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Aortic stenosis

Townsend, Terri MA, RN, CCRN-CMC, CVRN-BC

doi: 10.1097/01.CCN.0000457314.79995.1c
Department: Heart Beats
Free

Aortic stenosis occurs when the aortic valve opening becomes narrowed, resulting in left ventricular outflow obstruction. The most common cause of this progressive disorder is calcification of the valve leaflets. Risk factors for calcification include: hypertension, dyslipidemia, metabolic syndrome, and smoking.

Terri Townsend is a staff educator in the Medical/Surgical & ICU Community Hospital Anderson in Anderson, Ind.

The author has disclosed that she has no financial relationships related to this article.

Seventy-six year old Mrs. L was admitted to the hospital through the ED with increasing shortness of breath over 3-4 weeks, fatigue, and frequent cough.

She denied angina, dizziness, syncope, or nausea. Her health history included myocardial infarction (MI) with endovascular stent placement, dyslipidemia, hypertension, and hypothyroidism.

Home medications included: levothyroxine, aspirin, metoprolol, diltiazem, atorvastatin, and furosemide. She admitted to taking the furosemide “when she needed it,” rather than daily.

Initial vital signs were: BP 162/94, heart rate 92, respiratory rate 24, temperature 99.2° F (37.3° C), and oxygen saturation 94% on supplemental oxygen at 2 L/minute via nasal cannula.

She had a Grade 3/6 (moderately loud), harsh, crescendo-decrescendo systolic ejection murmur heard best at the right second intercostal space, with radiation to the carotids and left sternal border. Basilar pulmonary crackles were auscultated bilaterally. A 12-lead ECG demonstrated normal sinus rhythm with signs of left ventricular hypertrophy (LVH), left atrial hypertrophy and nonspecific ST segment and T-wave changes. A chest X-ray indicated mild pulmonary congestion and cardiomegaly. The cardiologist made the diagnosis of heart failure secondary to aortic stenosis.

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What is aortic stenosis?

Aortic stenosis occurs when the aortic valve opening becomes narrowed, resulting in left ventricular outflow obstruction. The most common cause is calcification of the valve leaflets, and is most often seen in older adult patients.

While it's rarely seen in patients younger than 50 years old, without congenital valvular abnormality, calcific aortic valve disease affects approximately 4% of North Americans and Europeans older than 75.1

Even though previously thought to be a consequence of aging, recent evidence demonstrated that calcific aortic valve disease is a progressive disorder with multiple physiologic processes resulting in the buildup of calcium on the valve leaflets. Risk factors for calcification include: hypertension, dyslipidemia, metabolic syndrome, and smoking.2 The mechanical stress of blood moving across the valve at high pressure (due to hypertension) triggers an inflammatory response and leads to tissue remodeling within the layers of the valve.2

As plaque builds up on the valve leaflets and progresses to calcification, the left ventricle encounters more and more resistance to systolic ejection (increased afterload). As a result, the ventricle has to generate a higher systolic pressure to overcome the increased afterload. The ventricle compensates by increasing the thickness of the ventricular wall, called concentric hypertrophy, much like a body builder's skeletal muscles increase in size to accommodate the weights he lifts. Over time, the hypertrophic ventricle becomes less compliant and the left ventricular end-diastolic pressure increases. Blood backs up into the left atrium and pulmonary veins, increasing left atrial pressure. This enlarges the left atrium and causes left atrial hypertrophy. In order to complete ventricular filling the left atrium must contract more forcefully and also contributes to hypertrophy. The higher diastolic pressure also decreases coronary artery blood flow, increases myocardial workload, and increases myocardial oxygen consumption. As cardiac output and ejection fraction fall, the increased left ventricular pressure is transmitted back to the lungs, and may cause pulmonary edema.1,3 (See Left ventricular hypertrophy.)

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Diagnosing aortic stenosis

The standard for diagnosing aortic stenosis is the transthoracic echocardiogram.1 Aortic stenosis is graded based on blood flow through the aortic valve during systole (aortic jet velocity), mean aortic pressure gradient, and aortic valve area. (See Grades of aortic valve stenosis)

Mrs. L's echocardiogram noted mild LVH, normal left ventricular systolic function with an ejection fraction of 65% (normal, by echocardiography is greater than or equal to 55%) mild mitral regurgitation, and normal pulmonic and tricuspid valves. The right ventricle was normal in size and function, and the left atrium was mildly dilated. Her aortic valve had severe calcific stenosis, with a mean pressure gradient of 65 mm Hg, aortic jet velocity of 4.82 m/s, and an aortic valve area of 0.34 cm2. A cardiothoracic surgeon was consulted for aortic valve replacement.

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Treating aortic stenosis

The only effective treatment for patients with severe symptomatic aortic stenosis is either surgical or transcatheter replacement of the aortic valve. Patients can be asymptomatic for many years, but as the disease progresses, signs and symptoms will ultimately develop. Once the signs and symptoms begin to appear (angina, exertional syncope, heart failure), the mean life expectancy is 2-3 years without treatment. Once the disease progresses to the severe stage, untreated patients have a less than 30% survival rate in 3 years, and 50% to 60% die within 2 years.1

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Definitive surgical treatment consists of removal of the calcified valve and replacement with a bioprosthetic or mechanical valve. Surgical valve replacement is also indicated for patients who have severe aortic stenosis and a need for other surgical heart intervention.4

Percutaneous aortic balloon valvotomy (placing a balloon across the stenotic aortic valve and inflating/deflating to widen the valve opening, reducing the degree of stenosis) is an option for patients who are poor surgical risk, or who require bridge treatment prior to surgical replacement.

A newer minimally invasive procedure for aortic valve replacement is transcatheter aortic valve replacement (TAVR) also known as transcatheter aortic valve implantation (TAVI). TAVR has been developed as a treatment for patients with severe symptomatic aortic stenosis considered inoperable or at high risk for surgical aortic valve replacement.

As many as 30% of older adult patients with symptomatic aortic stenosis aren't considered surgical candidates due to multiple comorbidities increasing the risk of sternotomy and cardiopulmonary bypass to dangerously high levels.5 These patients previously had to settle for palliative treatment with very limited hope for survival. Now, however, there is a less-invasive new approach to valve replacement. Transcatheter aortic valve replacement utilizes a transfemoral approach to place a prosthetic valve. There have been over 50,000 such valve replacements performed worldwide, and have provided many older adults with a better quality of life than they would have otherwise. In this procedure, the native valve is left in place and dilated to accommodate the prosthetic one, which is placed by balloon dilation.5

An alternative transcatheter valve replacement approach is through a small incision in the chest and entering the heart through the aorta or left ventricular apex (transapical). Mortalities are nearly the same for patients undergoing either surgical or transcatheter valve replacement.2

Strict medical management is paramount for patients who aren't candidates for any invasive procedures. Symptom management of angina, heart failure, and syncope is accomplished with the right combination of vasodilators, beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, inotropic agents, and supplemental oxygen.

Occasionally, severe symptoms of low coronary perfusion can be treated with intra-aortic balloon pump therapy. Medically managed patients require extensive education on symptom management, coping skills, and assessment of support systems.

A cardiac catheterization showed no change in Mrs. L's coronary arteries since her endovascular stent placement 3 years ago. Mrs. L underwent successful surgical aortic valve replacement with a porcine valve. After an uncomplicated postoperative course, she was discharged home, where she continued improving.

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Take-home points

Aortic stenosis is a chronic, degenerative disease, associated with high mortality if left untreated. Understanding the disease progression and symptoms can assist in prompt diagnosis and early intervention. While traditional surgical replacement is the definitive treatment, new advances in transcatheter aortic valve replacement offer hope to those patients who were previously not surgical candidates. Both procedures demonstrate improved survival, quality of life, and functional status.

Medical management for patients who aren't able or willing to have a replacement is a challenging undertaking to help relieve debilitating symptoms and maintain hemodynamic stability.

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REFERENCES

1. Cary T, Pearce J. Aortic stenosis: pathophysiology, diagnosis, and medical management of nonsurgical patients. Crit Care Nurse. 2013;33(2):58–72.
2. Coté N, Mahmut A, Bosse Y, et al. Inflammation is associated with the remodeling of calcific aortic valve disease. Inflammation. 2013;36(3):573–581.
3. Rajamannan NM, Evans FJ, Aikawa E, et al. Calcific aortic valve disease: not simply a degenerative process: a review and agenda for research from the National Heart and Lung and Blood Institute Aortic Stenosis Working Group. Executive summary: calcific aortic valve disease-2011 update. Circulation. 2011;124(16):1783–1791.
4. Shah RV, Desai NR, O'Gara PT. Asymptomatic severe aortic stenosis: silence of the lambs. Circulation. 2010;122(17):1734–1739.
5. Contrera P, Cushing M. AANA Journal Course: update for nurse anesthetists—part-4—transcatheter aortic valve replacement. AANA J. 2013;81(5):399–408.
6. Wagner G. Marriott's Practical Electrocardiography, 11th ed. 2008. Philadelphia: Lippincott, Williams, & Wilkins.
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