rivaroxaban or apixa ban once approved); and those with a score of 2 or higher should take warfarin or dabigatran (or rivaroxaban or apixaban), as should patients with AF and mitral stenosis or artificial heart valves. The best aspirin dose has not been determined, but most doctors recommend 81 to 325 milligrams (mg) a day. The dose of warfarin should be adjusted to maintain an INR (international normalized ratio) result of 2.0 to 3.0. The standard dose of dabigatran is 150 mg twice a day. Researchers are working hard to improve the management of AF. But for now, the tried and true will serve most patients well: slow the racing heart, consider restoring normal rhythm if symptoms persist, and reduce the risk of stroke by preventing clots. Atrial fibrillation is an old problem, but it can be treated effectively, whether by standard therapy or new innovations. on call with Harvey B. Simon, M.D., Editor Penile shortening post-prostatectomy Q I am trying to decide between a radical prostatectomy and radioactive seed therapy for my newly diagnosed prostate cancer. All the doctors I ve consulted say I have very early disease (PSA 4.9, Gleason score 6) and that I should be cured either way. I m basing my decision on side effects, but I need more information on one thing I learned about on the Internet, penile shortening. AI won t try to advise you about your choice of treatment, since there is no clear answer as to which is best. In addition to the options you re considering, many men would also consider external beam radiation therapy, and older men might consider deferred treatment or active surveillance (see Harvard Men s Health Watch, May September 2008). Penile shortening is a common consequence of the radical prostatectomy operation, but since it s of minor significance, it s not usually discussed in detail. The shortening is evident within the first 7 to 10 days after surgery, but even then, it averages less than 4/10 of an inch. Penile length often returns toward normal over the next year, particularly in men who recover erectile function. It s wise to consider the pros and cons of each treatment modality. The most important side effects are erectile dysfunction, urinary incontinence, and to a lesser degree, rectal problems. Compared to these, minor penile shortening is less likely to bother most men. That s the long and short of it. Visit the Harvard Health Blog online: By mail: Harvard Men s Health Watch 10 Shattuck St., 2nd Floor Boston, MA Send us a question for On call Harvey B. Simon, M.D., Editor, Harvard Men s Health Watch By (Please write On call in the subject line.) Because of the volume of correspondence we receive, we can t answer every question, nor can we provide 8 Harvard Men s Health Watch November 2011 personal medical advice.


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