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Severe Aortic Stenosis

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The aortic valve is one of four valves in the human heart. It is located between the left ventricle and aorta. In 99% of the population, it is trileaflet in structure. Two primary disease processes can affect the aortic valve: aortic insufficiency and aortic stenosis. In aortic insufficiency, blood flows back into the left ventricle from the aorta during the relaxation phase (diastole) due to a leaky valve. Aortic stenosis creates a pressure gradient during contraction (systole) between the left ventricle and aorta due to the valve failing to open fully.1

According to the American Heart Association, more than 5 million Americans are diagnosed with valvular heart disease each year. More than 5% of the population has diseases of the aortic and mitral valve. An estimated 1.5 million people in the United States are affected by aortic stenosis, and approximately 500,000 of them have the severe form. Nearly half of these people are symptomatic.2 Aortic stenosis is an insidious disease with a long latency period of 10 to 20 years followed by rapid progression after appearance of symptoms. This results in a high mortality rate of approximately 50% in the first 2 years, if left untreated.3

Etiology

In adults, three conditions cause aortic stenosis: progressive wear and tear of a congenital bicuspid aortic valve; degenerative breakdown with aging; and scarring of the valve due to rheumatic disease. The most common cause is degenerative, also known as senile calcific aortic stenosis. During the aging process, protein collagen of the valve leaflets is replaced with calcium deposits. The calcium deposits causes scarring, thickening and stenosis of the valve, resulting in increased pressure across the valve.4

Risk factors associated with aortic stenosis include hypertension, hypercholesterolemia, diabetes mellitus and smoking.5 Why the aging process of calcification causes severe aortic stenosis in some people and not others is unknown, and it does not correlate with healthy lifestyle choices.4

 

Symptoms and Evaluation

Symptoms of aortic stenosis are directly related to the degree of narrowing of the aortic valve area. When the narrowing causes a greater than 50% reduction in the valve area, left ventricular pressure increases. This results in heart muscle thickness, stiffness, left ventricular dilatation, a decrease in cardiac output, and heart failure. The resulting classic symptoms of chest pain, syncope and heart failure occur. Chest pain is the first symptom and it eventually occurs in half of patients  with aortic stenosis. The syncope associated with aortic stenosis is secondary to the relaxation of blood vessels, causing the blood pressure to drop with the inability for the heart with aortic stenosis to compensate. This results in reduced blood flow to the brain. In addition, syncope can occur due to arrhythmias. Shortness of breath from heart failure occurs because the heart muscle is unable to compensate for the extreme pressure in aortic stenosis.4

Asymptomatic  patients with severe aortic stenosis have an excellent prognosis for survival, with a death rate less than 1% per year. However, the prognosis for symptomatic severe aortic stenosis patients is poor, with more than 50% of deaths occurring suddenly.5

Identifying patients with aortic stenosis requires careful history taking, physical examination and diagnostic testing. On physical exam, an ejection systolic murmur of aortic stenosis is best heard at the base of the heart with radiation to the carotids.6

Important tests used in diagnosing and evaluating aortic stenosis include: electrocardiogram, which can reflect a thickened heart muscle; chest x-ray, which may demonstrate aortic dilatation above the valve; echocardiogram that uses ultrasound to evaluate heart muscle and valves; and cardiac catheterization. Cardiac catheterization is the gold standard for evaluating aortic stenosis and provides pressure measurements simultaneously on both sides of the valve. A normal valve area is 3.0 cm2 and severe aortic stenosis is a valve area less than 0.7 cm2.4

Patients with aortic stenosis may not exhibit symptoms for several years. It is important for patients to be aggressively treated for underlying risk factors. A cardiologist should monitor for progression and identify when more aggressive treatment is needed.

 

Treatment

When the patient with severe aortic stenosis starts experiencing the classic symptoms of chest pain, syncope or shortness of breath, the prognosis is poor. Medical therapy such as the use of diuretics to treat heart failure provides only temporary relief.4 Surgical replacement of the aortic valve relieves symptoms and improves survival. This procedure has a low mortality rate in patients without serious coexisting conditions.3 The overall mortality rate is approximately 5%. Replacement valves are either bioprosthetic (porcine or bovine) with a life expectance of 10 to 15 years or a mechanical valve that can last up to 40 years. A mechanical valve requires lifelong anticoagulation with warfarin to prevent clots.4

The patient population in the United States is aging, and therefore many older patients are considered high risk for surgical aortic valve replacement, resulting in significant morbidity and mortality.1 At least 30% of patients with severe symptomatic aortic stenosis do not undergo surgical replacement of the aortic valve due to advancing age, severe left ventricular dysfunction or the presence of multiple comorbities.3 For these patients, a new technology has emerged, transcatheter aortic valve replacement (TAVR). In this article, only the transfemoral approach to aortic valve replacement will be discussed.

The evaluation and management of patients who undergo TAVR is a complex multidisciplinary process that involves interventional cardiologists, cardiovascular surgeons, imaging specialists, anesthesiologists and support staff. The procedure is best performed in a specialized hybrid procedural suite that has both catheterization lab and operating room capabilities.1 Prior to undergoing the procedure, thorough assessment, including an echocardiogram with specific measurements, frailty assessment and CT scan of the lower extremities, is required. Echocardiography criteria includes severe calcified valve leaflets with reduced systolic motion and a mean gradient of greater than 40 mm Hg or jet velocity greater than 4.0 m/s. A fragility assessment is completed to provide functional status of the patient and includes the Katz ADL, grip strength, 5-minute walk, etc.

The procedure is performed in a hybrid sterile environment with the patient under general anesthesia. A bioprosthetic valve is inserted through a catheter in the femoral artery to the calcific aortic valve. The procedure is performed under guidance of transesophageal echocardiogram. The bioprosthetic valve is crimped onto a balloon catheter and advanced across the calcified aortic valve. During rapid pacing of the right ventricle, the balloon is inflated, causing deployment of the heart valve and the support frame to the aortic valve annulus and leaflets.3 Two bioprosthetic valves are available in the United States in 2014: the Edwards Sapien prosthesis and the Medtronics CoreValve system.7

 

Outcomes

The results of a large multicenter, randomized clinical trial comparing TAVR with standard therapy in high-risk and nonsurgical candidates with severe aortic stenosis found that TAVR was superior to standard therapy.3 In addition, TAVR markedly decreased the rate of death from any cause, from cardiovascular causes and hospital readmissions. Patients who underwent TAVR had a significant reduction in symptoms as assessed with a 6-minute walk test and the New York Heart Association classification system. Hemodynamic performance of the bioprosthetic valve did not demonstrate any evidence of deterioration in the first year. The TAVR procedure is not without risks. The PARTNER trial reported more neurologic events, major bleeding and major vascular complications in the TAVR group as compared to standard therapy.3

 

Recovery & Follow-up

Postprocedure, immediate extubation, early ambulation once femoral assess is stable, and careful monitoring in the intensive care unit for any complications is recommended. The continuous monitoring includes fluid balance, evaluation of renal status and cardiac rhythm disturbances. Also important in the TAVR patient is evaluation for complications of the extremities, since a large catheter is placed in the femoral artery during the procedure. This includes lower extremity insufficiency, groin hematomas, pseudoaneurysms, and retroperitoneal bleeding.

When stable, the patient should be transferred to a telemetry unit and discharged when hemodynamically stable. Medication recommendations upon discharge include the preadmission medications in addition to dual antiplatelet therapy with aspirin and clopidogrel (Plavix) for at least 6 months to prevent thrombotic complications.8

The TAVR patient should follow up with the implanting physician within 30 days. An echocardiogram is performed to identify any procedure complications. Thereafter, follow-up at 6 months and 1 year with an echocardiogram is recommended. Closer evaluation may be needed in cases of paravalvular leak evidenced on the echocardiogram or change in clinical status.8

 

Future Trends

Treatment of severe aortic stenosis has evolved rapidly since the first TAVR procedure was performed in 2002. The once high-risk, inoperable patient with symptomatic severe aortic stenosis had a 50% mortality rate at 2 years and had no options available.3

Over the last decade, new technology has had a significant impact on these patients, with good outcomes and reports of survival ranging from 69% to 85% at 1 year after TAVR.7 TAVR has become the standard of care in these high-risk patients. This treatment is just the tip of the iceberg. Broader applications of TAVR, including the next generation of TAVR bioprosthetics, are in development and will contribute to advancing the treatment of severe aortic stenosis.9

               

Mary Blade is a nurse practitioner in the Ambulatory Care/Diagnostic Cardiology department at St. Vincent's Medical Center in Jacksonville, Fla.

               

References

1. Forrest JK. Transcatheter aortic valve replacement: design, clinical application, and future challenges. Yale J Bio Med. 2012;85(2):239-247.

2. Maryland Heart Center. Surgical Treatments. U.S. Aortic Stenosis Disease Prevalence & Treatment Statistics. University of Maryland Medical Center Website. http://www.umm.edu/heart/aortic-facts.htm

3. Leon MB, et al. Transcatheter aortic-valve Implantation for aortic stenosis in patients who cannot undergo surgery. N Eng J Med. 2010;363(17):1597-1607.

4. Kulick DL, Shiel WC. Aortic Valve Stenosis. Medicine.net. http://www.medicinenet.com/script/main/art.asp?articlekey=279

5. Xiushui M. Aortic Stenosis. Medscape reference website. http://emedicine.medscrape.com/article/150638-overview

6. Braunwald E. Valvular Heart Disease. In: Braunwald's Heart Disease: A textbook of Cardiovascular Medicine. Philadelphia, PA: Elsevier Saunders; 2012: 1468-1474.

7. Webb JG, Wood DA. Current status of transcatheter aortic valve replacement. J Am Coll Cardiol, 2012;60(6):483-492.

8. Holmes DR, et al. 2012 ACCF/AATS/SCAI/STS Expert Consensus Document on Transcatheter Aortic Valve Replacement. J Am Coll Cardiol. 2012;59(13):1201-1254.

9. Hu PP. TAVR and SAVR: current treatment of aortic stenosis. Clin Med Insights Cardiol. 2012;6:125-139.

               

 

               




     

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