Aortic valve stenosis

Introduction

The aortic valve is a flap-like opening located between the left side of the heart and the aorta. The aorta is the main artery carrying blood from the heart. Blood is pumped by the left ventricle across the aortic valve into the aorta and the arteries of the body. Aortic stenosis causes restricted systolic opening of the valve leaflets, with a mean transvalvular pressure gradient of at least 5-10 mmHg. When the degree of narrowing becomes significant enough to impede the flow of blood from the left ventricle to the arteries, heart problems develop.
In the Euro Heart Survey on Valvular Heart Disease, aortic valve stenosis was the most common valve abnormality. Aortic valve sclerosis is commonly defined as a focal or diffuse thickening of the aortic cusps with calcific nodules generally at the base of leaflets and transvalvular velocity at Doppler still in the normal range (Vmax <2 m/s).

Epidemiology

Prevalence

Rheumatic valve disease has declined dramatically in the United States during the past 50 years, and isolated rheumatic aortic valve is unusual in any event. With our aging population, calcific aortic stenosis accounts for the vast majority of aortic valve disease. In the elderly, mild thickening and/or calcification of a trileaflet aortic valve without restricted leaflet motion (ie, aortic sclerosis) affects about 25% of the population > 65 years of age. Calcific aortic stenosis, however, affects approximately 2% to 3% of those > 75 years. Thus not all patients with aortic sclerosis will go on to develop obstructive aortic valve disease.

Incidence

The approximate overall incidence of an anatomic bicuspid aortic valve is 1% to 2% of the population. Of these individuals, most will go on to present with aortic stenosis, while a minority will develop a regurgitant lesion. Particularly, the aortic valve sclerosis (aortic valve thickening and calcification without pressure gradient) seem to affect about one fourth of adults over 65 years of age, while the aortic valve stenosis is present in 2�9% of general population over 65 years of age; an increased prevalence of both sclerosis and stenosis with aging (48% and 4% in those over 85 years) is observed.
The relative frequency of the postinflammatory disease (i.e. post-rheumatic) decreased from 30% to 18% and the relative frequency of the bicuspid aortic valve changed from 37% to 33%; in contrast, the relative frequency of degenerative-calcific aortic stenosis (an "atherosclerotic" form of disease, see below) increased from 30% to 46%. These differences were striking in subjects older than 70 years.

Gender

Aortic stenosis due to bicuspid valves affects males three times more often than females, but late-life calcific disease of a trileaflet valve involves both sexes equally.

Age

Aortic stenosis can occur at any age (because the causes are different) but is usually asymptomatic until middle or old age. Until few years ago, aortic stenosis was considered a physiologic process related to aging without clinical relevance. However, aortic valve sclerosis is not observed in about 50% of people over 80 years old.

Causes and risk factors

A number of conditions contribute towards aortic stenosis. Three conditions that are known to cause aortic stenosis are:

Valvular causes

1. Calcification of a bicuspid valve

Bicuspid aortic valve is the most common cause of aortic stenosis in patients under age 65. Normal aortic valves have 3 thin leaflets called cusps. About 2% of people are born with aortic valves that have only 2 cusps (bicuspid valves). Although bicuspid valves usually do not impede blood flow when the patients are young, they do not open as widely as normal valves with 3 cusps. The turbulent blood flow causes excessive wear and tear leading to calcification, scarring, and reduced mobility of the valve leaflets over time. About 10% of bicuspid valves become significantly narrowed, resulting in the symptoms and heart problems of aortic stenosis.

2. Senile calcific aortic stenosis

The most common cause of aortic stenosis in patients 65 years and over is called "senile calcific aortic stenosis." With aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Once valve leaflet mobility is reduced by calcification, turbulence across the valve increases, causing scarring, thickening, and stenosis of the valve. Why this aging process progresses to cause significant aortic stenosis in some patients but not in others is not known.

3. Rheumatic fever

Rheumatic fever rarely causes isolated aortic stenosis. Rheumatic fever is a condition resulting from untreated infection by group A streptococcal bacteria. Damage to valve leaflets from rheumatic fever causes increased turbulence across the valve and more damage. The narrowing from rheumatic fever occurs from the fusion of the commissures of the valve leaflets. Rheumatic aortic stenosis usually occurs with some degree of aortic regurgitation. Under normal circumstances, the aortic valve closes to prevent blood in the aorta from flowing back into the left ventricle. In aortic regurgitation, the diseased valve allows leakage of blood back into the left ventricle as the ventricular muscles relax after pumping. These patients also have some degree of rheumatic damage to the mitral valve.

Subvalvular causes

• Subvalvular aortic stenosis
• Hypertrophic obstructive cardiomyopathy

Pathogenesis

Valvular aortic stenosis results in chronic left ventricular pressure overloading. At any stage of life, however, the natural history of aortic stenosis largely reflects the functional integrity of the mitral valve. As long as adequate mitral valve function is maintained, the pulmonary bed is protected from the systolic pressure overloading imposed by aortic stenosis. In contrast to mitral valve disease where the pulmonary circuit is directly involved, compensatory concentric left ventricular hypertrophy allows the pressure overloaded ventricle to maintain stroke volume with modest increases in diastolic pressure, and patients can remain asymptomatic for many years.Eventually, left ventricular hypertrophy results in either diastolic dysfunction with the onset of congestive symptoms or myocardial oxygen needs in excess of supply with the onset of angina.

Symptoms

Most patients with calcific aortic stenosis report knowing of a cardiac murmur for many years. Common symptoms of aortic stenosis include: coughing at night; fainting, especially with physical activity; fatigue; shortness of breath that worsens at night or with exertion; angina; and, visual impairments. Some patients may also experience exertional syncope, probably reflecting the inability to increase cardiac output and maintain blood pressure in response to vasodilation. Vasodepressor syncope, however, may be an operative mechanism in a portion of these syncopal episodes.

Signs

On physical examination, the harsh systolic diamond shaped (crescendo-decrescendo) murmur of aortic stenosis, loudest at the base of the heart and radiating to the carotids, is often, but not always, prominent. Low output states, obesity, or chronic lung disease may mask the findings. The murmur may radiate toward the cardiac apex, in which case the harsh component is lost; this finding may be mistaken for a second murmur. Other hallmarks of significant aortic valve stenosis include a single (pulmonic) component of the second heart sound and a sustained left ventricular apical impulse with a fourth heart sound. The slowly rising, low volume carotid arterial pulses of severe aortic stenosis may be noted in younger patients, but changes in arterial compliance often mask these findings in the elderly.

Assessment

Patients with typical findings of aortic stenosis should have a detailed history-taking session with inquiry into habitual activity levels and any changes in exercise tolerance. The onset of any of the classic symptoms of left ventricular outflow obstruction, namely angina, syncope, or heart failure, in a patient with valvular aortic stenosis indicates advanced valve disease and should be carefully and promptly evaluated. The severity of symptoms is not always related to the severity of the disease. In fact, people sometimes die suddenly from aortic stenosis without having had symptoms. Symptoms usually occur when the aortic valve area narrows to less than 1 square centimeter. Critical aortic stenosis is present when the valve area is less than 0.7 square centimeters.

Diagnosis

The electrocardiogram often shows changes of left ventricular hypertrophy. In rare instances, electrical conduction abnormality can also been seen.
The chest X-ray is seldom helpful, although occasionally heavy calcification of the valve or post-stenotic ascending aortic dilation may be seen.
With its widespread availability, two-dimensional and Doppler echocardiography has become the study of choice in the evaluation of patients with suspected valvular disease. Echocardiography allows assessment of the anatomy of the valve as well as chamber size and ventricular function. Doppler studies permit estimation of pressure gradients, as well as aortic valve area by employing the continuity equation.
With good quality echocardiography, cardiac catheterization is usually not required for diagnosis of patients with aortic stenosis. However, a cardiac catheterization is the gold standard in evaluating aortic stenosis. A pre-operative coronary angiography is generally performed in men over 40 years old and women over 50.

Treatment

Patients with (predominant) aortic stenosis fall into one of four categories of severity:

1. valve area > 1.2 cm2����������.mild
2. valve area 1.0 to 1.2 cm2��������.moderate
3. valve area 0.7 to 1.0 cm2��������.severe
4. valve area < 0.7 cm2����������.critical

1. Observation

Asymptomatic patients with mild to moderate aortic stenosis should have medical follow-up with regular inquiry as to changes in exercise tolerance or other symptoms. Serial echocardiographic examination should be based on an understanding of the natural history of the lesion, as outlined below. Patients should avoid strenuous activity, and particularly avoid post-prandial exertion. Infective endocarditis precautions following American Heart Association guidelines must be emphasized at each visit.

2. Antihypertensives

Hypertension occurs in about 20% to 30% of patients with mild to moderate aortic stenosis and should be managed with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers titrated slowly. Selected patients may be given modest doses of concomitant beta-blockers.
A supervised exercise tolerance test may provide helpful objective assessment in patients with echocardiographic evidence of moderate aortic stenosis who report atypical symptoms, who minimize complaints, or who are sedentary and therefore might not experience exercise intolerance. Functional limitation with inability to exercise to levels greater than 6 metabolic equivalents (METs) may, in some cases, be viewed as a "symptom." Stress testing is not advocated for patients with very severe left ventricular outflow obstruction.

2. Valve replacement

Symptomatic patients, ie, those with angina, syncope, dyspnea, with moderate, severe, or critical aortic stenosis should undergo valve replacement. Indications for aortic valve surgery include moderate aortic stenosis in patients requiring coronary bypass grafting and/or any other cardiac surgery, exercise-induced hypotension, and asymptomatic severe aortic stenosis with evidence of left ventricular dysfunction. Smoking cessation and diabetic control are mandatory after the replacement. Dental care should be completed with antibiotic prophylaxis before surgery.
The advantages and drawbacks of mechanical versus bioprosthetic valves should be discussed with the patient and his or her family. Often the choice of prosthesis is straightforward, but younger patients in particular may have special needs, which should be addressed Bioprosthetic valves offer the advantage of not requiring long-term oral anticoagulation, but have the drawback of relatively limited durability. In contrast, mechanical valves offer long-term durability, but require lifelong warfarin therapy. The generally accepted risk of serious bleeding with warfarin is on the order of 3% per year. Childbearing in women and vigorous sports activities in men are contra-indications to chronic oral anticoagulation with warfarin, and may figure importantly in the choice of valves. In general, bioprosthetic valves are preferred in patients over the age of 60 years and mechanical valves under the age of 50. Homograft aortic valve replacement with a cryopreserved cadaveric valve may offer specific advantages in patients with infective endocarditis or with disease of the aortic root. If significant narrowing of the coronary arteries is found, coronary artery bypass graft surgery (CABG) can be performed during aortic valve replacement surgery.

3. Balloon valvuloplasty

Balloon valvuloplasty is a technique that lowers the pressure across the valve by slightly enlarging the opening. This is usually done when someone is not stable enough for corrective surgery.
Current evidence indicates that calcific aortic stenosis progresses, on the average, at a rate of about 0.1 cm2 per year decline in valve area. To date, no medical therapy exists for the treatment of degenerative aortic stenosis. The possible impact of 'secondary prevention' measures, particularly lipid lowering with HMG-CoA reductase inhibitors (statins), on the progression of aortic stenosis is under investigation.

Follow up

Successful replacement of the valve restores normal blood flow. The long-term outcome is usually very good. Artificial valves wear out over a period of years. Their function is monitored, and the valves are replaced as necessary. A prosthetic heart valve commits a patient to continued infective endocarditis prophylaxis, regular cardiac follow-up, and often to continued medical therapy, including anticoagulation with warfarin for those with mechanical prostheses. Re-operation may be required for malfunction of the prosthetic valve. In addition, a small but not insignificant subset of patients may require implantation of a permanent pacemaker after valve surgery.

Prognosis and survival

Serious long-term effects of aortic stenosis without timely treatment include:

• congestive heart failure
• coronary heart disease
• enlargement of the left ventricle
• pulmonary edema
• sudden death (occurs in less than 1%)

With surgery, the patient can expect to live a normal life with necessary precautions as explained above.

Aortic aneurysm

 

 

Introduction

An aortic aneurysm is an abnormal bulge in the wall of the aorta. Enlargement of the aorta may be only mild in degree and termed "ectasia." In general, if the diameter of the aneurysm is more than 1.5 times the size of the normal aorta, it is called an aneurysm.
Although an aneurysm can develop anywhere along the aorta, abdominal aneurysms are more common than thoracic ones. An aortic aneurysm is serious because - depending on its size - it may rupture, causing life-threatening internal bleeding. The risk of an aneurysm rupturing increases as the aneurysm gets larger. The risk of rupture also depends on the location of the aneurysm. When detected in time, an aortic aneurysm can usually be repaired with surgery.

Epidemiology

Incidence

• Ruptured aortic aneurysm is the 13th leading cause of death in the US.
• More than 15,000 Americans die each year due to ruptured aneurysms, many of them needlessly.
• The number of aneurysms in the United States is increasing as the population increases.
• Many people don't even make it to the hospital, and those who do often die of complications.

Gender

Aneurysm is 5 times more common in men than in women.

Age

Clinically important aneurysms over 4 cm in diameter are present in about 1 percent of men between the ages of 55 and 64; the prevalence increases by 2 to 4 percent per decade thereafter.

Race and ethnicity

The disease is predominant in men of the white race. In black men, black and white women the incidence of aortic artery aneurysm (AAA) is identical.

Morbidity

38 to 50 percent of the AAA patients suffer from hypertension, 33 to 60% from coronary artery disease, 28% from cerebrovascular diseases and 25% from peripheral occlusive disease.

Causes and risk factors

• Age over 55 years (Risk increases with age)
• A family history of AAA is particularly concerning
• Smoking
• High blood pressure

Pathogenesis

Most aneurysms are caused by a breakdown in the proteins that provide the structural strength to the wall of the aorta. These proteins, called collagen and elastin can gradually deteriorate with age, but inflammation that is associated with atherosclerosis can accelerate this process even in younger people. There are also naturally occurring enzymes that cause the breakdown of collagen and elastin. An excess of these enzymes or other conditions that activate these enzymes may also contribute to the formation of an aneurysm, or its sudden growth. In rare cases an aneurysm may be caused by infection (mycotic aneurysms). There is still much to be learned about the cause of aneurysms and their growth, but fortunately we have successful, permanent treatments for AAA when they occur. Vascular surgeons have performed much of the basic research on aneurysm formation.

Types of Aortic Aneurysms

Aortic aneurysms are classified by shape, location along the aorta, and how they are formed.

True aneurysms and pseudoaneurysms

The wall of the aorta is made up of three layers: a thin inner layer of smooth cells called the endothelium, a muscular middle layer which has elastic fibers in it called the media, and a tough outer layer called the adventitia. When the walls of the aneurysm have all three layers, they are called true aneurysms. If the wall of the aneurysm has only the outer layer remaining, it is called a pseudoaneurysm. Pseudoaneurysms may occur as a result of trauma when the inner layers are torn apart.

Shape

• Fusiform aneurysms

Most fusiform aneurysms are true aneurysms. The weakness is often along an extended section of the aorta and involves the entire circumference of the aorta. The weakened portion appears as a generally symmetrical bulge.

• Saccular aneurysms

Occasionally an aneurysm may occur because of a localized weakness of the artery wall (saccular). Saccular aneurysms appear like a small blister or bleb on the side of the aorta and are asymmetrical. Typically they are pseudoaneurysms caused either by trauma (such as a car accident) or as the result of a penetrating aortic ulcer.

Location

• Thoracic aortic aneurysm (TAA)

A TAA is a diseased, weakened, and bulging section of the aorta in the chest. This condition, if not treated, could result in a rupture of the aorta, leading to life-threatening internal bleeding. The aneurysm may be caused by vascular disease, injury, or a genetic defect of the tissue. TAA is sometimes found in people with Marfan�s syndrome, which is characterized by many anomalies including elongated bones. It is also associated with Turner syndrome, which results from a missing X chromosome and is associated with dwarfism and arrested sexual development in addition to aortic aneurysm. TAA also can run in families independent of those two syndromes. Because it is difficult to diagnose victims often die young. People with TAA remain unaware of the risk they face because the slowly enlarging aorta does not cause any symptoms until it has reached a critical diameter. At that point, the aorta dissects or ruptures, both of which are life-threatening. Typically, the patient develops chest pain and usually goes to an emergency department to seek treatment.

• Abdominal aortic aneurysm (AAA)

More than 90% of abdominal aortic aneurysms originate below the renal arteries. The diameter is the most important predictor of aneurysm rupture with up to a 40% risk of rupture over 5 years for aneurysm > 5 cm. When they do rupture they tend to rupture leftward and posteriorly.

Symptoms and signs

Most aortic aneurysms have no symptoms. In fact, most are diagnosed on a chest X-ray or computerized tomography (CT) scan performed for evaluation of another condition, such as lung disease, or during routine exams. Symptoms may occur, however, due to the aneurysm pressing on nearby organs or tissue, or if the aneurysm leads to dissection. Symptoms of dissection include severe tearing pain in the chest or back, stroke, cold or numb extremities, or abdominal pain.

Screening

When aortic aneurysms are diagnosed early, treatment is safe and effective and the aneurysm is cured. AAA can be diagnosed by a simple ultrasound scan that can be performed in a few minutes without risk or discomfort.
Men between the ages of 65 and 75 who are or have been smokers should have a one-time ultrasound to screen for abdominal aortic aneurysm, according to a new recommendation from the U.S. Preventive Services Task Force. Nearly 70 percent of men in this age group have smoked and would benefit from routine screening to check for aneurysms.

Diagnosis

Most patients have no symptoms at the time an AAA is discovered. Aneurysms are often detected on tests that were performed for entirely different reasons. Abdominal aortic aneurysms may be diagnosed by a doctor during a physical exam, or sometimes patients notice a pulsating mass in their abdomen. The first hint of an aortic aneurysm may be an abnormal chest X-ray. Although AAA can be detected by physical examination, most are diagnosed today using an ultrasound scan or CAT scan, simple exams that are non-invasive and can be done as an outpatient. Magnetic resonance imaging (MRI) can also help. These exams also tell us about the size of the aneurysms � the key element to determine the need for treatment. Since major surgery was required in the past to repair an aortic aneurysm, that decision depended upon a comparison of the risk of rupture with risk of the surgery itself. Most doctors agree that for someone in good health, an AAA larger than 5 centimeters in diameter (about the size of a lemon) needs treatment. Smaller aneurysms may also need treatment if they cause symptoms (like back pain or abdominal pain), or tests show that the aneurysm has rapidly grown larger.

Treatment

1. Watch and wait

When detected in time, most ruptures can be prevented by repairing the aneurysms with an operation. Treatment for an aneurysm depends on its size and location and the general health of the person. If the aneurysm is small and without symptoms, a "watch-and-wait" approach may be suggested with regularly scheduled images of the aneurysm to check the size. However, if the aneurysm is large enough, or if the aneurysm is growing more than 1 centimeter per year, surgery may be the best option.
Women are more likely than men to die from aortic dissection according to one of the first studies of its kind reported. Aortic dissections may involve the ascending aorta alone, the descending thoracic and abdominal aorta alone, or the entire aorta. The risk of death depends on the extent of the dissection. It is highest for those aneurysms involving the ascending aorta. For that reason, most of these aneurysms are treated surgically as an emergency.

2. Medical treatment

Dissections of the descending thoracic aorta can often be treated with blood pressure control. The medical treatment of aortic dissection includes aggressive control of blood pressure and heart rate while the aorta heals. The risk of death with medical treatment of descending thoracic aortic dissection is about 10 percent. If surgery is required, however, the risk is higher at about 30 percent. Every effort is therefore made to treat these patients with medication.

3. Endovascular repair of AAA

Recent advances in catheter-based technologies have led to exciting new treatments for aortic aneurysms. Now, endovascular grafting technology allows surgeons to repair the AAA by delivering a graft through a small incision in the groin, rather than the traditional major open surgery. The endovascular method, approved by the FDA in 1999, allows the graft to be delivered via a catheter (tube) inserted in a groin artery. In the operating room, x-ray guidance is used for proper positioning of the graft. The graft is then expanded inside the aorta and held in place with metallic hooks rather than sutures. The hospital stay is usually only one or two days, and most patients can return to work or normal daily activities in about a week. Even patients with serious medical problems, once thought to be too sick, or too frail to have surgery for AAA, may have their aneurysm repaired using an endovascular graft. This can avoid the need for major open surgery and also eliminate the risk of fatal rupture if the AAA was not treated at all. It�s very important for patients to know that endovascular grafting may not be possible in every case. Endovascular grafts are specially manufactured and don�t �fit� for every case. Also, in many cases, standard surgery is still the best since we don�t have 50 years of experience with these newer procedures like we do with surgery. There may still be serious problems we haven�t anticipated.

4. Surgical resection

Surgery is usually required to repair an AAA, but modern, catheter-based technologies using endovascular grafts have made treatment less invasive in many cases. The combination of early diagnosis and modern treatment of aortic aneurysms can save countless lives lost due to aneurysm rupture each year.
Surgical treatment of AAA has been performed for almost 50 years and is a successful and durable procedure. In surgery the diseased part of the aorta is replaced with a Dacron or Teflon graft that is carefully matched to the normal aorta and is sewn in place by the surgeon. While ultimately curative, this operation requires a major abdominal incision and general anaesthesia, and the hospital stay averages 7-10 days for most patients. Even after uncomplicated surgery, it is often a month or two before patients can return to a full and normal life. Nevertheless, more than 90% of patients make a full recovery from surgery. After more than half a century of experience with these procedures we know that once patients have recovered, their aneurysms are permanently cured.

Follow up

Once the acute dissection has healed, adequate control of blood pressure may eliminate the need for surgery. Lifelong monitoring of diameter of the aorta is required because a previously dissected descending thoracic aorta may enlarge and rupture.

Prognosis and survival

Because the abdominal aorta is such a large blood vessel, a ruptured abdominal aneurysm is a life-threatening event. Fortunately, not all aneurysms rupture. Many grow very slowly and cause no symptoms or problems for many years. However, all have the potential to rupture and thus must be identified and treated or watched very carefully. The combination of earlier diagnosis with safer, simpler, and ever more successful treatments can prevent needless deaths due to ruptured abdominal aortic aneurysms. Timely suspicion and consultation with the family doctor and a simple ultrasound test can tell whether a person has aneurysm.
The length of the operation and the risks involved depends on the extent of the repair required, and on the patient's general health. Recovery time varies. Most people need at least a month or six weeks to recover from aneurysm surgery. The length of the hospital stay depends on the patient's condition and the operation performed, but it is typically a week.
Although endovascular surgery reduces recovery time to a few days, it still carries risk. And because the procedure is fairly new, long-term results are unknown. Complications can occur with this procedure, namely blood leaking from the graft, known as endoleak. For this reason, patients who have repair of their aortic aneurysms with stent-grafts are initially required to return for monitoring every six months.

Recent news and research

Cocaine users in their mid-40s are found to have more than four times the risk of coronary artery aneurysms as non-users as per the Journal of the American Heart Association. It is believed that cocaine predisposes to coronary artery aneurysms, and then the aneurysms themselves may predispose to heart attacks.
The Food and Drug Administration has approved a new device called GORE TAG Endoprosthesis System that is intended to prevent ruptures of descending thoracic aneurysms by making a new path for blood flow. It is the first endovascular grafting system approved to treat aneurysms of the thoracic aorta.

Benign Prostatic Hypertrophy Treatment & Management

Approach Considerations

Patients with mild symptoms (IPSS/AUA-SI score < 7) or moderate-to-severe symptoms (IPSS/AUA-SI score ≥8) of benign prostatic hyperplasia (BPH) who are not bothered by their symptoms and are not experiencing complications of BPH should be managed with a strategy of watchful waiting. In these situations, medical therapy is not likely to improve their symptoms and/or quality of life (QOL). In addition, the risks of treatment may outweigh any benefits. Patients managed expectantly with watchful waiting are usually re-examined annually.
Transurethral resection of the prostate (TURP) has long been accepted as the criterion standard for relieving bladder outlet obstruction (BOO) secondary to BPH. In current clinical practice, most patients with BPH do not present with obvious surgical indications; instead, they often have milder lower urinary tract symptoms (LUTS) and, therefore, are initially treated with medical therapy.
The era of medical therapy for BPH dawned in the mid 1970s with the use of nonselective alpha-blockers such as phenoxybenzamine. The medical therapeutic options for BPH have evolved significantly over the last 3 decades, giving rise to the receptor-specific alpha-blockers that comprise the first line of therapy.

Alpha-1–Receptor Blockade in Benign Prostatic Hyperplasia

A significant component of LUTS secondary to BPH is believed to be related to the smooth-muscle tension in the prostate stroma, urethra, and bladder neck. The smooth-muscle tension is mediated by the alpha-1-adrenergic receptors; therefore, alpha-adrenergic receptor–blocking agents should theoretically decrease resistance along the bladder neck, prostate, and urethra by relaxing the smooth muscle and allowing passage of urine.
BPH is predominantly a stromal proliferative process, and a significant component of prostatic enlargement results from smooth-muscle proliferation. The stromal-to-epithelial ratio is significantly greater in men with symptomatic BPH than in those with asymptomatic BPH.
The 3 subtypes of the alpha-1 receptor include 1a, 1b, and 1c. Of these, the alpha-1a receptor is most specifically concentrated in the bladder neck and prostate. Provided that the alpha-1a subtype is predominant in the prostate, bladder neck, and urethra, but not in other tissues, drugs that are selective for this receptor (ie, tamsulosin) may have a potential therapeutic advantage.
Tamsulosin is considered the most pharmacologically uroselective of the commercially available agents because of its highest relative affinity for the alpha-1a receptor subtype. In 2008, the US Food and Drug Administration (FDA) approved a new alpha-1a receptor selective blocker, silodosin (Rapaflo). It is indicated for treatment of the signs and symptoms of BPH.
The efficacy of the titratable alpha-blockers doxazosin and terazosin (Hytrin) is dose-dependent. Maximum tolerable doses have not been defined for any alpha-blocker; however, the higher the dose, the more likely the adverse events (orthostatic hypotension, dizziness, fatigue, ejaculatory disorder, nasal congestion). Despite the requirement for dose titration and blood pressure monitoring, these older, often less costly, alpha-blockers appear to be equally effective to tamsulosin and alfuzosin, and the 2010 AUA guidelines state that they remain reasonable choices for patients with moderate-to-severe LUTS due to BPH.^[2]
An approximately 4- to 6-point improvement is expected in IPSS/AUA-SI scores when alpha-blockers are used. Interestingly, alpha-blocker therapy has not been shown to reduce the overall long-term risk for acute urinary retention (AUR) or BPH-related surgery.^[7]
Hellstrom and Sikka reported in 2006 that the acute administration of tamsulosin effects ejaculatory function and ejaculate volume. Nearly 90% of study subjects experienced decreased ejaculate volume, and approximately 35% experienced anejaculation. In their study, subjects treated with alfuzosin or placebo did not experience anejaculation.^[8]

Alpha-adrenergic receptor blockers

The alpha-blocking agents administered in BPH studies can be subgrouped according to receptor subtype selectivity and the duration of serum elimination half-lives, as follows:

• Nonselective alpha-blockers - phenoxybenzamine
• Selective short-acting alpha-1 blockers - prazosin, alfuzosin, indoramin
• Selective long-acting alpha-1 blockers - terazosin, doxazosin, slow-release (SR) alfuzosin.
• Partially subtype (alpha-1a)–selective agents – tamsulosin, silodosin

Nonselective alpha-blockers

Phenoxybenzamine was the first alpha-blocker studied for BPH. It is nonselective, antagonizing both the alpha 1- and alpha 2-adrenergic receptors, which results in a higher incidence of adverse effects. Because of the availability of more alpha-1-receptor–specific agents, phenoxybenzamine is currently not often used for the treatment of BPH. The 2010 update to the AUA guideline for BPH retains the statement that insufficient data exist for a recommendation of phenoxybenzamine or of prazosin for treatment of LUTS secondary to BPH. This statement was originally published in the 2003 AUA BPH guidelines.^[2]

Phosphodiesterase-5 enzyme inhibitors

Statistically significant symptomatic improvements have been reported for patients with BPH receiving tadalafil. It has also been approved for the treatment of simultaneous BPH and erectile dysfunction (ED). Phosphdiesterase-5 (PDE5) inhibitors are known to mediate smooth muscle relaxation in the lower urinary tract.

Intraoperative floppy iris syndrome

Intraoperative floppy iris syndrome (IFIS) is characterized by miosis, iris billowing, and prolapse in patients undergoing cataract surgery who have taken or currently take alpha-1-blockers. It is particularly prevalent among patients taking tamsulosin. The 2010 AUA guideline recommends that clinicians ask patients about planned cataract surgery when offering alpha-blocker therapy for LUTS due to BPH. Alpha-blockers should not be initiated until cataract surgery is completed.^[2] Patients currently on alpha-blocker therapy must disclose this to their ophthalmologist prior to cataract surgery so that the appropriate preoperative and intraoperative precautions can be taken. Experienced ophthalmologists can thereby reduce the risk of complications from IFIS.^{[9, 2]}
In a review by Bell et al, exposure to tamsulosin within 14 days of cataract surgery was significantly associated with serious postoperative ophthalmic adverse events, specifically IFIS and its complications (ie, retinal detachment, lost lens or fragments, endophthalmitis). No significant associations were noted with exposure to other alpha-blocker medications or to previous exposure to tamsulosin or other alpha-blockers.^[10]

5-Alpha-Reductase Inhibitors in Benign Prostatic Hyperplasia

Hormonal medical management emerged from the discovery of a congenital form of pseudohermaphroditism secondary to DHT deficiency (due to a lack of 5-alpha-reductase activity). This deficiency produced a hypoplastic prostate. The two types of 5-alpha-reductase include type 1 (predominantly located in extraprostatic tissues, such as skin and liver) and type 2 (predominant prostatic reductase).
Inhibition of 5-alpha-reductase type 2 blocks the conversion of testosterone to DHT, resulting in lower intraprostatic levels of DHT. This leads to inhibition of prostatic growth, apoptosis, and involution. The exact role of 5-alpha-reductase type 1 in normal and abnormal prostatic development is undefined. 5-Alpha-reductase inhibitors improve LUTS by decreasing prostate volumes; thus, patients with larger prostates may achieve a greater benefit. Further, maximal reduction in prostate volume requires 6 months of therapy.

5-Alpha reductase inhibitors

Finasteride (Proscar), a 4-aza-steroid, has demonstrated 5-alpha type II–blocking activity, resulting in the inhibition of DHT-receptor complex formation. This effect causes a profound decrease in the concentration of DHT intraprostatically, resulting in a consistent decrease in prostate size. One third of men treated with this agent exhibit improvements in urine flow and symptoms.
Dutasteride (Avodart) has an affinity for both type 1 and type 2 5-alpha-reductase receptors. The significance of blockage of type 1 receptors is currently unknown.
Both finasteride and dutasteride actively reduce DHT levels by more than 80%, improve symptoms, reduce the incidence of urinary retention, and decrease the likelihood of surgery for BPH. Adverse effects are primarily sexual in nature (decreased libido, erectile dysfunction, ejaculation disorder).
Both finasteride and dutasteride may reduce serum prostate-specific antigen (PSA) values by as much as 50%. The decrease in PSA is typically maximally achieved when the maximal decrease in prostatic volume is noted (6 months). Thus, one must take this into account when using PSA to screen for prostate cancer.
One prospective, randomized, double-blind study by the Enlarged Prostate International Comparator Study (EPICS) was conducted to compare the efficacy of dutasteride to that of finasteride in men with symptomatic BPH. While this study was conducted over the course of only one year, the data suggest that both of these drugs were similarly effective in reducing prostate volume, improving Qmax, and LUTS for this population. The long-term outcomes are yet to be investigated.^[11]
Because these drugs interfere with the metabolism of testosterone, they are contraindicated in children and pregnant females. In addition, pregnant females or those who are considering conception should not handle crushed or broken tablets because of the potential for absorption and subsequent potential risk to a male fetus.
In patients with LUTS and enlarged prostates, 5-alpha-reductase inhibitors are believed to be appropriate and effective treatment.

5-Alpha reductase inhibitors and prostate cancer

On June 9, 2011, the US Food and Drug Administration announced revisions to the prescribing information for 5-alpha reductase inhibitors (5-ARIs). These agents include finasteride (Proscar, Propecia) and dutasteride (Avodart, Jalyn). 5-ARIs are indicated for benign prostatic hypertrophy and alopecia.
Data from 2 large, randomized, controlled trials observed an increased risk of being diagnosed with a more serious form of prostate cancer (high-grade prostate cancer) in trial participants taking 5-ARIs. The 2 trials are the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial. Both of these trials observed a decreased incidence of prostate cancer overall when preventive treatment included 5-ARIs, but an increased incidence of high-grade prostate cancer in men taking dutasteride or finasteride compared with placebo.^{[12, 13]}
The revised prescribing information recommends that prior to initiating therapy with 5-ARIs, perform appropriate evaluations to rule out other urological conditions, including prostate cancer, that might mimic benign prostatic hyperplasia (BPH).

Next Section: Combination Therapy

Combination Therapy

The alpha-1-receptor blockers provide rapid relief, while the 5-alpha-reductase inhibitors target the underlying disease process.^[7] The Medical Therapy of Prostatic Symptoms (MTOPS) trial demonstrated that combination therapy reduced the risk of progression and produced a greater improvement in IPSS than therapy with finasteride or doxazosin alone. The risks of AUR and BPH-related surgery were reduced with combination therapy or finasteride in comparison with doxazosin monotherapy.^[14]
The Symptom Management After Reducing Therapy (SMART-1) trial demonstrated that after 6 months of combination therapy, discontinuation of the alpha-1-blocker is possible in men with moderate LUTS. However, those with severe LUTS may require longer combination therapy.^[14]

Anticholinergic Agents

Historically, anticholinergics were discouraged in men with BPH because of concerns of inducing urinary retention. Trials have demonstrated a slight increase in PVR; however, AUR rates were low. Importantly, these trials consisted of patients with low baseline PVR.
The 2010 AUA BPH guidelines recommend anticholinergic agents for management of LUTS in patients who do not have an elevated PVR and whose LUTS are primarily irritative. Baseline PVR should be obtained prior to initiation of anticholinergic therapy, to assess for urinary retention.^[15] Caution with anticholinergics is recommended with patients whose PVR is greater than 250-300 mL.^[2]

Landmark Clinical Trials

Numerous phase II and phase III trials of drugs used in the treatment of BPH have been conducted. A few landmark studies are selected below.
The Proscar Long-Term Efficacy and Safety Study (PLESS), patients treated with finasteride (5 mg/d) were at a significantly lower risk of developing AUR or needing surgery.^[16] This was a multicenter, 4-year, double-blind, placebo-controlled study of 3,040 men. Men with PSA levels of more than 10 ng/mL and those with prostate cancer were excluded.
The Medical Therapy of Prostatic Symptoms (MTOPS) trial demonstrated that combination therapy with doxazosin and finasteride was well tolerated, and was superior to placebo and monotherapy with either agent. The primary endpoints of the study were reduction in AUA-SI score, AUR, recurrent infections, renal insufficiency, incontinence, changes in flow, and PSA level and a lower rate of invasive treatments. MTOPS was a multicenter, 4- to 6-year, double-blind, randomized, placebo-controlled trial of 3,047 men with symptomatic BPH.^[17]
In the Alfuzosin Long-Term Efficacy and Safety Study (ALTESS), alfuzosin (10 mg/d) decreased the risk of LUTS deterioration and significantly improved QOL and peak urinary flow rate. ALTESS was a 2-year, double-blind, placebo-controlled study of 1,522 men. Notably, these men had greater risk factors for BPH progression (ie, older age, higher IPSS scores, larger prostate size, lower Qmax, and higher PVR) than those in the MTOPS trial. Alfuzosin did not reduce the risk of AUR but tended to reduce the risk of surgery.^[18]
In the international real-life practice study of alfuzosin once daily (ALF-ONE), 3 years of alfuzosin (10 mg/d) decreased IPSS by one third, with significant improvements in nocturia and bother score. ALF-ONE was conducted in 689 European men with a mean age of 67.6 years. Clinical progression of worsening of IPSS (≥4 points) was seen in 12.4%, AUR in 2.6%, and requirement of BPH-related surgery in 5.7%. Alfuzosin was well tolerated, with dizziness the most common adverse effect (4.5%). Notably, symptom worsening during treatment and high PSA levels appeared to be the best predictors of clinical progression.^[19]
Four-year results in the Combination of Avodart and Tamsulosin (CombAT) study revealed that for men with prostate volumes of 30-58 mL, combination therapy with dutasteride (dual 5-alpha-reductase inhibitor) and tamsulosin (alpha-1-blocker) improved symptoms, urinary flow, and QOL better than monotherapy with either drug, although not in men who had a prostate volume of 58 mL or more.^[20] The adverse-effect profile of combination therapy was similar to that of monotherapy, although drug-related adverse events were more common with combination therapy.^[21] CombAT is a 4-year, multicenter, randomized, double-blind, parallel group study of 4,844 men aged 50 years or older with moderate-to-severe BPH symptoms (IPSS ≥12), prostate volume of 30 mL or greater, and a PSA level of 1.5-10 ng/mL. This study contributes to the standard of care shifting towards combined drug therapy in appropriately selected patients, while better defining the role of the alpha-blockers.^[15]

Phytotherapeutic Agents and Dietary Supplements

Phytotherapeutic agents and dietary supplements are considered emerging therapy by the AUA Guidelines panel and are not recommended for the treatment of BPH because of the lack of evidence at this time.
Pharmaceuticals derived from plant extracts are widely used throughout the world for the treatment of various medical ailments. In 1998, Americans spent a total of $3.65 billion on all herbal remedies. In France and Germany, plant extracts have a market share of up to 50% of all drugs prescribed for symptomatic BPH. In the United States, these agents are also popular and readily available.
The attraction to phytotherapeutic agents appears to be related to the perception of therapeutic healing powers of natural herbs, the ready availability, and the lack of adverse effects.
Most of the phytotherapeutic agents used in the treatment of LUTS secondary to BPH are extracted from the roots, seeds, bark, or fruits of plants listed below. Some suggested active components include phytosterols, fatty acids, lectins, flavonoids, plant oils, and polysaccharides. Some preparations derive from a single plant; others contain extracts from 2 or more sources.
Each agent has one or more proposed modes of action. The following modes of action are suggested:

• Antiandrogenic effect
• Antiestrogenic effect
• Inhibition of 5-alpha-reductase
• Blockage of alpha receptors
• Antiedematous effect
• Anti-inflammatory effect
• Inhibition of prostatic cell proliferation
• Interference with prostaglandin metabolism
• Protection and strengthening of detrusor

The origins of phytotherapeutic agents are as follows:

• Saw palmetto, (American dwarf palm; Serenoa repens, Sabal serrulata) fruit
• South African star grass (Hypoxis rooperi) roots
• African plum tree (Pygeum africanum) bark
• Stinging nettle (Urtica dioica) roots
• Rye (Secale cereale) pollen
• Pumpkin (Cucurbita pepo) seeds

Saw palmetto (American dwarf palm)

Extracts of saw palmetto berries are the most popular botanical products for BPH. The active components are believed to be a mixture of fatty acids, phytosterols, and alcohols. The proposed mechanisms of action are antiandrogenic effects, 5-alpha-reductase inhibition, and anti-inflammatory effects.
The recommended dosage is 160 mg orally twice daily. Studies show significant subjective improvement in symptoms without objective improvements in urodynamic parameters. Minimal adverse effects include occasional GI discomfort.
The 2010 AUA guidelines, based on more recent studies, do not detect a clinically meaningful effect of saw palmetto on LUTS. Further clinical trials are underway.^[2] In fact, in a double-blind, multicenter, placebo-controlled randomized trial at 11 North American clinical sites, saw palmetto extract was studied at up to 3 times the standard dose on lower urinary tract symptoms attributed to BPH. Saw palmetto extract was no more effective than placebo on the American Urological Association Symptom Index. No clearly attributable adverse effects were identified. Similar to the Saw Palmetto Treatment for Enlarged Prostates (STEP) study, saw palmetto was not found to be beneficial for the treatment of LUTS in men.^[22]

African plum tree (P africanum)

Suggested mechanisms of action include inhibition of fibroblast proliferation and anti-inflammatory and antiestrogenic effects. This extract is not well studied.

Rye (S cereale)

This extract is made from pollen taken from rye plants growing in southern Sweden. Suggested mechanisms of action involve alpha-blockade, prostatic zinc level increase, and 5-alpha-reductase activity inhibition. Significant symptomatic improvement versus placebo has been reported.

Treatment of Concomitant Erectile Dysfunction

It is recommended to first establish the alpha-1 blocker dose before treating the erectile dysfunction. The medication used to treat erectile dysfunction should be titrated to the lowest effective dose. Furthermore, sildenafil doses of greater than 25 mg should not be taken within 4 hours of any alpha-blocker.^{[23, 24, 25]}
In addition to treating erectile dysfunction, sildenafil may improve mild-to-moderate LUTS. Nitric oxide may mediate relaxation of the prostatic urethra and/or bladder neck. The utility of phosphodiesterase inhibitors in the treatment of LUTS has yet to be defined.^[26]
Recent trials have addressed the use of long-acting phosphodiesterase type 5 inhibitors (tadalafil) and have found them to be significantly better than placebo in improving the symptoms of BPH/LUTS.

Transurethral Resection of the Prostate

TURP is considered the criterion standard for relieving BOO secondary to BPH. The indications to proceed with a surgical intervention include the following:

• AUR
• Failed voiding trials
• Recurrent gross hematuria
• Urinary tract infection
• Renal insufficiency secondary to obstruction

Additional indications for surgical intervention include failure of medical therapy, a desire to terminate medical therapy, and/or financial constraints associated with medical therapy. However, TURP carries a significant risk of morbidity (18%) and mortality risk (0.23%). More recent techniques using bipolar cautery resection devices have lowered the morbidity associated with TURP.
TURP is performed with regional or general anesthesia and involves the placement of a working sheath in the urethra through which a hand-held device with an attached wire loop is placed. High-energy electrical cutting current is run through the loop so that the loop can be used to shave away prostatic tissue. The entire device is usually attached to a video camera to provide vision for the surgeon.
Although TURP is often successful, it has significant drawbacks. When prostatic tissue is cut away, significant bleeding may occur, possibly resulting in termination of the procedure, blood transfusion, and a prolonged hospital stay.
Irrigating fluid may also be absorbed in significant quantities through veins that are cut open, with possible serious sequelae termed transurethral resection syndrome (TUR syndrome). However, this is very rare and does not occur with saline irrigation used in bipolar devices. A urinary catheter must be left in place until the bleeding has mostly cleared.
The large working sheath combined with the use of electrical energy may also result in stricturing of the urethra.
The cutting of the prostate may also result in a partial resection of the urinary sphincteric mechanism, causing the muscle along the bladder outlet to become weak or incompetent. As a result, when the patient ejaculates, this sphincteric mechanism cannot keep the bladder adequately closed. The ejaculate consequently goes backwards into the bladder (ie, retrograde ejaculation), rather than out the penis. Additionally, if the urinary sphincter is damaged, urinary incontinence may result.
The nerves associated with erection run along the outer rim of the prostate, and the high-energy current and/or heat generated by such may damage these nerves, resulting in impotence.
TURP usually requires hospitalization.

Open Prostatectomy

This procedure is now reserved for patients with very large prostates (>75 g), patients with concomitant bladder stones or bladder diverticula, and patients who cannot be positioned for transurethral surgery.
Open prostatectomy requires hospitalization and involves the use of general/regional anesthesia and a lower abdominal incision. The inner core of the prostate (adenoma), which represents the transition zone, is shelled out, thus leaving the peripheral zone behind. This procedure may involve significant blood loss, resulting in transfusion. Open prostatectomy usually has an excellent outcome in terms of improvement of urinary flow and urinary symptoms.
More recently, laparoscopic simple prostatectomy has been performed at a number of institutions and appears to be feasible. However, prostatectomy performed in this fashion still appears to be associated with risk for significant blood loss. Experience to date with this procedure is limited.^[27]

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Next Section: Combination Therapy

Minimally Invasive Treatment

There is considerable interest in the development of other therapies to decrease the amount of obstructing prostate tissue while avoiding the above-mentioned adverse effects associated with TURP. These therapies are collectively called minimally invasive therapies.
Most minimally invasive therapies rely on heat to destroy prostatic tissue. This heat is delivered in a limited and controlled fashion, in the hope of avoiding the complications associated with TURP. They also allow for the use of milder forms of anesthesia, which translates into less anesthetic risk for the patient.
Heat may be delivered in the form of laser energy, microwaves, radiofrequency energy, high-intensity ultrasound waves, and high-voltage electrical energy. As in TURP, delivery devices are usually passed through a working sheath placed in the urethra, although they are usually of a smaller size than that needed for TURP. Devices may also simply be attached or incorporated into a urinary catheter or passed through the rectum, from which the prostate may also be accessed.
Keep in mind that many of these minimally invasive therapies are undergoing constant improvements and refinements, resulting in increased efficacy and safety. Ask urologists about the specifics of the minimally invasive therapies that they use and what results they have experienced.

Transurethral Incision of the Prostate

Transurethral incision of the prostate (TUIP) has been in use for many years and, for a long time, was the only alternative to TURP. It may be performed with local anesthesia and sedation. TUIP is suitable for patients with small prostates and for patients unlikely to tolerate TURP well because of other medical conditions. TUIP is associated with less bleeding and fluid absorption than TURP. It is also associated with a lower incidence of retrograde ejaculation and impotence than TURP.

Lasers

Lasers deliver heat to the prostate in various ways. Lasers heat prostate tissue, causing tissue death by coagulative necrosis, with subsequent tissue contraction; however, laser coagulation of the prostate in this specific sense has met with limited results.
Lasers have also been used to directly evaporate, or to melt away, prostate tissue, which is more effective than laser coagulation. Photoselective vaporization of the prostate produces a beam that does not directly come into contact with the prostate; rather, it delivers heat energy into the prostate, resulting in destruction/ablation of the prostate tissue.
Potassium-titanyl-phosphate (KTP) and holmium lasers are used to cut and/or enucleate the prostate, similar to the TURP technique. These are widely used laser techniques.
Transurethral vaporization/ablation with the KTP or holmium laser can be performed with general or spinal anesthesia and can be performed in an outpatient setting. Catheter time usually lasts less than 24 hours. Studies suggest that photoselective vaporization of the prostate can significantly improve and sustain symptomatic and urodynamic outcomes.
This procedure has been quite useful in patients who require anticoagulation for various medical conditions, since anticoagulation does not need to be interrupted for this procedure, thus further decreasing patient risk.^{[28, 29]}
Lasers may be used in a knifelike fashion to directly cut away prostate tissue (ie, holmium laser enucleation of the prostate), similar to a TURP procedure. The holmium laser allows for simultaneous cutting and coagulation, making it quite useful for prostate resection. Laser enucleation of the prostate has proved to be safe and effective for treatment of symptomatic BPH, regardless of prostate size, with low morbidity and short hospital stay.
TUR syndrome is not seen with this technique, because iso-osmotic saline is used for irrigation. Additionally, removed prostatic tissue is available for histologic evaluation, whereas vaporization/ablation technique does not provide tissue for evaluation. Holmium laser enucleation of the prostate may prove to be the new criterion standard for surgical management of BPH.^{[29, 30]}
Laser treatment usually results in decreased bleeding, fluid absorption, and length of hospital stay, as well as decreased incidence of impotence and retrograde ejaculation when compared with standard TURP. However, healing from laser treatment does not occur until after a period when dead cells slough; thus, patients may experience urinary urgency or irritation, resulting in frequent or uncomfortable urination for a few weeks.
The results of laser therapy vary from one another because not all wavelengths yield the same tissue effects. For example, interstitial lasers (eg, indigo lasers) are designed to heat tissue within the confines of the prostate gland and spread radiant energy at relatively low energy levels. They do not directly involve the urethral portion; thus, irritative symptoms following the procedure are potentially reduced.
Contact lasers such as KTP or holmium, on the other hand, are designed to cut and vaporize at extremely high temperatures They usually bring about more relief of urinary symptoms than treatment with medicines, but not always as much as is provided with TURP. However, KTP laser vaporization and holmium laser enucleation yield results that rival those of TURP.

Transurethral Microwave Therapy

The use of microwave energy, termed transurethral microwave therapy (TUMT), delivers heat to the prostate via a urethral catheter or a transrectal route. The surface closest to the probe (the rectal or urethral surface) is cooled to prevent injury. The heat causes cell death, with subsequent tissue contraction, thereby decreasing prostatic volume.
TUMT can be performed in the outpatient setting with local anesthesia. Microwave treatment appears to be associated with significant prostatic swelling; a considerable number of patients require a urinary catheter until the swelling subsides. In terms of efficacy, TUMT places between medical therapy and TURP. The 2010 AUA guidelines state TUMT is an effective option for partially relieving symptoms that may be considered in patients with moderate or severe LUTS secondary to BPH.^[31]

Transurethral Needle Ablation of the Prostate

Transurethral needle ablation of the prostate (TUNA) involves using high-frequency radio waves to produce heat, resulting in a similar process of thermal injury to the prostate as previously described. A specially designed transurethral device with needles is used to deliver the energy.
TUNA can be performed under local anesthesia, allowing the patient to go home the same day. Similar to microwave treatment, radiofrequency treatment is quite popular, and a number of urologists have experience with its use. Radiofrequency treatment appears to reliably result in significant relief of symptoms and better urine flow, although not quite to the extent achieved with TURP. The 2010 AUA guideline update considers TURP an appropriate and effective treatment option for moderate or severe LUTS.^[2]

High-Intensity Ultrasound Energy Therapy

High-intensity ultrasound energy therapy delivers heat to prostate tissue, with the subsequent process of thermal injury. High-intensity ultrasound waves may be delivered rectally or extracorporeally and can be used with the patient on intravenous sedation. Urinary retention appears to be common with its use.
High-intensity ultrasound energy also produces moderate results in terms of improvement of the urinary flow rate and urinary symptoms, although its use is now relatively limited compared with the more popular TUNA and TUMT.
High-intensity ultrasound is considered investigational at this time and should not be offered outside of clinical trials.

Mechanical Approaches

Mechanical approaches are used less commonly and are usually reserved for patients who cannot have a formal surgical procedure. Mechanical approaches do not involve the use of energy to treat the prostate.
Prostatic stents are flexible devices that can expand when put in place to improve the flow of urine past the prostate. Their use has been associated with encrustation, pain, incontinence, and overgrowth of tissue through the stent, possibly making their removal quite difficult. To date, their full role and long-term effects are not fully known.

Diet

Data from the Prostate Cancer Prevention Trial revealed that a diet low in fat and red meat and high in protein and vegetables may reduce the risk of symptomatic BPH. Additionally, regular alcohol consumption was associated with a reduced risk of symptomatic BPH, but this is to be interpreted cautiously given the untoward effects of excessive alcohol consumption.^[32]

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Long-term Monitoring

Patients with BPH who have symptoms significant enough to be placed on medication should be evaluated during office visits to discuss the efficacy of the medication and potential dose adjustment. These visits should take place at least biannually. Patients should undergo DRE and PSA screening at least annually.