**Surgical Valve Replacement (Bioprosthetic vs. Mechanical)**

Stamenko Šušak, Lazar Velicki, Dušan Popović and Ivana Burazor

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/53687

## **1. Introduction**

The aortic valve separates the left ventricular outflow tract from the aorta. It is a tricuspid valve consisting of three semilunar cusps and the aortic valve annulus. The aortic valve annulus is a collagenous structure lying at the level of the junction of the aortic valve and the ventricular septum, which is the nadir of the aortic valve complex. This area is also referred to as the aortic ring and serves to provide structural support to the aortic valve complex. The annulus is shaped like a crown and extends to the level of the aortic sinuses. It attaches to the aortic media distally and the membranous and muscular ventricular septum proximally and anteriorly. There are 3 aortic valve cusps, each half-moon shaped or semilunar in appearance. A small dilatation of the proximal aorta is associated with each cusp; collectively, these are referred to as the sinuses of Valsalva or aortic sinuses, named after the Italian anatomist Antonio Valsalva. Their association with the respective coronary ostia identifies them: left, right, and posterior (or noncoronary).[1]

Aortic stenosis (AS) is one of the most common diseases of the aortic valve. The most common causes of AS are degenerative calcification, bicuspid aortic valve and rheumatic etiology. Age – related degenerative calcific AS is currently the most common cause of AS in adults and most frequent reason for aortic valve replacement (AVR).[2] That atherosclerosis is a cause of AS is derived primarily from five pieces of evidence: 1) that patients with familial homozygous hyperlipidemia usually develop calcific deposits on the aortic aspects of their aortic valve cusps at a very young age, usually by the teenage years (These individuals have serum total cholesterol levels *>*800 mg/dl from the time of birth.); 2) that progression of AS can be slowed by lowering total and low-density lipoprotein cholesterol levels by statins; 3) that patients *>*65 years of age with AS involving a three-cuspid aortic valve (unassociated with mitral valve

© 2013 Šušak et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

disease) usually have extensive atherosclerosis involving the major epicardial coronary arteries and usually other systemic arterial systems; 4) that serum total cholesterol levels and concomitant coronary bypass grafting tend to be higher in patients with AS involving threecuspid aortic valves than in patients of similar age and sex without AS or with congenitally bicuspid aortic valves; and 5) that histologic study of three-cuspid stenotic aortic valve demonstrates features similar to those in atherosclerotic plaques.[2] Rare causes of aortic stenosis include obstructive, infective endocarditis, Paget's disease, renal failure, drug induced, familial hypercholesterolemia, systemic lupus erythematosus, irradiation, and ochronosis.[3] As the valves stenosis, valvular abnormality produces turbulent flow, which traumatizes the leaflets and eventually leads to progressive cell proliferation, extracellular matrix production, and calcification of the valve. It is degenerative process that leads to proliferative and inflammatory changes that leading to calcification of the aortic valve. Progressive calcification leads to immobilization of the cusps.[3]

sensitive to diffuse subendocardial ischemic injury, which may result in both systolic and diastolic dysfunction. As the obstruction progresses to a critical level, the high afterload "overwhelms" the left ventricle and systolic function begins to decrease. With continued severe afterload excess, myocyte degeneration and fibrosis occurs and produces irreversible left ventricular systolic dysfunction. In these patients, both the high afterload and the intrinsic myocardial disease significantly increase wall stress and a vicious cycle of deterioration in

The evaluation of aortic stenosis is based upon the history, the physical examination, and a comprehensive echocardiography. For most patients, two-dimensional echocardiography readily identifies the calcified stenotic aortic valve, and Doppler echocardiography reliably estimates the severity of aortic stenosis in the majority of patients. Many patients with aortic stenosis will remain asymptomatic for decades. The diagnosis of aortic stenosis is usually made in the asymptomatic patient on the basis of a systolic murmur on auscultation and confirmed by echocardiography. Symptoms, when they occur, usually consist of one or more of the classic triad of exertional dyspnea, angina, and syncope. Following symptom onset, there is a high mortality rate with an average survival of 2–3 years. The development of symptoms therefore is a critical point in the natural history of patients with aortic stenosis. Sudden death rarely is the initial manifestation of severe aortic stenosis, occurring at a rate of less than 1% per year in asymptomatic patients.[3] Two-dimensional and Doppler echocardiography is the imaging modality of choice for the diagnosis and quantification of aortic stenosis. Short-axis images from two-dimensional echocardiography demonstrate the number of aortic cusps and the degree of cusp fusion or restricted cusp opening in valvular aortic stenosis. Two dimensional echocardiography is also useful for determining the status of the left ventricle and the degree of hypertrophy. Left atrial enlargement indicates concomitant diastolic dysfunction. The

does not produce symptoms until the valve reaches one-fourth of its normal dimension.[4] The

There is no effective medical therapy for AS. AVR is the only effective treatment for severe aortic stenosis in adults. Following AVR for AS, one can expect resolution of symptoms, left ventricular hypertrophy (LVH) regression, and improved left ventricular (LV) systolic function secondary to reduced afterload. Importantly, postoperative survival is similar to age-

Normal < 2.5 - 3 to 4 Mild 2.5 to 2.9 < 25 1.5 to 2 Moderate 3 to 4 25 to 40 1 to 1.5 Severe > 4 > 40 < 1

**Mean gradient (mm Hg)**

. Reduction of the normal area usually

Surgical Valve Replacement (Bioprosthetic VS Mechanical)

http://dx.doi.org/10.5772/53687

363

**Aortic valve area (cm2)**

ventricular function ensues.[3]

normal area of the adult aortic valve is 3.0 to 4.0 cm2

**(m per second)**

graduation of AS is given in Table 1.

**Severity Aortic jet velocity**

**Table 1.** Classifications of Aortic Stenosis Severity4

The pathophysiology of valvular aortic stenosis is one of progressive obstruction and the resultant compensatory changes. With increasing left ventricular outflow tract obstruction, there is pressure hypertrophy of the left ventricle. Left ventricular cavity size and systolic function is initially maintained, as the increase in left ventricular wall thickness acts as a compensatory mechanism to normalize wall stress. The development of pressure hypertrophy is initially a beneficial adaptation. However, this hypertrophy may result in reduced coronary flow reserve and oxygen supply–demand mismatch. These hypertrophied hearts are also more

**Figure 1.** Normal aortic valve and stenotic aortic valve

sensitive to diffuse subendocardial ischemic injury, which may result in both systolic and diastolic dysfunction. As the obstruction progresses to a critical level, the high afterload "overwhelms" the left ventricle and systolic function begins to decrease. With continued severe afterload excess, myocyte degeneration and fibrosis occurs and produces irreversible left ventricular systolic dysfunction. In these patients, both the high afterload and the intrinsic myocardial disease significantly increase wall stress and a vicious cycle of deterioration in ventricular function ensues.[3]

The evaluation of aortic stenosis is based upon the history, the physical examination, and a comprehensive echocardiography. For most patients, two-dimensional echocardiography readily identifies the calcified stenotic aortic valve, and Doppler echocardiography reliably estimates the severity of aortic stenosis in the majority of patients. Many patients with aortic stenosis will remain asymptomatic for decades. The diagnosis of aortic stenosis is usually made in the asymptomatic patient on the basis of a systolic murmur on auscultation and confirmed by echocardiography. Symptoms, when they occur, usually consist of one or more of the classic triad of exertional dyspnea, angina, and syncope. Following symptom onset, there is a high mortality rate with an average survival of 2–3 years. The development of symptoms therefore is a critical point in the natural history of patients with aortic stenosis. Sudden death rarely is the initial manifestation of severe aortic stenosis, occurring at a rate of less than 1% per year in asymptomatic patients.[3] Two-dimensional and Doppler echocardiography is the imaging modality of choice for the diagnosis and quantification of aortic stenosis. Short-axis images from two-dimensional echocardiography demonstrate the number of aortic cusps and the degree of cusp fusion or restricted cusp opening in valvular aortic stenosis. Two dimensional echocardiography is also useful for determining the status of the left ventricle and the degree of hypertrophy. Left atrial enlargement indicates concomitant diastolic dysfunction. The normal area of the adult aortic valve is 3.0 to 4.0 cm2 . Reduction of the normal area usually does not produce symptoms until the valve reaches one-fourth of its normal dimension.[4] The graduation of AS is given in Table 1.


**Table 1.** Classifications of Aortic Stenosis Severity4

disease) usually have extensive atherosclerosis involving the major epicardial coronary arteries and usually other systemic arterial systems; 4) that serum total cholesterol levels and concomitant coronary bypass grafting tend to be higher in patients with AS involving threecuspid aortic valves than in patients of similar age and sex without AS or with congenitally bicuspid aortic valves; and 5) that histologic study of three-cuspid stenotic aortic valve demonstrates features similar to those in atherosclerotic plaques.[2] Rare causes of aortic stenosis include obstructive, infective endocarditis, Paget's disease, renal failure, drug induced, familial hypercholesterolemia, systemic lupus erythematosus, irradiation, and ochronosis.[3] As the valves stenosis, valvular abnormality produces turbulent flow, which traumatizes the leaflets and eventually leads to progressive cell proliferation, extracellular matrix production, and calcification of the valve. It is degenerative process that leads to proliferative and inflammatory changes that leading to calcification of the aortic valve.

The pathophysiology of valvular aortic stenosis is one of progressive obstruction and the resultant compensatory changes. With increasing left ventricular outflow tract obstruction, there is pressure hypertrophy of the left ventricle. Left ventricular cavity size and systolic function is initially maintained, as the increase in left ventricular wall thickness acts as a compensatory mechanism to normalize wall stress. The development of pressure hypertrophy is initially a beneficial adaptation. However, this hypertrophy may result in reduced coronary flow reserve and oxygen supply–demand mismatch. These hypertrophied hearts are also more

Progressive calcification leads to immobilization of the cusps.[3]

362 Calcific Aortic Valve Disease

**Figure 1.** Normal aortic valve and stenotic aortic valve

There is no effective medical therapy for AS. AVR is the only effective treatment for severe aortic stenosis in adults. Following AVR for AS, one can expect resolution of symptoms, left ventricular hypertrophy (LVH) regression, and improved left ventricular (LV) systolic function secondary to reduced afterload. Importantly, postoperative survival is similar to agematched controls after AVR for AS when performed prior to the development of LV dysfunc‐ tion or congestive heart failure (CHF). Similarly, incomplete regression of LVH after AVR has been associated with adverse outcomes such as reduced long-term survival. Contrary to the immediate improvement in systolic performance, diastolic dysfunction may persist for several more years after AVR. In fact, Gjertsson et al. recently evaluated diastolic dysfunction in AS and found that the proportion of patients with moderate-to-severe diastolic dysfunction actually increased with time after AVR despite normalization of LV mass and appropriate adjustments for senile diastolic dysfunction. Finally, AVR is associated with improved quality of life scores, particularly among the elderly, and has been found to be similar to age-matched individuals without heart disease. [3,5,6]

**•** However, on the other hand, breathlessness on exercise may be difficult to interpret in patients with only low physical activity, particularly the elderly, making decisionmaking more difficult. There is no strict age limit for performance of exercise testing and it is

reasonable to propose it in patients > 70 years old who are still highly active.[8]

Patients with severe AS undergoing coronary artery bypass surgery, surgery of the ascending aorta, or

Asymptomatic patients with severe AS and systolic LV dysfunction (LVEF < 50%) unless due to other

Asymptomatic patients with severe AS and abnormal exercise test showing fall in blood pressure

Patients with moderate AS undergoing coronary artery bypass surgery, surgery of the ascending aorta

Asymptomatic patients with severe AS and moderate-to-severe valve calcification, and a rate of peak

Asymptomatic patients with severe AS and abnormal exercise test showing complex ventricular

Asymptomatic patients with severe AS and excessive LV hypertrophy (≥ 15 mm) unless this is due to

AS with low gradient (< 40 mmHg) and LV dysfunction with contractile reserve IIaC

AS with low gradient (< 40 mmHg) and LV dysfunction without contractile reserve IIbC

In last 50 years, the varieties of prostheses that have become available for use are numer‐ ous. An ideal aortic prosthesis would be simple to implant, widely available, possess long-term durability, would have no intrinsic thrombogenicity, would not have a predilec‐ tion foe endocarditis and would have no residual transvalvular pressure gradient. Such a valve does not currently exist. Currently available options include mechanical valves, stented biological valves, stentless biological valves, allograft valves and pulmonary auto‐

on another valve

below baseline

or another valve

arrhythmias

hypertension

**Table 2.** Indications for AVR in AS

velocity progression ≥ 0.3 m/s per year

cause

**Patients with severe AS and any symptoms IB**

Asymptomatic patients with severe AS and abnormal exercise test showing symptoms on exercise IC

IC

365

Surgical Valve Replacement (Bioprosthetic VS Mechanical)

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IC

IIaC

IIaC

IIaC

IIbC

IIbC

The American College of Cardiology (ACC) and the American Heart Association (ACH) have jointly developed guidelines in which they published indications for AVR:

	- **•** Patients who have severe AS and presented with one or more of its classical symptoms (angina, syncope, heart failure, etc.)
	- **•** Patients who have severe AS and required coronary artery bypass surgery, surgery on the aorta or other heart valves
	- **•** Patients who have severe AS and left ventricle systolic dysfunction (ejection fraction less than 50 %)
	- **•** Patients who have moderate AS and required coronary artery bypass surgery, surgery on the aorta or other heart valves
	- **•** Asymptomatic patients with severe AS with abnormal exercise test, or an increase in transaortic gradient during exercise, or left ventricle systolic dysfunction (ejection fraction less than 50 %), or left ventricular dilatation, or significantly elevated left ventricular diastolic pressure. [7]

The European Society of Cardiology (ESC) has also developed guidelines in which they published indications for AVR (Table 2).[8] They strongly recommended early AVR in all symptomatic patients with severe AS.

Management of asymptomatic patients requires careful weighing of benefits against risks. Early elective surgery at these patients can only be recommended in selected patients, at low operative risk. This could be the case in:


**•** However, on the other hand, breathlessness on exercise may be difficult to interpret in patients with only low physical activity, particularly the elderly, making decisionmaking more difficult. There is no strict age limit for performance of exercise testing and it is reasonable to propose it in patients > 70 years old who are still highly active.[8]


#### **Table 2.** Indications for AVR in AS

matched controls after AVR for AS when performed prior to the development of LV dysfunc‐ tion or congestive heart failure (CHF). Similarly, incomplete regression of LVH after AVR has been associated with adverse outcomes such as reduced long-term survival. Contrary to the immediate improvement in systolic performance, diastolic dysfunction may persist for several more years after AVR. In fact, Gjertsson et al. recently evaluated diastolic dysfunction in AS and found that the proportion of patients with moderate-to-severe diastolic dysfunction actually increased with time after AVR despite normalization of LV mass and appropriate adjustments for senile diastolic dysfunction. Finally, AVR is associated with improved quality of life scores, particularly among the elderly, and has been found to be similar to age-matched

The American College of Cardiology (ACC) and the American Heart Association (ACH) have

**•** Patients who have severe AS and presented with one or more of its classical symptoms

**•** Patients who have severe AS and required coronary artery bypass surgery, surgery on

**•** Patients who have severe AS and left ventricle systolic dysfunction (ejection fraction

**•** Patients who have moderate AS and required coronary artery bypass surgery, surgery

**•** Asymptomatic patients with severe AS with abnormal exercise test, or an increase in transaortic gradient during exercise, or left ventricle systolic dysfunction (ejection fraction less than 50 %), or left ventricular dilatation, or significantly elevated left

The European Society of Cardiology (ESC) has also developed guidelines in which they published indications for AVR (Table 2).[8] They strongly recommended early AVR in all

Management of asymptomatic patients requires careful weighing of benefits against risks. Early elective surgery at these patients can only be recommended in selected patients, at low

**•** Those with echocardiographic predictors of poor outcome suggested by the combination of a markedly calcified valve with a rapid increase in peak aortic velocity of ≥ 0.3 m/s per year

**•** If the exercise test is abnormal, particularly if it shows symptom development, which is a

**•** The rare asymptomatic patients with depressed LV function not due to another cause

jointly developed guidelines in which they published indications for AVR:

individuals without heart disease. [3,5,6]

(angina, syncope, heart failure, etc.)

the aorta or other heart valves

on the aorta or other heart valves

ventricular diastolic pressure. [7]

symptomatic patients with severe AS.

operative risk. This could be the case in:

strong indication for surgery in physically active patients.

**a.** Definite indications:

364 Calcific Aortic Valve Disease

less than 50 %)

**b.** Possible indications:

In last 50 years, the varieties of prostheses that have become available for use are numer‐ ous. An ideal aortic prosthesis would be simple to implant, widely available, possess long-term durability, would have no intrinsic thrombogenicity, would not have a predilec‐ tion foe endocarditis and would have no residual transvalvular pressure gradient. Such a valve does not currently exist. Currently available options include mechanical valves, stented biological valves, stentless biological valves, allograft valves and pulmonary auto‐ graft valves. Commonly in us are mechanical and biological prostheses.[9] When selecting between mechanical and biologic heart valves, the surgeon and patient must balance the risks and benefits of each choice.
